Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

LSS Year 1 > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

1
Q

In what cavity does the heart lie?

A

In the mediastinum

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

What is the pericardium?

A

Fibroserous sac surrounding the heart and it’s great vessels

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

What are the layers that make up the pericardium?

A 
Consists of 2 layers:
- Fibrous
- Serous
Serous has two parts:
- Parietal: lines fibrous
- Visceral: adheres to heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How does blood flow around the heart, starting in the right atrium?

A

Blood flows from right atrium, through the tricuspid valve into the right ventricle. It then flows through the pulmonary semilunar valve into the pulmonary artery to the lungs, becomes oxygenated and returns to the lungs in the pulmonary veins into the left atrium. It flows through the mitral valve into the left ventricle and is then pumped through the aortic semilunar valve into the ascending aorta

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

What vessels feed into the right atrium?

A

Superior and inferior vena cava

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

What vessel leaves the right ventricle?

A

The pulmonary trunk (left and right pulmonary artery)

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

What vessels enter the left atrium?

A

Pulmonary veins (left and right superior and inferior)

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

What vessel leaves the left ventricle?

A

Aorta

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

What vessels branch off the aortic arch?

A

1) Brachiocephalic truck (right subclavian artery and right common corotid artery)
2) Left common corotid artery
3) Left subclavian artery

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

What veins feed into the superior vena cava?

A

Left and right internal jugular vein and subclavian vein feed into the left and right brachiocephalic vein which feeds into the the superior vena cava

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

What tendons connect the tricuspid valve to the papillary muscles?

A

Chordae tendineae

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

What is the function of chordae tendineae?

A

Prevents the tricuspid valve from prolapse or inversion into the right atrium

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

What is the function of the papillary muscles?

A

Connects to the tricuspid valve with the chordae tendineae to prevent inversion or prolapse

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

What cusps make up the tricuspid valve?

A

1) Anterior cusp
2) Septal cusp
3) Posterior cusp

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

What cusps make up the pulmonary valve?

A

1) Anterior semilunar cusp
2) Right semilunar cusp
3) Left semilunar cusp

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

What valves make up the mitral valve?

A

1) Anterior cusp

2) Posterior cusp

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

What are trebeculae carnae?

A

Papillary muscles which pulls on chordae tendineae and aid blood flow, preventing suction

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

What are the nodes of the heart?

A

Sinoatrial (SA) node

Atrioventricular (AV) node

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

What are the internodal tracts of the left atrium?

A

1) Anterior internodal tract
2) Middle internodal tract
3) Posterior internodal tract

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

What node causes contraction of the atria?

A

sinoatrial node (SA)

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

What are the conduction tracts of the atria?

A

Anterior, middle and posterior internodal tract and Bachmann’s bundle

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

What are the conduction tracts of the ventricles?

A

Left and right bundle branch

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

What node causes contraction of the ventricles?

A

Atrioventricular node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What is the function of Purkinje fibres?

A

They carry the contraction impulse from the left and right bundle branch to the myocardium of the ventricles

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

How big are ventricular cells?

A

100μm long and 15μm wide

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

Where is calcium stored in the heart?

A

In the sarcoplasmic reticulum

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

What calcium channel is found on T-tubules?

A

L-type Ca channel

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

What channel allows Ca to leave the sarcoplasmic reticulum in the heart?

A

Ryanodine receptors

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

How is Ca removed from the cytoplasm, back into the sarcoplasmic reticulum in the heart?

A

SR Ca ATPase

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

What exchanger keeps the level of Ca at a steady state inside cardiac cells?

A

Na/Ca exchanger

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

How much Ca needed for contraction comes from the SR?

A

70%

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

What is the relationship between Ca and force of contraction?

A

Sigmoidal

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

What is the relationship between length (stretch) of cardiac muscle and the force of contraction?

A

Increasing length of muscle increases the force of contraction (up to a point- over-stretching will pull myofilaments apart and reduce force)

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

What is passive force in cardiac muscle?

A

The recoil of muscle due to stretch (elastic elements of the muscle)

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

What type of contraction do cardiac muscle have?

A

Isometric and isotonic

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

What has more passive force? Cardiac or skeletal muscle?

A

Cardiac

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is more compliant? Cardiac or skeletal muscle?

A

Skeletal

Cardiac is more resistant to stretch due to properties of ECM and cytoskeleton

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

Why does the heart use isometric contraction?

A

To increase the pressure in the ventricles

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

Why does the heart use isotonic contraction?

A

Shortens fibres to eject blood from the ventricles

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

What is preload?

A

Initial stretch on the muscle which prior to contraction

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

What is afterload?

A

Weight which is not apparent to the muscle in the resting state and is only encountered when muscle has started to contract

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

What effect does the afterload have on the amount of shortening of a muscle fibre?

A

The heavier the afterload the less shortening that occurs and the slower it occurs

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

What effect does preload have on the shortening of muscle with increasing afterload?

A

A larger preload allows muscle fibres to increase their shortening with a larger afterload

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

What is preload in the heart?

A

The blood filling the ventricles and stretching the resting ventricular walls is preload Stretch or filling determines the preload

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

What is preload in the heart dependent upon?

A

Venous return to the heart

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

What are the possible measures of preload in the heart?

A

End-diastolic volume
End diastolic pressure
Right atrial pressure

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

What is afterload in the heart?

A

The load against which the left ventricle ejects blood after opening the aortic valve

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

What are the possible measures of afterload in the heart?

A

Diastolic arterial blood pressure

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

What does an increase in afterload cause in terms of muscle shortening?

A

Decreases the amount of isotonic shortening

Decreases the velocity of shortening

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

What is the Frank-Starling relationship?

A

Increased diastolic fibre length increases ventricular contraction
(The more blood returned to the heart the more blood the heart will pump out)
Cardiac output exactly balances the augmented venous return

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

What two factors affect the Frank-Starling relationship?

A

1) Changes in the number of myofilament cross bridges that interact (between myosin and trophonin)
2) Changes in the Ca sensitivity of the myofilaments

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

What happens to calcium sensitivity when muscle fibre length increases?

A

Calcium sensitivity increases

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

What are the two possible reasons why Ca sensitivity increases when muscle fibre length increases?

A

1) Troponin C has higher affinity for Ca at longer lengths due to conformational change in protein
2) Decreased myofilament lattice spacing increases the probability of forming strong binding cross-bridges

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

What is work done? (by the heart)

A

Stroke work

Stroke work = SV x P

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

What is stroke work?

A

Volume of blood ejected during each stroke (SV) times the pressure at which the blood is ejected (P)
Stroke Work = SV x P

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

What is stroke volume?

A

The volume of blood ejected during each stroke

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

What occurs in diastole?

A

Ventricular relaxation during which the ventricles fill with blood
Split into four sub-phases

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

What occurs in systole?

A

Ventricular contraction when blood is pumped into the arteries
Split into two sub-phases

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

What is end-diastolic volume - end-systolic volume?

A

Stroke volume

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

What is the formula for ejection fraction?

A

EF = SV/EDV

Stroke volume / end-diastolic volume

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

What occurs in atrial systole?

A

Atria contract, adding to blood already in the ventricle. Atrial contraction complete before ventricle contraction. Gives a small increase in pressure (a wave)
On ECG this is initiated with the P wave

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

What is the ECG QRS complex?

A

Ventricle depolarisation

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

If you hear a heart sound in atrial systole what causes this?

A

A problem with the tricuspid valve or mitral valve

S4

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

What is isovolumic contraction?

A

Blood has filled the ventricles and they start to contract. Ventricle depolarisation causing contraction. This builds pressure but aortic and atrioventricular valves are closed so pressure builds
Isometric contraction

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

When do you hear the “lub” S1 heart sound?

A

During isovolumic contraction

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

What is rapid ejection?

A

Pressure in the ventricle exceeds pressure in the aorta and blood is forced out
Isotonic contraction
Large change in volume
This is the c wave
Nothing happening on ECG (electrically silent)

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

What is reduced ejection?

A

End of systole
aortic and pulmonary valves begin to close
Blood flow from ventricles decreases, ventricular volume decreases more slowly. Semilunar valves close
ECG- T wave due to ventricular repolarisation
Ca pumped back into SR and out of cell

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

What is isovolumic relaxation?

A

Beginning of diastole
Pressure is decreasing in the ventricles but volume doesn’t change (as muscle fibres relax)
Dichrotic notch- rebound pressure against aortic valve due to vessel wall relaxation
“dub” S2 sound

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

What is rapid ventricular filling?

A

AV valves open and blood flows from the atria into the ventricle. Ventricular volume increases and atrial pressure falls
S3 heart sound due to signify turbulent ventricular filling. Can be due to severe hypertension or mitral incompetence

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

What is reduced ventricular filling?

A

Diastasis

Ventricular volume increases more slowly

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

On what side of the heart are pressure the highest?

A

The left side

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

On what side of the heart are the volumes the highest?

A

Equal on both sides

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

What is the average pressure on the left side of the heart?

A

120/80mmHg

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

What is the pressure on the right side of the heart?

A

25/5mmHg

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

What is a pressure-volume loop?

A 
Pressure increase (1→2): End-diastolic volume→ isovolumetric contraction (full ventricle)
Volume decrease (2→3): Isovolumetric contraction  → end systolic volume (blood ejected)
Pressure decrease (3→4): End systolic volume → Isovolumetric relaxation (muscles relaxes and pressure drops)
Volume increase (4→1): Isovolumetric relaxation → end diastolic volume
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Where are the preload and afterload on the pressure-volume loop?

A

Preload: Point 1
Afterload: Point 2

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

What happens to stroke volume is you increase afterload (e.g. hypertension)

A

Increased afterload decreases the amount of shortening. This decreases stroke volume

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

What three things effect stroke volume?

A

1) Preload
2) Afterload
3) Contractility

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

What is cardiac contractility? What causes it to increase?

A

The contractile capability (or strength of contraction) of the heart
It is increased by sympathetic stimulation

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

What measure gives cardiac contractility?

A

Ejection fraction

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

Increasing or decreasing contractility does what to volume and pressure in the heart?

A

Increasing contractility increases pressure and volume

Decreasing contractility decreases volume and pressure

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

During exercise what happens to contractility and end diastolic volume?

A

They increase

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

At rest (diastole) what are cardiac cell membranes permeable to?

A

Only K

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

What causes the refractory period of a cardiac action potential?

A

Na channel inactivation. They recover from this when the membrane is repolarised

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

What controls the duration of contraction of the heart?

A

The duration of action potential

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

What is the absolute refractory period of cardiac action potential?

A

Time during which no action potential can be initiated regardless of stimulus intensity

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

What is the relative refractory period of cardiac action potential?

A

Period after absolute refractory period where an action potential can be elicited but only with stimulus strength larger than normal

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

What is the full recovery time of cardiac action potential?

