Cardiovascular System Flashcards

1
Q

Describe the structure of the pericardium?

A

Parietal pericardium- strong outer fibrous layer
Intrapericardial space- lubricating fluid
Visceral pericardium- inner serosal layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the fibrous layer of the pericardium attached to? Why?

A

Sternum and mediastinal portions of the left and right pleurae
Keeps the pericardial sac firmly anchored within the thorax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What structures emerge from the pericardium?

A

Superiorly: aorta, pulmonary artery, superior vena cava
Inferiorly: inferior vena cava

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why do we need a cardiovascular system?

A

All cells require oxygen and release carbon dioxide

Diffusion is not efficient over long distances. Rate of diffusion is proportional to square of the distance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why doesn’t the left ventricle receive all oxygen and nutrients from the oxygenated blood within its ventricular cavity? Where does it receive its oxygen and nutrients from?

A

Some cells are supplied with blood directly from the ventricular cavity through tiny vascular channels known as thebesian veins.
There is a large distance from the source of oxygen to some of the cells in its thick muscle wall.
Majority of the left ventricle is supplied with blood from the left coronary artery which branches into the anterior interventricular artery and the circumflex artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Which arteries branch off the aortic arch?

A

Brachiocephalic trunk- supplies right upper limb, head and neck
Left common carotid artery- supplies head and neck
Left subclavian artery- supplies left upper limb with some branches to the head and thorax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the location of the heart.

A

The heart is enclosed in the mediastinum, the medial cavity of the thorax. It extends 12-14cm from the second rib to the fifth intercostal space. It is superior to the diaghragm. It is anterior to the vertebral column and posterior to the sternum. The lungs are lateral to the heart and partially obscure it.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the valves in the heart?

A

Mitral valve- two cusps- between left atrium and left ventricle
Tricuspid valve-three cusps- between right atrium and right ventricle
Aortic valve- semilunar, three cusps- between left ventricle and aorta
Pulmonary valve- semilunar, three cusps- between right ventricle and pulmonary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where are the output vessels of the heart located?

A

The base of the heart consists of the hearts output vessels; the ascending aorta which leads on to the aortic arch and the pulmonary trunk which splits into the two pulmonary arteries.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the different layers of the heart?

A

Endocardium - layer of endothelial cells lining chambers
Myocardium - thick layer of cardiac muscle cells
Epicardium/ visceral pericardium- layer of connective tissue/adipose tissue through which pass the larger blood vessels and nerves that supply the heart muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Where is the fossa ovalis? What is this?

A

It is a depression in the right atrium of the heart at the level of the interatrial septum. It is the remnant of the opening between the atria in the foetus as blood flow to the lungs and double circulation only begins after birth with the baby’s first breath.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are trabeculae carnae? Where are they?

A

Irregular muscle ridges in the heart. They are present in the right and left ventricular walls giving them a spongelike appearance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What structures prevent the inversion of of the mitral and tricuspid valve cusps during systole?

A

3 papillary muscles in RV which hold thin string like chordae tendinae which attaches to the edges of the tricuspid valve leaflets
2 papillary muscles in LV which hold thin string like chordae tendinae which attaches to the ended of the mitral valve leaflets

Contraction of the papillary muscles prior to other regions of the ventricle tightens the chordae tendinae and the valve is forced closed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What controls the opening and closing of the pulmonic and aortic valves?

A

During relaxation of the ventricles, elastic recoil of the pulmonary arteries forces blood back toward the heart, distending the valve cusps towards one another closing the valve. Therefore, there is slight backflow of blood into the ventricles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Which vessels enter the atria and where from?

A

The superior vena cava enters the right atrium superiorly. The inferior vena cava and coronary sinus enter the right atrium inferiorly
The four pulmonary veins enter the left atrium posteriorly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How is the left side of the heart adapted to the pumping blood at a higher pressure than the right side of the heart?

A

Structures on the left side of the heart are approximately three times thicker than structures on the right side of the heart.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What do the grooves on the surface of the heart indicate?

A

Anterior and posterior interventricular grooves (interventricular sulcus)
—> inter ventricular septum
Anterior and posterior atrioventricular grooves (coronary sulcus)
—>boundary between atria and ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Where are impulses in the ventricles first transmitted to and why?

A

Impulses within the His-Purkinje fibres are transmitted first to the papillary muscles and then throughout the walls of the ventricles so the papillary muscles contract before the ventricles. This coordination prevents the regurgitation of blood through the AV valves.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Where do the right and left coronary arteries originate from and how do they reach the heart?

A

The root of the aorta just above the aortic valve cusps. The left main coronary artery arises in the left aortic sinus and the the right coronary artery arises in the right aortic sinus. After their origin, these vessels pass anteriorly one on each side of the pulmonary artery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe the position of the atria relative to the ventricles?

A

The atria are positioned slightly posteriorly and to the right of the ventricles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What factors affect the rate of diffusion in the cardiovascular system?

A

Surface area- higher capillary density in metabolically active tissues
Diffusion resistance- nature of the molecule and the barrier (exchange occurs in capillaries), proportional to square root of the distance
Concentration gradient- substance which is used by tissues will have a lower concentration in capillary blood than arterial blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What factors affect how much lower the concentration of a substance is in the capillary blood than the arterial blood?

A

Rate of use by the tissue
Rate of blood flow through the capillary bed- the lower the blood flow, the lower the capillary concentration. Blood flow must be high enough to maintain a sufficient concentration gradient and must match the tissues metabolic needs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How will capillary density and perfusion rate vary between a tissue that is not very metabolically active and a tissue that is very metabolically active?

A

The tissue that is metabolically active will have:

  • a higher capillary density
  • greater perfusion rate (greater rate of blood flow)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is perfusion rate?

A

The rate of blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which organs require high, constant flow of blood to them?

A

Brain
Kidneys
Heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

During exercise, blood flow to which tissues increases?

A

Heart
Brain
Skeletal muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the normal rate of blood flow? What can this increase to during exercise?

A

Normal-5 litres per minute

Exercise-25 litres per minute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What causes cardiac tamponade?

A

Excess fluid building up relatively rapidly in the pericardial space.
The heart becomes compressed due to the inextensible fibrous pericardial layer
Compression of the heart leads to cardiac tamponade
Pressure of the fluid means that the heart cannot fully fill during diastole leading to a smaller stroke volume and smaller cardiac output.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

When is pericardiocentesis required?

A

Fluid from pericardial space to be removed for testing

Fluid from pericardial space to be removed to relieve compression after a cardiac tamponade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Where is the transverse pericardial sinus? What is its relevance?

A

Posterior to the pulmonary trunk and the ascending aorta, superior to the left atrium and anterior to the superior vena cava.
A clamp can be placed here during a heart lung bypass so that there is no blood leaving the heart without damaging the pericardium. The heart lung bypass machine receives blood from the inferior and superior vena cava, oxygenates the blood and transfers it to the aortic arch.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Where is the oblique sinus?

A

Small concavity in the pericardium, posterior to the heart bound by pulmonary veins on either side.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What happens if a major coronary artery is blocked?

A

Myocardial infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

There is not a very high pressure gradient between the veins and the right atrium. What valves prevent the backflow of blood from the right atrium into the vessels?

A

Incomplete valves
Inferior vena cava - eustachian valve
Coronary sinus - thebesian ring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Why is mitral stenosis more common than tricuspid stenosis?

A

The entrance of the left atrium into the left ventricle is smaller than the entrance of the right atrium into the right ventricle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

At what rate should blood flow to the brain be at all times?

A

750ml per minute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the major components of the cardiovascular system?

A
Heart- pump 
Arteries - distributing vessels
Arterioles - resistance vessels- restricting blood flow to easily perfused areas so that blood can flow to those often vulnerable parts that are not easily perfused
Capillaries- exchange vessels
Veins - capacitance vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the role of capacitance vessels? Which blood vessels are capacitance vessels?

A

Veins store blood (without an increase in pressure) to cope with temporary imbalances between the amount of blood returning to the heart and the amount that is required to pump out. This gives the cardiovascular system the ability to cope with changes in cardiac output.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the mediastinum?

A

The intervening region in the thoracic cavity between the right and left pleural cavities occupied by the lungs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

How do we prevent all of our blood from going to t he most easily perfused areas and how do we allow blood to flow to areas that are difficult to perfuse?

A

Resistance vessels restrict blood flow to drive supply to areas that are difficult to perfuse.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Explain how resistance and capacitance vessels work together to meet demand during exercise?

A

In exercise, more blood needs to flow to the heart muscle, skeletal muscle and cardiac muscle
Resistance vessels restrict flow to other organs by constricting and dilate to allow blood to flow to these organs

Cardiac output increases so there is less blood stored in capacitance vessels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Is the output greater from the right or left hand side of the heart?

A

Neither- its the same. Any difference would cause oedema.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the typical pressure in the left an right ventricle?

A

Left ventricle
120 systole / 10 diastole

Right ventricle
25 systole/ 4 diastole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What does systole mean?

A

Contraction and ejection of blood from ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What does diastole mean?

A

Relaxation and filling of ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

At rest, what is the typical stroke volume?

A

70ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

At rest, what is typical heart rate?

A

70 beats per minute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What embryonic tissue gives rise to the CVS?

A

Splanchnic Mesoderm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

How do we prevent all blood from going to the most easily perfused areas and how do we allow blood to reach the brain against gravity?

A

Resistance vessels restrict blood flow to drive supply to hard to perfuse areas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is the purpose of capacitance vessels?

A

Enable CVS to vary amount of blood pumped around the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Why are resistance and capacitance vessels important?

A

Blood supply must change to meet demand and this is achieved by a balance between blood in these vessels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is typical pressure in the left and right atrium?

A

Left atrium= 8-10 mm Hg

Right atrium = 0-4 mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is typical pressure in the aorta and pulmonary artery?

A

Aorta- 120 systole/ 80 diastole mm Hg

Pulmonary artery- 25 systole/ 10 diastole mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

How is a cardiac action potential different to other action potentials and why is it different?

A

It is relatively longer because it lasts for the duration of a single contraction (beat) of the heart.
Duration of cardiac action potential = 280 ms
Duration of skeletal muscle action potential = 2-5 ms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

During which phase in the cardiac cycle are both the mitral and aortic valves open?

A

NEVER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

When do the mitral and tricuspid valves open at the same time?

A

ALWAYS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What is the function of the papillary muscles and chordae tendinae?

A

They prevent inversion of the cusps of the mitral and tricuspid valves.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Which phases of the cardiac cycle occur during systole?

A

Phase 2: Isovolumetric contraction
Phase 3: Rapid ejection
Phase 4: Reduced ejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Which phases of the cardiac cycle occur during diastole?

A

Phase 5: Isovolumetric relaxation
Phase 6: Rapid filling
Phase 7: Reduced filling
Phase 1: Atrial contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is the typical duration of systole at 67 beats per minute

A

0.35 seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is the typical duration of diastole at 67 beats per minute?

A

0.55 seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

As heart rate increases, how does the cardiac cycle change?

A

Each cardiac cycle is shorter.

Systole stays the same length but diastole shortens.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

When does the length of systole change?

A

NEVER

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

The mitral/tricuspid valves are open. The aortic and pulmonary valves are closed.
What stages of the cardiac cycle could the heart be in?

A

Diastole
Phase 6: Rapid filling
Phase 7: Reduced filling
Phase 1: Atrial contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

The mitral/tricuspid valves and aortic/pulmonary valves are all closed.
Is the heart in systole or diastole?

A

Could be in systole.
Phase 2: Isovolumetric contraction

Could be in diastole.
Phase 5: Isovolumetric relaxation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

When do the mitral/tricuspid valves open?

At what point in the cardiac cycle does this occur?

A

When pressure in the atria exceeds pressure in the ventricles.
Pressure in the atria gradually rises due to venous return until it exceeds pressure in the ventricles after phase 5-Isovolumetric relaxation.
This marks the beginning of
Phase 6: Rapid filling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is the A wave?

A

Atrial pressure rises due to atrial systole during phase 1 (atrial contraction) of the cardiac cycle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is the C wave?

A

Atrial pressure increases slightly due to closing of the mitral valve during phase 2 (Isovolumetric contraction) of the cardiac cycle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is the X descent?

A

Atrial pressure initially decreases as the atrial base is pulled downward as the ventricle contracts during phase 3 (rapid ejection) of the cardiac cycle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What is the V wave?

A

Atrial pressure gradually rises due to continued venous return from the lungs during phase 4 (reduced ejection) of the cardiac cycle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What is the dicrotic notch?

A

There is a slight rise in aortic pressure as the aortic valve closes during phase 5 (isovolumetric relaxation) of the cardiac cycle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What is the Y descent?

A

Atrial pressure decreases after opening of the mitral valve during phase 6 (rapid filling) of the cardiac cycle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What is the P wave?

A

Signifies onset of atrial depolarisation on an electrocardiogram.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is the QRS complex?

A

Signifies onset of ventricular depolarisation on an electrocardiogram.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is the T wave?

A

Signifies ventricular repolarisation on an electrocardiogram.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Which phase in the cardiac cycle marks the end of systole?

A

Phase 4: Reduced ejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Which phase in the cardiac cycle marks the end of diastole?

A

Phase 1: Atrial contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

When in the cardiac cycle can S1 be heard?

A

Beginning of Phase 2- Isovolumetric contraction, as the mitral/tricuspid valves close.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

When in the cardiac cycle can S2 be heard?

A

Beginning of phase 5- isovolumetric relaxation as the mitral/pulmonary valves close.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

When in the cardiac cycle can s3 be heard?

A

During phase 6- rapid ventricular filling. This is usually silent but can sometimes be heard in children and is a sign of pathology in adults.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What proportion of ventricular filling does atrial contraction account for?

A

10%

Passive filling driven by venous pressure accounts for 90% of the filing of the ventricles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is typical end diastolic volume?

A

120ml

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Atrial contraction usually accounts for the final 10% of ventricular filling. Does this value tend to increase or decrease with age?

A

It increases because venous pressure in the elderly decreases so there is less passive filling of the ventricles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Which heart sound caused by the opening of valves?

A

NONE - they are caused by the closing of valves.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Where can S1 be heard at its loudest?

A

At the apex of the heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Where can closing of the aortic valve and pulmonary valve be most clearly heard?

A

Aortic valve- 2nd intercostal space, right sternal edge

Pulmonary valve- 2nd intercostal space, left sternal edge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Where can closing of the tricuspid and mitral valve be heard the clearest?

A

Tricuspid valve
4th intercostal space, left sternal edge

Mitral valve
5th intercostal space, mid-clavicular line

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is stenosis?

A

Valve does not open enough. There is an obstruction to blood flow when the valve is usually open.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What is regurgitation?

A

Valve does not open fully. Back leakage when valve should be closed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Is abnormal valve function more common in the left or right side of the heart?

A

Left

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

What are the common causes of aortic valve stenosis? (3)

A

Degenerative (senile calcification/fibrosis)
Congenital (bicuspid form of valve)
Chronic rheumatic fever- inflammation - commissural fusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What are the effects of aortic valve stenosis?

A

Less blood can get can get through valve.
> increased left ventricle pressure–> LV hypertrophy
> left sided heart failure–> syncope, angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What are the effects of aortic valve regurgitation?

A

Blood flows back into left ventricle during diastole
Increases stroke volume
Systolic pressure increases
Diastolic pressure decreases
Bounding pulse (head bobbing, Quinke’s sign- beds of nails flush in colour with each heart beat)
LV hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What are the common causes of aortic valve regurgitation? (2)

A

Aortic root dilation- leaflets pulled apart

Vlavular damage- endocarditis rheumatic fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What are the common causes of mitral valve stenosis?

A

99.9% cases caused by rheumatic fever (autoimmune)
Commissural fusion of valve leaflets
Harder for blood to flow from left atria to the left ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What are the common causes of mitral valve regurgitation?

A

REMEMBER Chordae tendinae and papillary muscles normally prevent prolapse in systole
-Myxomatous degeneration can weaken tissue leading to prolapse
Other causes:
-Damage to papillary muscle after heart attack
-Left sided heart failure leads to LV dilation which can stretch valve
-Rheumatic fever can lead to leaflet fibrosis which disrupts seal formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

How does aortic valve stenosis cause angina?

A

Less blood can get through the valve. This causes left sided heart failure leading to angina.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What is syncope?

A

Insufficient blood flow to the CNS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

How does aortic valve stenosis cause microangiopathic haemolytic anemia?

A

Red blood cells are damaged as blood is transported under very high pressure through a very narrow gap.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

What type of abnormal valve function results in increased systolic pressure and decreased diastolic pressure?

A

Aortic valve regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What sound is characteristic of aortic valve stenosis?

A

Crescendo-decrescendo murmur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

What sound is characteristic of aortic valve regurgitation?

A

Early decrescendo diastolic murmur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What heart sound is characteristic of mitral valve stenosis?

A

Snap as valve opens

Diastolic rumble

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What sound is characteristic of mitral valve regurgitation?

A

Holosystolic murmur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What does afterload mean?

A

The load the heart must eject blood against (roughly equivalent to aortic pressure).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

What does preload mean?

A

Amount the ventricles are stretched (filled) in diastole- related to the end diastolic volume or central venous pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

What does total peripheral resistance mean?

A

Sometimes referred to as systemic vascular resistance- resistance to blood flow offered by all the systemic vasculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

What happens to pressure of blood in a vessel as it encounters resistance?

A

The pressure that the blood exerts drops as it flows through ‘a resistance’.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Which blood vessels offer the greatest resistance and how can they increase resistance?

A

Arterioles. Constriction of the arterioles increases resistance.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

How does constriction of the arterioles change arterial and venous pressure without a change in cardiac output?

A

Venous pressure decreases

Arterial pressure increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What are the effects of dilation of arterioles/pre-capillary sphincters and not changing cardiac output on arterial and venous pressure?

A

Arterial pressure decreases

Venous pressure increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

What are the effects of increased total peripheral resistance and not changing cardiac output on venous and arterial pressure?