A

The time at which a normal AP can be elicited with normal stimulus

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

What is tetanus? (muscle contraction)

A

When re-stimulation of muscle and rapid action potential firing causes a summation of contraction

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

How does muscle excitation differ in skeletal and cardiac muscle?

A

Skeletal muscle repolarises very early in the contraction phase allowing re-stimulation and tetanus
Cardiac muscle cannot be re-excited until the contraction is well underway so cannot be tetanised

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

What are the phases of cardiac action potential?

A 
Phase 0= Upstroke
Phase 1= Early repolarisation
Phase 2= Plateau
Phase 3= Repolarisation
Phase 4= Resisting membrane potential (diastole)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is required early in phase 2 which is essential for contraction?

A

Ca influx required to trigger Ca release from intracellular stores.

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

What are three dihydropyridine Ca channel antagonists which inhibit Ca influx?

A

1) Nifedipine
2) Nitrendipine
3) Nisoldipine

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

What K current is responsible for fully repolarising the cell?

A

IK1
It is large and flows during diastole. It stabilises the resting membrane potential reducing the risk of arrhythmias by requiring a large stimulus to excite the cells

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

What channel does not exist in the SA node?

A

IK1

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

What four components make up the heart’s conduction system?

A

1) Sinoatrial nodes (SA node)
2) Inter-nodal fibre bundles
3) Atrioventricular node (AV node)
4) Ventricular bundles (bundle branches and Purkinje fibres)

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

Where are gap junctions found in cardiac cells?

A

At intercalated discs

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

What causes an upward and downward deflection on an ECG?

A

Upward: When a wave of depolarisation is moving towards the positive electrode OR when a wave of repolarising current is moving away from the positive electrode
Downward: When a wave of depolarisation is moving away from the positive electrode

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

What are the waves on an ECG and what part of the cardiac cycle are they?

A

P wave: atrial depolarisation
QRS wave: ventricular depolarisation
T wave: Ventricular repolarisation

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

How many leads in an ECG?

A

12

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

How many limb leads are there on an ECG?

A

6

two columns on the left

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

How are limb leads recorded?

A

Four electrodes, one on each limb

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

Which limb is neutral in a limb lead ECG?

A

Right leg

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

What is shown on an ECG in Lead I?

A

Potential difference between right arm (-ve) → left arm (+ve)
Anything that goes in this direction will be positive in this lead

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

What is shown on an ECG in Lead II?

A

The most common direction of the heart
Potential difference between right arm (-ve) and left leg (+ve)
Anything that goes in this direction will be positive in this lead

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

What is shown on an ECG in Lead III?

A

Potential difference between left arm (-ve) and left leg (+ve)

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

How do depolarisation and repolarisation show on an ECG>

A

Depolarisation towards the positive electrode is upwards deflection
Depolarisation away from the positive electrode is a downwards deflection
Repolarisation is OPPOSITE

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

What are P and QRS expected to be in leads I and II?

A

Positive

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

What are the three augmented leads from an ECG?

A

aVR
aVL
aVF

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

What is shown on an ECG in Lead aVR?

A

Potential difference between an average of left arm and left leg (-ve) and the unipole of right arm (+ve)
It is augmented because it is a combination of two leads

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

What is shown on an ECG in Lead aVL?

A

Potential difference between an average of right arm and left leg (-ve) and the unipole of left arm (+ve)
It is augmented because it is a combination of two leads

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

What is shown on an ECG in Lead aVF?

A

Potential difference between an average of right arm and left arm (-ve) and the unipole of left leg (+ve)
It is augmented because it is a combination of two leads

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

How long is one small square on an ECG? (time)

A

40ms

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

How long is one large square on an ECG? (time)

A

0.2 seconds

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

What is a normal QRS axis?

A

-30° to +90°

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

How do you calculate QRS axis?

A

Two vectors 90° to each other so you cover all directions of electrical activity
e.g. QRS=I + aVF

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

When would limb leads show left axis deviation?

A

Is the QRS calculation is -30° to -90°

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

When would limb leads show right axis deviation?

A

Then the QRS calculation is +90° to +210°

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

What is the difference between limb lead and chest lead measurements?

A

They are on a completely different plane
Limb leads: frontal plane (sagital section through the body)
Chest leads: horizontal plane

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

Where do the chest leads go?

A 
V1: 4th IC space, right sternal margin
V2: 4th IC space, left sternal margin
V3: Midway between V2 and V4
V4: 5th IC space, MCL
V5: Horizontal to V4 at anterior axillary line
V6: Horizontal to V4 at midaxillary line
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

What is the Wilson’s central terminal?

A

Summation pole of right arm, left arm and left leg (average potential across the body)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

How are chest leads measured? What are the negative and positive poles?

A

Measured potential difference from Wilson’s central terminal (-ve) to the chest lead (+ve)

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

What is a normal duration and amplitude of the P wave in lead II?

A

Duration:

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

What is a normal PR interval?

A

0.12-0.20s

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

What is a normal QRS complex duration and amplitude?

A

Duration:

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

What is a normal Q wave duration and amplitude?

A

Duration:

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

What is a normal QT interval duration?

A

0.38-0.42s

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

What is a normal ST segment?

A

Should be ‘isoelectric’

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

What is a normal T wave?

A

May be inverted in III, aVR, V1 and V2 without being abnormal

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

What is sinus tachycardia? How would you identify it on an ECG?

A

Increased heart rate (normal amplification of the heart- just faster- get it when exercising)
P wave is normal
Atrial rate 100-200bpm
Regular ventricular rhythm
Ventricular rate is 100-200bpm
One P wave precedes every QRS complex
Often physiological response (hypovolaemia, sepsis, stress etc)

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

How do you work out heart rate from an ECG?

A

300 / number of large squares in between QRS complexes

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

What is atrial fibrillation? How would you identify it on an ECG?

A

Atria contract at different times (not synchronous)
Heart rate: Atria- 350-650bpm; Ventricle-slow to rapid
Rhythm: irregular
P wave: fibrillatory (fine to course)
QRS:

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

What is atrial flutter? How would you identify it on an ECG?

A

Undulating sawtoothed baseline F (flutter) waves
Atrial rate: 250-350bpm
Regular ventricular beating: 150bpm with 2:1 atrioventricular block (4:1 is also common)

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

What is AVNRT?

A

Atrioventricular nodal reentrant tachycardia
Narrow-complex tachycardia with regular QRS complexes
P waves often buried within QRS or just after QRS
Reentrant circuit within AV node
Adenosine responsive (for treatment)

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

What is preexcitation syndrome?

A

Abnormally short PR interval (

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

What are the three types of heart block (AV nodal block)?

A

1st degree: Prolonged PR interval
2nd degree: Mobitz Type I (Wenckeback), Mobitz Type II
3rd degree: Complete heart block

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

What is a first degree heart (AV) block?

A

Prolonged P wave- takes slightly longer for the atrial depolarisation to get to the ventricles
(slightly diseases AV node)

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

What is a second degree heart (AV) block? What are the two type?

A

Delay between the atrial and ventricle depolarisation and also intermittently non-conducted atrial depolarisation down to the ventricle
Mobitz type I is progressively elongated PR interval until the P-wave is non-conducted
Mobitz type II is non-conducted beats (e.g. 2:1 ratio)

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

What is a third degree heart (AV) block?

A

Absolutely no atrial impulses getting down to the ventricles, completely unrelated waves on ECG
Would present with collapse, need CPR and treatment with permanent pacemaker

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

What are bundle branch blocks? What are the signs visible on an ECG?

A

One of the two bundles that branch from the AV node has a conduction block due to disease. One side will depolarise normally and one will depolarise a lot more slowly (cell-to-cell, not through Purkinje fibres)
ECG: QRS complex widens or morphology changes

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

What is the characteristic morphology of the QRS complex in a right bundle branch block?

A

“Rabbit ears” in V1 and V2 chest leads

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

What is the characteristic morphology of the QRS complex in a left bundle branch block?

A

Deep V or W in V1 and V2 chest leads

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

What is a ventricular (broad complex) tachycardia?

A 
Potentially lethal
>120ms
Extremely irregular rhythm that leads to drop in blood pressure, drop in cardiac output, no pulse and cardiac arrest. Leads (usually) to ventricular fibrillation
Heart rate: 300-600
Absent P wave
Monomorphic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Where is the reservoir of blood stored?

A

In the venules and veins

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

In what vessels does the majority of the exchange occur?

A

Capillaries

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

What is the formula for pressure difference (Darcy’s law)?

A

△P = Q x R

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

What is the formula for mean blood pressure?

A

= cardiac output x resistance

MBP = CO x PVR (TPR)

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

In what vessels is mean blood pressure the highest?

A

In large arteries

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

In what vessels does most of the pressure change take place?

A

In small arteries and arterioles

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

What are the three variables that resistance to blood flow depend upon?

A

1) Fluid viscosity
2) The length of the tube
3) Inner radius of the tube

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

How do the three variables that resistance to blood flow depend on vary in people?

A

Fluid viscosity: Not fixed but is mostly constant
Length of tube: Fixed
Radius of tube: Variable- the main determinant of resistance

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

Generally what is resistance equal to

A

radius⁴

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

At rest what is the rate of blood flow and what is the percentage blood flow to the organs?

A 
5L/min
GI tract: 20%
Kidneys: 20%
Brain: 15%
Muscle: 15%
Skin: 5%
Heart: 5%
Bone: 3%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

During excercise what is the rate of blood flow and what is the percentage blood flow to the organs?

A 
25L/min
MUSCLE: 80%
Heart: 5%
Kidneys: 4%
GI tract: 3%
Brain: 3%
Bone: 1%
Skin:
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

What is laminar flow?

A

Where the flow of fluis follows a smooth path flowing in layers/streamlines; paths which never interfere with one another. The velocity of the fluid is constant at any one point

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

What is turbulent flow?

A

Irregular flow characterised by tiny whirlpool regions and associated with pathophysiological changes to the endothelial lining of the blood vessels. The velocity of the fluid is not constant at every point

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

Where is the flow fastest in a vessel? Why is this? What does it cause?

A

In the middle because adhesive forces act on the fluid in the periphery of the vessel.
Creates parabolic velocity profile

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

What is the shear rate?

A

The velocity gradient at any point

a tangent to the parabolic velocity profile

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

What is shear stress?

A

The shear rate multiplied by the viscosity of the fluid

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

What does high shear stress do to the physiology of endothelial cells? Where do you find high shear stress?

A

Found in laminar flow, promotes endothelial cell survival, alignment in the direction of flow and secretion of vasodilators and anticoagulants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

What does low shear stress do to the physiology of endothelial cells? Where do you find low shear stress?

A

Found in turbulent flow. Promotes endothelial proliferation and apoptosis, shape change and secretion of vasoconstrictors, coagulators and platelet aggregators

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

What is pulse pressure?

A

systolic blood pressure - diastolic blood pressure

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

What are Korotkoff sounds?

A

Turbulent flow in an artery heard when taking blood pressure

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

How can you calculate mean blood pressure?

A

≈ diastolic blood pressure + 1/3 pulse pressure

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

Why does aortic blood pressure not fall in the same way as ventricular blood pressure?

A

Due to the elasticity of the aorta and large arteries which buffer the change in pulse pressure.

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

What is Windkessel?

A

The dampening effect of arteries which recoil slowly, maintaining diastolic flow.

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

What happens to arterial compliance as you age? What effect does this have?

A

Compliance decreases as you get older. This dampens the Windkessel effect which causes pulse pressure to increase

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

What is Laplace’s relationship?

A 
T = P x r
Tension = Pressure x r
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

What is the formula for circumferential stress?

A

σ = (P x r)/ h

= tension / wall thickness

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

How does Laplace’s law relate to an aneurysm?

A

The radius of the vessel wall increases. This means for the same internal pressure the inward force from the muscular wall must also increase, but because the muscle fibres have weakened they cannot produce the force necessary so the aneurysm continues to expand
50% of ruptured aneurysms are fatal

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

What is the compliance of a vessel?

A

The relationship between the transmural pressure and the vessel volume. It depends on vessel elasticity

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

How does venous compliance compare to arteriole compliance?

A

Ten-twenty times greater compliance in veins

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

How does smooth muscle contraction effect the veins?

A

Increasing smooth muscle contraction decreases venous volume and increases venous pressure. Can manipulate the volume stored in the veins and therefore return more blood to the heart and increase cardiac output

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

What effect does gravity have on hydrostatic pressure?

A

Varies with height but is around 100mmHg. The major effect of gravity is on the distensible veins in the legs ad the volume of blood contained in them

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

What is syncope?

A

Fainting

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

What occurs when counter the effect of gravity when you go from sitting to standing?

A

1) Activation of SNS to
- constrict venous smooth muscle
- constrict arteries (↑ resistance and maintain BP)
- ↑ heart rate + force of contraction and maintain CO
2) Myogenic venoconstriction
3) Use of muscle and respiratory ‘pumps’ to improve venous return

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

How does skeletal muscle pump affect blood flow?

A

Contraction of muscles and contract the veins which moves blood towards the heart

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

How does the respiratory pump affect blood pressure?

A

Breathing heavier pulls diaphragm down which decreases the pressure in the thoracic cavity slightly, allowing more blood to come back to the right atrium

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

What problems do you get if you have poor compensatory mechanisms to counter the effect of gravity?

A

1) Varicose veins- incompetent valves cause dilated superficial veins in the leg
2) Oedema- prolonged elevation of venous pressure (even with intact compensatory mechanisms

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

What is the function of the vascular endothelium? (5)

A

1) Vascular tone management: Secrete and metabolise vasoactive substances
2) Thrombostasis: Prevents clots forming or molecules adhering to wall
3) Absorption and secretion: Allows passive/active transport via diffusion/channels
4) Barrier: Prevents atheroma development
5) Growth: Angiogenesis; mediates cell proliferation

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

How is vascular function controlled? (4)

A 
Within the circulation:
- Hormones (e.g. adrenaline)
- Drugs (e.g ACE inhibitor)
- Shear stress
In the nerves
- Neurotransmitters
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
182
Q

What are the mediators of vascular function? (5)

A

1) Nitric oxide (NO)
2) Prostacyclin (PGO2)
3) Thromboxane A2 (TXA2)
4) Endothelin-1 (ET-1)
5) Angiotensin II (Ang II)

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

What are the actions of nitric oxide? (3)

A

1) Smooth muscle
- relaxation
- inhibition of growth
2) Myocytes
- increased blood flow
- increased contractility
3) Platelets
- inhibits aggregation

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

What are the actions of prostacyclin? (3)

A

1) Smooth muscle
- relaxation
- inhibition of growth
2) Myocytes
- increased blood flow
- increased contractility
3) Platelets
- inhibits aggregation

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

What are the actions of thromboxane A2? (3)

A

1) Smooth muscle
- contraction
2) Myocytes
- reduced blood flow
3) Platelets
- activation
- stimulates aggregation

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

What are the action of endothelin-1? (2)

A

1) Smooth muscle
- CONTRACTION
- stimulation of growth
2) Myocytes
- reduced blood flow
- increased contractility

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

What are the actions of angiotensin II? (2)

A

1) Smooth muscle
- contraction
- stimulation of growth
2) Myocytes
- reduced blood flow
- remodelling
- fibrosis

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

What is the mechanism of action nitric oxide?

A

Inside Endothelial Cell

1) G protein couple receptor binds ligand (e.g. acetyl choline)
2) Activates phospholipase C
3) Phospholipase C converts PIP2 into
- IP3
- DAG
4) IP3 causes an influx of Ca2+ into the cytosol from ER
5) ↑ Ca2+ activates eNOS (endothelial Nitric Oxide Synthase)
6) eNOS produces NO (L-arginine + O2 → L-citrulline + NO)
7) NO diffuses out of cells to vascular smooth muscle cells
8) NO upregulates guanylyl cyclase which converts GTP→cGMP
9) cGMP activates protein kinase G
10) Protein kinase G triggers relaxation

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

What upregulates eNOS? (2)

A

1) Increase in intracellular Ca2+

2) Shear stress (mechanoreceptor in vessel wall)

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

How is arachidonic acid produced? (2)

A

1) Phospholipid converted to arachidonic acid using phospholipase A2
2) DAG lipase converts DAG to arachidonic acid

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

How is prostacyclin produced from arachidonic acid?

A

1) COX1 and COX2 convert archidonic acid to PGH2 (prostaglandin H2)
2) Prostacyclin synthase converts PGH2 to prostacyclin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
192
Q

How is thromboxane A2 produced from arachidonic acid?

A

1) COX1 and COX2 convert arachidonic acid to PGH2 (prostaglandin H2)
2) Thromboxane synthase converts PGH2 to thromboxane A2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
193
Q

What are the actions of prostacyclin once it has been produced? (2)

A

1) Binds to prostacyclin receptor on vascular muscle cell

2) Travels out into lumen

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

What is the mechanism of action of prostacyclin when it binds to receptor on vascular smooth muscle?

A

1) Prostacyclin binds to receptor and activates adenylate cycles
2) AC converts ATP to cAMP
3) cAMP upregulates protein kinase A
4) Protein kinase A causes relaxation

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

What are the possible actions of thromboxane A2 once it has been produced?

A

1) Binds to receptors on platelets

2) Binds to receptors on vascular smooth muscle cell

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

What is the mechanism of action when thromboxane A2 binds to platelets?

A

1) Thromboxane A2 binds to TPα receptor
2) This activates the platelets
3) Also causes production of more thromboxane A2 from arachidonic acid
4) This causes activation of other platelets (chain reaction)

197
Q

What is the mechanism of action when thromboxane A2 binds to vascular smooth muscle?

A

1) Thromboxane A2 binds to TPβ receptor
2) Activates phospholipase C
3) Phospholipase C converts PIP2 into IP3
4) IP3 causes contraction of vascular smooth muscle

198
Q

What is the mechanism of production of endothelin-1?

A

1) Endothelial cell nucleus produces pro-endothelin-1

2) Endothelin converting enzyme (ECE) converts pro-endothelin-1 into endothelin-1

199
Q

Where is endothelin-1 derived from?

A

The nucleus of the endothelial cell

200
Q

What receptors can endothelin-1 bind to on vascular smooth muscle? What happens when endothelin-1 binds these receptors? What does this cause?

A

ETA and ETB
When endothelin-1 binds it activates phospholipase C which converts PIP2 to IP3.
This causes vascular smooth muscle contraction

201
Q

What is the mechanism when endothelin-1 binds to ETB on an endothelial cell?

A

1) Upreglates eNOS
2) eNOS produces NO (L-arginine + O2 → L-citrulline + NO)
3) NO released from cell and enters vascular smooth muscle
4) Causes relaxation

202
Q

What determines whether endothelin-1 causes contraction or relaxation?
Typically what does endothelin-1 cause?

A

The expression of receptors

Typically causes contraction

203
Q

Give 6 examples of endothelin-1 antagonists

A

1) Prostacyclin (PGI2)
2) NO
3) ANP
4) Heparin
5) HGF
6) EGF

204
Q

Give 4 examples of endothelin-1 agonists

A

1) Adrenaline
2) ADH
3) Angiotensin II
4) IL-1

205
Q

Where is angiotensinogen produced?

A

In the liver

206
Q

Where is renin produced?

A

In the kidney

207
Q

What is the mechanism of the renin-angiotensin-aldosterone axis?

A

1) Angiotensinogen converted to angiotensin I by renin
2) Angiotensin I is converted to angiotensin II by ACE (angiotensin converting enzyme)
3) Angiotensin II increases water retention and vascular resistance
4) Causes increased blood pressure

208
Q

Where is ACE located?

A

A membrane protein on endothelial cells in the lungs and in kidneys

209
Q

What are the five actions of angiotensin II? What do they do?

A 
INCREASED WATER RETENTION:
1) ADH secretion
2) Aldosterone secretion
3) Tubular sodium reabsorption
INCREASED VASCULAR RESISTANCE
4) Sympathoexcitation
5) Arteriolar vasoconstrication
210
Q

What does angiotensin II do?

A

Increase blood pressure

211
Q

What is the mechanism by which angiotensin II causes contraction of vascular smooth muscle?

A

1) Angiotensin II binds AT1 receptor which activates phospholipase C. This converts PIP to IP3 which causes contraction
2) Angiotensin II binds to AT1 receptor which binds SRC which causes growth (angiogenesis) and also has a limited effect on contraction.

212
Q

What is the mechanism by which bradykinin causes vascular smooth muscle relaxation?

A

1) Bradykinin binds to B1 receptor on endothelial cells
2) This converts PIP2 to IP3
3) IP3 produces NO
4) NO leaves endothelial cell and enters vascular smooth muscle and causes vasodilation

213
Q

How is the action of bradykinin on vascular smooth muscle prevented?

A

Bradykinin is broken down by ACE inhibitor making it inactive

214
Q

What are the different methods of increasing nitric oxide bioavailability? Are these dependent on the endothelium? Give examples (3)

A

1) Stimlate the production of NO
- Endothelium-dependent
- e.g. Acetylcholine
2) ‘Donate’ ready to use NO
- Endothelium- independent
- e.g. GTN, nicorandil, ISMN
3) Enhance the effects of NO
- prevent counterproductive processes
- viagra

215
Q

What is the mechanism from NO-donors?