A

Arterial pressure increases

Venous pressure decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

What are the effects of increasing cardiac output and having no change in total peripheral resistance on venous and arterial pressure?

A

Arterial pressure increases

Venous pressure decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

In a clinical setting, does hypertension refer to arterial or venous pressure?

A

Arterial pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

How do we facilitate changes in demand for blood without changing arterial or venous pressure?

A

Tissues require more blood.
Arterioles and pre-capillary sphincters dilate.
Peripheral resistance decreases so more blood flows to these tissues.
To counteract arterial pressure decreasing and venous pressure increasing cardiac output increases as this increases arterial pressure and decreases venous pressure.
Cardiac output increases by intrinsic and extrinsic mechanisms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

How can cardiac ouput be increased?

A

EXTRINSIC MECHANISMS
Greater activity of sympathetic nervous system:
Increase in heart rate
Increase in stroke volume by increasing contractility (changing the slope of the frank starling curve)

INTRINSIC MECHANISMS
Increase in stroke volume by:
Increased preload- increased end diastolic volume and increased venous pressure
Decreased afterload (aortic impedance) - decreased end systolic volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Stroke volume is about ____% of normal end diastolic volume.

A

67%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What is the relationship between venous pressure and filling of the heart?

A

The greater the venous pressure, the more the heart fills.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

When does the ventricle stop filling in a healthy heart?

A

The ventricle fills until the walls stretch enough to produce an intraventricular pressure equal to venous pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What kind of a curve can be plotted to show the relationship between venous pressure and ventricular pressure?
State the labels of the axis.

A

Compliance curve
X axis = LV volume (ml)
Y axis = LV pressure (mmHg)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

What does a significant increase in venous pressure cause?

A

In lungs - pulmonary oedema

In peripheries- peripheral oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What is typical end diastolic volume and the pressure in the left ventricle when it is this full?

A
EDV = 120ml 
Pressure = 10 mm Hg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

How would left ventricular hypertrophy affect compliance?

A

More difficult to stretch
Therefore, decreased compliance.
Pressure increases to a higher value with the same value of end diastolic volume.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

What is the difference between ventricular dilation and hypertrophy?

A

Simple dilatation- the walls do not materially decrease in thickness, but the cavities of the heart are enlarged
Hypertrophic dilatation-the cavities enlarge and the walls increase in thickness.
Atrophic dilatation-the cavities are enlarged and the walls of the heart become thin
Hypertrophy-the walls increase in thickness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

How does ventricular dilation affect compliance?

A

Dilated left ventricles causes increased compliance as the ventricle stretches more. The pressure in the ventricle is lower with the same value of end diastolic volume than in a healthy ventricle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Is ventricular hypertrophy or dilation more likely to cause an increased end diastolic pressure?
What are the implications of this?

A

Hypertrophy. Less room for blood. Decreased compliance. As venous pressure increases, LV end-diastolic pressure increases to a greater extent than usual. As LV end-diastolic pressure increases, stroke volume increases up to a certain point after which the actin and myosin filaments are too far apart from one another and stroke volume decreases (Frank-starling law).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Explain how decreased compliance can cause eventual decrease in stroke volume.

A

Decreased compliance. As venous pressure increases, LV end-diastolic pressure increases to a greater extent than usual. As LV end-diastolic pressure increases, stroke volume increases up to a certain point after which the actin and myosin filaments are too far apart from one another and stroke volume decreases (Frank-starling law).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Explain how increased compliance can result in decreased stroke volume.

A

Increased compliance. More room for blood. As venous pressure increases, LV end-diastolic pressure increases to a lesser extent than usual. Decreased end-diastolic pressure results in a lower stroke volume due to less stretching of the actin and myosin filaments. (Frank-starling law).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Explain the Frank-Starling law of the heart.

A

Increasing venous return in diastole, increases LV end diastolic pressure and causes an increase in stroke volume up to a certain point.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

What are the axis on a starling curve.

A

X axis = left ventricular end diastolic pressure/ left ventricular volume/ venous pressure
Y axis = stroke volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Why is the Frank-starling curve steeper in cardiac muscle than skeletal muscle?

A

In both cardiac and skeletal muscle, an increased sarcomere length decreases overlap between the actin and myosin filaments and increased the force of contraction.
In cardiac muscle, there is also an increase in calcium sensitivity as the muscle fibres are stretched.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

How does Starling’s law of the heart ensure that both sides of the heart pump maintain the same output?

A

As stroke volume on the right side of the heart increases, venous pressure to the left side of the heart increases so stroke volume on the left side of the heart increases…

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Why is it important that cardiac output of both sides of the heart is the same?

A

More blood pumped to lungs than returns to the heart—> pulmonary oedema

More blood pumped to the peripheries than returns to the heart—> peripheral oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What causes increased arterial pressure?

A

Increased peripheral resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What effect does hypertension have on stroke volume?

A

Increased afterload decreases stroke volume as the heart has to pump out against a higher pressure.
Caused by increased peripheral resistance which decreases venous pressure causing a decrease in stroke volume. Cardiac output decreases.

Eventually causes left ventricle hypertrophy as ventricle has to contract against a high pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

What factors determining cardiac ouput are controlled by the autonomic nervous system?

A

Contractility

Heart rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Explain what happens to cardiac output after eating a meal.

A
Vasodilation in the gut 
Peripheral resistance decreases
Arterial pressure decreases 
Venous pressure increases
Stroke volume increases so cardiac output increases

The fall in arterial pressure suppresses the parasympathetic nervous system and stimulates the sympathetic nervous system.
Heart rate increases
Contractility increases
Cardiac output increases

Cardiac output increases
Increases arterial pressure
Decreases venous pressure
Returns system back to normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Explain what happens to cardiac output when you stand up.

A

Venous pooling
Venous pressure decreases.
Decreased stroke volume. Decreased cardiac output.
Arterial pressure decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Why can’t venous pooling be rectified by intrinsic mechanisms?
What happens instead?

A

Both venous and arterial pressures are lowered

Intrinsic mechanisms would normally increase peripheral resistance to increase arterial pressure and decrease venous pressure.

This would further decrease venous pressure.

Therefore, the autonomic nervous system is involved with the baroreceptor reflex. This increased heart rate and increases total peripheral resistance so that arterial pressure increases and venous pressure does not fall further.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What happens if the baroreceptor reflex and autonomic nervous system do not work during venous pooling?

A

Postural hypotension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

What happens to cardiac output during exercise?

A

Initially muscle pumping and venoconstriction increases venous pressure and returns more blood to the heart, increasing stroke volume.
Later, decreased total peripheral resistance increases venous pressure further.
Very early response of increased heart rate via decreased parasympathetic drive and increased sympathetic drive.
Increased contractility due to increased sympathetic drive - without this, increased venous pressure alone would move ventricular function to the top part of the Starling curve.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

What would happen if only venous return increased during exercise?
What is also increased during exercise to prevent this from occurring?

A

If only venous return increased, then ventricular function would be shifted to the flat part of the frank starling curve.
Increasing contractility couples with increased venous return to cope to prevent this from occurring.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Why can murmurs be heard during exercise in normal individuals?

A

Turbulent flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

A murmur is heard in an individual who is at rest. What could this be caused by?

A

Disturbed flow through a valve due to stenosis

Back flow through an incompetent valve due to regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Describe the difference between centrifuging unclotted whole blood and clotted whole blood.

A

Unclotted whole blood
Plasma
Buffy coat
Red blood cells

Clotted whole blood
Serum
Clot

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

The fluid collected from clotted blood is…

A

Serum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

The fluid collected from unclotted blood is…

A

Plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

How can you prevent blood from clotting?

A

Add an anti-coagulant eg. Heparin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

Finish the following equation

Serum = plasma -

A

Clotting factors

Particularly fibrinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

Increased total blood viscosity leads to…

A

Sludging of blood in peripheries. Peripheries feel colder.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

What is the most common cause of increased blood viscosity?

A

Multiple myeloma
Cancer of plasma cells- a malignant clone of plasma cells produces immunoglobulins in large quantities which increases the viscosity of the blood.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

What causes increased blood viscosity? (4)

A

Multiple myeloma- increased plasma cells
Polycythaemia- increased red blood cells
Thrombocythaemia- increased thrombocytes
Leukaemia- increased white blood cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

Why is it clinically useful to measure plasma viscosity?

A

Minor changes in plasma viscosity can result from raised levels of acute phase proteins (eg. Fibrinogen, complement factors and C-reactive protein). Acute phase proteins increase in response to inflammation. Therefore, minor changes in plasma viscosity can be used to measure the inflammatory response. In recent years, we have been able to measure C-reactive protein (CRP) and this is more commonly used to measure inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

What is the difference between turbulent and laminar blood flow?

A

Turbulent flow- blood flowing in all directions in the vessel and continually mixes within the vessel.

Laminar flow- blood flows in streamlines with each layer of blood remaining the same distance from the wall.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

Describe normal blood flow.

A

Laminar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

When is blood flow turbulent?

A
Increased blood flow and the rate of blood flow becomes too great
Blood passes an obstruction in a vessel
Blood makes a sharp turn
Blood passes over a rough surface
Increased resistance to flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

Why might you hear a murmur in anaemic patients?

A

Limited number of red blood cells.
Heart rate to increase cardiac output so oxygen can be transported around the body quick enough
Results in turbulent flow which can be heard as a murmur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

Why might you hear a murmur in a patient with thyrotoxicosis?

A

Increased T3 and T4
Causes increased sensitivity to catecholamines
Increased chronotropy and inotropy
Turbulent flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

What units is pressure measured in?

A

Psi (pounds per square inch)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

What are the units for blood flow?

A

Volume per unit time ml/min or l/hour

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

Give an equation for calculating kinetic energy.

A

1/2 x m x v squared

M= mass
V= velocity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

There must be a difference in ____ to feel a pulse.

A

Pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

Why can’t a pulse be felt in blood vessels that are not compliant?

A

Volume does not change in response to pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

Describe how flow, pressure, velocity and kinetic energy changes distally and proximally to a stenosis in an artery.

A

Proximal to the stenosis, flow is less, pressure is greater, velocity is lower and kinetic energy is lower
Distal to the stenosis, flow is less, pressure is less, velocity is higher and kinetic energy is higher

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

When palpated, what can be felt at a stenosis?

A

A thrill

Blood vessel vibrates due to the high velocity and kinetic energy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

On auscultation, what can be heard if there stenosis of a peripheral artery/heart valve?

A

Peripheral artery
Bruit - sounds like a plane taking off

Heart valve
Murmur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

What is a stenosis?

A

Narrowing of a blood vessel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

Eventually, what might occur distally to a stenosis in an an artery?

A

Distal to the stenosis, blood hits the wall of the artery at high velocity and high kinetic energy. This causes a post stenotic dilatation of the blood vessel as the wall of the artery dilates. Bursting of this is an aneurysm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

What causes critical ischaemia?

A

One stenosis followed by another stenosis.

Distal to the second stenosis, flow is further decreased and may stop flowing completely.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

Where is critical ischaemia common?

A

Legs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

Why is it usually difficult to find an elderly persons pulse in the femoral artery?

A

As people age, arteries often calcify and become less compliant. Volume does not increase in response to an increase in pressure so a pulse cannot be felt.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

What are the changes in flow, pressure and velocity when there is greater peripheral resistance?

A

Flow and pressure decreases

Velocity increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

What are the changes in flow, pressure and velocity when peripheral resistance is decreased?

A

Flow and pressure increases

Velocity decreases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

In an descending aorta pressure tracing, what creates the anacrotic limb?

A

Systolic uptake
Pressure in the descending aorta increases rapidly during systole as blood is ejected out of the ventricles as they contract and the elastic walls of the aorta stretches.

Peak systolic pressure
This is the highest pressure in the descending aorta.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
174
Q

In a descending aorta pressure tracing, what creates the dicrotic limb?

A

Systolic decline
Pressure decreases as the ventricles relax and less blood is ejected from the ventricles

Dicrotic notch
The pressure in the aorta exceeds that in the left ventricle and the aortic valve closes. This is the end of systole. There is a slight increase in pressure as blood collects in the aorta.

Diastolic run off
Pressure decreases as blood flows down the aorta and the aortic wall recoils

End diastolic pressure
This is the lowest pressure in the aorta as there is no flow of blood from the ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
175
Q

Give an equation for calculating pulse pressure.

A

Pulse pressure = peak systolic pressure - end diastolic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
176
Q

In an average person, what is the value of pulse pressure?

A

120 - 80 = 40 mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

How do we measure blood pressure?

A

Sphygomanometer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

How can mean arterial pressure be estimated?

A

Diastolic pressure + 1/3 pulse pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
179
Q

In an average person, what is the value of mean arterial pressure?

A

80 + 13 = 93 mm Hg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
180
Q

What are the implications of mean arterial pressure being below 70 mm g?

A

Organ perfusion is impaired

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
181
Q

When measuring blood pressure, how can you make the reading as accurate as possible?

A

Cuff must go around at least 80% of the arm.

An undersized cuff can give a false reading of blood pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

What can affect the accuracy of a blood pressure reading?

A

The height at which blood pressure is measured due to the effect of gravity. Venous and arterial pressure is greater at a lower height when standing up.
The size of the cuff. An undersized cuff can give a false reading of blood pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
183
Q

What is retrograde flow?

A

Retrograde flow is when the blood bounces back slightly. It can occur in the arterial system and is greatest when peripheral resistance is high.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
184
Q

What is the effect of peripheral resistance on retrograde flow?

A

Greater peripheral resistance—> greater retrograde flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
185
Q

What determines the volume of a pulse?

A
  1. The force with which the left ventricle is able to eject the blood into the arterial system to develop a normal shock wave.
    Weaker force —> reduced pulse volume—> thready pulse
  2. Pulse pressure. This is the major determinant of how strong the pulse is.
    Greater pulse pressure—> increased pulse volume—> bounding pulse

Pulse pressure= peak systolic pressure - end diastolic pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
186
Q

What is a thready pulse?

A

Pulse volume is lower than usual

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
187
Q

What are the causes of a thready pulse?

A

LV failure
Aortic valve stenosis
Hypovolaemia (severe dehydration/bleeding)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
188
Q

Why does bradycardia produce a bounding pulse?

A

Bradycardia- greater amount of time spent in diastole than usual. End diastolic pressure reaches a smaller value than normal. Pulse pressure increases and pulse volume increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
189
Q

Why does low peripheral resistance cause a bounding pulse?

A

Low peripheral resistance caused by vasodilation- diastolic run off occurs more quickly as blood rushes out of the aorta to the peripheries. End diastolic pressure reaches a smaller value within the same period of time. Pulse pressure increases and pulse volume increases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
190
Q

What are the common causes of congenital heart defects? (3)

A

Genetic
Downs, turner’s syndrome, marfan’s syndrome

Environmental
Teratogenicity from drugs, alcohol etc.

Maternal infections
Rubella, toxoplasmosis etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
191
Q

Give the approximate percentage saturation of haemoglobin in the different chambers of the heart.

A
Left atrium- 99%
Left ventricle- 99%
Aorta- 99%
Right atrium- 67%
Right ventricle- 67% 
Pulmonary arteries- 67%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

Give the average pressures in the different chambers of the heart

A
Right atrium- 0-4mmHg 
Right ventricle- 25/3 mmHg 
Pulmonary arteries- 25/10mmHg
Left atrium - 8-10 mmHg
Left ventricle- 120/7mmHg 
Aorta-120/80mmHg
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

What is a shunt?

A

A communication between two sides of the circulation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
194
Q

What is cyanosis?

A

Bluish discolouration skin, nail beds and mucous membranes due to unsaturated haemoglobin entering the systemic circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
195
Q

When does the cardiogenic field appear and why?

A

In the 3rd week of development because nutrient and gas exchange needs of the rapidly growing embryo can no longer be met by diffusion alone so the developing cardiovascular system is formed to deliver these substances over long distances.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
196
Q

How is the primitive heart tube formed?

A

The endocardial tubes are brought together during embryonic folding and fuse in the midline.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
197
Q

Describe the primitive heart tube.

A

Cranial end

Aortic roots (2 vessel outlet) 
Truncus arteriosus 
Bulbus cordis
Ventricle 
Atrium 
Sinus venosus (4 vessel inlet)

Caudal end

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
198
Q

What is the truncus arteriosus destined to be?

A

The roots and proximal portions of the pulmonary trunk and aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
199
Q

What is the bulbus cord is destined to be?

A

Part of the right ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
200
Q

What is the primitive ventricle destined to be?

A

The left ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

What is the primitive atrium destined to be?

A

Most of the right atrium and some of the right ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
202
Q

What is the cardiogenic field?

A

A zone within the mesoderm consisting of blood pools and tiny vessels. There is a space which will be the pericardial cavity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
203
Q

What is the sinus venosus destined to be?

A

Right atrium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
204
Q

What happens during looping of the primitive heart tube?

A

The tube elongates.
It runs out of room.
Twists and folds up placing the inflow cranially and dorsally to the outflow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
205
Q

From which structures in the primitive heart tube is the right atrium developed from?

A

Most of the primitive atrium
Sinus venosus
This recieves venous drainage from the body (venue cavae) and the heart (coronary sinus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
206
Q

From which structures in the primitive heart tube does the left atrium develop from?

A

A small portion of the primitive atrium
Absorbs proximal parts of pulmonary veins
Receives oxygenated blood from the lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
207
Q

What explains why an adults left atrium has a smooth inner surface whereas their right atrium has a rough inner surface?

A

The left atrium mainly develops from proximal parts of the pulmonary veins which has a smooth inner surface whereas the right atrium mainly develops from the primitive atrium which has a rough inner surface.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
208
Q

What ensures the heart occupies fully the pericardial sac?

A

Looping in the fourth week of embryonic development

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
209
Q

What is the difference between adult and foetal circulation?

A

There is a double circulation in series in an adult but in a foetus, the lungs do not work so there is no requirement for this double circulation.
Oxygenation and removal of carbon dioxide occurs at the placenta for a foetus.
Shunts are required to maintain foetal life but these must be reversible at birth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
210
Q

What shunts are present in a foetal circulation and what is the purpose of these?

A

Ductus venosus- between inferior vena cava and the liver to prevent all blood entering the liver

Ductus arteriosus- between the aorta and pulmonary trunk which is right to left to ensure all highly oxygenated blood is pumped to the foetus

Foramen ovale-between the atria which is right to left to ensure that blood enters the left atria and hence the left ventricle so that blood can enter the systemic circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
211
Q

In which vessel is the most oxygenated blood in a foetus?

A

The inferior vena cava which comes from the placenta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
212
Q

How do the shunts close when a baby is born?

A

Ductus venosus-physiological closure
Placental support is removed

Ductus arteriosus
Ductus arteriosus undergoes a muscular spasm and closes

Ductus venosus and ductus arteriosus become fibrotic and close.

Foramen ovale-mechanical closure
Left atrial pressure increases
Septum primum closes firmly against septum secondum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
213
Q

Which aortic arches in the foetus form the arch of the aorta and the pulmonary artery?

A

Arch 4 LHS = arch of the aorta

Arch 6 RHS = pulmonary artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
214
Q

How many aortic arches are there in a foetus?

A

6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
215
Q

Which nerve loops around the aortic arch?

A

Left recurrent laryngeal nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
216
Q

How does the atrial septal wall form?

A

Neural crest cells migrate into the developing heart making a shaft of tissue called endocardial cushions.

Endocardial tissues create a crescent shaped wedge down the roof of the atria towards the atrioventricular canal called the septum primum. The hole is the Ostium primum which allows right to left shunt.

Septum secundum forms and the foramen ovale forms.

This forms a right to left shunt.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
217
Q

Why is atrial septal defect common?

A

There is a complex process in producing the atrial septum. Atrial septal defect can arise due to problems in forming either septum primum or septum secondum.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
218
Q

What are the two components of the ventricular septum?

A

Muscular

Membranous

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
219
Q

Why does inadequate formation of endocardial cushions or endocardial cushions in the incorrect place cause ventricular septal defect?

A

The muscular portion of the septum which forms the majority of the septum grows upwards towards the fused endocardial cushions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
220
Q

What is the interventricular foramen and how is it closed?

A

The interventricular foramen is the gap formed when the muscular portion of the septum grows upwards towards the endocardial cushions.
This is closed by the membranous portion of the interventricular septum formed by connective tissue derived from endocardial cushions to fill the gap.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
221
Q

Describe septation of outflow tracts.

A

Endocardial cushions appear in the truncus arteriosus.
As they grow towards each other, they twist around each other to form a spiral septum.
This connects the left ventricle to the aorta and connects the right ventricle to the pulmonary trunk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
222
Q

What is transposition of the great arteries?

A

The aorta arises from the right ventricle.

The pulmonary trunk arises from the left ventricle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
223
Q

What is tetralogy of fallot?

A

Large ventricular septal defect
Overriding aorta
Right ventricular outflow tract obstruction (pulmonary stenosis)
Right ventricular hypertrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
224
Q

Why are neural crest cells important?

A

They migrate to from the endocardial cushions which are the foundation of atrial septation, ventricular septation and septation of the outflow tracts.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
225
Q

How can alcohol affect the development of a foetus?

A

Low concentrations of alcohol can kill or damage these cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
226
Q

What type of shunting does tetralogy of fallot cause?

A

Right to left shunting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
227
Q

What causes coarctation of the aorta?

A

Narrowing of the aortic lumen in the region of the former ductus arteriosus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
228
Q

What is eisenmenger syndrome?

A

The condition of severe pulmonary vascular obstruction that results from chronic left to right shunting through a congenital heart defect. The elevated pulmonary vascular resistance causes reversal of the original shunt and systemic cyanosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
229
Q

When can patent foramen ovale cause a problem?

A

Takes on significance if the right atrial pressure becomes elevated (due to pulmonary hypertension or right heart failure) leading to right to left shunting since the higher left atrial pressure causes functional closure of the flap valve.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
230
Q

Coarctation of the aorta affects blood flow to some regions of the body. Which regions of the body are and are not affected?

A

Because vessels to the head and upper limbs usually emerge proximal to the coarctation, the blood supply to these regions is not compromised.
However, blood flow to the rest of the body is reduced.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
231
Q

If no shunt existence, would transposition of the great arteries be compatable with life?

A

Compatible with life in uterus because flow through ductus arteriosus and foramen ovale allows communication between the two circulations.

After birth, without any intervention, TGA is not compatable with life because oxygenated blood does not reach systemic tissues.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
232
Q

On examination, what is noticeable about the femoral pulse of patients with coarctation of the aorta?

A

Femoral pulses are weak and delayed.

An elevated blood pressure in the upper body is common.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
233
Q

Give some examples of acyanotic congenital heart defects.

A
Left to right shunts: 
Atrial septal defect (ASD)
Patent foramen ovale (PFO)
Ventricular septal defect (VSD)
Patent ductus arteriosus (PDA)
Obstructive lesions:
Aortic stenosis (Hypoplasia) 
Pulmonary stenosis (Valve, outflow, branch)
Coarctation of the aorta
Mitral stenosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
234
Q

Give some examples of cyanotic congenital heart defects.

A
Complex, right to left shunts
Tetralogy of Fallot
Tricuspid Atresia
Transposition of the great arteries 
Hypoplastic left heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
235
Q

What is hypoplastic left heart?

A

Left ventricle and ascending aorta fail to develop properly.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
236
Q

What influences the course of the recurrent laryngeal nerves?

A

Caudal shift of the development heart and expansion of the developing neck region
The need for a foetal shunt between the pulmonary trunk and aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
237
Q

What is the difference between the upstroke in an action potential in cardiomyocytes and pacemaker cells?

A

Cardiomyocytes = Na+ influx via the opening of fast type Na+ channels due to depolarisation.

Pacemaker cells = Ca2+ influx via the opening of L-type Ca2+ channels due to depolarisation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
238
Q

What is the difference between the Na+ channels involved in an action potential in cardiomyocytes and pacemaker cells?

A

Cardiomyocytes
Fast type Na+ channels-responsible for upstroke in AP

Pacemaker cells
Slow type Na+ channels- responsible for ‘pacemaker potential’

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
239
Q

What is pacemaker potential?

A

Slow Na+ channels slowly open and the resting membrane potential depolarises steadily from its most negative value of -60mV in pacemaker cells.
They activate more with hyperpolarisation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
240
Q

What is the main difference between the shape of an action potential in a pacemaker cell and in a cardiomyocyte?

A

Plateau phase in cardiomyocytes

Ca2+ influx and K+ outflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
241
Q

Describe how movement of ions changes in a cardiac action potential in cardiomyocytes.

A

Phase 0 –> Na+ influx
Phase 1 –> transient K+ efflux
Phase 2 –> Ca2+ influx and K+ efflux
Phase 3 –> K+ efflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
242
Q

Describe how movement of ions changes in a cardiac action potential in pacemaker cells.

A

Slow Na+ influx
Fast Ca2+ influx
K+ outflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
243
Q

Slow voltage gated Na+ channels are activated by depolarisation.
True or false

A

False
Activated by hyperpolarisation
They are HCN channels
Hyperpolarisation activated cyclic nucleotide gated channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
244
Q

Which region of the heart depolarises fastest?

A

SA node- therefore, this sets the rhythm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
245
Q

Where are pacemaker cells found?

A

SA node and AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
246
Q

Do purkinje fibres have a stable resting potential?

A

No they have slow type Na+ channels that allows Na+ to continuously leak in.
But does not depolarise as fast as SA node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
247
Q

Which regions of the heart have the capacity to set the rhythm of the heart?

A

Those which do not have a stable resting potential due to continuous influx of Na+ :
SA node
AV node
Purkinje fibres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
248
Q

Describe the terms asystole and fibrillation in terms of electrical activity of the heart.

A

Asystole- action potentials fail

Fibrillation- electrical activity becomes random

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
249
Q

What is normal plasma K+ concentration?

A

3.5-5.5 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
250
Q

What is hyperkalaemia?

A

> 5.5mmol/L of K+ in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
251
Q

Why cardiac myocytes sensitive to changes in K+ concentration?

A

Their resting membrane potential is very close to Ek (-90mV)

There are many different kinds of K+ channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
252
Q

What is hypokalaemia?

A

<3.4mmol/L of K+ in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
253
Q

Describe the effect of hyperkalaemia on an action potential cardiac myocytes.

A

EK is less negative
Inactivates some of the voltage gated Na+ channels
Slow upstroke

Narrows action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
254
Q

What are the consequences of hyperkalaemia on the heart and what do the extent of the consequences depend upon?

A

Asystole- the heart can stop because of the slower upstroke of the action potential

May initially get an increase in excitability

Depends on extent of hyperkalaemia and how quickly hyperkalaemia develops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
255
Q

What are the treatments for hyperkalaemia and when should they be given?

A

Calcium gluconate
Insulin + glucose
These won’t work if the heart has already stopped

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
256
Q

Define mild, moderate and severe hyperkalaemia.

A

Mild hyperkalaemia = 5.5-5.9mmol/L
Moderate hyperkalaemia = 6.0-6.3 mmol/L
Severe hyperkalaemia> 6.5mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
257
Q

Why can calcium gluconate be given as a treatment for hyperkalaemia?

A

Calcium makes the heart less excitable because it is a bivalent cation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
258
Q

Why is glucose given together with insulin in the treatment of hyperkalaemia?

A

To prevent hypoglycaemia
If you gave insulin alone, this would increase uptake of glucose from the blood and would cause hypoglycaemia.
Insulin increases uptake of K+ into cardiac myocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
259
Q

What is the effect of hypokalaemia on action potentials in cardiac myocytes?

A

Decreased plasma K+ concentration
Allosteric effect reducing the conductance of voltage gated K+ channels so downstroke of AP is slower
Leads to a longer action potential

Early reactivation of some voltage gated Ca2+ channels as some of the membrane repolarises
Leads to early after depolarisations (EADs) and hence oscillations in membrane potential
Ventricular fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
260
Q

What are the effects of hypokalaemia on the heart?

A

Oscillations in membrane potential—>Ventricular fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
261
Q

When is hypokalaemia dangerous?

A

In patients

  • with existing heart problems
  • people on anti-arrhythmic drug
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
262
Q

Describe excitation-contraction coupling in cardiac cells?

A

Depolarisation open L-type Ca2+ channels in the T-tubule system
Localised Ca2+ entry opens CICR channels in the sarcoplasmic reticulum
Close link between L-type channels and Ca2+ release channels (but they’re not directly connected)

25% enters across the sarcolemma, 75% released from SR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
263
Q

What happens at a cellular level with the relaxation of cardiac myocytes?

A

Ca2+ in the cardiac myocytes is returned to resting levels
Most is pumped back into the SR as 75% of Ca2+ came from here, some exits across the membrane
Ca2+ ATPase is activated (high affinity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
264
Q

Where in the vascular wall are smooth muscle cells found?

A

Tunica media

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
265
Q

Describe excitation contraction coupling in smooth muscle cells.

A

Opening of voltage gated Ca2+ channels due to depolarisation allows Ca2+ to enter

A1 adrenoreceptors activate and Ca2+ is released from SR via activation of phospholipase C and creation of iP3 which binds to SR

Ca2+ binds to calmodulin. Ca2+ activates myosin light chain kinase which phosphorylates the myosin light chain to permit activation with actin.

DAG stimulates PKC which inhibits myosin light chain phosphatase. This allows sustained vasoconstriction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
266
Q

Does troponin C have a role in contraction in smooth muscle cells?

A

No. Ca2+ binds to calmodulin.
This activated myosin light chain kinase
Myosin light chain kinase phosphorylates the myosin light chain to permit interaction with actin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
267
Q

Describe what happens in the cell during relaxation of smooth muscle cells.

A

Myosin light chain phosphatase dephosphorylates the myosin light chain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
268
Q

How is contraction in smooth muscle cells in arterioles different to contraction in cardiac myocytes?

A

Ca2+ binds to calmodulin which activates myosin light chain kinase in smooth muscle

Ca2+ binds to troponin C in cardiac muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
269
Q

How does the body coordinate its response to exercise and stress?

A

Autonomic nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
269
Q

How does the autonomic nervous system control the activity of the cardiovascular system?

A

Can change:
Rate
Force of contraction of heart
Peripheral resistance of blood vessels (arteriolar/venous constriction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
269
Q

We can divide the autonomic nervous system into sympathetic and parasympathetic branches.
This division is based on….

A

Anatomical grounds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
270
Q

What is the origin of parasympathetic nerves?

A

Cranial and sacral origin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
271
Q

What is the origin of sympathetic nerves?

A

Thoracic and lumbar origin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
272
Q

What is the enteric nervous system?

A

Network of neurones surrounding GI tract

Normally controlled via sympathetic and parasympathetic fibres

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
273
Q

What branch of the nervous system is dominant under basal conditions?

A

Parasympathetic nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
274
Q

Where are alpha 1 adrenoreceptors found?

A

Smooth muscle of blood vessels- vasoconstriction
Pupil of eye. Dilation
Sweat glands - increased sweat release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
275
Q

If you activate the sympathetic nervous system, is sympathetic drive to all tissues regulated?

A

No, sympathetic drives to different tissues is independently regulately

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
276
Q

What happens if you denervate a heart?

A

It beats at a faster rate to about 100 beats per minute because parasympathetic nervous system dominates at rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
277
Q

At rest, which nerve innervates the heart?

A

Vagus nerve-10th cranial nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
278
Q

What muscarinic and adrenergic receptors are present on the heart?

A

M2

B1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
279
Q

What influence does the parasympathetic nervous system have on the heart?

A

Decreases heart rate (negative chronological effect)

Decreases AV node conduction velocity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
280
Q

What influence does the sympathetic nervous system have on the heart?

A

Increases heart rate (positive chronograph)

Increases force of contraction (positive inotropy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
281
Q

What is the difference between what sympathetic and parasympathetic pre-ganglionic nerves innervate in the heart?

A

Sympathetic
Innervates: SA node, AV node, myocardium

Parasympathetic
Innervates: SA node, AV node

282
Q

Where are the sympathetic and parasympathetic postganglionic nerves that innervate the heart?

A

Sympathetic
Post ganglionic nerves come from the paravertebral disc/sympathetic trunk

Parasympathetic
Post ganglionic nerves are within the epicardium or within walls of heart at SA node and AV node

283
Q

Explain sensory input to the cardiovascular centre in the medulla oblongata.

A

Baroreceptors which are sensitive to stretch in:
Carotid sinus of internal carotid artery - arterial pressure
Aortic arch - arterial pressure

Atrial receptors - venous pressure

Sensory (afferent neurones) from the baroreceptors/atrial receptors go to the cardiovascular centre in the medulla oblongata

The cardiovascular centre in the medulla oblong at a acts as a control centre and alters the activity of the efferent preganglionic nerves which go to the heart and vessels

284
Q

What sets the rhythm of the heart?

A

Action potentials in the sa node

Slow depolarising pacemaker potential eventually causing the opening of Ca2+ channels responsible for upstroke

285
Q

Describe the membrane potential changes in pacemaker cells associated with sympathetic input.

A

Sympathetic effect mediated by beta 1 adrenoreceptor GPCR
Increase cAMP
Speeds up pacemaker potential—>Increases slope

286
Q

Describe the membrane potential changes in pacemaker cells associated with decreases in heart rate.

A

Parasympathetic effect mediated by M2 GPCR
Increase K+ conductance and decrease cAMP
Decreases slope of pacemaker potential

287
Q

How does the sympathetic nervous system increase inotropy?

A

Noradrenaline
B1 adrenoreceptors in myocardium
cAMP —> activates PKA
-phosphorylation of Ca2+ channels increases Ca2+ entry during the plateau of the AP
-increased uptake of Ca2+ in sarcoplasmic reticulum
-increased sensitivity of contractile machinery to Ca2+
All lead to increased force of contraction

288
Q

Does most vasculature get sympathetic or parasympathetic innervation?

A

Sympathetic innervation

289
Q

How does the sympathetic nervous system cause vasodilatation?

A

Activating beta 2 adrenoreceptors causes vasodilation

290
Q

Which receptors arteries and veins have to control vasodilation and vasoconstriction

A

a1 adrenoreceptors

Coronary, skeletal and liver vasculature also have b2 adrenoreceptors

291
Q

Increased sympathetic tone is…

A

Vasoconstriction

292
Q

Decreased sympathetic tone is…

A

Vasodilation

293
Q

What is the difference between adrenaline which activates alpha 1 adrenoreceptors and beta 2 adrenoreceptors in vasculature?

A

Alpha 1 - noradrenaline from sympathetic nervous system and circulating adrenaline at high plasma concentrations of adrenaline (higher affinity of a1)

Beta 2 - circulating adrenaline at physiological concentration (higher affinity for b2)

294
Q

Vasodilation in arteries is caused by activation of which receptors?

A

B2 - only some tissues eg. Skeletal muscle, myocardium and liver

Usually vasodilation is just a lack of sympathetic tone

295
Q

Vasoconstriction of arteries is caused by activation of which receptors?

A

Alpha 1

296
Q

How does activation of beta 2 adrenoreceptors cause vasodilation?

A

Increases cAMP
Activates PKA
Opens K+ channels and inhibits myosin light chain kinase and phosphorylates myosin light chain kinase
Relaxation of smooth muscle

297
Q

How does activation of alpha 1 adrenoreceptors cause vasoconstriction?

A

Stimulates ip3 production
Increase of intracellular calcium from stores and via influx of extracellular calcium
Contraction of smooth muscle

298
Q

What is the main method for ensuring adequate perfusion of skeletal and coronary muscle?

A

Active tissue produces more metabolites eg. Adenosine, K+, H+, increased co2

Local increases in metabolites has a strong vasodilator effect

299
Q

The vagus nerve is just a motor neurone.

True or false.

A

False
It is a sensory and motor neurone
Sensory - from baroreceptors in aortic arch
Motor - to AVN and SAN

300
Q

When is the baroreceptor reflex important?