A

1) Exogenous NO enters the vascular smooth muscle
2) Converted to guanylyl cyclase
3) Guanylyl cyclase converts GTP to cGMP
4) cGMP upregulated protein kinase G which causes relaxation of smooth muscle

216
Q

What is the self regulation mechanism of cGMP? Pharmacologically what is this used for?

A

cGMP is broken down to GMP by Phosphodieaterase (PDE5) which prevents too much vascular smooth muscle relaxation.
Downregulating the effects of phosphodiesterase is the mechanism of viagra

217
Q

What is the effect of low-dose aspirin on prostacyclin?

A

Slight reduction
Predominantly produced in endothelial cells. When COX enzymes are disabled the nucleus generates some more and can replace them

218
Q

What is the effect of low-dose aspirin on thromboxane?

A

Thromboxane synthase is predominantly produced in platelets. They are unable to produce more COX enzymes when disabled by so thromboxane levels get gradually lower with each dose of aspirin

219
Q

What does low-dose aspirin do to each COX enzyme?

A

COX-1: Aspirin acetylation inactivated enzyme

COX-2: Aspirin acetylation switches its function (to generating protective lipids)

220
Q

What is the difference in concentration between intracellular and extracellular [Ca2+]?

A

Up to 20,000 times greater extracellularly
Intracellular [Ca2+]: 100nmol/L
Extracellular [Ca2+]: 2mmol/L

221
Q

What are the neurotransmitters in a normal sympathetic neurone that acts on an effector organ?

A

Acetylcholine in sympathetic trunk

Noradrenaline in synapse with effector organ

222
Q

What are the two uptake mechanisms for noradrenalin in a sympathetic neuron?

A

Uptake 1: A recycling system where neuradrenaline gets back into the neuron and is used again or degraded
Uptake 2: Occurs in the effector cell where it is broken down by enzymes (e.g. COMT)

223
Q

How and where does synthesis of noradrenalin occur?

A

Occurs in terminal varicosity

1) Tyrosine enters terminal varicosity and is converted to DOPA.
2) DOPA converted to dopamine
3) Dopamine stored in vesicles
4) Dopamine converted to noradrenaline in vesicl

224
Q

What is the release of neurotransmitter (e.g. noradrenaline) dependent on?

A

ATP

225
Q

What are the two groups of effects of adrenoceptors?

A

1) EXCITATORY effects on smooth muscle- α-adrenoceptor-mediated
2) RELAXANT effects on smooth muscle, stimulatory effects on heart (by cAMP)- β-adrenoceptor mediated

226
Q

What are the three types of β-adrenoceptors? Where are they found?

A

1) β1-adrenoceptors located on
- cardiac muscle
- smooth muscle of the GI tract
2) β2-adrenoceptors located on
- bronchial, vascular and uterine smooth muscle
3) β3-adrenoceptors: found on fat cells and possibly smooth muscle of GI tract. Involved in thermogenesis but few in humans

227
Q

What are the two different types of α-adrenoceptor? Where are they located? What is their role?

A

1) α1-adrenoceptor: located post-synaptically i.e. predominantly on effector cells
- important in mediating constriction of resistance vessels in response to sympathomimetric amines
2) α2-adrenoceptor: located on presynaptic nerve terminal membrane
- their activation by released transmitter causes negative feedback inhibition of further transmitter release
- some are post-synaptic on vascular smooth muscle

228
Q

What reaction are α1-adrenoceptors coupled to?

A

Phosphorylation of GDP which causes activation of phospholipase C. This converts PIP2 to IP3 and DAG. IP3 in turn causes a release of stored calcium, activating Ca2+ dependent protein kinase

229
Q

What reaction are β-adrenoceptors coupled to?

A

Activate adenylyl cyclase to convert ATP to cAMP

230
Q

What reaction are α2-adrenoceptors coupled to?

A

Inhibit adenylyl cyclase, lowering the amount of cAMP produced from ATP. This increases the effectiveness of intracellular calcium

231
Q

What catecholamines act on the α1-adrenoceptor?

A

Noradrenaline
Adrenaline
Phenylephrine
Dopamine: weak effects

232
Q

What catecholamines act on the α2-adrenoceptor?

A

Noradrenaline
Adrenaline
Phenylephrine

233
Q

What catecholamines act on the β1-adrenoceptor?

A

Noradrenaline
Adrenaline
Isoprenaline
Dopamine: weak effects

234
Q

What catecholamines act on the β2-adrenoceptor?

A

Adrenaline

Isoprenaline

235
Q 
What happens to the following if noradrenaline is intravenously infused into a patient:
Systolic BP
Diastolic BP
Mean BP
Heart rate
A

Systolic BP: ↑↑↑ (increased cardiac contractility)
Diastolic BP: ↑↑ (increased vasoconstriction)
Mean BP: ↑↑
Heart rate: ↓ (reflex bradycardia- effect of baroreceptors)

236
Q 
What happens to the following if adrenaline is intravenously infused into a patient:
Systolic BP
Diastolic BP
Mean BP
Heart rate
A

Systolic BP: ↑↑ (increases contractility)
Diastolic BP: ↓ (reduced peripheral resistance)
Mean BP: ↑
Heart rate: ↑ (direct β effect on the heart)

237
Q 
What happens to the following if isoprenaline is intravenously infused into a patient:
Systolic BP
Diastolic BP
Mean BP
Heart rate
A

Systolic BP: ↑ (direct increase in contractility)
Diastolic BP: ↓↓ (potent vasodilator effect)
Mean BP: ↓ or →
Heart rate: ↑↑ (direct effect on the heart)

238
Q

What adrenoceptors are found in the skin and viscera?

A

α-adrenoceptors

239
Q

What factors regulate renin release? (3)

A

1) Sodium: NaCl reabsorption at macula densa
2) Blood pressure in pre-glomerular vessels
3) β1-receptor activation in the kidney (if the sympathetic nervous system is inactive)
…all activate renin release

240
Q

What do β-blockers do?

A

Block β1 receptor on the kidney which inhibits renin release

241
Q

What do ACE inhibitors do?

A

Block ACE which prevents the conversion of renin to angiotensin II

242
Q

What do α2 agonists do?

A

Prevent the activation of β1 receptors in the kidney which prevents the activation of renin release

243
Q

How do NSAIDs effect renin release?

A

Increase the release of renin

244
Q

What are angiotensin II type 1 (AT1) receptors? What do they do, where are they found? What is their role in pharmacology?

A

G-protein coupled; Gi and Gq, also coupled to phospholipase A2
Located in blood vessels, brain, adrenal, kidney and heart
Activation of AT1 receptors increases BP
Blocking them stops this (antihypertensive)

245
Q

What is the role of of Angiotensin II? What are the two types of response?

A

RAPID PRESSOR RESPONSE (minutes)
- direct vasoconstriction
- enhanced action of peripheral noradrenaline (increased release, decreased uptake)
- increased sympthatic discharge
- release of catecholamines from adrenal
SLOW PRESSOR RESPONSE
- direct effects to increase Na+ reabsorption in proximal tubule
- synthesis and release of aldosterone from adrenal cortex
- altered renal hemodynamics (renal vasoconstriction, enhanced adrenaline effects in kidney)

246
Q

What are the haemodynamic effects of angiotensin II on cardiovascular structure? What do they cause (2)

A

1) Increased preload and afterload
2) Increased vascular wall tension
Causes vascular and cardiac hypertrophy and remodelling

247
Q

What are the non-haemodynamic effects of angiotensin II on cardiovascular structure? (3)

A

1) Increased expression of proto-oncogenes
2) Increased production of growth factors
3) Increased synthesis of extracellular matrix proteins
Causes vascular and cardiac hypertrophy and remodelling

248
Q

What is the family of enzymes called which synthesise angiotensin II? What effect do they have on the production of angiotensin II?

A

Chymase enzymes
They will produce angiotensin II from angiotensin I and sometimes angiotensinogen even when ACE inhibitors are given at maximal dose

249
Q

What are the two side effects that occur when taking angiotensin II type 1 blockers?

A

1) Cough: due to excess bradykinin build up in the lung

2) Angioedema: pseudoallergy similar to anaphylaxis

250
Q

What is a uricosuric effect?

A

Where the kidney is stimulated to get rid of more uric acid

251
Q

What are the physiological effects of aldosterone?

A

Maintains body content of Na+, K+, (and H2O)

1) Increased Na+ retention (and H2O retention)
2) Increased K+ excretion (and H+ excretion)

252
Q

What effect do high levels of K+ have on aldosterone?

A

Increase release of aldosterone to bring down the levels of K+

253
Q

What disease are high levels of aldosterone associated with?

A

Cardiovascular disease

254
Q

What is the formula for bloow flow?

A

F=△P/R

Flow= pressure gradient / vascular resistance

255
Q

What is the relationship between flow and pressure gradient?

A

The are directly proportional

256
Q

If you halve the radius of a blood vessel what does this do to the resistance?

A

Increases it 16 fold

257
Q

What is normal MAP (mean arterial pressure)?

A

93mmHg

258
Q

What is a normal pressure in venules?

A

Only a few mmHg in any tissue

259
Q

What is vascular tone? When is this maintained? Why?

A

Arteriolar smooth muscle normally displays a state of partial contraction. It allows the capacity to both increase and decrease the flow to a tissue

260
Q

What are the two functions that are accomplished by arterioles independently adjusting their radii?

A

1) Blood flow matched to metabolic needs of specific tissues (depending on body’s momentary needs): regulated by local (intrinsic) controls; independent of nerve or hormone
2) Help regulate arterial blood pressure: regulated by extrinsic controls

261
Q

What is active hyperemia? What type of control of the microcirculation is this?

A

The mechanism for local regulation.
When a tissue becomes more metabolically active the oxygen consumption increases, resulting in lower oxygen in the capillaries. This CHEMICAL change signal to the arterioles, causing vasodilation
This is an intrinsic control

262
Q

What are the different types of intrinsic control of the microcirculation?

A

1) Chemical
2) Physical
- temperature
- stretch

263
Q

How does the intrinsic control of the microcirculation respond to temperature? What is the medicinal application of this?

A

A decrease in temperature on the arteriole (e.g. in the skin) causes constriction of vessels. This diverts blood flow away from the cold to try and retain heat.
If you have an injury applying an ice pack diverts blood flow from the area which will reduce swelling

264
Q

What is myogenic vasoconstriction? What type of control of the microcirculation is this?

A

If blood pressure goes up the stretch detected by the arterioles (which is not linked to an increased metabolic demand) the tissue does not want the increased blood supply which causes vasoconstriction (autoregulation)
This is an intrinsic control

265
Q

What is the formula for cardiac output? (MAP)

A

CO=MAP/TPR

266
Q

Consider α receptors and β receptors. Which receptors are responsible for constricting and which receptors are responsible for dilating?

A

α receptors are responsible for constricting

β receptors are responsible for dilating

267
Q

What type of nerves innervate blood vessels?