A

When maintaining blood pressure over short term

Compensates for moment to moment changes in arterial blood pressure

301
Q

Why is the baroreceptor reflex not that useful in responding to long term increases in blood pressure?

A

Baroreceptors re-set to higher levels with persistent increases in blood pressure

302
Q

Why would you not give propranolol as a drug to treat hypertension to an asthmatic?

A

It is a non-selective B1/B2 antagonist
Slows heart rate and reduces force of contraction (b1)
Acts on bronchial smooth muscle to cause bronchoconstriction (b2)

303
Q

How can adrenoreceptors be used in the treatment of hypertension?

A

A1 antagonist

B1-selective antagonist

304
Q

What can muscarinic agonists be used in the treatment of?

A

Glaucoma

Activates constriction papillae muscle- agonises m3 receptor

305
Q

What can Muscarinic antagonists be used in the treatment of?

A

Asthma, antagonises m3 receptors

Dilation of pupils for examination, antagonises m3 receptors

306
Q

What properties of the CVS does the autonomic nervous system control?

A

Total peripheral resistance
Distribution of flow
Cardiac output - heart rate and force of contraction

307
Q

What is the effect of venoconstriction?

A

Increases return of blood to the heart

308
Q

Why can left ventricle failure cause mitral valve regurgitation?

A
LV dilation 
More room for blood 
Increased compliance 
Stretched mitral valve
Mitral valve regurgitation
309
Q

Why can mitral valve regurgitation cause left ventricle failure?

A
Blood leaks back into left atrium
Increases preload 
More blood enters left ventricle in subsequent cycles 
Causes left ventricle hypertrophy
Left ventricle failure
310
Q

How can left atria dilation cause atrial fibrillation?

A

The walls of the atria stretch and there is more room for blood.
Pacemaker cells become ‘irritated’.
Leads to atrial fibrillation

311
Q

How can atrial fibrillation cause thrombus formation?

A

Individual fibrils contract not in synchrony with one another.
Blood remains stagnant in the atria.
Leads to thrombus formation

312
Q

How can increased left atrial pressure lead to dysphagia?

A

Increase LA pressure
LA dilation
Oesophagus compression
Dysphagia

313
Q

How can mitral valve stenosis lead to right ventricle hypertrophy?

A

Increased left atrial pressure

Pulmonary hypertension

Right ventricle hypertrophy

314
Q

Why are people who are born with a bicuspid form of an aortic valve more prone to aortic valve stenosis?

A

Mechanical stress which is usually distributed over three leaflets is now only distributed over two leaflets.

315
Q

Why does chronic rheumatic fever cause valve stenosis?

A

Repeated inflammation and repair leads to fibrosis of valves and hence stenosis

316
Q

How does aortic valve stenosis lead to syncope and angina?

A
Less blood can get through valve
Increase left ventricle pressure
Left ventricle hypertrophy
Left sided heart failure
Insufficient blood flow to CNS = syncope
Insufficient blood flow to heart = heart
317
Q

How can aortic valve stenosis cause microangiopathic haemolytic anaemia?

A

Damage to red blood cells as blood is being transported under a very high pressure through a very narrow gap

318
Q

Which valvular disease increases pulse pressure?

A

Aortic valve regurgitation
Blood flows back into LV during diastole
Increases stroke volume
Systolic pressure increases and diastolic pressure decreases

319
Q

What are the signs of increased pulse pressure?

A

Bounding pulse - head bobbing and quinke’s sign (nail beds change colour with pulse)

320
Q

Which shunts allow the bypass of the pulmonary circulation?

A

Ductus arteriosus

Foramen ovale

321
Q

Why is the baroreceptor reflex not sufficient for long term regulation?

A

Works well to control acute changes in blood pressure
Does not control sustained increases because the threshold for baroreceptor firing resets after a short period- it responds to changes

322
Q

Which of these are altered in the short term regulation OR long term regulation of blood pressure?

Heart rate
Total peripheral resistance
Force of contraction
Sodium concentration in extracellular fluid \

Give reasons why

A

Short term- heart rate, TPR, force of contraction
To cause: vasoconstriction/dilation, changes in CO

Long term-sodium concentration in extracellular fluid
To cause: increase/decrease in blood volume

323
Q

Where is renin released from?

A

Juxtaglomerular apparatus in kidney

324
Q

What stimulates the release of renin?

A
  • Reduced NaCl concentration in distal tubule
  • Reduced perfusion pressure in the kidney detected by baroreceptors in afferent arteriole (going into the kidney- reflects peripheral arteriole blood pressure)
  • Sympathetic stimulation to juxtaglomerular apparatus increases release of renin
325
Q

State two equations that can be used to calculate mean arterial blood pressure.

A

Mean arterial BP = CO x TPR

Mean arterial BP = diastolic pressure + 1/3 pulse pressure

326
Q

What does the baroreceptor reflex do?

A

Controls and produces a rapid response to acute changes in blood pressure by:

  • adjusting sympathetic and parasympathetic inputs to the heart to alter CO
  • adjusting sympathetic input to peripheral resistance vessels to alter TPR
327
Q

What are the four parallel neurohumoral pathways that control circulating volume and hence blood pressure?

A

Renin-angiotensin-aldosterone system
Sympathetic nervous system
Antidiuretic hormone
Atrial natriuretic peptide (ANP)

328
Q

What does angiotensin converting enzyme (ACE) do? (2)

A

Stimulates the conversion of angiotensin I to angiotensin II

Kininase enzyme that breaks down the vasodilator bradykinin into peptide fragments so causes vasoconstriction

329
Q

What is the main kind of receptor that angiotensin II binds to?

A

Angiotensin II receptor 1 (AT1) =

GPCR

330
Q

What are the effects of angiotensin II on:

  1. Arterioles
  2. Kidneys
  3. Adrenal cortex
  4. Sympathetic nervous system
  5. Hypothalamus
A
  1. Vasoconstriction
  2. Stimulates Na+ reabsorption
  3. Stimulates release of aldosterone
  4. Increases noradrenaline released
  5. Stimulates ADH release, increasing thirst sensation
331
Q

Where does aldosterone exert its effects?

A

Principal cells of collecting ducts

332
Q

What does aldosterone do? (2)

A
  • activates apical Na+ channel and apical K+ channel

- increases basolateral Na+ extrusion via Na+/K+ ATPase

333
Q

What would you predict about the potassium levels in an individual who has high aldosterone levels?

A

Low potassium levels
Aldosterone stimulates basolateral Na+/K+ ATPase to promote extrusion of Na+ into capillaries but in turn decreases K+ concentration in capillaries

334
Q

Why can ACE inhibitors be used in the treatment of hypertension?

A

The inhibit ACE so

  • prevent the conversion of angiotensin I to angiotensin II (so all the effects of this including release of aldosterone are inhibited)
  • prevent the conversion of bradykinin into peptide fragments by ACE.
335
Q

How is the sympathetic nervous system involved in long term control of blood pressure?

A

High levels of sympathetic activation causes:

-reduced renal blood flow:
Vasoconstriction of arterioles to kidneys
Decreased glomerular filtration rate-decreased Na+ excretion

  • activation of apical Na+/H+ exchanger and basolateral Na+/K+ ATPase in proximal convolutions tubule
  • stimulates renin released from juxtaglomerular renal cells
336
Q

Where is ADH produced and released from?

A

Produced in hypothalamus but secreted by pituitary gland by neurocrine secretion

337
Q

What are the effects of ADH?

A
  • formation of concentrated urine by retaining water by leading to increased transcription of aquaporins
  • stimulates Na+ reabsorption by acting on the thick ascending limb and stimulating the Na+/K+/Cl- co-transporter
  • vasoconstriction
338
Q

What stimulates the release of ADH?

A

Plasma osmolarity

Severe hypovolaemia

339
Q

When are elevated levels of ANP found in the bloodstream?

A

Hypervolaemia

340
Q

Where is ANP stored and released?

A

Atrial myocytes

341
Q

What stimulates release of ANP?

A

High level of stretching by low pressure volume sensors in the atria

342
Q

What are the effects of ANP?

A

Vasodilation of afferent arterioles
Increased blood flow to kidneys to increase glomerular filtration rate
Inhibits Na+ rebasorption along the nephron

343
Q

Which long term mechanism of controlling blood pressure works in the opposite direction to other neurohumoral regulators?

A

Natriuretic peptides- ANP and BNP

344
Q

Define the stages of hypertension.

A

Stage 1 hypertension = 140/90mmHg
Stage 2 hypertension = 160/100 mmHg
Severe hypertension > or equal to 180 systolic
> or equal to 110 diastolic

345
Q

What is accelerated hypertension?

A

A rapid increase in blood pressure which causes damage to blood vessels

346
Q

What is the difference between primary and secondary hypertension?

A

Primary- cause cannot be defined

Secondary-cause can be defined

347
Q

How can renal artery stenosis of one kidney result in hypertension?

A

Occlusion of the renal artery
Fall of perfusion pressure in that kidney
Increased renin production
Activation of RAAS
Vasoconstriction and Na+ retention at other kidney
Hypervolaemia
Hypertension

348
Q

Give some adrenal causes of hypertension.

A

Cushing’s syndrome- excess secretion of glucocorticoid cortisol from adrenal cortex

Conn’s syndrome- mineralocorticoid aldosterone secreting adenoma in adrenal cortex

Tumour of the adrenal medulla-secretes catecholamines adrenaline and noradrenaline

349
Q

Give some non-pharmacological approaches to treating hypertension.

A

Exercise
Diet
Reduced Na+ intake
Reduced alcohol intake

350
Q

Which organs are commonly affected by hypertension?

A
Brain 
Eyes
Heart
Kidneys 
Arteries
351
Q

What effect can hypertension have on the eyes?

A

Hypertension causes arterial damage
Leading to weakened vessels
Leading to retinopathy

352
Q

How can hypertension cause heart failure?

A

Increased afterload
Left ventricular hypertrophy
Heart failure

353
Q

How can hypertension cause a myocardial infarction?

A

Increased afterload
Increased myocardial oxygen demand
Myocardial ischaemia
Myocardial infarction

354
Q

Describe what shock is.

A

Acute condition of general inadequate blood flow throughout the body

355
Q

What is common in all types of shock?

A

A drop in arterial blood pressure

356
Q

Which types of shock occur due to a fall in cardiac output?

A

Cardiogenic shock
Mechanical shock
Hypovolaemic shock

357
Q

Which types of shock occur due to a drop in total peripheral resistance?

A

Anaphylactic shock

Septic shock

358
Q

List some common causes of cardiogenic shock.

A

MI—> damage to left ventricle
Serious arrhythmias—> profound bradycardia/tachycardia
Acute worsening of heart failure—> at rest, BP cannot be maintained

359
Q

What is cardiogenic shock?

A

Inadequate tissue perfusion, resulting in generalised lack of oxygen supply to cells because the ventricle cannot eject enough blood.

360
Q

How is cardiogenic shock different to heart failure?

A

Heart failure is a chronic condition. With heart failure, patients have an adequate blood pressure which may change if they exert themselves but at rest, they are not in an acutely life threatening condition.
Cardiogenic shock refers to acute failure of the heart to maintain cardiac output so blood pressure can no longer be maintained for vital organs to be adequately perfused, making it acutely life threatening.

361
Q

What is cardiac arrest?

A

Unresponsiveness associated with lack of pulse

The heart has stopped or ceased to pump effectively

362
Q

Can someone be in cardiac arrest if an ECG shows there is electrical activity present in their heart/

A

Yes- cardiac arrest can be due to a loss of electrical and/or mechanical activity

Pulseless Electrical Activity= presence of electrical activity but loss of mechanical activity

363
Q

What is asytole?

A

Loss of electrical and loss of mechanical activity of the heart

364
Q

Describe how defibrillation works in the management of cardiac arrest.

A

Electrical current delivered to the heart
Depolarises all of the cells
Puts them into a refractory period
Allows coordinated electrical activity to restart

365
Q

Why is adrenaline given in the management of cardiac arrest?

A

Enhances myocardial function

Vasoconstriction—>increases peripheral resistance

366
Q

What is mechanical shock?

A

Inadequate tissue perfusion, resulting in generalised lack of oxygen supply to cells because:

  • there is a restriction on filling of the heart
  • there is obstruction to blood flow through the lungs
367
Q

Which type of shock can be caused by cardiac tamponade?

A

Mechanical shock

368
Q

How can a pulmonary embolism lead to mechanical shock?

A

Embolus occludes a large pulmonary artery
– Pulmonary artery pressure is high
– Right ventricle cannot empty
– Central venous pressure high
– Reduced return of blood to left heart
– Limits filling of left heart
– Left atrial pressure is low
– Arterial blood pressure low
– Shock

369
Q

How might an embolus reach the lungs?

A

• Typically due to deep vein thrombosis
• Potion of thrombus breaks off
• Travels in venous system to right side of the heart
• Pumped out via pulmonary artery to lungs
• The effect of this will depend on the size of the embolus

370
Q

How much blood loss can the body usually tolerate without causing any signs of hypovolaemic shock?

A

20%

371
Q

What does the severity of hypovolaemic shock depend upon?

A

Amount and speed of blood loss

372
Q

List some common causes of hypovolaemic shock.

A

Haemorrhage
Severe diarrhoea
Vomiting
Excessive loss of Na+

373
Q

What is internal transfusion and when does it occur?

A

Vasoconstriction (increased TPR) reduces capillary hydrostatic pressure and there is a net movement of fluid into capillaries
This occurs when there is peripheral vasoconstriction because low arterial pressure is detected by baroreceptors

374
Q

What is the danger of the compensatory response that occurs in hypovolaemic shock?

A

– Peripheral vasoconstriction to increase blood pressure impairs tissue perfusion
– Tissue damage due to hypoxia
– Release of chemical mediators – vasodilators – TPR falls
– Blood pressure falls dramatically
– Vital organs can no longer be perfused
– Multi system failure

375
Q

In which type of shock would you see
Warm, red extremities initially but
Cold clammy extremities as it progresses

A

Septic shock

376
Q

Describe the management of septic shock.

A

Fluid resuscitation to maintain BP

Vasosuppressants required due to peripheral vasoconstriction and leaky capillaries

377
Q

How can septic shock cause a decrease in cardiac output in addition to a drop in total peripheral resistance?

A

TPR
Vasodilation—>reduced arterial pressure

SV
Capillaries become leaky resulting in reduced blood volume

378
Q

What is hypovolaemic shock?

A

Inadequate tissue perfusion, resulting in generalised lack of oxygen supply of cells due to loss of circulating fluid volume.

379
Q

What is normovolaemic shock?

A

Inadequate tissue perfusion, resulting in generalised lack of oxygen supply to cells due to uncontrolled falls in peripheral resistance ie. sepsis or anaphylaxis

380
Q

Give some features of the cells involved in the conducting system of the heart.

A
  • consists of specialised cells (lost their contractile ability)
  • able to generate action potentials
  • conduct impulses very rapidly to all subendocardial regions of the ventricles - results in depolarisation of myocytes and coordinated contraction of atria and ventricles
381
Q

In which direction do the ventricles depolarise?

A

From endocardium to epicardium (His-purkinje system is in the endocardium)

Starts with the interventricular septum, following rapidly by the apex and free wall of the ventricles. Last part to be depolarised is the base of the ventricles.

382
Q

Which group of cells in the heart have the fastest rate of depolarisation and what is the significant of this?
Where is this found?

A

Sinoatrial node
Fastest rate of depolarisation so sets sinus rhythm
At junction between right atrium and superior vena cava

383
Q

Where does electrical activity pause after coming from the sinoatrial node? Why?

A

Atrioventricular node
At base of right atrium
Slow rate of depolarisation so electrical activity is delayed here by about 120-200ms
This allows time for atrial contraction

384
Q

What is the only conducting path from the atria to the ventricles under normal conditions?

A

Bundle of His
Continuous with AV node
Atrial impulse cannot travel from atria to ventricles due to the fibrous non-conductive connective tissue separating them

385
Q

Does the left or right bundle branch conduct slightly faster than the other? Why?

A

Left bundle branch because the left ventricular muscle wall is thicker.

386
Q

What are purkinje fibres?

A

Fine branches of Bundle of His

Rapid spread of depolarisation throughout ventricular myocardium to allow synchronised contraction (4 metres/sec)

387
Q

Describe how excitation normally spreads through the heart.

A
  1. The electrical events start with depolarisation of the sinoatrial node and is followed by depolarisation of the myocytes of the right and left atria.
  2. The wave of depolarisation is delayed by about 100-200ms at the AV node, allowing time for atrial contraction.
  3. Depolarisation can only spread from the atria to the ventricles via the Bundle of His. It is thereafter rapidly conducted to all parts of the ventricles by the His-Purkinje system.
388
Q

What is the electrical axis of the heart?

A

The overall direction of the wave of depolarisation.

This is directed towards the apex somewhat to the left of the inter-ventricular septum in the normal heart.

389
Q

How does repolarisation of the heart occur?

A

All of the ventricular myocardial cells depolarise before any start to repolarise. Repolarisation does not follow the same sequence across the heart, as the cells at the outside of the ventricle (epicardium) repolarise first, so the direction of spread of repolarisation is opposite to that of depolarisation.

(Therefore, the duration of the action potential of the cells in the epicardium is short)

390
Q

What is an electrocardiogram?

A

An ECG records changes on the extracellular surface of cardiac myocytes during a wave of depolarisation and repolarisation
From the surface of the body
Using electrodes pasted on the skin

391
Q

Depolarisation wave going towards the positive recording electrode.

Upwards or downwards deflection on an ECG?

A

Upward

392
Q

Repolarisation going away from positive recording electrode.

Upward or downward deflection on an ECG?

A

Upward deflection

393
Q

Depolarisation going away from the positive recording electrode.

Upwards or downwards deflection on an ECG?

A

Downwards deflection

394
Q

Repolarisation going towards the positive recording electrode.

Upward or downward deflection on an ECG?

A

Downward deflection

395
Q

What determines the amplitude of a deflection on an ECG?

A

The amplitude (height) of the deflection depends on
• the size of muscle changing potential
• how fast depolarisation occurs
• how directly the wave of activity is travelling towards the electrode
◦ directly towards /away yields a large signal
◦ obliquely towards/away yields a smaller signal
◦ spread at right angles yields no signal

396
Q

Where is the R-R interval measured and what does this indicate?

A

Peak to peak of R-waves

Shorter interval - faster heart rate

397
Q

Where is the QRS complex measured and what does this indicate?

A

Start of Q wave to end of S wave

Wider QRS complexes are associated with ventricular depolarisations that are not initiated by the normal conductance mechanism.

Normal QRS is less than or equal to 3 small boxes

398
Q

Where is the P-R interval measured and what does this indicate?

A

Start of P-wave to start of Q wave

Longer P-R intervals indicate slow conduction from the atria to the ventricle (first degree heart block)

Normal PR interval = 3-5 small boxes

399
Q

Where is the ST segment measured and what does this indicate?

A

End of S wave to start of T wave

The ST segment should be isoelectric. If it is raised or depressed, this indicates myocardial infarction or ischaemia.

400
Q

Where is the Q-T interval measured and what does this indicate?

A

Start of Q-wave to end of T-wave

A prolonged Q-T interval suggests prolonged repolarisation of the ventricles. This can lead to arrhythmias as occur in long QT syndrome.

Varies with heart rate. Upper limit of corrected QT interval: 11-12 small boxes

401
Q

What does the p wave on an ECG represent?

A

Start of the P wave is SA node depolarisation

Majority of it is atrial depolarisation

402
Q

What is atrial depolarisation represented as on an ECG?

A

P wave

403
Q

What does the Q wave on an ECG represent?

A

Depolarisation of the myocardium in intraventricular septum

Septum depolarises from left to right
Produces a small downward deflection because it is moving obliquely away.

404
Q

What does the R wave on an ECG represent?

A

Depolarisation of apex and free ventricular wall

upward because depolarisation moving directly towards electrode
Large because large muscle mass – more electrical activity
If left ventricle was hypertrophies – Then R wave will be correspondingly taller

405
Q

What does the S wave represent?

A

End of depolarisation as depolarisation has spread to the base of the ventricles.

Downwards because moving away
Small because not moving directly away

406
Q

What does the T wave represent?

A

Ventricular repolarisation

Upward because it is repolarisation moving away from the electrode

407
Q

Which waves of an ECG would you use to infer about what is occurring in ventricular muscle?

A

QRS complex

408
Q

Which region on an ECG represents the pause of electrical activity at the AV node and conduction via Bundle of His?

A

Flat line segment

409
Q

How many electrodes are placed on the body for an ECG and where are they placed?

How many views/leads of the heart does this generate?

A

10 electrodes
4 on the limbs
6 on the chest

12 views of the heart

410
Q

Which ECG leads are looking at the inferior surface of the heart?

A

Lead II, III, aVF

411
Q

Which leads look at the left side (lateral) of the heart?

A

Lead I and aVL

V5 and V6

412
Q

Which lead is a mirror image of lead II?

A

aVR

413
Q

What are the limb leads in an ECG?

In what plane do they view the heart?

A

Leads II, III, aVF - inferior view
Leads I, aVL - LHS view
Lead aVR - mirror image of lead II

Vertical plane

414
Q

What are the chest leads in an ECG?

A

V1 and V2 - septal leads
face the right ventricle and septum

V3 and V4 - anterior leads
face the apex and anterior wall of ventricles

V5 and V6 - lateral leads
face the left ventricle

415
Q

Which leads look at the right ventricle and septum of the heart?

A

V1 and V2

416
Q

Which leads look at the apex and anterior wall of ventricles?

A

V3 and V4

417
Q

How can you tell if an ECG is in sinus rhythm?

A

Sinus rhythm = depolarisation initiated by sinus node

  • is the rhythm regular?
  • heart rate? (60-100bpm)
  • are there p waves?
  • are p waves upright in leads I, II?

-Is PR interval is normal (3-5 small boxes)?

  • is every p wave followed by QRS?
  • every QRS preceded by a p wave?
  • normal QRS width (≤3 small boxes)
418
Q

Is sinus arrhythmia pathological?

A

No. Sinus rhythm changes with respiration so small irregularity is not seen as pathological, it is good because it shows the sympathetic nervous system is working.

419
Q

How is heart rate calculated from a rhythm strip for a regular heart rhythm?

A

Heart rate = 300/how many large squares there are between each R wave

420
Q

How is heart rate calculated from a rhythm strip for an irregular heart rhythm?

A

Find number of QRS complex in 6 seconds (30 large squares)

Then x 10

421
Q

Why may there be an abnormal heart rhythm?

A
  • abnormal impulse formation

- abnormal conduction

422
Q

Where in the heart may rhythms arise from?

A

Supraventricular rhythms

  • sinoatrial node
  • ectopic atrial foci
  • atrioventricular node

Ventricular rhythms
-ventricle

423
Q

How are supraventricular rhythms conducted and how do they present on an ECG?

A

Conducted into and within ventricles by His-Purkinje system
Normal ventricular depolarisation

Normal (narrow) QRS complex
Depending on origin of impulse, P wave will vary

424
Q

How are ventricular rhythms conducted and how do they present on an ECG?

A
  • from a focus/foci in ventricle
  • conduction not via normal His-purkinje system
  • depolarisation takes longer
  • wide (> 3 small boxes) QRS complex - rhythms from different foci will have different shapes
  • depending on the origin of the impulse, the P wave and QRS complex will vary allowing us to diagnose the arrhythmia
425
Q

What is an ectopic impulse?

A

Ectopic impulses from subsidiary pacemakers are normally suppressed by more rapid impulses from above.
However, if an ectopic focus depolarises early enough, prior to the arrival of the next sinus impulse, it may “capture” the ventricles, producing a premature contraction.
Premature contractions (“ectopics”) are classified by their origin — atrial (PACs), junctional (PJCs) or ventricular (PVCs).

426
Q

What is the rate of a normal sinus rhythm?

A

60-100 beats per minute

427
Q

What is the rate of sinus bradycardia?

A

< 60 beats per minute

428
Q

What is the rate of sinus tachycardia?

A

> 100 beats per minute

429
Q

What happens to electrical conduction in atrial fibrillation?

A
  • Multiple atrial foci (supraventricular escape rhythm)
  • Impulses are random and chaotic
  • Atria quiver rather than contract
  • Impulses arrive at AV node at rapid irregular rate
  • Only some conducted to ventricles at irregular intervals when the AV node is not refractory
  • Ventricles depolarise and contract normally
430
Q

How does atrial fibrillation present on an ECG?

A
  • Absence of isolectric baseline (Wavy baseline)
  • No p waves
  • Irregular R-R intervals
  • QRS complex normal (narrow)
  • Irregularly irregular rhythm
431
Q

What are the physiological consequences of atrial fibrillation?

A

• CO maintained in most cases as atrial contraction only accounts for 10% of filling in diastole
• Blood remains stagnant in the appendage of the atria
• Clots form in the atria
◦ Left atria- embolism in peripheral arteries eg. cerebral arteries —> stroke
◦ Right atria- embolism in the pulmonary artery

432
Q

What is heart block?

A

Heart block = AV conduction block

Delay or failure of conduction of impulses from the atria to the ventricles via the AV node and Bundle of His

433
Q

What is an escape rhythm?

A

When an alternative pacemaker takes over the role of the SAN in initiating the heart beat.

434
Q

What can cause heart block?

A
  • most commonly, acute MI

- degenerative changes

435
Q

In which type of heart block are ventricular escape rhythms involved?

A

Complete heart block/third degree heart block

436
Q

What happens in first degree heart block and how is it presented on an ECG?

A

What happens?
• Delay at AV node and Bundle of His

Presentation on ECG?
• P wave normal
• PR interval prolonged > 5 small squares (0.2 seconds)
• QRS normal

437
Q

What is Mobitz type 1/Wenkebach phenomenon second degree heart block and how does it present on an ECG?

A

What happens?
-Delay at AV node and one beat is not transmitted to allow the AVN to repolarise

Presentation on ECG?

  • progressive lengthening of PR interval > 5 small squares
  • until one P is not conduced
  • cycle begins again
438
Q

What causes mobitz type 1/wenkebach phenomenon second degree heart block?

A

Ischaemic damage

439
Q

What happens in mobitz type 2 second degree heart block and how does it present on an ECG?

A

What happens?
-AV node fails to conduct heart beat with no warning

Presentation on ECG?

  • PR interval normal (3-5 small squares)
  • sudden absent QRS complex
440
Q

Does mobitz type 1 or mobitz type 2 second degree heart block have a high risk of progression to complete heart block?

A

Mobitz type 2

441
Q

What happens in third degree heart block/complete heart block and how is this presented on an ECG?

A

What happens?
• Atrial depolarisation is normal
• Impulses are not conducted to ventricles at all
• Ventricular pacemaker (slower to depolarise) takes over (ventricular escape rhythm)
• Heart rate is often too slow to maintain blood pressure and perfusion

Presentation on ECG?
• P waves present
• P-P intervals constant (about 93 bpm)
• R-R intervals constant and much slower (about 37 bpm)
• P-R intervals variable from beat to beat- P waves have no relationship with QRS complex
• Wide QRS complexes
• Very slow rate (30-40 beats per minute)

442
Q

Both atrial fibrillation and ventricular fibrillation result in a significant loss of cardiac output.

True or false.

A

False

Atrial fibrillation doesn’t usually result in a significant loss of cardiac output as atrial contraction only accounts for the final 10% of filling of the ventricles.

443
Q

What happens to form a ventricular ectopic beat and what are the consequences of this on depolarisation of the ventricles?

A
  • Ectopic focus in ventricle muscle which randomly produces a beat (this is not a ventricular escape rhythm which would occur after a pause and is regular- it is ONE random beat initiated in the ventricles in between normal beats which are conducted by the SAN which occurs as cells in the ventricle have been able to depolarise before conduction of depolarisation from the SAN- usually due to ischaemia)
  • Impulse not spread via fast His-purkinje system
  • Slower depolarisation of ventricle
444
Q

How does a ventricular ectopic beat present on an ECG?

A

Wide QRS complex (> 3 small boxes) in the middle of sinus rhythm
QRS complex different in shape to usual QRS

445
Q

What is the difference between an ectopic beat and an escape rhythm?

A

An ectopic beat is one random beat initiated somewhere other than the SAN in between normal beats conducted by the SAN

An escape rhythm occurs after a pause and is regular

446
Q

What are the consequences of ventricular ectopic beats?

A

Usually asymptomatic and normal

447
Q

What happens in ventricular tachycardia and how does it present on an ECG?

A

What happens?
• Run of 3 or more ventricular ectopics
• It is a broad complex tachycardia

Presentation on ECG?
• Run of 3 or more abnormally shaped, wide QRS complexes

448
Q

What are the consequences of ventricular tachycardia?

A
  • Persistent ventricular tachycardia is a dangerous rhythm that requires urgent treatment
  • High risk of ventricular fibrillation
449
Q

How is ventricular tachycardia treated?

A

Use defibrillator to depolarise all of the heart muscle cells and put them into a refractory period so that the SAN depolarises first and a sinus rhythm is established

450
Q

What is ventricular fibrillation and how does it present on an ECG?

A

What happens?
• Abnormal, chaotic, fast ventricular depolarisation
• Impulses from numerous ectopic sites in ventricular muscle
• No co-ordinated contraction
• Ventricles quiver
• No cardiac output

Presentation on ECG?

  • no recognisable QRS complexes
  • no heart beat/pulse
451
Q

What are the consequences of ventricular fibrillation?

A

Cardiac arrest

452
Q

How is ventricular fibrillation treated?

A

Use defibrillator to depolarise all of the heart muscle cells and put them into a refractory period so that the SAN depolarises first and a sinus rhythm is established

CPR

453
Q

Why can people live a normal life with atrial fibrillation but ventricular fibrillation causes cardiac arrest?

A

Atrial depolarisation is where impulses are conducted irregularly to ventricles.

  • ventricular depolarisation occurs
  • coordinated ventricular contraction occurs
  • cardiac output is present
  • pulse and heart rate is irregularly irregular

Ventricular fibrillation is where ventricular depolarisation is chaotic

  • no coordinated ventricular contraction
  • no cardiac output
  • no pulse or heart beat
  • require CPR and immediate defibrillation to restore rhythm
454
Q

In what condition is the pulse and heart rate irregularly irregular?

A

Atrial fibrillation

455
Q

What causes myocardial ischaemia and which part of the muscle is most vulnerable to ischaemia?

A

-reduced perfusion of myocardium due to coronary atherosclerosis
-major coronary arteries lie on epicardial surface so subendocardial muscle is furthest away and most vulnerable to ischaemia
• Flow is during diastole- if diastole is short (rapid heart rate), there is less time for flow when arteries are narrowed (atherosclerosis)
• Does not affect all parts of the heart
• Changes may only be seen during exercise (STABLE ANGINA) . If severe reduction of lumen size, there are ischaemic changes at rest (UNSTABLE ANGINA)

456
Q

How does myocardial ischaemia (NSTEMI) present on an ECG?

A

• Changes seen in leads facing affected area
• Need to look at P-QRST in all 12 leads
• Ischaemia of subendocardial region—>
◦ leads facing affected area show ST segment depression
◦ T wave inversion - due to abnormal current during depolarisation

457
Q

What causes a myocardial infarction?

A
  • Complete occlusion of lumen by thrombus
  • Muscle injury extends full thickness from endocardium to epicardium
  • If perfusion is not re-established, muscle necrosis will follow which can be detected using blood tests
458
Q

How does a myocardial infarction (STEMI) present on an ECG?

A

• Changes shown on leads facing affected area
• Need to look at P-QRST for all 12 leads
• Ischameia of full thickness from endocardium to epicardium—>
◦ Leads in affected area show ST segment elevation - abnormal repolarisation

459
Q

How does a previous myocardial infarction present on an ECG?

A

Pathological large Q wave
> 1 small square wide
> 2 small squares deep
Depth more than a quarter of the height of the subsequent R wave

460
Q

Pathological Q waves on an ECG
(>1 small square wide)
(>2 small squares deep)

Indicate…

A

A previous myocardial infarction

461
Q

ST depression and T wave inversion on an ECG indicate…

A

Ischaemia of subendocardial region

NSTEMI

462
Q

ST elevation indicates…

A

Ischaemia of full thickness from endocardium to epicardium

STEMI

463
Q

What is hyperkalaemia?

A

plasma potassium >5.5mmol/L

464
Q

What are the effects of hyperkalaemia on action potentials in cardiomyocytes?

A

> 5.5 mmol/L plasma potassium
More K+ in extracellular environment than usual
Ek is less negative
Resting membrane potential is less negative
Cardiomyocyte action potential:
-is narrower
-slower upstroke - Na+ channels are inactivated
Heart is less excitable as hyperkalaemia worsens
Conduction problems

465
Q

How does hyperkalaemia present on an ECG?

A

7mmol/L - high T wave
8 mmol/L - prolonged PR interval, depressed ST segment, high T wave
9mmol/L - P wave absent, AV block
10mmol/L - ventricular fibrillation

466
Q

What is hypokalaemia?

A

< 3.5 mmol/L

467
Q

What is the effect of hypokalaemia on action potentials in cardiomyocytes?

A

Less K+ in extracellular environment than usual
Ek is more negative than usual
Resting membrane potential is more negative
Effect on action potentials in cardiomyocytes:
-downstroke slower - allosteric effect of K+ channels so K+ enters more slowly
-wider action potential
-early after depolarisations - some cells repolarise more quickly than others
Early after depolarisations can lead to ventricular fibrillation

468
Q

How does hypokalaemia present on an ECG?

A
3.5mmol/L = low T wave 
3mmol/L = low T wave, high U wave 
2.5mmol/L = low T wave, high U wave, low ST segment
469
Q

What is the difference between the P-R interval and the P-R segment?

A

P-R interval
Start of P wave to beginning of Q wave

P-R segment
End of P wave to beginning of Q wave

470
Q

What is a left cardiac axis deviation?

A

The overall direction of ventricular depolarisation is upward and to the left.(

471
Q

When do you get left cardiac axis deviation? (3)

A
  1. Conduction block of the anterior branch of the left bundle
  2. Inferior MI (left anterior descending artery affected)
  3. Left ventricular hypertrophy
472
Q

What is a right axis cardiac axis deviation?

A

When the overall direction of ventricular depolarisation is downwards and to the right (>+90degrees)

473
Q

When do you get right cardiac acids deviation?

A
  1. Right ventricular hypertrophy

2. RHS MI (right anterior descending artery affected)

474
Q

How does left axis deviation present on an ECG?

A

Look at leads I, III, aVF

If QRS is positive in lead I and negative in aVF, it is left axis deviation
Lead I and Lead aVF are leaving each other (start with lead I)

475
Q

How does right axis deviation present on an ECG?

A

Look at QRS in leads I, III, aVF

QRS in lead I is negative and positive in lead III or aVF
Lead I and aVF are reaching for each other (start with lead I)

476
Q

If someone has a normal cardiac axis (-30 degrees to +90 degrees), how would leads I and and aVF appear?

A

QRS complexes positive in both

477
Q

Lead I is positive. Lead aVF is negative.

What does this show?

A

Left cardiac axis deviation

478
Q

Lead I is negative. Lead aVF is positive.

What does this show?

A

Right cardiac axis deviation

479
Q

Patient is experiencing pain slightly to the left hand side of their chest which is worse when coughing and breathing

Other symptoms:

  • cough with mucus
  • breathlessness
  • feeling generally unwell
  • high temperature

Diagnosis?

A

Respiratory problem.

Probably…

Pneumonia
(Inflammation of the tissue in one or both of the lungs usually caused by bacterial infection)

480
Q

Patient has sudden well localised sharp pain in their chest which is worse when breathing or coughing.

Other symptoms:

  • sudden shortness of breath
  • feeling light headed
  • pain, redness and swelling in right calf
  • coughing

Diagnosis?