A

Sympathetic

268
Q

What are the different types of extrinsic control of the microcirculation?

A

1) Neural

2) Hormonal

269
Q

Give examples of hormones which cause vasoconstriction?

A

1) Vasopressin

2) Angiotensin

270
Q

What is the role of adrenaline and noradrenaline in regulation of arterial blood pressure?

A

They act like noradrenaline and adrenaline released from nerves, enhancing the sympathetic response

271
Q

What pressure does blood leave the arterioles?

A

37mmHg

272
Q

What is the diameter of a capillary?

A

7μm

273
Q

What is the thickness of a capillary wall?

A

1μm

274
Q

Why is the capillary density of a tissue important?

A

Higher metabolically active tissues need denser capillary networks. Harder working cells need to be nearer to capillaries

275
Q

What tissues have the most dense capillary networks?

A

Skeletal muscle= 100 cm2/g
Myocardium/ brain= 500cm2/g
Lung= 3500cm2/g
(for gas exchange rather than metabolic

276
Q

What is the most common type of capillary structure?

A

Continuous

has H2O filler gap junctions which allow for transfer of small electrolytes for example.

277
Q

What are the different types of capillary structure?

A

1) Continuous
2) Fenestrated
3) Discontinuous

278
Q

What is the capillary structure of the blood brain barrier?

A

Really tight junctions between endothelial cells of the blood brain barrier. This allows the brain to have really tight control over the things that get to the brain

279
Q

What is bulk flow?

A

Where a volume of protein free plasma filters out of the capillary, mixes with the surrounding interstitial fluid and is reabsorbed

280
Q

What is hydrostatic pressure?

A

The pressure that forces fluid out of the gap junctions of capillaries and into tissues

281
Q

What is oncotic pressure?

A

The force drawing fluid back into the capillaries- created by proteins and plasma

282
Q

What are Starling forces?

A

Hydrostatic pressure and oncotic pressure that must balance

283
Q

What is ultrafiltration?

A

When pressure inside the capillary > pressure in the interstitial fluid

284
Q

What balance of pressures causes reabsorption of fluid back into the capillaries?

A

If inward driving pressures > outward driving pressures across the capillary

285
Q

The cardiovascular system is a closed loop. What is the lymphatic system?

A

Blind ended

286
Q

Where are the major points where the lymph is returned to the cardiovascular system?

A

Right lymphatic duct

Thoracic duct

287
Q

How much fluid is returned to the blood stream per day through the lymph?

A

3L/day

288
Q

What balance of fluids causes oedema?

A

Rate of production>rate of removal

289
Q

What disease causes parasitic blockage of the lymph nodes?

A

Elephantiasis

290
Q

What is the formula for stroke volume?

A

SV= EDV-ESV

Stroke volume = end-diastolic volume - end-systolic volume

291
Q

What is the formula for cardiac output? (HR)

A

CO=HRxSV

292
Q

What is central venous pressure? What does it determine?

A

Mean pressure in the right atrium. The amount of blood flowing back to the heart

293
Q

In veins, constriction determines what?

A

Compliance and venous return

294
Q

In arterioles, constriction determines what?

A
  • Blood flow to the organs they serve
  • Mean arterial blood pressure
  • The pattern of distribution of blood to organs
295
Q

What is ANP? Where is it secreted? What does it do?

A

Atrial Natriuretic Peptide
Secreted from the cardiac atria
Vasodilator

296
Q

What vessels are innervated by the sympathetic nervous system?

A

All vessels except capillaries, precapillary sphincters and some metarterioles

297
Q

What adrenoceptor does noradrenaline preferentially bind to? What does this cause?

A

α1-adrenoceptor

Causes smooth muscle contraction and vasoconstriction

298
Q

What is the vasomotor centre? Where is it located? What does it do?

A

The vasomotor centre is composed of a vasoconstrictor (pressor) area, a vasodilator (depressor) area and a cardioregulatory inhibitory area
It transmits impulses distally through the spinal cord to almost all blood vessels
Higher centers of the brain (e.g. hypothalamus) can exert powerful excitatory effects on the VMC.
Lateral portions: control heart activity by influencing heart rate and contractility
Medial portion: transmits signals via vagus nerve to heart that tend to decrease heart rate

299
Q

What cardiac innervation causes increased heart rate?

A

1) Increased activity of sympathetic nerves to heart
2) Increased plasma adrenaline
3) Decreased activity of parasympathetic nerves to heart

300
Q

How is the force of cardiac contraction controlled?

A

Increased Ca influx

Increased Ca uptake into intracellular stores

301
Q

What are the intrinsic controls of increasing stroke volume?

A

Increased venous return increases atrial pressure
These increase end-diastolic ventricular volume
Increased respiratory movements decrease intrathoracic pressure which assists increasing end-diastolic ventricular volume. These (Starling’s law) increase stroke volume

302
Q

What are the extrinsic controls of increasing stroke volume?

A

1) Increased activity of sympathetic nerves to heart

2) Increased plasma adrenaline

303
Q

Where are the baroreceptors located?

A

In the aortic arch and the common carotid

304
Q

What nerve innervates the aortic arch baroreceptor? (to the vasomotor centre)

A

Vagus nerve

305
Q

What nerve innervates the common carotid baroreceptor? (to the vasomotor centre)

A

Glossopharyngeal nerve

306
Q

What pressure does the common carotid respond to? And what temperature is it most sensitive at?

A

Responds to: 60-180mmHg

Most sensitive: 90-100mmHg

307
Q

How does rest affect the heart rate, stroke volume and blood vessels. Answer with reference to both the sympathetic and parasympathetic nervous system?

A

1) Increased parasympathetic stimulation of the heart decreases the heart rate
2) Decreased sympathetic stimulation of the heart decreases the heart rate and stroke volume
3) Decreased sympathetic stimulation to the blood vessels produces vasodilation

308
Q

What mechanisms increase venous pressure (4) and explain the mechanism to increase atrial pressure?

A

1) Increased blood volume
2) Increased activity of sympathetic nerves to veins
3) Increased skeletal muscle “pump”
4) Increased respiratory movements
Cause:
Increased venous pressure
Increased venous return
Increased atrial pressure

309
Q

Explain the mechanism from haemorrhage to control venous pressure

A

1) ↓ blood volume
2) ↓ venous pressure
3) ↓ venous return to heart
4) ↓ atrial pressure
5) ↓ ventricular end diastolic volume
6) ↓ stroke volume
7) ↓ arterial blood pressure
8) ↓ cardiac output
Baroreceptor feedback and reciprocal innervation
9) ↑ sympathetic discharge to veins
10) ↑ venous constriction
11) ↑ venous pressure

310
Q

Why might the transition from supine to standing induce a hypotensive effect? (Starling’s law)

A

Standing → supine = ↑ hydrostatic pressure in the blood vessels of the legs
This causes a reduction in effective circulating volume
↑ ventricular filling during diastole (end-diastolic volume) → ↑ volume of ejected blood during the resulting systolic contraction (stroke volume)
→ hypotension (transient)

311
Q

What is autotransfusion? (an extra compensatory mechanism to haemorrhage)

A

Where hydrostatic pressure drops and the colloid osmotic pressure rises causing fluid to flow into the circulation, raising blood volume

312
Q

What happens to total peripheral resistance when you exercise? What changes cause this?

A

Heart and lungs + skeletal muscle- vasodilation
Skin has decreased sympathetic stimulation= vasodilation
GIT and kidney have increased sympathetic stimulation= vasocontriction

313
Q

What is the mechanism by which a haemostatic plug forms in response to vessel injury?

A

1) Vessel constriction
2) Formation of an unstable platelet plug
- platelet adhesion
- platelet aggregation
3) Stabilisation of the plug with fibrin
- blood coagulation
4) Dissolution of clot and vessel repair
- fibrinolysis

314
Q

During haemostasis what is the mechanism of platelet adhesion?

A

1) Removal of endothelial layer causes exposure of collagen
2a) Von Willebrand factor binds to the collage and captures platelets by binding to Glp1b (platelet receptor) OR
2b) Glpa platelet receptors bind directly to collagen
(This is because of differences in flow rates of the vasculature
3) Platelets then release important cofactors (ADP and prostaglandins)

315
Q

What causes platelet aggregation in haemostasis?

A

Release of cofactors (ADP and thromboxane) cause platelets to clump together by the GlpIIB/IIIa receptor

316
Q

What does thrombin do?

A

It is an important enzyme that activates platelets to clump

317
Q

What changes occur to a platelet when it has been activated?

A

1) Change shape
2) Change membrane composition
3) Present new or activated proteins on their surface

318
Q

Where are most clotting factors produced?

A

In the liver

319
Q

Where is von Willebrand factor produced?

A

In endothelium (in high concentration)

320
Q

Where is clotting factor V produced?

A

In megakaryocytes

321
Q

What is the mechanism of the intrinsic blood coagulation pathway?

A

1) XII→XIIa
2) XI→XIa
3) IX→IXa
4) X→Xa (catalysed by VIIIa and PI)

322
Q

What is the mechanism of the extrinsic blood coagulation pathway?

A

Tissue factor (from vessel damage) binds to VIIa and this directly converts X→Xa

323
Q

What is the common pathway for blood coagulation?

A

1) Prothrombin → thrombin (IIa) catalysed by Xa
2) Thrombin converts fibrinogen to fibrin
3) Fibrin crosslinks (proteolytic cleavage) creating an insoluble clot

324
Q

What is the mechanism of fibrinolysis?

A

tPA (tissue plasminogen activator) converts plasminogen into plasmin which starts to break down the fibrin clot

325
Q

What is the fibrin clot broken down into?

A

Fibrin degradation products (FDP)

326
Q

How does the coagulation pathway amplify?

A

Thrombin activates VIIIa to create more Xa which creates more thrombin

327
Q

What are the different types of coagulation inhibitory mechanisms?

A

1) Direct inhibition

2) Indirect inhibition

328
Q

Give an example of the direct inhibition coagulation inhibitory mechanism

A

Antithrombin (sometimes known as antithrombin III), which is an inhibitor of thrombin and other clotting proteinases

329
Q

Give an example of the indirect inhibition coagulation inhibitory mechanism

A

Inhibition of thrombin generation by the protein C anticoagulant pathway

330
Q

What is the only role of antithrombin?

A

To regulate the activity of coagulation

331
Q

What does heparin do?

A

Heparin accelarates the action of antithrombin.

Heparin is used for immediate anticoagulation in venous thrombosis and pulmonary embolism

332
Q

How does the indirect coagulation inhibitory mechanism work?

A

The protein C pathway down-regulates thrombin generation by inactivating factor Va and VIIIa

333
Q

What coagulation inhibitory mechanism failure are risk factors for thrombosis? (4)

A

1) Antithrombin deficiency
2) Protein C deficiency
3) Protein S deficiency
4) Factor V Leiden (not so easily inactivated by protein C)

334
Q

What are the characteristics of abnormal bleeding?