A

Pulmonary embolism
(DVT has broken off, entered the right atrium and lodged in the pulmonary artery causing a blockage in the pulmonary circulation)

481
Q

Patient has poorly localised, retrosternal, central chest pain which radiates to the jaw, neck and shoulders.
The quality of the pain is dull, feels like a ‘heaviness’ in the chest.
This pain is aggravated by exertion.

Diagnosis?

A

Ischaemic damage to the heart

Lack of blood supply to the heart secondary to ischaemic heart disease

482
Q

Patient has retrosternal, central chest pain localised to the front of the chest.
The quality of the pain is sharp.
The pain is worse when lying flat, when breathing and coughing.
It is relieved when sitting up and leaning forward.

Diagnosis?

A

Pericarditis
Inflammation of pericardial sac often secondary to a viral illness

Pericardial rub may be heard on auscultation

483
Q

What does saddle-shaped ST elevation on an ECG indicate?

A

Pericarditis

484
Q

Patient has a sharp pain their chest which radiates to their back.

What condition is this a typical presentation of?

A

Aortic dissection
Tear in the wall of the aorta so blood flows in between the layers of the blood vessel leading to aortic rupture and decreased blood flow to organs

485
Q

Patient has a burning, central chest pain which feels as though it is running up the chest.
It is worse when lying flat and after eating certain foods.

Which condition is this a typical presentation of?

A

Acid reflux from stomach into oesophagus

486
Q

Patient has sharp, well localised chest pain on one side of their chest.
This area is tender to palpate. It is worse during inspiration and when coughing.

What condition is this a typical presentation of?

A

Rib fracture or costochondritis

487
Q

What is the difference between pleural/pericardial pain and ischaemic chest pain?

A

Pleural/pericardial pain is somatic.
-there are sensory impulses through somatic spinal nerves
Pleura - intercostal and phrenic nerves
Pericardial - phrenic nerves
-It is well localised and sharp
-it is aggravated by movement of the chest wall (inspiration and coughing)

Ischaemic chest pain is visceral.

  • there are sensory impulses through autonomic nerves with pain in organs
  • it is poorly localised and dull
  • it is aggravated by exertion
488
Q

Describe the pathophysiology of ischaemic heart disease.

A
  • Begins with atherosclerosis
  • Build up of fat in the walls of the arteries over time.
  • Coronary arteries are small so does not take long for this fatty deposit to narrow the lumen.
  • Fibrous cap forms on top of this fatty deposit
  • This fibrous cap can rupture
489
Q

What are the risk factors for ischaemic heart disease?

A
Modifiable risk factors:
• Smoking
• Hypertension
• Hypercholesterolaemia
• Diabetes
• Obesity
• Sedentary lifestyle

Non-modifiable risk factors:
• Advanced age
• Family history
• Male

490
Q

What is stable angina?

A

Pathophysiology?
Fixed narrowing of coronary artery due to atherosclerosis.

What?
Heart tissue ischaemia only when metabolic demands of cardiac muscle are greater than what can be delivered via coronary arteries.

491
Q

Patient has retrosternal, central chest pain.
Quality is dull.
Worse with exertion.
Relieved by rest.
Patient does not look particularly unwell and clinical examination is normal.

What is this a typical presentation of?

A

Stable angina

Fixed narrowing of coronary artery due to atherosclerosis. Heart tissue ischaemia only when metabolic demands of cardiac muscle are greater than what can be delivered by coronary arteries.

492
Q

How is stable angina treated?

A

GTN spray - relieves pain

493
Q

What is unstable angina?

A

Pathophysiology
Narrowing of coronary artery due to atherosclerosis.

What?
Heart tissue ischaemia at rest as usual metabolic demands cannot be delivered by coronary arteries.

494
Q

Patient has retrosternal, central chest pain.
Quality is dull
Pain occurs at rest
It is worse with exertion. Patient has noticed an acute deterioration in what causes it to come on, previously mild exercise did not cause chest pain but now it does.

On clinical examination, patient appears sweaty, anxious and pale.

What is this a typical presentation of and what are the implications of this?

A

Unstable angina

Risk of deteriorating further —> NSTEMI/STEMI
Heart may fail and CO may be compromised

495
Q

How is unstable angina managed?

A

GTN spray does not relieve pain

Patient admitted to hospital for surgical intervention

496
Q

Patient has dull, severe retrosternal central chest pain.
Pain occurs at rest and persists for longer than 15 mins.
It is worse with exertion. Patient has noticed acute deterioration in what causes it to come on. Previously, mild exercise did not cause chest pain but now it does.
Nothing makes it better.
Patient appears generally unwell and there is noticeable increased sympathetic output - sweaty, pallor, nauseous.

What is this a typical presentation of?

A

Myocardial infarction

497
Q

What are acute coronary syndromes?

A

Acute myocardial ischaemia caused by atherosclerotic coronary artery disease.
Atheromatous plaques rupture with thrombus formation causing an acute increased occlusion in an already partially occluded lumen leading to ischaemia.
It is a spectrum of increasing occlusion from a common pathophysiological mechanism.

498
Q

Which of these does an acute coronary syndrome include?

  • stable angina
  • unstable angina
  • NSTEMI
  • STEMI
A

All except stable angina

499
Q

Describe the investigations for MI.

A

ECG
-look at ST segments, T waves, pathological Q waves

Blood tests
-troponin - indicates cardiac myocyte death (NSTEMI/STEMI)

500
Q

An ECG shows
ST segment elevation and hyperacute T waves.
What does this indicate?

A

STEMI has occurred minutes-hours ago

501
Q

An ECG shows ST elevation and T wave inversion. What does this indicate?

A

STEMI has occurred hours-1 day ago

502
Q

How would unstable angina and a NSTEMI present on an ECG.

How would you determine whether the diagnosis is unstable angina or NSTEMI?

A

Presentation on ECG?
• ST segment depression
• T wave flattening or inversion

Check troponin
• NSTEMI = positive because there is cardiomyocyte death
• STEMI = negative because there is no cardiomyocyte death

503
Q

What is heart failure?

A

Heart failure is a state ‘in which the heart fails to maintain an adequate circulation for the needs of the body despite an adequate filling pressure’.

In heart failure the heart can no longer produce the same amount of force (or cardiac output) for a given level of filling

504
Q

What are the causes of heart failure?

A

It is often the final and most severe manifestation of nearly every form of cardiac disease
• Ischaemic heart disease (coronary artery disease) is the primary cause
• Hypertension
• Non-ischaemic dilated cardiomyopathy
◦ Infectious- viral, bacterial, myobacterium
◦ Alcohol/drugs/poisoning
◦ Pregnancy
◦ Idiopathic
• Valvular heart disease/congenital
• Restrictive cardiomyopathy eg. Amyloidosis
• Hypertrophic cardiomyopathy
• Pericardial disease
• High-output heart failure - heart cannot keep up with CO required
• Arrhythmia

505
Q

What is arrhythmia?

A

Heart beat is irregular, too fast or too slow.

506
Q

How can we increase cardiac output?

A
  1. Increase preload (venous capacity). Increase end diastolic volume to increase stroke volume.
  2. Decrease afterload (aortic and peripheral impedance. Decrease end stroke volume to increase stroke volume.
  3. Increase contractility. Decrease end stroke volume to increase stroke volume.
  4. Increase heart rate
507
Q

How can preload be changed to increase cardiac output?

A
Increase preload (venous capacity). Increase EDV. Increase stroke volume.
The force developed in the myocardium depends on the degree to which the fibres are stretched (or the heart is filled). Within a physiological range, the greater the venous pressure, the larger the ventricular volume during diastole, the more the fibres are stretched before stimulation and the greater the force of the next contraction. (Frank-Starling Law)

PROOF
Muscle is passively stretched and then stimulated to contract while its ends are held at fixed positions (isometric contraction). The total tension, generated by the fibres is proportional to the length of the muscle at the time of stimulation as stretching causes there to be greater overlap between actin and myosin.

508
Q

How can afterload be changed to increase cardiac output?

A
Decrease afterload (aortic and peripheral impedance) . Decrease ESV. Increase stroke volume.
The pressure generated by the ventricle and the size of the chamber at the end of each contraction depends on the load against which the ventricle contracts but is independent to the stretch on the myocardial fibres before contraction. 

PROOF
Fibres are allowed to shorten during stimulation against a fixed load (isotonic contraction). The final length of the muscle at the end of contraction is determined by the magnitude of the load and is independent of the length of the muscle before stimulation.

509
Q

How can contractility be changed to increase stroke volume?

A

Increase contractility. Decrease ESV. Increase stroke volume.
Contractility reflects chemical and hormonal influences on cardiac contraction.
The sympathetic nervous system affects contractility by the release of adrenaline/noradrenaline
Increased contractility increases the cycling rate of actin-myosin cross bridge formation.

PROOF
When contractility is enhanced, the relationship between initial fibre length and force is shifted upwards so that a greater total tension develops with isometric contraction at any given preload.
When contractility is enhanced, the fibre contracts to a greater extent and achieves a shorter final fibre length with isotonic contraction at any given afterload.

510
Q

What is normal CO, SV, ESV, EDV and hence ejection fraction?

A
CO = 5 litres/min
SV = 75ml
LV end systolic volume = 75ml
LV end diastolic volume = 150ml
Ejection fraction = 50% +
511
Q

What is the difference between systolic dysfunction and diastolic dysfunction?

A
Diastolic dysfunction (decreased EDV)- preserved ejection fraction 
1. Impaired ventricular relaxation and filling

Systolic dysfunction (increased ESV)- reduced ejection fraction

  1. Increased afterload
  2. Impaired ventricular contractility

Many patients demonstrate both systolic and diastolic abnormalities.

512
Q

What are the causes of systolic dysfunction due to increased afterload?

A
  1. Advanced aortic stenosis
  2. Uncontrolled severe hypertension

This chronic pressure overload causes an increased resistance to flow.

513
Q

What are the causes of systolic dysfunction due to impaired contractility?

A
  1. Coronary artery disease (MI, transient myocardial ischaemia)
  2. Chronic volume overload (mitral regurgitation, aortic regurgitation)
  3. Dilated cardiomyopathies

These cause destruction of myocytes, abnormal myocyte function or even fibrosis resulting in reduced ability of the myocytes to contract.

514
Q

What are the common causes of diastolic dysfunction?

A

Impaired diastolic filling:

  1. Left ventricular hypertrophy
  2. Restrictive cardiomyopathy
  3. Myocardial fibrosis
  4. Transient myocardial ischaemia
  5. Cardiac tamponade

These either impair early diastolic relaxation which is energy dependent or increase the stiffness of the ventricular wall.

515
Q

How is a change in contractility change the Starling curve?

A

A decrease in contractility is seen as a shallower slope on the frank starling curve.

516
Q

What happens in systolic heart failure?

A

End diastolic volume increases. Stroke volume decreases.

Normal venous return is added to the increased end systolic volume that has remained in the ventricle due to incomplete emptying.
End diastolic volume increases above normal
End systolic volume remains elevated.
Reduced ejection fraction

There is a compensatory rise in stroke volume to remain cardiac output
End diastolic volume increases further and there is a high end diastolic pressure. During diastole, pressure is transmitted to the atrium through the open mitral valve/tricuspid valve to
Pulmonary veins and capillaries from the left ventricle —> pulmonary oedema
Systemic veins and capillaries from right ventricle —> systemic oedema

To cope with the increased volume, hypertrophy of the ventricle occurs. Eccentric hypertrophy - synthesis of new sarcomeres in series with the old causing the myocytes to elongate. The radius of the ventricular wall enlarges proportional to the increase in wall thickness.

517
Q

What happens as a consequence of left ventricular systolic function?

A
  • High end diastolic volume —> increased LV capacity (capacity>150ml)
  • Reduced end systolic volume and reduced ejection fraction—> Reduced cardiac output (compensatory mechanism to increase CO by increasing end diastolic volume is not sufficient)
518
Q

How is the capacity of the left ventricle increased as in left ventricular systolic dysfunction?

A

Dilation of the left ventricle via thinning of the myocardial wall
◦ Fibrosis and necrosis of myocardium
◦ Activity of matrix proteinases

519
Q

What is the significance of thinning of the myocardial wall and dilation of the left ventricle in left ventricular systolic dysfunction?

A
  • Further loss of muscle—> loss of contractility
  • Conductive tissue may affected —> uncoordinated or abnormal myocardial contraction —> cardiac arrhythmias

• Changes to the extracellular matrix
Increase in collagen (I, III) from 5% to 25%
Slippage of myocardial fibre orientation

• Changes of cellular structure and function
◦ Myocytolysis and vacuolation of cells
◦ Myocyte hypertrophy
◦ Sarcoplasmic reticulum dysfunction
◦ Changes to calcium availability and receptor regulation

  • Mitral valve incompetence
  • Greater exposure to neuro-hormonal activation
520
Q

What happens in diastolic heart failure?

A

In diastole, filling of the ventricle is dependent on higher than normal pressures.
Pressure transmitted to the atrium through open mitral/tricuspid valves to
Pulmonary veins and capillaries capillaries from left ventricle —> pulmonary oedema
Systemic veins and capillaries from right ventricle —> systemic oedema

To cope with the increased pressure, the myocardium hypertrophies. Concentric hypertrophy - synthesis of new sarcomeres in parallel with the old so the wall thickness increases without proportional chamber dilatation.

521
Q

Who tends to get diastolic heart failure?

A

Elderly and female

Often history of hypertension/diabetes/obesity

522
Q

Which side of the heart does diastolic heart failure tend to affect?

A

Left ventricle as it is this ventricle that is under higher pressure so more likely to be less compliant due to left ventricle hypertrophy, myocardial fibrosis, transient myocardial ischaemia etc.

Left ventricle filling becomes dependent on high left atrial pressure.

Right ventricle systolic dysfunction can result from high left atrial and pulmonary artery pressure

523
Q

Right sided heart failure rarely occurs on its own.

A

True

524
Q

What are the symptoms of left sided heart failure?

A

• Dyspnea = breathlessness on exertion
due to pulmonary venous congestion and decreased cardiac output
• Dulled mental status
reduced cerebral perfusion
• Impaired urine output
decreased renal perfusion
• Orthopnea = laboured breathing while lying flat relieved by sitting upright (how many pillows do you use when you sleep?)
redistribution of intramuscular blood from lower portions of the body to the lungs after lying down
• Paroxysmal nocturnal dyspnoea = severe breathlessness that awakens the patient from sleep
gradual resorption into the circulation of lower extremity interstitial oedema after lying down with expansion of intravascular volume and increased venous return to heart and lungs
• Lethargy
decreased cardiac output

525
Q

What would a typical clinical examination of a patient with left sided heart failure show?

A

• Tachycardia
increased sympathetic nervous system activity
• Basal pulmonary crackles
popping open of small airways during inspiration that had been closed off by oedema fluid
• S3 or S4
S3= in adults with systolic heart failure caused by abnormal filling of the dilated chamber
S4= late diastolic sound from forceful atrial contraction into a stiffened ventricle common where there is increased LV compliance in diastolic dysfunction

526
Q

In what kind of heart failure is S3 and S4 heard? Why?

A
S3= in adults with systolic heart failure caused by abnormal filling of the dilated chamber 
S4= late diastolic sound from forceful atrial contraction into a stiffened ventricle common where there is increased LV compliance in diastolic dysfunction
527
Q

Why is the right ventricle able to accept a wider range of filling volumes without marked changes in its filling pressure than the left ventricle?

A

It is a thin-walled highly compliant chamber that accepts blood at low pressures and ejects against a low pulmonary vascular resistance.

528
Q

Why is the right ventricle more susceptible to failure when there is a sudden increase in afterload compared to the left ventricle? Give an example of when this happens.

A

Acute pulmonary embolism

It has a thin wall that’s relatively less muscular.

529
Q

The most common cause of right-sided heart failure is the present of left-sided heart failure. Why?

A

Left sided heart failure increases pulmonary vascular pressure.
This increases afterload for the right ventricle.
Leads to right sided systolic heart failure.

530
Q

Isolated right heart failure is less common. When might this occur?

A

Diseases of the lung parenchyma or pulmonary vasculature.

531
Q

What are the symptoms and signs of right sided heart failure?

A

Relate to distension and fluid accumulation in areas drained by the systemic veins:

  • fatigue, dyspnoea, anorexia, nausea
  • increased jugular vein pressure
  • tender, smooth hepatic enlargement
  • dependent pitting oedema
  • ascites
  • pleural effusion
532
Q

What compensatory mechanisms are present in patients with hear failure to buffer the fall in cardiac output and help preserve blood pressure to perfuse vital organs?

A

Long term control of blood pressure is via neurohormonal alterations:

  1. Sympathetic nervous system
  2. Renin-angiotensin-aldosterone system
  3. Increased production of ADH
  4. ANP

However, these have the effect of making an already struggling heart work harder.

533
Q

What are the effects of arteriolarconstriction on TPR and CO?

A

Increases TPR but decreases CO

BP = TPR x CO

534
Q

What are the long-term deleterious effects of the sympathetic nervous system in a patient with heart failure?

A

Chronic sympathetic release of noradrenaline causes:
• down-regulation of cardiac β-adrenergic receptors and up-regulation of inhibitory G proteins, contributing to a decrease in the myocardium’s sensitivity to circulating catecholamines and a reduced inotropic response
• Induces cardiac hypertrophy myocyte apoptosis and necrosis
• Stimulates RAAS
• Reduction in heart rate variability—> increased risk of cardiac arrhythmias

535
Q

What are the long-term deleterious effects of angiotensin II and aldosterone?

A

Chronically elevated levels of AII and aldosterone have additional detrimental effects. They provoke the production of cytokines (small proteins that mediate cell–cell communication and immune responses), activate macrophages, and stimulate fibroblasts, resulting in fibrosis and adverse remodeling of the failing heart.

536
Q

Describe what endothelin is and how it changes in heart failure.

A

Secreted by vascular endothelial cells.
Causes local vasoconstriction
There are increased levels in patients with heart failure so is used as a prognostic sign as it correlates with indices of severity.

537
Q

Describe how natriuretic peptide release is affected in heart failure. Why is it beneficial?

A

Elevated ANP/BNP demonstrates there is a high level of stretching of the heart. This is caused by increased stroke volume which occurs in systolic heart failure. Therefore, ANP/BNP can be used to diagnose heart failure along with other factors.

538
Q

How do prostaglandins E2 and I1 change in patients with heart failure?

A

They increase in concentration as their production is stimulated by noradrenaline and RAAS
They act as vasodilator on the afferent renal arterioles to attenuate effects of noradrenaline and RAAS
Taking NSAIDS blocks synthesis of these and reduces vasodilation.

539
Q

How does nitric oxide change in heart failure?

A

It is a potent vasodilator produced by endothelial cells via NO synthase.
In heart failure, NO synthase may be blunted
There is a loss of vasodilation balance

540
Q

What does bradykinin do to decrease blood pressure?

A

Promotes natriuresis
Vasodilation
Stimulates production of prostaglandins

541
Q

How does tumour necrosis factor (alpha-TNF) change in heart failure?

A

Increased in heart failure

It depresses myocardial function and has a role in cachexia

542
Q

How is there increased vasoconstriction in patients with heart failure?

A
  • Increased sympathetic output
  • RAAS
  • Reduced NO
  • Increased endothelin
543
Q

What does increased vasoconstriction lead to in patients with heart failure?

A
  • reduction of skeletal muscle mass
  • renal failure
  • anaemia
544
Q

What is the consequence of increasing arteriolar blood pressure in patients with heart failure?

A

Afterload increases and this decreases stroke volume decreasing cardiac output further.

545
Q

How can increasing heart rate further reduce the performance of the failing heart?

A

It increases the metabolic demand of the heart

546
Q

Give an equation that links

Osmotic pressure
Hydrostatic pressure
Net filtration pressure

A

Net filtration pressure = hydrostatic pressure - osmotic pressure

547
Q

Is peripheral oedema a sign of right or left sided heart failure?

A

Peripheral oedema occurs due to right-sided heart failure.

Failure of the right side of the heart to pump effectively raises venous pressure and therefore capillary pressure.

An increased capillary hydrostatic pressure favours the movement of water out of the capillaries.

548
Q

Is pulmonary oedema a sign of right or left sided heart failure?

A

Pulmonary oedema occurs due to left sided heart failure

Failure of the left side of the heart to pump effectively raises left atrial pressure and thus the pressure of vessels in the pulmonary system.

Since these vessels have a low resistance this also causes an increase in pulmonary artery pressure.

Presentation:
-breathless

549
Q

Why would diuretics be used to treat left sided heart failure?

A

Diuretics
• Promote elimination of Na+ and water through the kidney
• Reduce intravascular volume
• Reduce venous return to heart
• Reduced end-diastolic volume without a significant decrease in SV. Preload is decreased
• Diastolic pressure of left ventricle falls out of the range that causes pulmonary congestion

Limitations
Only used where there is peripheral oedema or pulmonary congestion due to the risk of decreasing stroke volume too much that cardiac output will be compromised (especially in a patient operating on the steep portion of the frank-starling curve- best used when on flat portion where it is moved towards the steep portion)

550
Q

Why are venous vasodilators used to treat right sided heart failure?

A

—>Venous vasodilators - nitrates
• Increase venous capacitance
• Decrease venous return to the heart
• Decrease end-diastolic volume and decrease preload
• Diastolic pressure of left ventricle falls out of the range that causes pulmonary congestion

Limitations
Only used where there is peripheral oedema or pulmonary congestion due to the risk of decreasing stroke volume too much that cardiac output will be compromised (especially in a patient operating on the steep portion of the frank-starling curve- best used when on flat portion where it is moved towards the steep portion)

551
Q

What are the main categories of drugs used in the treatment and management of heart failure?

A

Diuretics

Vasodilators

Inotropic drugs

Beta blockers

Aldosterone antagonist therapy

552
Q

What are the types of tachycardic arrhythmia?

A
  • ectopic pacemaker activity
  • afterdepolarisations
  • atrial flutter/atrial fibrillation
  • re-entry loop
553
Q

What are the types of bradycardic arrhythmia?

A
  • sinus bradycardia (sick sinus syndrome, extrinsic factors such as drugs)
  • conduction block (problems at AV node or bundle of His, extrinsic factors such as drugs)
554
Q

What is sick sinus syndrome?

A

Malfunction of the sinus node
Normally, the sinus node produces a regular, steady pattern of signals.
With sick sinus syndrome, the pattern is irregular - they may have a heart rhythm that is too low or too fast

Typically occurs in elderly people

555
Q

What is ventricular tachycardia?

A

Tachycardia which originates from the Bundle of His, purkinje fibres or ventricular myocytes (ectopic pacemaker activity, afterdepolarisations)

556
Q

What is supraventricular tachycardia?

A

Tachycardia which arises from the atria or AV node (atrial fibrillation/atrial flutter, re-entry loop)

557
Q

Why is ventricular tachycardia dangerous?

A

Can lead to ventricular fibrillation

Cardiac output cannot be maintained in ventricular fibrillation and this is a life-threatening situation which must be reversed.

558
Q

What arrhythmia can arise due to a damaged ischaemic area of myocardium?

A

Ectopic pacemaker activity is activated in damaged area of ischaemic myocardium as it becomes constantly depolarised and spontaneously active. This dominates over the SA node.

559
Q

How can arrhythmias be caused by premature firing of action potentials?

A

After depolarisations (triggered activity) following an action potential

560
Q

What are delayed after-depolarisations and when do they occur?

A

There should be approximately a 700ms pause between one action potential and another in a cardiomyocyte.

In delayed, after-depolarisations there are delayed after-depolarisations before this 700ms pause.

This is likely to happen when intracellular Ca2+ is high. Eg. Drugs such as cardiac glycosides

561
Q

The duration of an action potential is measured by what interval on an ECG?

A

Q-T

562
Q

What are early after-depolarisations and when are they likely to occur?

A

Early after-depolarisations occur during the plateau phase of the ventricular action potential

They are more likely to happen if the action potential is prolonged (longer QT interval) eg. Hypokalaemia, certain drugs

563
Q

What causes a re-entry loop?

A

Incomplete conduction damage (unidirectional block)

Excitation can take a long route to spread the wrong way through the damaged area setting up a circus of excitation

564
Q

What causes atrial flutter or atrial fibrillation?

A

Conditions which put extra stretch or pressure on the atria eg. Mitral stenosis

565
Q

What is the difference between atrial flutter and atrial fibrillation?

A

Atrial flutter - regularly irregular rhythm (sawtooth pattern)

Atrial fibrillation - irregularly irregular rhythm (wavy baseline)

566
Q

Several small re-entry loops in the atria leads to…

A

Atrial fibrillation

567
Q

What is AV nodal re-entry?

A

Fast and slow pathways in the AV node create a re-entry loop.

568
Q

What is Wolff-Parkinson-White syndrome?

A

An accessory pathway between the atria and ventricles creates a fixed re-entry loop

569
Q

What are the four classes of anti-arrhythmic drugs?

A
  1. Na+ channel blockers
  2. Beta-adrenoreceptor antagonists
  3. K+ channel blockers
  4. Ca2+ channel blockers
570
Q

Describe how lidocaine works?

A

Class 1 - blocks voltage gated Na+ channels

Damaged area of myocardium has sustained depolarisation and more Na+ channels open.

Lidocaine binds to Na+ channels in open or inactive state during the phases of the refractory period of the action potential when Na+ channels should be inactive or closed. It is use-dependent (the degree of block is proportional to the rate of nerve stimulation) so preferentially blocks damaged depolarised tissue

It dissociates rapidly so has little effect in normal cardiac tissue.
It blocks depolarisation but dissociates in time for the next action potential.

571
Q

When is lidocaine used?

A

Sometimes used following MI because damaged areas of myocardium may be depolarised and fire automatically (risk of ectopics leading to VF)

Because…

More Na+ channels are open in depolarised damaged tissue. Lidocaine blocks these Na+ channels that are in open or inactive form and is use-dependent.

BUT not used prophylactically following MI, people showing ventricular tachycardia generally use other drugs.

572
Q

Local anaesthetics are use-dependent. What does this mean?

A

The degree of block is proportional to the rate of nerve stimulation.

573
Q

Propranolol and atenolol are examples of…

A

Beta adrenoreceptor antagonists

574
Q

How do beta-adrenoreceptor antagonists work and how do they affect the heart?

A

Block sympathetic action by acting on beta adrenoreceptors on the heart

  • decrease slope of pacemaker potential in SA node - decreases heart rate
  • slow conduction in AV node - prevents supraventricular tachycardias and slows ventricular rate in patients with atrial fibrillation
  • reduces inotropy - reduces oxygen demand and hence reduces myocardial ischaemia which is beneficial for patients following an MI
575
Q

Why are beta blockers used following a myocardial infarction?

A

A myocardial infarction can cause increased sympathetic input to the heart to maintain cardiac output

Beta blockers decrease this sympathetic input to the heart, reducing heart rate to prevent ventricular arrhythmias from arising due to this increased sympathetic activity.

Beta blockers reduce heart rate and the force of contraction which reduces the workload and hence the oxygen demand of the heart. This reduces the chance of further myocardial ischaemia.

576
Q

How do drugs that block K+ channels work and why can they be pro-arrhythmic?

A

Prolongs action potential by blocking K+ channels so prevents repolarisation.

This lengthens the absolute refractory period (time during which Na+ channels are in inactive state)

In theory, it was thought this should prevent another action potential from occurring too soon.

However, it causes early after depolarisations which can lead to arrthymias.

577
Q

K+ channel blockers are not generally used because they can be pro-arrhythmic. Amiodarone is an exception. Why?

A

K+ channel blockers are not usually used because they prolong the action potential and increase the risk of early after depolarisations leading to arrhythmia.

Although amiodarone is a type III anti-arrhythmic, it has other actions in addition to blocking K+ channels.

Therefore, it is effective in treating supraventricular tachycardia associated with Wolff-Parkinson-White syndrome
It is also effective at suppressing arrhythmias post-MI.

578
Q

The upstroke of the action potential in SA node pacemaker cells is due to…

A

Opening of voltage gated Ca2+ channels

Ca2+ influx

579
Q

How does verapamil work?

A

Class IV - blocks L-type Ca2+ channels

Decreases slope of action potential at SA node

Decreases AV nodal conduction

Decreases force of contraction (negative inotropy)
(Blocks L-type Ca2+ channels in plateau phase in ventricular myocytes and this prevents high intracellular Ca2+ triggering further Ca2+ release from SR)

Some coronary and peripheral vasodilation

580
Q

How does dihydropyridine work?

A

L-type Ca2+ channel blocker

Acts on vascular smooth muscle so causes vasodilation

(Does not act on L-type Ca2+ channels in the heart because these are a different sub-type)

581
Q

What is adenosine used to treat and how is it administered?

A

Doesn’t fit into any of the classes

Administered intravenously

Useful for terminating supraventricular tachycardia

582
Q

How does adenosine act to terminate supraventricular tachycardia?

A

Acts on A1 receptors (purinergic receptors) at AV node (GPCR)

Has a very short half-life (10 seconds)

Beta-gamma subunit binds to potassium channels and increases K+ conductance
This hyperpolarises cells of the conducting tissue to prevent re-entry loops and hence atrial fibrillation/flutter.

583
Q

What is the aim of therapeutic intervention for heart failure?

A

-positive inotropes to increase cardiac output (not routinely used)
Cardiac glycosides - improves symptoms but not long-term outcome
B-adrenergic agonists

-drugs which reduce workload of the heart
Reduce afterload and preload

584
Q

Digoxin is an example of a…

A

Cardiac glycoside

585
Q

How do cardiac glycosides work?

A

Na+/K+ exchanger blocked
Intracellular Na+ concentration increases
Rise in extracellular Na+ leads to decrease in activity of NCX
Intracellular Ca2+ concentration increases
More Ca2+ stored in SR
This results in an increased force of contraction

Increased vagal activity which:

  • slows heart rate initiated at SA node
  • slows AV conduction
586
Q

When are cardiac glycosides used?

A

Heart failure when there is an arrhythmia such as atrial fibrillation

587
Q

Which drug is used in cardiogenic shock?

A

Beta adrenoreceptor agonists eg. Dobutamine

Increases myocardial contractility

588
Q

Which drug would be used in acute but reversible heart failure eg. Following cardiac surgery?

A

Beta 1 adrenoreceptor agonists eg. Dobutamine

Increase myocardial contractility

589
Q

Which types of drugs reduce the workload of the heart?

A

Diuretics eg. ACE inhibitors (reduces preload and afterload)

Beta adrenoreceptor antagonists (reduce heart rate and contractility)

590
Q

Angiotensin II antagonists are sometimes used instead of ACE inhibitors because they do not have the side effect of a dry cough. Why?

A

ACE inhibitor inhibits ACE.
Functions of ACE:
• Breaks down bradykinin which has vasodilatory effects (causes dry cough)
• Converts angiotensin I to angiotensin II so blocks the effects of angiotensin II

Angiotensin II antagonist only blocks the effects of angiotensin II which includes:
• Vasoconstriction
• Aldosterone release

591
Q

Why are ACE inhibitors used in the treatment of chronic heart failure?

A

-reduce afterload
Decrease vasomotor tone –> decrease blood pressure

-reduce preload
Reduce fluid retention —> reduce blood volume

Reduces workload of the heart

592
Q

What is the aim of therapeutic intervention to treat angina?

A

-reduce workload of the heart
Beta adrenoreceptor blocker
Ca2+ antagonists
Organic nitrates

-Improve blood supply to the heart
Organic nitrates
Ca2+ channel antagonists

593
Q

The left coronary artery fills with blood during which stage of the cardiac cycle?

A

Diastole - backflow of blood as aortic valve closes

During systole there is pressure of the left myocardium that prevents filling

594
Q

Give some examples of organic nitrates.

A

Glyceryl trinitrate (GTN)

Isoorbide dinitrate

595
Q

How do organic nitrates work?

A

Reaction of organic nitrates with thiols in vascular smooth muscle causes NO2- to be released

NO2- is reduced to NO

NO a powerful vasodilator:
NO activates guanylate cyclase. This increases cGMP which lowers intracellular Ca2+ causing relaxation of vascular smooth muscle

MAINLY Venodilation - primarily works by dilating the veins decreasing preload

Dilation of collateral coronary arteries - improving blood supply to the heart

596
Q

Organic nitrates dilate arterioles in the treatment of angina.

True or false?

A

False (arterioles are fully dilated in the ischaemic region)

597
Q

Name some cardiovascular conditions which have an increased risk of thrombus formation.

A

Atrial fibrillation

Acute myocardial infarction

Mechanical prosthetic valves

598
Q

Which drugs are used to minimise the risk of thrombus formation?

A

Anticoagulants:

Heparin - activates antithrombin III which inhibits thrombin. Used acutely for short term action)

Warfarin - antagonises action of vitamin K which is a co-factor for many clotting factors (2, 7 9 10)

Anti-platelet drugs:

Aspirin - inhibits cyclo-oxygenase from forming prostaglandins and thromboxane. Thromboxane causes platelet aggregation.

599
Q

Which anti-thrombotic drug is used acutely for short term acton?

A
Heparin (IV)
Fractionated heparin (subcutaneous injection)
600
Q

Which anti-thrombotic drug is used following an acute MI or to patients at high risk of MI?

A

Aspirin - clots that form in the arterial system tend to be platelet rich

601
Q

Which anti-thrombin drug is used in the long term prevention of thrombosis

A

Warfarin

602
Q

Which drug is used in the treatment of hypertension and heart failure?

A

ACE inhibitors

Reduce afterload and preload

603
Q

What are the therapeutic targets in the treatment of hypertension?

A

Lower blood volume

Lower cardiac output

Lower peripheral resistance

604
Q

What drugs are used to treat hypertension?

A
ACE inhibitors 
Ca2+ channel blockers selective for vascular smooth muscle
Diuretics 
Beta blockers 
Alpha 1 adrenoreceptor antagonist
605
Q

What aspects of the arterial and venous system can be measured using a Doppler?

A

Velocity and direction of flow

606
Q

Can a Doppler be used to measure flow?

A

No, flow is volume per unit time

Doppler can be used to measure velocity.
This can be used to infer flow.

607
Q

Where are deep veins found?

A

In muscles

608
Q

Where are superficial veins found?

A

Within subcutaneous fat

609
Q

Where are perforating veins found?

A

Connect superficial veins to deep muscles

610
Q

Is the direction of flow in veins from superficial to deep OR from deep to superficial?

A

Superficial to deep

611
Q

What is the significance of deep fascia in the lower limb?

A

Deep fascia is tightly attached to muscles in one compartment.

When the muscles contract, pressure increases in a compartment so blood is forced to flow in through the veins. (Calf pump)

612
Q

What are the deep veins of the lower limb?

A

External iliac vein
Femoral vein
Popliteal vein

613
Q

What are the superficial veins of the lower limb?

A

Long saphenous vein

Short saphenous vein

614
Q

How can you find the long saphenous vein?

A

Anterior to the medial malleolus

615
Q

What are varicose veins?

A

Varicose veins are tortuous, twisted or lengthened veins

616
Q

Explain the pathophysiology of varicose veins.

A

The vein wall is inherently weak in varicose veins, which leads to dilatation and separation of valve cusps so that they become incompetent.

617
Q

What symptoms are felt along varicose veins?

A

Heaviness

Tension

Aching

Itching

618
Q

What are the common complications of varicose veins?

A

Result from vein itself:

  • haemorrhage
  • thrombophlebitis

Result from venous hypertension:

  • oedema
  • skin pigmentation
  • varicose eczema
  • lipodermatosclerosis
  • venous ulceration
619
Q

What is thrombophlebitis?

A

Venous thrombosis - produces inflammatory response including pain

620
Q

What is venous ulceration a result of?

A

Venous hypertension

621
Q

What causes venous hypertension?