A

Bleeding that is:

  • Spontaneous
  • Out of proportion to the trauma/injury
  • Unduly prolonged
  • Restarts after appearing to stop
335
Q

What is primary haemostasis?

A

Formation of an unstable platelet plug
Platelet adhesion
Platelet aggregation

336
Q

What are the different types of deficiency or defect that can occur in primary haemostasis? Give examples of each (3)

A

1) Collagen- vessel wall (e.g. steroid therapy, age, scurvey)
2) Von Willebrand factor (e.g. Von Willebrand disease- genetic deficiency)
3) Platelets (e.g. aspirin and other drugs, thrombocytopaenia)

337
Q

What stimulates the coagulation system to form a haemstasis plug?

A

Collagen

Tissue factor

338
Q

What is the pattern of bleeding in a patient with defects of primary haemostasis?

A
  • Immediate
  • Easy bruising
  • Nose bleeds (prolonged: >20 mins)
  • Gum bleeding
  • Menorrhagia (anaemia)
  • Bleeding after trauma/surgery
  • Petechiae (specific for thrombocytopenia)
339
Q

What is secondary haemostasis?

A

Stabilisation of the plug with fibrin (blood coagulation)

340
Q

What coagulation factor is usually lacking in haemophilia?

A

Factor VIII

341
Q

What defects can occur in secondary haemostasis?

A

1) Genetic (e.g. haemophilia: FVIII or FIV deficiency
2) Liver disease (acquirder- most coagulation factors are made in the liver)
3) Drugs (warfarin-inhibits synthesis, other block function)
4) Dilution (results from volume replacement)
5) Consumption (Disseminated intravascular coagulation)

342
Q

What is disseminated intravascular coagulation?

A

Generalised activation of coagulation- Tissue factor
Associated with sepsis, major tissue damage, Consumes and depletes coagulation factors and platelets
Activation of fibrinolysis

343
Q

What is the pattern of bleeding with a defect in secondary haemostasis?

A

1) Often delayed (after primary haemostasis)
- Prolonged
2) Deeer: joints and muscles
3) Not from small cuts (primary haemostasis is ok)
4) Nosebleeds are rare
5) Bleeding after truama/surgery
6) After intramuscular injection

344
Q

What is the role of Von Willebrand factor in primary haemostasis?

A

It helps capture platelets onto collagen

345
Q

A bleeding time test is performed on a patient with haemophilia A by making a small blade incision on the forearm. What is the likely outcome?

A

A normal result: bleeding stops after

346
Q

What is thrombosis?

A

1) Intravascular coagulation
2) Inappropriate coagulation
3) Coagulation inside a blood vessel
4) Coagulation not preceded by bleeding
5) Thrombi may be venous or arterial

347
Q

What are the effects of thrombosis?

A

1) Obstructed flow of blood
- Artery → myocardial infarction, stroke, limb ischaemia
- Vein → pain and swelling
2) Embolism
- Venous emboli, to lungs (pulmonary embolus)
- Arterial emboli, usually from heart, may cause stroke or limb ischaemia

348
Q

What is the prevalence of a venous thrombo-embolism?

A 
Overall:
1 in 1000 (young)
1 in 10,000 (older)
Incidence doubles with each decade
Cause of 10% of hospital deaths
(25000 preventable deaths per annum)
349
Q

What causes some people to get thrombosis?

A

Genetic constitution
Effect of age and previous illnesses and medication
Acute stimulus

350
Q

What is Virchow’s triad?

A

Blood
Vessel wall
Flow
Shows the three contributory factors to thrombosis which may be inherited or acquired

351
Q

Deficiency of which anticoagulant proteins, major regulatory proteins, causes an increased risk of thrombosis?

A

1) Antithrombin
2) Protein C
3) Protein S

352
Q

Which coagulant proteins/ activity causes increased risk of thrombosis when increased

A

1) Factor VIII
2) Factor II and others
3) Factor V Leiden (increased activity due to activated protein C resistance)
4) Thrombocytosis

353
Q

What are the clinical and laboratory features of thrombophilia?

A 
Clinical
- Thrombosis at a young age
- 'idiopathic thrombosis'
- Multiple throboses
- Thrombosis whilst anticoagulated
Laboratory
- Identifiable cause of increased risk (AT deficiency, Factor V Leiden, global measures of coagulation activity)
354
Q

What conditions alter blood coagulation and increase risk of thrombosis?

A
  • Pregnancy
  • Malignancy
  • Surgery
  • Inflammatory response
355
Q

A low plasma level of antithrombin is likely to result in?

A

An increased risk of post-operative thrombosis

356
Q

The increased risk of thrombosis associated with the COCP is likely to be the result of:

A

Reduced concentration protein S

357
Q

What happens to factors when you have bleeding?

A

INCREASE fibrinolytic factors and anticoagulant proteins

DECREASE coagulation factors and platelets

358
Q

What happens to factors when you have thrombosis?

A

DECREASE fibrinolytic factors and anticoagulant proteins

INCREASE coagulation factors and platelets

359
Q

What are the treatment and prevention options for thrombosis?

A 
Increase anticoagulants (e.g. heparin)
Decrease coagulants (e.g. warfarin and antiplatelets)
360
Q

What are the complications associated with increased blood pressure?

A

1) Increased size and thickness of the left ventricle
2) Increased wall thickness in large arteries
3) Changes in microvasculature
4) Increased risk of heart attack and stroke

361
Q

What is primary hypertension?

A

Hypertension which doesn’t have a known secondary cause

362
Q

What is secondary hypertension?

A

Hypertension which is caused by another medical condition

363
Q

What is the world’s number one risk factor for death?

A

Hypertension

364
Q

What are the different genetic causes of hypertension?

A

Monogenic

Complex polygenic

365
Q

What are environmental causes of hypertension

A

1) Dietary salt
2) Obesity/overweight, lack of excise
3) Alcohol, pre-natal environment (birthweight)
4) pregnancy (pre-eclampsia)
5) Other dietary factors and environment exposure

366
Q

What is the cause of monogenic hypertension?

A

Problem in the way the kidney handles salt

367
Q

What is primary hypertension typically associated with? (5)

A

1) Increased total peripheral resistance
2) Reduced arterial compliance (higher pulse pressure)
3) Normal cardiac output
4) Normal blood volume/ extracellular volume
5) Central shift in blood- secondary to reduced venous compliance

368
Q

What accounts for the elevated pulmonary vascular resistance in hypertension?

A

1) Active narrowing of arteries
- vasoconstriction (probably short-term)
2) Structural narrowing of arteries
- growth and remodelling (adaptive)
3) Loss of capillaries
- rarefraction (adaptive/damage)

369
Q

What is isolated systolic hypertension? What causes it?

A

Systolic BP ≥ 140
Diastolic BP ≤ 90
Due to increasing stiffness of medium/large arteries
Pulse wave reflected and is greater by the time it reached brachial artery (amplified rather than diminished)

370
Q

What is the single most important factor in influencing vascular damage

A

Pulse pressure

371
Q

Why is the kidney thought to be involved in hypertension?

A

Exerts a major influence on blood pressure though regulation of sodium/water/ECF
Impaired renal function is the commonest cause of secondary hypertension
Salt intake it strongly linked with blood pressure
Hypertension has been “transplanted” with the kidney in rats

372
Q

What are the major risks attributable to elevated blood pressure?

A

Increased risk of:

  • coronary heart disease
  • stroke
  • peripheral vascular disease/ atheromatous disease
  • heart failure
  • atrial fibrillation (indirect effect on left atrium which becomes expanded and stretched)
  • dementia/ cognitive impairment
  • retinopathy (changes in the vasculature in the retina- particularly arterioles)
373
Q

How does hypertension affect the risk of congestive heart failure?

A

Increases the risk 2-3 fold

374
Q

How does hypertension affect the large arteries?

A

It causes the the media and intima to widenand increases the risk of atherosclerosis

375
Q

What are the characteristics of grade IV retinopathy?

A

1) Papilledema- swelling of the optic disc
2) Very severe complication with very high mortality
3) Not untreatable

376
Q

What happens to the microvasculature with hypertension?

A

Reduced capillary density
Elevated capillary pressure
(impaired perfusion, increased peripheral vascular resistance, damage and leakage)

377
Q

What happens to the kidney with hypertension?

A

Cortex of the kidney is thinned
Renal dysfunction is common in hypertension (increased microalbumin excretion in urine)
(Especially with hyperglycaemia) can lead to progressive renal failure and end stage renal disease

378
Q

What happens to mean blood pressure and pulse pressure with age?

A

Both rise with age

379
Q

What is the major factor for the rise in blood pressure with age?

A

Dietary salt intake

380
Q

What are the non-modifiable risk factors for atherosclerosis?

A

Age
Sex
Genetic background

381
Q

What are the potentially modifiable risk factors for atherosclerosis?

A 
Smoking
Lipids (high cholesterol)
Blood pressure
Diabetes
Obesity
Lack of exercise
382
Q

Which of the following is known to significantly increase cardiovascular risk by acting as atherosclerotic risk factor?

a) High level of high density lipoprotein cholesterol
b) High level of low density lipoprotein cholesterol decreased in familial hypercholersterolaemia
c) Hepatitis B infection
d) Malaria
e) Blood pressure lowering medication
f) Clotting factor VIII deficiency

A

b) High level of low density lipoprotein cholesterol decreased in familial

383
Q

If risk factors for atherosclerosis are general why is atherosclerosis focal?

A

Turbulence is the reason people develop some types but not others

384
Q

What are the progressive steps of atherosclerosis?

A

1) Coronary artery at lesion-prone location. Adaptive thickening of smooth muscle
2) Type II lesion. Macrophage foam cells in smooth muscle layer
3) Type III (preatheroma). Small pools of extracellular lipid deposit in smooth muscle
4) Type IV (atheroma). Core of extracellular lipid in smooth muscle
5) Type V (fibroatheroma) Fibrous thickening of smooth muscle
6) Type VI (complicated lesion). Fissure and haematoma. Thrombus formation in smooth muscle

385
Q

What components make up a low density lipoprotein?

A 
Core= triglyceride and cholesterol esters
Phospholipid coat (lipid monolayer) containing cholesterol molecules, and apoproteins (docking molecules)
386
Q

What is subendothelial trapping of LDL and what modifications occur?

A

Low density lipoproteins leak through the endothelial barrier and are trapped by binding to sticky matrix carbohydrates (proteoglycans) in the sub-endothelial layer. They are then susceptible to modification.
LDL becomes oxidatively modified by free radicals
Oxidised LDL is phagocytosed by macrophages and stimulates chronic inflammation (forming foam cells)

387
Q

What is familial hyperlipidemia?