A

Calf muscle pump failure

622
Q

What causes calf muscle pump failure?

A

‘Failure’ of calf muscle contraction - immobility, obesity, reduced hip, knee and/or ankle movement

Deep vein incompetence

Volume overload - superficial vein incompetence

623
Q

What is the main predisposing factor for arterial thrombosis?

A

Abnormality of the lining of vessel wall (eg. Atherosclerosis)

624
Q

What is the main predisposing factor for venous thrombosis?

A

Abnormality of flow - stasis

625
Q

Does stasis in veins always cause venous thrombosis?

A

In reality, it is usually stasis plus another factor eg.

Surgery
Oral contraceptive pill
Dehydration
Cancer

626
Q

Platelets are a major component of both arterial and venous thrombi.

True or false?

A

FALSE

Arterial thrombosis in response to bleeding involves platelets, extrinsic and then intrinsic pathways. Arterial thrombi are platelet rich

Venous thrombosis does not involve platelets in a major way, initially the intrinsic pathway is involved and then the extrinsic. Venous thrombi are fibrin rich

627
Q

What are venous thrombi rich in?

A

Fibrin

628
Q

How does the body stop bleeding from high pressure arteries?

A

Initially vasoconstriction

Platelets

Extrinsic and then intrinsic pathways

(Arterial thrombi are platelet rich)

629
Q

How does the body stop bleeding in low pressure veins?

A

Venoconstriction

Particular the intrinsic pathway and then both pathways

(Venous thrombi are fibrin rich)

630
Q

Why is cardiac pain brought on by exercise and stress in angina?

A

Sympathetic drive increases

Heart rate increases

Diastole decreases

Filling of coronary arteries is during diastole, so filling of coronary arteries decreases.

631
Q

What are the causes of calf muscle pump failure?

A
  • failure of calf muscle contraction - immobility, obesity, reduced hip, knee and/or ankle movement
  • deep vein incompetence
  • volume overload - superficial vein incompetence
632
Q

How can a retrograde circuit result in calf muscle failure?

A

Incompetence of valve in saphenous vein resulting in backflow in the saphenous vein.

Blood flows through perforating veins from this superficial vein into deep veins every time blood is ejected by the calf pump.

This results in calf pump failure due to volume overload.

633
Q

Is a bounding pulse usually caused by a change is end systolic pressure or end diastolic pressure?

A

Usually caused by decreased end diastolic pressure

Eg. Bradycardia

634
Q

Which palpable pulse is a good representation of aortic pulse?

A

Carotid pulse

635
Q

What are the signs of DVT?

A

Produces inflammatory response:

  • calor - skin warmth, pyrexia
  • dolor - pain, calf tenderness
  • functio laesa - cannot walk
  • rubor - blue-red discolouration
  • tumor - oedema

Others:

  • muscle induration - increase in the fibrous elements in muscle resulting in reduced elasticity
  • distended, warm superficial veins
636
Q

What happens to capillary hydrostatic pressure if arterioles are constricted?

A

Capillary hydrostatic pressure falls

Pressure drop across the system is greater as you increase the resistance.

637
Q

What happens to arterial pressure and venous pressure if arterioles are constricted?

A

Arterial pressure increases

Venous pressure decreases

638
Q

Why does heart failure cause oedema but hypertension generally does not?

A

In hypertension, arterioles are constricted. This increases arterial pressure but decreases capillary hydrostatic pressure and decreases venous pressure, if pumping remains the same.

In heart failure, there is decreased venous return to the heart. This increases venous pressure and increases hydrostatic pressure in the capillaries.

Increased capillary hydrostatic pressure results in more fluid leaving the capillaries than returns. This results in oedema due to a build up of tissue fluid.

639
Q

How does left sided heart failure cause oedema?

A
  • left ventricle cannot empty so well
  • left atrial pressure is higher
  • higher pressure in pulmonary veins and pulmonary capillaries
  • higher pulmonary capillary pressure causes pulmonary oedema
640
Q

What can cause pulmonary oedema?

A
  • increased pressure in pulmonary veins (left sided heart failure)
  • pulmonary hypertension
641
Q

Systolic pressure in the arteries equates to the systolic pressure in the corresponding ventricles. Why is diastolic pressure in arteries greater than that of its corresponding ventricle?

A

Elastic recoil

642
Q

How can chronic lung disease lead to right ventricular failure?

A

Hypoxic pulmonary vasoconstriction ensures optimal ventilation/perfusion ratio. (Alveolar hypoxia results in vasoconstriction of pulmonary vessels - opposite to what normally happens in systemic circulation)

  • in chronic lung disease, there are poorly ventilated alveoli. These are less perfused by vascular resistance to optimise gas exchange.
  • this increases pressure in the pulmonary artery. Increases afterload
  • harder for right ventricle to pump —> right sided heart failure
643
Q

How does the pulmonary circulation respond to hypoxia differently to the systemic circulation?

A

Chronic hypoxia in the lungs causes smooth muscle cells in arterioles to contract. This results in vasoconstriction.
(Hypoxia pulmonary vasoconstriction ensures optimal ventilation/perfusion ratio)

In the systemic circulation, hypoxia triggers vasodilation to increase blood flow and hence oxygen delivery to the hypoxic region.

644
Q

How does systolic right sided heart failure cause peripheral oedema?

A
  • poor pumping of right ventricle
  • right ventricular end systolic volume is increased (systolic dysfunction)
  • more difficult to fill right ventricle
  • increased right atrial and systemic venous pressure
  • increased capillary hydrostatic pressure in systemic circulation —> systemic oedema
645
Q

Why can ACE inhibitors be used for both heart failure and hypertension?

A

-reduce peripheral resistance by preventing production of Ang II
HF - reduced preload
BP - reduced blood pressure

  • reduce blood volume through preventing production of AngII
  • HF - heart has to work less hard
646
Q

How does stimulation of beta 2 adrenoreceptors cause vasodilation?

A

Adrenaline/noradrenaline binds to beta 2 adrenoreceptors and changes its conformation.

The change in conformation on the activated adrenoreceptor increases its affinity for the G-alpha q protein.

The GPCR-G protein interaction causes the GDP on the alpha sub-unit of the G protein to change to GTP.

Once GTP binds to the alpha sub-unit, the alpha sub-unit loses affinity for the beta-gamma sub-unit so they seperate

The alpha-subunit binds to phospholipase C and stimulates it. Phospholipase C converts PiP2 to IP3 and DAG.

IP3 binds to IP3 receptors on the SER/SR inducing the release of Ca2+ in the cytosol from the SER/SR. Ca2+ binds to calmodulin. The Ca2+-calmodulin complex stimulates myosin light chain kinase.

Myosin light chain kinase phosphorylates myosin light chain so that actin binding sites are exposed.

DAG stimulates protein kinase C. Protein kinase C inhibits myosin light chain phosphatase, preventing the phosphate from being removed from myosin light chain, maintaining contraction and hence vasoconstriction.

647
Q

Why is surgery associated with DVT?

A
  • immobility prior to surgery
  • no calf muscle pump during surgery
  • immobility after surgery
  • surgery is trauma, the body’s response to trauma includes a pro-thrombotic state
648
Q

What is peripheral artery disease?

A

Peripheral artery disease is a disease which results in stenosed peripheral arteries.

It can be acute or chronic.

649
Q

Why might someone with chronic peripheral artery disease be asymptomatic?

A

Collateral circulation develops in response to a stenosis.

650
Q

Where is natural collateral circulation particularly common?

A

Across joints such as elbow and knee.

651
Q

What are the consequences of acute peripheral artery disease?

A

Acute limb ischaemia

Fixed mottling

Gangrene

652
Q

What is the difference between acute and chronic peripheral artery disease?

A

Acute peripheral artery disease - the limb goes from a normal blood supply to a greatly impaired blood supply over a period of minutes. There is no chance for collateral vessel development (which takes weeks/months).

Chronic peripheral artery disease - the limb goes from a normally blood supply to an impaired blood supply over months. There is a chance for collateral vessel development.

653
Q

What is the most common cause of acute limb ischaemia?

A

Embolism (from heart or abdominal aortic aneurysm)

654
Q

The limb has gone from a normal blood supply to a greatly impaired blood supply over a period of minutes. How long does the patient have for this to be reversed for the limb to be recovered?

A

6 hours

655
Q

After 6 hours of greatly impaired blood supply to a limb, why does the limb have to be amputated for the patient to survive?

A

Dead tissue releases intracellular potassium

Hyperkalaemia - makes Ek less negative, inactivates Na+ channels, slower upstroke, narrower action potential
Leads to asystole

656
Q

What are the signs and symptoms of acute limb ischaemia?

A

6 P’s

Pain 
Paralysis 
Paraesthesia 
Pallor
Perishing cold
Pulseless 

(These are the 6 P’s of compartment syndrome)

657
Q

What is fixed mottling?

A

Spotting with patches of colour that won’t blanch

It is a sign of irreversible ischaemia (dry gangrene is a late sign of irreversible ischaemia >2 weeks)

658
Q

How does chronic peripheral arterial disease present?

A

-intermittent claudication (equivalent to stable angina)

  • critical ischaemia
  • –> rest pain (equivalent to unstable angina)
  • –> ulceration/gangrene (equivalent to myocardial infarction)
659
Q

What does intermittent claudication mean?

A

Pain in the muscles of the lower limb elicited by walking and exercise

Pain relieved rapidly by stopping exercise for a few minutes even whilst standing up

660
Q

Which muscles are affected by claudication?

A

Calf muscles

  • gastrocnemius
  • soleus
  • plantaris
661
Q

Where can you find the femoral pulse?

A

Mid-inguinal point

Mid-way between the pubis symphysis and ASIS

(REMEMBER THIS IS DIFFERENT TO THE MIDPOINT OF THE INGUINAL LIGAMENT WHERE THE FEMORAL NERVE IS)

662
Q

Where can the popliteal pulse be found?

A

Deep in the popliteal fossa and is difficult to feel.

663
Q

Where can the pedal pulses be found?

A

Dorsal pedis artery - lateral to the tendon of extensor hallucis longus

Posterior tibial artery - just behind the medial malleolus

664
Q

The dorsal pedis artery is a continuation of…

A

Anterior tibial artery

665
Q

In a normal person with no peripheral vascular disease, which pulses should you be able to feel and where?

A

Femoral pulse - mid-inguinal point
Popliteal pulse - popliteal fossa
Dorsalis pedis pulse - lateral to tendon of EHL
Posterior tibial pulse - behind medial malleolus

666
Q
Patient has the following pulses absent:
Femoral pulse 
Popliteal pulse
Dorsalis pedis pulse 
Posterior tibial pulse 

They are also experiencing bilateral buttock, thigh and calf claudication.

Diagnosis?

A

Aortoilliac occlusion

667
Q

Patient has absent right lower limb pulses

They are experiencing right buttock, thigh and calf claudication

Diagnosis?

A

Common iliac occlusion

668
Q

What would be the signs and symptoms of a left external iliac occlusion?

A

Right thigh and calf claudication

Absent right femoral pulse, popliteal pulse, dorsalis pedis pulse, posterior tibial pulse

669
Q

The following pulses are absent in a patient:

  • popliteal pulse
  • dorsalis pedis pulse
  • posterior tibial pulse

The femoral pulse is present

The patient is experiencing right calf claudication.

Diagnosis?

A

Superficial femoral artery occlusion

670
Q

What occlusion is the commonest finding in patients with claudication?

A

Superficial femoral artery occlusion

671
Q

Why do patients with rest pain due to critical ischaemia complain that it is worse at night?

A
  • gravity is not forcing blood to feet as it would if patient was standing
  • metabolic activity of feet is high to keep feet warm
  • cardiac output is reduced when sleeping
672
Q

Describe what is happening in rest pain caused by critical ischaemia.

A

Ischaemia = hypoxia due to reduced blood supply

The ischaemia is so severe that at rest the foot, skin, muscles, bones are ischaemic at rest.

This means that there is not enough oxygen to provide for the cells basic metabolic requirements.

673
Q

If rest pain caused by critical ischaemia is left untreated, it will progress to…

A

Ulceration/gangrene

674
Q

Why is a classic place for gangrene/ulceration on the anterior shin?

A

Blood supply to the anterior shin is poor

675
Q

Do you get fixed mottling in acute or chronic ischaemia?

A

Acute ischaemia

676
Q

What is substance P?

A

Substance P is a neuropeptide that is released locally when there is ischaemia.

It increases the sensitivity of pain afferents in muscle.

677
Q

Presenting complaint:

Pain in the foot that comes on when the patient goes to bed and is relieved by hanging the foot out of the bed.

Diagnosis?

A

Critical ischaemia - rest pain

678
Q

In ischaemic tissue, what is thought to be a key factor in stimulating pain afferents?

A

Low pH

Substance P (neuropeptide)

679
Q

Ischaemia is a relative phenomenon. Explain what this means.

A

Degree of ischaemia depends on whether you have enough blood supply to meet metabolic demands.

680
Q

What is the difference between ischaemia and infarction?

A

Ischaemia - reversible damage due to lack of oxygen

Infarction - irreversible damage due to lack of oxygen with cell death (necrosis)

681
Q

What are the different types of ischaemic damage to the heart?

A

Stable angina

Unstable angina

Myocardial infarction

682
Q

Why might a young person with normal coronary vessels with thyrotoxicosis get angina/have an MI?

A

-increased heart rate
Decreasing time for diastole
Reduced filling of coronary arteries

-increases metabolic rate
Increased metabolic demand
Blood supply may not be sufficient to meet this metabolic demand

683
Q

What is the difference between ischaemia and infarction?

A

Ischaemia - reversible damage due to lack of oxygen

Infarction - irreversible damage due to lack of oxygen with cell death (necrosis)

684
Q

What is referred pain?

A

Visceral and somatic afferents synapse in similar place in spinal cord.

The brain cannot tell if the pain is coming from the skin or heart.

685
Q

The sympathetic nervous system is activated in patients with an MI. What are the signs and symptoms of this?

A
  • diaphoresis (sweating)
  • nausea
  • systemic vasoconstriction (Pallor)
  • tachypnoea
686
Q

Why is the sympathetic nervous system activated in a patient with MI?

A
  • reduced cardiac output due to MI. Decreased arterial pressure
  • pain and anxiety from MI
687
Q

What can cause palpitations?

A
  • sinus tachycardia
  • increased awareness of normal heartbeat
  • arrhythmias
688
Q

What is the difference between dyspnoea, orthopnoea and paroxysmal nocturnal dyspnoea?

A

Dyspnoea - difficulty breathing

Orthopnoea - shortness of breath when lying flat

Paroxysmal nocturnal dyspnoea - shortness of breath that wakes the patient up at night

689
Q

Why does dyspnoea occur at night and why is it relieved by sitting up?

A

When lying flat, increased venous return to right side of the heart. More blood is in the lungs so there is increased hydrostatic pressure and more oedema is formed.

690
Q

What diseases apart from pulmonary oedema causes dyspnoea that is worse at night?

A

Asthma

691
Q

What is a postural hypotension?

A

Drop in systolic pressure over 20mmHg when standing

692
Q

What can cause postural hypotension?

A
Venous pooling 
Impaired vasomotor tone eg. Diabetic autonomic neuropathy 
Reduced muscle tone 
Hypovolaemia 
Drugs antihypertensives
Addison's disease
693
Q

Why might Addison’s disease result in postural hypotension?

A

Decreased aldosterone —> aldosterone increases transcription and activity of Na+/K+ ATPase. This increases Na+ retention and hence water retention
Decreased cortisol —> increases blood pressure

694
Q

What is Buerger’s test?

A

-elevation pallor
In an ischaemic leg, elevation to less than 20 degrees may cause pallor

-rubor of dependency
Hang leg off edge of bed
Leg reverts to pink colour more slowly than normal
Goes through normal pinkness to reddish colour
Dilation of arterioles in an attempt to get rid of metabolic waste ‘reactive hyperaemia’

695
Q

What is ‘sunset foot’

A

Foot becomes parodoxically pink - becomes hyperaemic due to lactate causing vasodilation

Can take six weeks of ischaemia to develop

696
Q

What is the difference between moveable mottling?

A

Moveable mottling
Press and the spots blanch because there is still some blood supply

Fixed mottling
Press and spots will not blanch because there is nowhere for the blood to move - capillaries are thrombosed - no blood supply

697
Q

When would you get a regularly irregular rhythm?

A

2nd degree heart block - intermittent failure of conduction between atria and ventricles

698
Q

In atrial fibrillation the strength of the pulse varies. Why?

A

Variable filling time of the ventricles

699
Q

In the case of a ventricular ectopic, there is a compensatory pause. It is in fact, the next ‘normal beat’ that is strong and felt by the patient. Why?

A

There is a longer time in diastole.

Ventricles are able to fill to a larger volume in diastole and pump a larger volume of blood than usual in systole

End systolic pressure has increased because the ventricles are pumping a larger volume.

700
Q

What are the causes of a thready pulse?

A

Poor cardiac output eg. Hypovolaemia

701
Q

What causes a bounding pulse?

A

Low peripheral resistance - causes lower diastolic blood pressure

Bradycardia

702
Q

Why does raising the arm exaggerate a bounding pulse?

A

Increased pulse pressure as blood falls away more profoundly.

703
Q

Why is S2 split on inspiration?

A

In inspiration:
Chest wall moves out
Diaphragm flattened
Decreased (negative) pressure so air rushes into lungs and more blood drawn into right side of heart
Pulmonary valve closes after aortic valve – giving a split second heart sound

704
Q

Why can you hear right sided murmurs better on inspiration?

A

Chest wall moves out
Diaphragm flattened
Decreased pressure so air rushes into lungs and more blood drawn into right side of heart
Blood flowing through tricuspid and pulmonary valves increases,
therefore can hear right sided murmurs better

705
Q

Why can you hear left sided murmurs better on expiration?

A

Chest wall moves in
Diaphragm moves up
Increases pressure so air rushes out of lungs and more blood pushed out of heart
Blood flowing through mitral and aortic valves increases, therefore can hear left sided murmurs better