A

An autosomal genetic disease causing massively elevated cholesterol (20mmol/L) due to a failure to clear LDL from the blood
Xanthomas and early atherosclerosis; if untreated fatal myocardial infarction before 20 years old
Causes fat deposits in the skin

388
Q

What are the two types of macrophage scavenger receptor?

A

Macrophage scavenger receptor A

Macrophage scavenger receptor B

389
Q

What is macrophage scavenger receptor A? What does it do?

A

CD204
Binds to oxidised LDL
Binds to Gram-positive bacteria like Staphylococci and Streptococci
Binds to dead cells

390
Q

What is macrophage scavenger receptor B? What does it do?

A

CD36
Binds to oxidised LDL
Binds to malaria parasite
Binds to dead cells

391
Q

What are foam cells?

A

Very very fatty macrophages

392
Q

What activates macrophages within plaques?

A

Modified lipoproteins or free intracellular cholesterol

393
Q

What do macrophages express/ secrete once they have been activated in plaques?

A

1) Cytokine mediators (e.g. TNFα, IL-1, MCP-1) that recruit more monocytes
2) Chemoattractants and growth factors for VSMC
3) Proteinases that degrade tissue (e.g. the fibrous cap)
4) Tissue factor that stimulates coagulation upon contact with blood

394
Q

What oxidative enzymes do macrophages produce to modify native LDL?

A

1) NADPH Oxidase
- superoxide O2
2) Myeloperoxidase
- HOCl hypochlorous acid (bleach) from ROS + Cl-
- HONOO Peroxynitrite

395
Q

What cytokines do plaque macrophages express?

A

1) Interleukin-1→ upregulates vascular cell adhesion molecules 1 VCAM-1
2) VCAM-1→ mediates tight monocyte binding

396
Q

What chemokines do plaque macrophages express?

A

1) MCP-1 (monocyte chemotactic protein-1)

2) MCP-1 binds to a monocyte G-protein coupled receptor CCR2

397
Q

What complementary growth factors are released by macrophages and what do they do?

A

They recruit vascular smooth muscle cells and stimulate them to proliferate and deposit ECM

1) Platelet derived growth factor→ VSMC chemotaxis, survival and mitosis
2) Transforming growth factor beta→ increased collagen synthesis and matrix deposition

398
Q

What does macrophage metalloproteinases do?

A

Family of ∼28 homologous enzymes
Activate each other by proteolysis. Degrade collagen
Catalytic mechanism based on Zn

399
Q

What can happen if an atherosclerotic plaque ruptures?

A

Blood coagulation at the site of rupture may lead to an occlusive thrombus and cessation of blood flow

400
Q

What are the characteristics of vulnerable and stable plaques?

A

1) Large soft eccentric lipid-rich necrotic core
2) Thin fibrous cap
3) Reduced VSMS and collagen content
4) Increased VSMS apoptosis
5) Infiltrate of activated macrophages expressing MMPs

401
Q

What causes atherosclerotic plaque macrophages to die by apoptosis?

A

OxLDL derived metabolites are toxic (e.g. 7-keto-cholesterol)
Macrophage foam cells have protective systems that maintain survival in face of toxic lipid loading
Once overwhelmed macrophages die by apoptosis
Releases macrophage tissue factor and toxic lipids into the ‘central death zone’ called lipid necrotic core
Thrombogenic and toxic material accumulates, walled off, until plaque ruptures which causes it to meet the blood

402
Q

What is NFκB? What activates it, what does it do?

A 
A transcription factor, the master regulator of inflammation
Activated by numerous stimuli:
- scavenger receptors
- toll-like receptors
- cytokine receptors
Switches on numerous inflammatory genes
- matrix metalloproteinases
- inducible nitric oxide synthase
403
Q

What does tissue factor (secreted by macrophages) do?

A

Stimulates coagulation on contact with blood

404
Q

Ruptured plaques:

a) Have an excess of structurally strong collagen synthesised by an excess of vascular smooth muscle cells
b) Have excess of activated macrophages containing excess lipids
c) Are safe since they do not cause thrombosis or myocardial infarction
d) Are mechanically stablised due to insufficient expression of proteases by macrophages?

A

b) have excess of activated macrophages containing excess lipid

405
Q

Atherosclerotic risk factors:

a) Are expected to decrease globally leading to a decrease in CVD worldwide
b) Include high blood pressure, diabetes, hyperlipidaemia, smoking, age and anatomically localising branches and bends
c) Are not worth treating since atherosclerosis is fundamentally a degenerative disease
d) Do not modify vascular and leukocyte cell functions

A

b) Include high blood pressure, diabetes, hyperlipidaemia, smoking, age and anatomically localising branches and bends

406
Q

Low density lipoprotein:

a) Is decreased in familial hypercholesterolemia
b) May be modified in vessel wall to a form that activates macrophages like a pathogen would
c) Is formed in vessel walls and carries cholesterol back to the liver
d) Is characterised by the presence of a lipid bilayer
e) Is not measured clinically since there are no worthwhile ways to reduce its level

A

b) May be modified in vessel wall to a form that activates macrophages like a pathogen would

407
Q

What is the first system to develop during embryonic development?

A

Blood vessels

408
Q

Where do haematopoietic stem cells originate from?

A

Hemogenic endothelium

409
Q

What is the structure of a blood vessel?

A 
Lumen
Endothelium (Tunica Intima)
Internal Elastic Tissue
Smooth Muscle (Tunica Media)
External Elastic Tissue
Fibrous Connective Tissue (Tunica Adventitia)
410
Q

What cells make up the wall of vessels in the microcirculation?

A

Endothelial cells surrounded by pericytes

411
Q

In the vessel wall what types of cells give rise to vascular stem cells?

A

Pericytes

Adventitial progenitor cells (APCs)

412
Q

What can vascular stem cells differentiate into?

A

All cell types that constitute blood vessels

Specific cells of their native tissue

413
Q

In response to injury what does activation of vascular stem cells result in?

A

Mature progenitor cells for vascular repair

414
Q

Dysregulated signalling of vascular smooth muscle cells causes what?

A

Abnormal activation and reprogramming producing various types of premature cells:
Synthetic smooth muscle cells
Dysfunctional endothelial cells
Adipocytes
Osteoblasts
Chondrocytes
All contributing to maladaptive vascular remodelling and eventually causing vascular disease

415
Q

What is the function of an adult resident vascular smooth muscle cells when it differentiates into a mature progenitor cell?

A

Homeostasis, repair and regeneration

416
Q

What are endothelial progenitor cells?

A

Bone marrow-derived or tissue resident stem cells that can differentiate into mature endothelial cells

417
Q

Endothelial progenitor cells can be used for what?

A

1) Biomarkers of cardiovascular disease
2) Therapeutic agents (e.g. for ischaemic conditions)
3) Tool to study moleculer mechanisms of disease
4) As autologous vectors for gene therapy

418
Q

What is angiogenesis?

A

The growth of new blood vessels from pre-existing blood vessels

419
Q

What is vasculogenesis?

A

The differentiation of precursor cells (angioblasts) into endothelial cells and the de novo formation of a primitive vascular network

420
Q

What conditions have shown improvement with treatment with endothelial progenitor cells?

A

Limb ischaemia
Myocardial infarction
Tumour vascularisation

421
Q

What circulating cells express endothelial cell markers?

A

Haematopoietic stem cells and endothelial progenitor cells
Circulating mature endothelial cells, shed off the vessel wall
Myeloid cells can differentiate to endothelial cells in culture

422
Q

Why do labs measure circulating endothelial progenitor cells? What do the results mean?

A

As a risk factor for disease

Low EPC colonies = High cardiovascular risk

423
Q

What is the problem with measuring endothelial progenitor cells as a risk factor for disease?

A

There are no surface markers of EPCs that are unique to this cell.
Most commonly used markers CD34, AC133 and KDR are also found on haematopoietic stem cells

424
Q

What are the most commonly measured surface markers for endothelial progenitor cells?

A

CD34, AC133 and KDR

425
Q

Where are peripheral blood endothelial progenitor cells derived from?
What mediates their angiogenic abilities?

A

Derived from monocytes/macrophages

Their angiogenic effects are most likely mediated by growth factor secretion

426
Q

What is the definition criteria for endothelial progenitor cells?

A

1) Circulating cells with clonal potential
2) Able to differentiate into mature endothelial cells
3) Contribute to angiogenesis in vivo

427
Q

What are the different types of genetic and epigenetic dysfunction of endothelial cells?

A

Genetic: von Willebrand disease
Epigenetic: Smoking related disorders (COPD)

428
Q

What is von Willebrand factor?

A

A large plasma glycoprotein produced by megakaryocytes and endothelial cells.
It mediates platelet adhesion to sub-endothelium, is the carrier for factor VIII and regulates inflammation and angiogenesis

429
Q

What is the most common congenital bleeding disorder?

A

Von Willebrand disease

430
Q

What are the different types of von Willebrand disease and their cause in relation to von Willebrand factor?

A

Type 1 and 3: deficiency

Type 2: dysfunction

431
Q

COPD increases cell senescence in which cells?

A

Lung fibroblast, epithelial and endothelial cells

432
Q

Cardiovascular disease increases cell senescence in which cells?

A

Endothelial cells: atherosclerotic plaques and arteries

433
Q

How does coronary artery disease present?

A

1) Sudden cardiac death
2) Acute coronary syndrome
- Actue myocardial infarction
- Unstable angina
3) Stable angina pectoris
4) Heart failure
5) Arrhythmia

434
Q

What factors increase the risk of coronary heart disease?

A 
Tobacco use
Physical inactivity
Harmful use of alcohol
Unhealthy diet accounts result in:
- Hypertension
- Obesity
- Diabetes mellitus
- Hyperlipidaemia
435
Q

How many deaths does cardiovascular disease account for per year?

A

∼17 million worldwide

88,000 in UK

436
Q

Where is cardiovascular disease the leading cause of death?

A

Developed and low/medium income countries

437
Q

How many myocardial infarctions occur in the UK per year?

A

124,000

438
Q

How many cases of stable angina are there in the UK?

A

∼2 million

439
Q

What effect does stenosis have on coronary flow?

A

Increasing stenosis diameter causes decreasing flow

440
Q

What is angina pectoris? What provokes and relieves it?

A

Discomfort in the chest, jaw, shoulders, arms or back.
Provoked by exertion or emotional stress
Relieved by rest or s.l. GTN in

441
Q

What are the treatment strategies for coronary heart disease? (3)

A

1) Prevent atherosclerosis progression and risk of death/ MI
- Education
- Lifestyle modification
- Aspirin, statins, ACE inhibitors
2) Reduce myocardial oxygen demand
- HR (β blockers, Ca antagonists, If blockers)
- Wall stress (ACE inhibitors, Ca antagonists)
- Metabolic modifiers
3) Improve blood supply
- Vasodilators (nitrates, nicorandil, Ca antagonists)
- Revascularisation (PCI, CABG)

442
Q

What are the different types of acute coronary syndrome?

A

1) Inflammation
- Systemic
- Local
2) Plaque
- Rupture
- Erosion
3) Thrombosis

443
Q

What mechanisms underly myocardial infarction?

A

1) Myocardial cell death arising from interrupted blood flow to the heart
- Coronary plaque rupture
- Coronary plaque erosion
- Coronary dissection
2) Mechanisms of myocardial cell death
- Oncosis
- Apoptosis

444
Q

What factors can effect Virchow’s triad?

A

1) Abnormal vessel wall
- Endothelial dysfunction
- Inflammation
- Atherosclerosis
2) Abnormal blood flow
- Endothelial dysfunction
- Turbulent flow at bifurcations and stenoses
- Stasis
3) Abnormal blood constituents
- Endothelial dysfunction
- Hypercoagulability
- Abnormal platelet function
- Altered fibrinolysis
- Metabolic factors
- Hormonal factors

445
Q

What is a white thrombus? Where are they found? What treatment is beneficial?

A

Platelet rich
Common in arterial thrombosis (high pressure/ turbulent circulation)
Benefit from antiplatelet therapy

446
Q

What is a red thrombus? Where are they found? What treatment is beneficial?

A

Fibrin rich, with trapped erythrocytes
Common in venous or low pressure situations (stasis)
Benefit from anticoagulant or antifibrinolytic therapy

447
Q

What is the definition of acute MI?

A

Detection of a rise or fall in a biomarker (troponin) with at least one value >99th centile upper reference limit AND at least one of:

  • Symptoms suggestive of ischaemia
  • New or presumed new ST-T changes or LBBB on ECG
  • Development of pathological Q waves on ECG
  • Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
  • Identification of intracoronary thrombus on angiography or at autopsy
448
Q

What are the treatment options to manage an acute thrombosis?

A

1) Thrombectomy
2) Drugs
- Oral antiplatelets: aspirin, clopidogrel, prasugrel, ticagrelor
- SC anticoagulants: LMWH, fondaparinux
- IV antiplatelets: GpIIb/IIIa inhibitors
- IV anticoagulants: bivalirudin, fibrinolytics, Factor Xa inhibitors

449
Q

What are the treatment options to manage a recurrent thrombosis?

A

1) Oral antiplatelet drugs
2) Anticoagulants
- Direct thrombin inhibition
- Factor Xa inhibitors

450
Q

What are the options to achieve plaque stabilisation?

A

1) Mechanical
- Stent
2) Drugs
- Statins (high dose)
- ACE inhibitors

451
Q

What are the options to manage LV remodelling?

A

1) Non-drug
- CRT-P/D
- Progenitor cells
2) Drugs
- β blockers
- ACE inhibitors
- Angiotensin receptor blockers
- Aldosterone receptor antagonists

452
Q

What is an embolism?

A

An obstruction in a blood vessel due to an object (e.g. thrombus) getting stuck while travelling through the bloodstream

453
Q

What is a TIA?

A

Transient ischaemic attack (stroke)

454
Q

What are the different types of transient ischaemic attack?

A

1) Embolic
- ICA plaque rupture
- Intracardiac (e.g. AF, old MI, valve disease)
- Intracardiac commuication
2) Haemorrhagic
- Vascular malformation
- Hypertension
- Tumor
- Iatrogenic

455
Q

What are the treatment options for an embolic stroke?

A
  • Fibrinolysis
  • Clot extraction
  • Antiplatelet drugs
  • Modify atherosclerotic risk factors
  • Endarterectomy, stene
  • Hole closure
456
Q

What are the treatment options for a hemorrhagic stroke?

A
  • Coil/clip aneurysm
  • Withdraw pro-haemorrhagic medication
  • Control hypertension
457
Q

What are the symptoms of pulmonary embolsim?

A

Dyspnoea, chest pain, hypotension and shock

458
Q

What is the aetiology of deep vein thrombosis?

A
  • Trauma
  • Orthapedic surgery
  • Malignancy
  • Autoimmune disease
  • Thrombophilia
  • Immobility
459
Q

What are the treatment options for deep vein thrombosis?

A

Anticoagulation
Fibrinolysis
Thrombectomy

460
Q

What are the treatment options for a pulmonary embolism

A

Anticoagulation
Fibrinolysis
Mechanolysis
IVC filter

461
Q

What is heart failure?

A

A clinical syndrome caused by an abnormality of the heart and recognised by a characteristic pattern of haemodynamic, renal, neural and hormonal responses
Patients have low blood pressure and salt and water retention

462
Q

What is the prevalence of heart failure?

A

1-3%
10% in those over 75 years
22 million worldwide

463
Q

What is the incidence of heart failure?

A

2 million new cases annually worldwide

464
Q

What are the general causes of heart failure?

A

1) Arrhythmias
2) Valve disease
3) Pericardial disease
4) Congenital heart disease (holes in the heart)
5) Myocardial disease (caused by CHD, myocardial infarction)

465
Q

What is the leading cause of death in Europe?

A

Coronary heart disease

466
Q

What are the causes of restrictive cardiomyopathy?

A

1) Associated with fibrosis (diastolic dysfunction)
- elderly
- hypertrophy
- ischaemia
- scleroderma
2) Infiltrative disorders (amyloidosis, sarcoid disease, inborn errors of metabolism, neoplasia
3) Storage disorders (haemochromatosis and haemosiderosis, Fabry disease, glycogen storage disease
4) Endomyocardial disorders (Endomyocardial fibrosis, hypereosinophilic syndrome, carcinoid, metastases, radiation damage)

467
Q

What are the causes of death in heart failure?

A

1) Progression of heart failure
- Increased myocardial wall stress
- Increased retention of sodium and water (oedema and pooling of fluid in the lungs)
2) Sudden death
- Opportunistic arrhythmia
- Acute coronary event (often undiagnosed)
3) Cardiac event
- e.g. myocardial infarction
4) Other cardiovascular event
- e.g. stroke, PVD
5) Non-cardiovascular cause

468
Q

What is cardiomyopathy?

A

Heart disease in the absence of a known cause and particularly coronary artery disease, valve disease and hypertension

469
Q

What percentage of heart failure is caused by cardiomyopathy?

A

Approximately 5%

470
Q

What is the most common type of cardiomyopathy?

A

Hypertrophic cardiomyopathy

471
Q

What are the infectious causes of dilated cardiomyopathy?

A
  • Viruses and HIV
  • Rickettsia
  • Bacteria
  • Mycobacteria
  • Fungus
  • Parasites
472
Q

What toxins and poisons cause dilated cardiomyopathy?

A
  • Ethanol
  • Cocaine
  • Metals
  • Carbon dioxide or hypoxia
473
Q

What are the causes of dilated cardiomyopathy?

A

1) Idiopathic dilated cardiomyopathy
2) Genetic and/or familial cardiomyopathies
3) Infectious causes
4) Toxins and poisons
5) Drugs
6) Metabolic disorders
7) Collagen disorders
8) Autoimmune cardiomyopathies
9) Peri-partum cardiomyopathy
10) Neuromuscular disorders

474
Q

What are the different types of hormonal mediators in heart failure?

A

Constrictors
Dilators
Growth factors

475
Q

What are the different types of hormonal mediators that cause constriction in heart failure?

A 
Noradrenaline
Renin/ angiotensin II
Endothelin
Vasopressin
NPY
476
Q

What are the different types of hormonal mediators that cause dilation in heart failure?

A 
ANP
Prostaglandin E2 and metabolites
EDRF
Dopamine
CGRP
477
Q

What are the different types of growth factor hormonal mediators in heart failure?

A 
Insulin
TNF alpha
Growth hormone
Angiotensin II
Catecholamines
NO
Cytokines
Oxygen radicals
478
Q

What are the symptoms of heart failure?

A
  • Ankle swelling
  • Exertional breathlessness
  • Fatigue
  • Orthopnoea
  • PND
  • Nocturia
  • Anorexia
  • Weight loss
479
Q

What size is a normal heart on an X-ray?

A
480
Q

What size is a enlarged heart on an X-ray?

A

> 50% is enlarged

481
Q

What is the grading system used for heart failure?

A

NYHA classification of functional capacity
(New York Heart Association)
Class I to IV

482
Q

What is the management algorithm for heart failure?

A

1) Establish that patient has heart failure
2) Determine aetiology of heart failure
3) Identify concomitant disease relevant to heart failure
4) Assess severity of symptoms
5) Predict prognosis
6) Anticipate complications
7) Choose appropriate treatment
8) Monitor progress and tailor treatment

483
Q

What are the objectives of treatment in chronic heart failure?

A

1) Prevention
- Myocardial damage (occurence, progression of damage, further damaging episodes)
- Reoccurence (symptoms, fluid accumulation, hospitalisation)
2) Relief of symptoms and signs
(Eliminate oedema and fluid retention, increase exercise capacity, reduce fatigue and breathlessness)
3) Prognosis
(Reduce mortality)

484
Q

What lifestyle changes are introduced to someone with heart failure?

A
  • Weight reduction
  • Discontinue smoking
  • Avoid alcohol excess
  • Exercise
485
Q

What medical treatments are introduced as the first stage of management in heart failure?

A
  • Treat HTN, diabetes, arrhythmias
  • Anticoagulation
  • Immunisation
  • Sodium/ fluid restriction
486
Q

What are the treatments introduced as the second stage of management in heart failure?

A
  • Diuretics
  • ACE inhibitors / ARAs
  • β-blockers
  • Aldosterone antagonists (spironolactone)
  • Digoxin
  • Devices (cardiac resynchronisation, ICD)
487
Q

What are the pharmacological treatments used in a new diagnosis of heart failure and what treatments are added as the disease progresses?

A

New Diagnosis

1) Start ACE inhibitor and titrate upwards (or ARA if ACE-intolerant)
2) Add β-blocker and titrate upwards (providing no contraindication and patient is stable. Usually as outpatient)
3) Add spironolactone (if patient remains moderately to severely symptomatic (NYHA III / IV)
4) Seek specialist advice for further options

488
Q

What are the possible treatment options for severe heart failure?

A

1) IV drugs
- Diuretics or combination of diuretics
- Nitrates
- Positive inotropes- dopamine/dobutamine
2) Fluid control
- Haemofiltration
- Peritoneal dialysis or haemodialysis
3) Devices
- ICD or pacing
- Intraaortic balloon pump
- Ventricular assist device, total artificial heart
4) Surgery
- CABG for “hibernation”
- Valve surgery
- Cardiomyoplasty, volume reduction/restriction
- Transplantation

LSS Year 1 (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions