Brainscape's Knowledge GenomeTM

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


See full index

ESA 2 > CVS > Flashcards

CVS Flashcards

1
Q

What is afterload? And what is it roughly equivalent to?

A

The pressure in the wall of the left ventricle during ejection. Ie the load the heart must eject blood against.
Roughly equivalent to aortic pressure

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

What is preload?

A

The amount of stretch on the ventricles during diastole

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

What is preload related to?

A

End diastolic volume

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

What is total peripheral resistance?

A

The resistance to blood flow offered by all systemic vasculature

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

What happens to pressure as it reaches resistance?

A

The pressure drops

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

Constricting arterioles decrease pressure where and increase pressure where?

A

Decrease pressure in the venous side while increasing pressure on the arteriole side

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

What happens to pressures during vasodilation? (Peripheral resistance decreased)

A

Reduction in the arteriole side, increase in the venous side

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

What happens to the pressures if you increase peripheral resistance EG vasoconstriction

A

An increase in arteriole pressure and a decrease in venous pressure

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

If you increase cardiac output (SVxHR) but keep peripheral resistance the same what will happen to arteriole and venous pressures?

A

Increase in arteriole

Decrease in venous

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

If you keep the total peripheral resistance the same but decrease the cardiac output (SVxHR) what will happen to the venous and arteriole pressures?

A

venous pressure will increase and arteriole pressure decrease.

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

If a tissue needs more blood, what needs to happen?

A

Dilation of precapillary sphincters

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

If precapillary sphincters dilate what will happen to total resistance?
What does the heart need to do in response?

A

Reduction in total peripheral resistance

Heart needs to increase cardiac output to maintain BP.

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

How does the heart detect the fall in blood pressure due to something like dilation of a pre-capillary sphincter?

A

Baroreflex

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

What is cardiac output?

A 
The amount of blood ejected in 1 minute. 
Stroke volume (end systolic volume-end diastolic volume) x HR
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

In ventricular filling, when should the ventricles stop filling ?

A

When they reach the pressure of the veins

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

What does the ventricular compliance curve describe?

A

With increased venous pressure, increased heart filling occurs.

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

The ventricular compliance curve can be increased and decreased in disease state. That can be problematic due to the association of this curve with what law?

A

Starlings law of the heart

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

What does starlings law of the heart state?

A

The more the heart is stretched (within reason) the greater the force of contraction

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

Starlings law of the heart is linked to what curve associated with the cardiac myocytes

A

Length tension curve of sarcomeres

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

In theory why does increased stretch increase contraction?

A

More exposed binding sites for the actin-myosin power stroke.

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

On top of the intrinsic control from stretch what other extrinsic factors can alter contractility?

A

Adrenaline and sympathetic stimulation

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

When aortic pressure increases as a result of an increase in total peripheral resistance what happens to heart filling?

A

Venous pressure reduces, thus a decrease in filling of the heart.

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

When we exercise total peripheral resistance falls. Explain why? And what happens next (dismissing sympathetic stimulation)

A

Heart and muscles require more oxygen therefore vasodilation.
A decrease in total peripheral resistance increases venous pressure.
More blood pushed back to heart and increased filling
Increased filling, increased stretch, increased cardiac output

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

Blood entering the right atria is from where?

A

Superior and inferior vena cava and coronary sinus

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

Blood leaving the right atria into the right ventricle, goes through what valve?

A

tricuspid

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

Blood leaves the right ventricle through what vessel and what valve

A

Pulmonary artery, Pulmonary valve

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

Blood from enters the left atria from where?

A

Pulmonary vein

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

Blood from the left atria reaches the left ventricle, passing through what valve

A

Mitral

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

Blood is ejected from the left ventricle through what valve and into what vessel

A

Aortic valve, into the aorta

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

What is seen on the left and right apical areas of the heart, closely wrapped around major vessels

A

Oracles

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

What causes a valve to open or close?

A

Pressure changes

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

What stops inversion of the mitral and tricuspid valves during systole?

A

Papillary muscles attached via chordae tondonae

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

What is the pressure roughly, in the left atrium

A

8-10mmHg

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

What is the pressure of the left ventricle roughly in systole and diastole

A

Systole 120 mmHg

Diastole 10 mmHg

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

What is the pressure in the right atrium roughly

A

0-4 mmHg

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

What is the pressure in the right ventricle during systole and diastole

A

Systole- 24mmHg

Diastole 4 mmHg

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

What is the pressure in the pulmonary artery during systole and diastole?

A

Systole- 24mmHg

Diastole 10mmHg

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

In what direction does the conduction system cause contraction. At a local myocytes level and globally in the ventricles

A

From inner to out, endocardial to epicardial

From the apex upwards

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

How many stages of the cardiac cycle are there?

A

7

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

The first stage of the cardiac cycle (usually thought of as) is atrial contraction;
What happens in regards to filling?

A

Final 10% of ventricle filled

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

During atrial contraction what position are the valves in?

A

tricuspid and mitral are open

Aortic and pulmonary are closed

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

What is the ventricle volume considered at the end of atrial contraction?

A

End Diastolic Volume

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

What follows atrial contraction?

A

Isovolumetric contraction

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

What heart sound is produced with isovolumetric contraction and why?

A

S1

Ventricle pressure exceeds atrial and causes closure of mitral and tricuspid valves

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

What happens to the volume of the ventricles with the s1 heart sound?

A

Volume stays the same (isovolumetric contraction)

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

What follows isovolumetric contraction?

A

rapid ejection

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

What is happening during the rapid ejection phase at both the ventricles and atria

A

The ventricle pressure exceeds the aorta, opening the aortic valve (same on other side) rapid decrease in ventricular volume
Blood is filling the atria

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

What follows rapid ejection?

A

reduced ejection

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

What is occurring, in relation to pressures in reduced ejection

A

A decline in ventricle pressure and a slow increase in atrial pressure

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

What follows reduced ejection?

A

Isovolumetric relaxation

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

What causes the aortic valve to close?

A

Brief backflow due to decreased ventricular pressure

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

What heart sound is produced when the ventricular pressure falls inducing back flow?

A

S2- closure of aortic valve

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

What volume does isovolumetric relaxation relate to?

A

end systolic volume

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

What follows isovolumetric relaxation?

A

Rapid filling

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

What happens in rapid filling, and what might be heard

A

Ventricular pressure below atrial so the mitral valve opens.

S3 can be heard sometimes

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

What is the final stage between rapid filling and atrial contraction? And what volume does it relate to?

A

Reduced filling

Ventricles reaching inherent relaxed volume (90%)

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

What is a typical stroke volume? What does that equate as?

A

80ml roughly

EDV-ESV

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

A heart at rest beat cycle lasts 0.9 seconds. How long is systole and how long is diastole?

A

.55 diastole

.35 systole

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

Which part of the cardiac cycle decreases with an increase in heart rate?

A

Duration of diastole

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

What does S1 represent

A

Closure of mitral valve

LUB

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

What does s2 represent?

A

Closure of aortic and pulmonary valve

DUB

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

What is S3 known as? And is it ever normal?

A

Ventricular Gallop

Normal in children

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

What causes heart sound s3 in an adult

A

A sudden deceleration of blood flow into the left ventricle

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

What does the prescence of s3 indicate

A

Congestive heart failure

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

what are some causes of aortic stenosis

A

Degenerate
Congenital
Rheumatic fever

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

What effect does aortic stenosis have on blood flow?
What is the resultant pressure change?
How does the body adapt to this?

A

Less blood through the aortic valve
Raises LV pressure
Hypertrophy of the left ventricle

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

What long term effect does having a hypertrophic left ventricle and aortic stenosis have?

A

Left sided heart failure
Angina (more tissue to perfuse)
Syncope

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

What effect can aortic stenosis have on RBC count? Why?

A

Decrease due to shearing forces inducing a microangiopathic haemolytic anaemia

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

What causes aortic valve regurgitation?

A

Aortic root dilation (leaflets pulled apart)
Valvular damage- endocarditis, rheumatic fever,
LV dilation
Myxomatous degeneration post heart attack

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

What is the main cause of mitral valve stenosis

A

Rheumatic fever (99.9%)

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

Where does pressure increase in Israel valve stenosis?

A

Left atria, venous system

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

What part of the heart is likely to become hypertrophic in mitral stenosis

A

The Right ventricle

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

What happens to the left atria in mitral valve stenosis

A

Left atria dilates

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

Where are some symtoms of mitral valve stenosis

A

Pulmonary oedema, dyspnoea, pulmonary HTN

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

How is MAP calculated?

A

Diastolic pressure + 1/3 of pulse pressure

OR

Cardiac output (stroke volume heart rate) x total peripheral resistance.

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

What is haemodynamic shock?

And what is circulatory shock?

A
  1. Acute condition of inadequate blood flow throughout the body
  2. A catastrophic fall in arterial pressure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

In reference to the MAP, what can we stipulate shock can be a result of?

A

CO x TPR

Therefore a fall in either can result in shock

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

What is the bodies natural response to avoid shock?

A

Altering either TPR or CO

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

In a nutshell shock can be due to what 4 methods?

A

Cardiogenic
Mechanical
Hypovolaemia
Excessive vasodilation

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

What is cardiogenic shock?

A

A failure of the pumping action of the heart. Eg ventricle not fully emptying

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

What is mechanical shock?

A

An obstruction e.g ventricle cant fill

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

Is cardiac arrest part of haemodynamic shock?

A

No, but shock can progress to cardiac arrest

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

What is cardiac arrest

A

Unresponsiveness associated with lack of pulse

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

What is asystole

A

Loss of electrical and mechanical activity in the heart

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

What is PEA in the heart

A

Pulseless electrical activity

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

What is ventricular fibrillation?
When can it commonly occur?
What does it often lead to?

A

Uncoordinated electrical activity of the ventricles
Following MI, electrolyte imbalances and arrythmias
Cardiac arrest

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

What’s the difference between BLS and ALS

A

Basic- just compressions

Advances- defib

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

How does a defibrilator work?

A

Depolarises the cells into refractory period, giving time for coordinated activity to restart

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

Why is adrenaline given in shock

A

Increases cardiac output and peripheral resistance

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

In cardiogenic shock. Is the filling an issue?

A

No the heart fills but it doesnt pump correctly

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

In cardiogenic shock what clinical sign can sometimes be spotted? Why is this?

A

Raised JVP due to increased central venous pressure

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

What happens to arterial blood pressure in cardiogenic shock?

A

Decreases

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

In cardiogenic shock, what organ in particular suffers from a lack of perfusion? What clinical sign might occur?

A

Kidney

Oliguria (reduced urine output)

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

Is filling of the heart an issue in mechanical shock?

A

Yes, there is a restriction to filling

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

Give an example of something that can cause mechanical shock

A

Cardiac tamponade

Massive Pulmonary emobilsim

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

What happens to pressures in arterial and venous systems with mechanical shock?

A

Increase in venous, decrease in arterial

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

How would a massive PE cause mechanical shock?

A

If it occluded a large pulmonary artery so that the right ventricle cant fully empty
Back pressure increases venous pressure while decreasing arterial.

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

what is hypovolaemic shock commonly due to?

A

Haemorrhage

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

How much blood loss is likely to cause hypovoelemic shock?

A

20% upwards

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

In hypovolaemic shock what happens to venous and arterial pressures

A

Venous pressure falls, leading to arterial pressure to fall

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

What is the bodies response to hypovoelimic shock?

A

Baroreflex induces vasoconstriction, tachycardia, increased force of contraction (chrontropy and inotropy)

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

What is internal transfusion in shock?

A

A reduction in the capillary hydrostatic pressure causing a net movement of fluid into the capillaries

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

Given the physiology behind hypovoelemic shock what patient signs would be present?

A

Weak pulse, pale, tachycardia and cold

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

Aside from haemorrhage what else can cause hypovoelemia ?

A

Severe burns

Excessive diarrhoea or vomiting (due to loss of Na)

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

What is ‘shutdown’ in relation to tissue perfusion

A

Peripheral vasoconstriction reducing tissue perfusion

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

What can occur due to ‘shutdown’

A

Damage due to hypoxia
Local release of vasodilators causing further bp fall
Multi system failure

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

What longer term response aims to restore blood volume

A

RAAS and ADH

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

How long would a 20% loss of blood take to restore (given adequate salt and water intake)

A

3 days

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

What is normovoelemic shock?

A

A distributive shock caused by loss of resistance (vasodilation)

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

What can commonly cause a distributive shock?

A

Sepsis- toxic shock

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

How does toxic shock occur

A

Endotoxins released by circulating bacteria cause vasodilation.
Secondly capillaries become leaky in response

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

When is it septic shock?

A

When there is persisting hypotension that requires treatment to maintain DESPITE fluid resuscitation

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

What other common form of shock is distributive?

Not toxic/septic

A

Anaphylactic

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

What causes distributive shock in anaphylaxis?

A

Mast cells secrete histamine that cause massive vasodilation

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

What else occurs in anaphylactic shock (aside from mass vasodilation)

A

Bronchoconstriction and laryngeal oedema

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

What treatment is required in anaphylactic shock and why?

A

Adrenaline for its vasoconstrictive effects

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

What sets the resting membrane potential in a cardiac myocyte

A

K+ permeability

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

Why isn’t the cardiac myocytes resting potential equal to Ek

A

Due to small permeability to other ion species at rest

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

What is the result of an action potential in a cardiac myocyte

A

Calcium influx leading to contraction

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

A cardiac myocytes action potential has what additional stage when compared to a axon potential

A

Plateau following depolarisation

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

What is happening to a cardiac myocyte during diastole?

A

Maintains resting potential

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

What is the first stage of a cardiac action potential and what are the rough voltages

A

Opening of voltage gated sodium channels.

Depolarising the cell from -85 to +20mv

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

During the cardiac myocytes action potential what brings the voltage from +20mv to 0mv

A

Transient outward flow of K+

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

What is happening during the plateau phase of a cardiac myocytes

A

Opening of voltage gated calcium L type channels with opening of K+ channels

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

What occurs to bring the cardiac myocyte out of the plateau phase?

A

Inactivation of calcium channels.

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

What is special about the sinoatrial nodes electrical activity

A

It is spontaneously active, transmitting electrical impulses across the heart

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

Does the sinoatrial node have a resting membrane potential?

A

No, the most negative it will be is -60 (but slowly depolarising)

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

What is the pacemaker potential

A

Funny current. Slow depolarisation caused by influx of Na+

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

What channels are responsible for the funny current

A

Hyperpolarisation activated cyclic nucleotide gated channels (HCN)

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

Once the funny current reaches threshold what happens

A

L type calcium channels open to cause upstroke before voltage gated potassium channels open

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

HCN channels activate what messengers

A

Cyclic AMP and cyclic GMP

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

Why does the SA node set the rhythm

A

It’s cells are the quickest to depol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q 
The SA node being  \_\_\_\_ causes \_\_\_\_\_
1 slow
2 failing
3. Quick
4. Random
A
  1. Bradycardia
  2. Asystole
  3. Tachycardia
  4. Fibrilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What is the normal range for plasma levels of K

A

3.5-5.5 mmol

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

Why does plasma K have to be tightly controlled in relation to the heart

A

It’s levels are important for resting potential

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

In hyperkalemia what happens to the resting potential of the cell

A

It is less negative

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

Why is having a less negative RMP dangerous?

A

It can lead to Na channels remaining inactivated.

Initial excitability followed by potential inability to fire action potential

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

How can we treat hyperkalaemia in regards to preventing cardiac arrest

A 
Calcium glauconate (makes heart more excitable)
Insulin and glucose ( Insulin promotes K moving into the cell)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What effect does hypokalaemia have on action potentials?

A

Lengthens them and delays repolarisation

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

What is EAD and what can it result in

A

Early after depolarisations- VF

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

In contraction coupling what is the effect of depolarisation?

A

L type calcium channels open in t tubule

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

In contraction coupling, when calcium enters the cells what happens

A

Localised induced calcium release (in myocytes from sarcolemma and sarcoplasmic reticulum)

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

What does calcium bind to in contraction coupling

A

Troponin

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

When calcium binds to troponin what happens

A

Conformational change shifting tropomyosin revealing the actin binding site.

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

How is calcium returned back to normal level after contraction?

A

Most pumped back into sarcoplasmic reticulum via SERCAtpase, some out of the cell membrane via Na/C exchange and sarcolemma calcium atpase.

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

What nervous system co-ordinates the bodies response to exercise and stress?

A

ANS

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

What are the 2 divisions of the ANS

A

Sympathetic and parasympathetic

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

What is the main function of the ANS

A

Regulate physiological functions- HR, Body temp, BP

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

What activity of the ANS is increased with stress?

A

Sympathetic

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

When is parasympathetic ANS more dominant?

A

Under basal conditions

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

What receptor is found in the pupil of the eye to signal for dilation (contract radial muscle)

A

Alpha 1

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

The airways of the lungs have what receptors for sympathetic effect? What do they do in the lungs?

A

Beta 2

Relax

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

What receptor in the heart is there for sympathetic effect? What does it do?

A

Beta 1

Increase rate and force of contraction

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

Sweat glands have what 2 receptors for sympathetic effect? What do they do?

A

Alpha 1- localised secretion

Muscarinic 3- generalised secretion

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

What receptor in the pupil of the eye recieves parasympathetic stimulation? What does it do?

A

M3

Contraction (contracts sphincter muscle)

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

What receptor in the lungs recieves parasympathetic? What does it do?

A

M3

Contracts

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

What receptor in the heart recieves parasympathetic input? What’s the outcome?

A

M2

Decrease rate

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

If sympathetic drive to the heart increases, does that mean other sympathetically regulated activity is increased?

A

No different tissues independently regulate

BUT- on some occasions there is a more co-ordinated response

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

The ANS controls what in the cardiovascular system (4)

A

Heart rate
Force of contraction
Peripheral resistance of blood vessels
Amount of venoconstriction

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

What does the AND not do in the cardiovascular system

A

Initiate electrical activity

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

At rest the heart is normally under what influence?

A

Vagal

Parasympathetic dominating

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

The vagus nerve is what cranial nerve?

A

10 (x)

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

Where does the vagus nerve synapse?

A

Epicardial surface within walls of heart at SA and AV node

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

What do the post-ganglionic cells of the vagus nerve release?

A

ACh

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

What receptors does the vagus nerve act on? What 2 effects?

A

M2
Decrease rate
Decrease AV conduction velocity

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

Where do the postganglionic fibres of the sympathetic nervous input to the heart come from?

A

Sympathetic trunk

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

What does the sympathise trunk innervate?

A

SA, AV and myocardium

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

What do the sympathetic trunk nerves release?

A

Noradrenaline

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

What receptors does the sympathetic nervous system act on? And what are the effects (2)

A

Beta 1

Increase rate and increase force

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

Where is the cardiovascular centre in the brain

A

Medulla oblongata

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

What makes the funny current in the heart?

A

Turning on of a slow Na+ conductance

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

What sets the rhythm of the heart

A

AP firing in the SA node (sinus rhythm)

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

What effect does sympathetic activity heave on the funny current?

A

Increases the slope

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

How does the sympathetic nervous system increase the slope of the SA node funny current?

A

Beta 1 receptors
Gs protein
Increase cAMP

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

What effect does parasympathetic activity have on the funny current?

A

Decreases the slope

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

how does parasympathetic activity decrease the slope of the funny current in the SA node?

A

M2 receptors

  1. Gi- inhibits adenyl cyclase
  2. Ggamma- increases K+ conductance to cell.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
177
Q

How does noradrenaline acting on a B1 receptor increase the force of contraction?

A 
Gs-> increase cAMP
Activate protein kinase A
Phosphoryalates calcium channels
Intracellular calcium increases sarcoplasmic release.
Increased contraction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
178
Q

Most arteries and veins have what receptors?

A

Alpha 1

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

Coronary and skeletal muscle vasculature have what receptors?

A

Beta 2

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

What allows for vasodilation to occur?

A

Vasomotor tone

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

Decreased sympathetic output to alpha 1 receptors results in what?

A

Vasodilation

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

Increased sympathetic output to alpha 1 receptors causes what?

A

Vasoconstriction

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

Circulating adrenaline has a higher affinity for what receptors?

A

Beta 2 compared to alpha 1

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

Circulating adrenaline having a higher affinity for beta 2 receptors compared to alpha 1 causes what?

A

Vasodilation of vessels with beta 2 (skeletal, myocardium, liver)

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

At very high levels of adrenaline in the body what does circulating adrenaline do?

A

Activate both beta 2 and alpha 1

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

How do beta 2 adrenoreceptors cause vasodilation

A

Increased cAMP->PKA-> potassium channels and inhibition of myosin light chain kinase-> relaxation

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

How does activation of alpha 1 receptors cause vasoconstriction?

A

Stimulates Ip3-> pip/dag-> increases calcium influx causing contraction.

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

What tissues produce more metabolites?

A

Active ones

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

What effect do local increases in metabolites have (eg adenosine, K+, H+, PCO2)

A

Strong vasodilator effects

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

What’s the most important for ensuring adequate perfusion of skeletal and coronary muscles?

A

Metabolites compared to beta 2 receptors

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

What receptors detect low pressure in the cardiac system?

A

Atrial receptors

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

Where are baroreceptors for the CVS system located?

A

Carotid sinus

Aortic arch

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

What is the baroreceptor reflex?

A

Increase MAP detected
Afferent to medulla
Efferent to heart and vessels
Vassolidation and bradycardia

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

What happens to barroreceptors when high BP persists

A

Re set to higher pressure

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

What are sympathomimetics?

A

Alpha adrenoreceptor and beta adrenoreceptor agonists

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

What are cholinergics?

A

Muscarinic agonists and antagonists

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

What sympathomimetic is used to restore function in cardiac arrest?

A

Adrenaline

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

What beta 1 agonist may be given in cardiogenic shock?

A

Dobutamine

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

What is salbutamol?

A

Beta 2 agonist

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

What is the action of a non selective beta1/2 antagonist like propranolol?

A 
Slow heart rate and force of contraction (b1)
Causes bronchoconstriction (b2)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
201
Q

What is used instead of a non selective b1/b2 antagonist ?

A

Selective b1 atenolol.

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

One cholinergic agonist and its use

A

Pilocarpine

Activator constrictor papillae

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

One cholinergic antagonist and its use?

A

Tropicamide

Dilate pupils

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

What is the short term regulator of blood pressure

A

Baroreceptors reflex

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

What does the baraoreceptor reflex adjust?

A

Sympathetic and parasympathetic input to the heart to alter cardiac output and TPR

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

Does the baroreceptor reflex have a sustained control on blood pressure

A

no

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

What is controlled in the long term management of blood pressure?

A

Sodium balance

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

How does controlling sodium balance alter blood pressure?

A

Controls the extracellular fluid volume

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

If you lower extracellular fluid what volume has been reduces?

A

Plasma volume

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

What are the four parallel neurohormonal pathways that control circulating volume (therefore bp)

A

Renin angiotensin aldosterone system
Sympathetic nervous system
Antidiuretic hormone
Atrial natriuretic peptide

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

Where is renin released from?

A

Granular cells of juztaglomerular apparatus (JGA)

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

What are 3 factors that stimulate renin release

A

Reduced NACL to distal tubule
Reduced perfusion pressure in kidney
Sympathetic stimulation to JGA increases renin release

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

Reduced perfusion in the kidney causing release of renin is detected by what?

A

Baroreceptors in afferent arteriole

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

Where are macula densa cells located?

A

Distal tubule

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

What can macula dense detect a change in?

A

NaCl delivery

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

Where does the sympathetic stimulation go in RAAS control?

A

Juxtaglomerular apparatus

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

What does renin do?

A

Convert circulating angiotensinogen to angiotensin 1

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

What happens to circulating angiotensin 1?

A

Angiotensin converting enzyme converts it into angiotensin 2

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

What are the 3 main effects of angiotensin 2?

A

Vasoconstriction
Na+ reabsorbtion
Aldosterone stimulation

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

Where does aldosterone come from?

A

Adrenal cortex

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

How many type of ang 2 receptors are there?

A

2

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

What receptor does ang 2 have its main action on?

A

AT1

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

What type of receptor is a AT1 receptor

A

G protein coupled for angiotensin2

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

Where are 5 sites of the AT1 receptor?

A 
Arteriole
Kidney
Sympathetic NS
Adrenal cortex
Hypothalamus
225
Q

Ang 2 stimulation to an AT1 receptor in the arterioles has what effect?

A

Vasoconstriction

226
Q

Ang 2 stimulation to an AT1 receptor in the Kidney has what effect?

A

Stimulates Na+ reabsorbtion

227
Q

Ang 2 stimulation to an AT1 receptor in the sympathetic nervous system has what effect?

A

Increased release of Noradrenaline

228
Q

Ang 2 stimulation to an AT1 receptor in the adrenal cortex has what effect?

A

Aldosterone release

229
Q

Ang 2 stimulation to an AT1 receptor in the hypothalamus has what effect?

A

Stimulates ADH release, increases thirst sensation

230
Q

Where does aldosterone principlely act?

A

Cells of collecting duct

231
Q

What are 3 actions of aldosterone on the cells of collecting ducts

A

Na+ reabsorbtion
Activate apical Na+ channel and apical K+ channel
Increase basolateral Na+ extrusion

232
Q

What is the link between Angiotensin converting enzyme (ACE) and bradykinin?

A

ACE breaks down bradykinin

233
Q

If ACE breaks down bradykinin what is the effect and why

A

Vasoconstriction because bradykinin is a vasodilator

234
Q

Why do you get a dry cough when taking an ACE inhibitor

A

Accumulation of bradykinin (vasodilator) as no longer getting broken down

235
Q

What are some examples of ACE inhibitor

A

Captopril, lisinopril, enalapril

236
Q

High levels of sympathetic stimulation does what to renal blood flow?

A

Decreases it

237
Q

Why does high levels of sympathetic stimulation reduce renal blood flow?

A

Vasoconstriction of arterioles

238
Q

Why does decreased renal blood flow due to sympathetic stimulation increase blood pressure

A

Decreased glomerular filtration rate resting in decreased Na excretion

239
Q

The sympathetic nervous system can directly stimulate renin release and reduce blood flow to the kidney, how else can it alter blood pressure?

A

Activate apical Na/H exchanger in proximal convoluted tubule

240
Q

The 3 mechanisms of sympathetic stimulation on plasma volume control are?

A

Change arteriole flow to kidney
Stimulate renin release
Stimulate Na reabsorbtion in proximal convoluted tubule

241
Q

What is the main role of ADH

A

Increase water reabsorbtion in distal nephron

242
Q

What’s another name for ADH

A

Vasopressin

243
Q

What is ADH release stimulated by?

A

Increases in plasma osmolality

Severe hypovolaemia

244
Q

How does ADH act on Na+ reabsorbtion

A

Stimulates apical Na/K/Cl co-transporter in thick ascending limb

245
Q

atrial natriuretic peptide does what to afferent arteriole?

A

Vasodilates

246
Q

What effect does increased blood pressure have on GFR

A

Increases it

247
Q

What effect does ANP have on sodium along the nephron?

A

It inhibits Na reabsorbtion

248
Q

What system works in the opposite direction to RAAS, ADH, sympathetic stimulation in BP control

A

ANP

249
Q

What can cause loss of sodium in urine? Neurohormonal control mechanism

A

ANP

250
Q

What is loss of sodium in the urine called?

A

Natriuretic

251
Q

What do prostaglandins act as a buffer against and why?

A

Buffer against excessive vasoconstriction (SNS, RAAS) because they are local vasodilators

252
Q

What’s the effect of PGE2 on GFR

A

Enhances it and reduces Na reabsorbtion

253
Q

What is dopamine formed from in the kidney?

A

Circulating L-DOPA

254
Q

Where are dopamine receptors present in relation the the kidney?

A

Renal blood vessels
Cells of proximal convoluted tubule
Thick ascending loop TAL

255
Q

What does dopamine cause in the kidney?

A

Vasodilation and increased renal blood flow

256
Q

What does dopamine do to NaCl in the kidney? How?

A

Reduce reabsorbtion

Inhibits NH exchanger and Na/K in PCT and TAL

257
Q

What are the 3 stages of hypertension

A

Stage 1,2 and severe

258
Q

What is hypertensions main cause? 95% of cases

A

Unknown

259
Q

If the cause of HTN is unknown what is it called

A

Primary HTN

260
Q

What are some examples of secondary HTN

A

Renovascular disease, Chronic renal disease, Cushing

261
Q

Primary hypertension is what?

A

Sustained blood pressure of a diastolic above 90 or a systolic above 140

262
Q

How does renovascular disease cause secondary HTN

A

Reduced renal perfusion

Increased renin + RAAS activation

263
Q

How does renal parenchymal disease cause secondary HTN

A

Na+ and water retention due to inadequate GFR

264
Q

If the secondary HTN is due to an adrenal cause what is likely being secreted?

A

Aldosterone

265
Q

What can HTN lead to?

A

Heart failure, MI, stroke, renal failure

266
Q

What is the effect on afterload with HTN

A

Increased afterload

267
Q

What can become damaged in HTN

A

Arterioles

I

268
Q

If you have increased afterload what are 2 possible effects?

A

Left ventricular hypertrophy

Increased myocardial oxygen demand

269
Q

If you have arterial damage, what are 2 possible effects?

A

Atherosclerosis, weakened vessels

270
Q

How do you treat secondary HTN

A

Treat the cause

271
Q

What are some non pharmacological treatments for HTN

A

Exercise
Diet
Reduced Na intake
Reduced alcohol intake

272
Q

What pharmacological treatment for blood pressure affects the RAAS system

A

ACE inhibitors

273
Q

What effects does ACE have?

A

Diuretic and vasodilatory

274
Q

What is the purpose of an L type calcium channel blocker in HTN treatment?

A

Vasodilation

275
Q

What vasodilator is primarily used to treat HTN

A

L-type calcium channel blocker

276
Q

In principle what other vasodilator (not an L-type calcium channel blocker) can be used to treat HTN ? Why is it often not?

A

Alpha 1 receptor blocker

Can cause postural Hypotension

277
Q

Why are beta blockers less commonly used in the treatment of HTN?

A

Beta blocker decrease sympathetic output which does lower bp but only used if other indicators eg previous MI

278
Q

What else can be used tot treat HTN if you have an ACE inhibitor and an L type calcium blocker?

A

Diuretic

279
Q

How does a diuretic lower BP

A

Inhibits Na/Cl cotransproter in distal tubule

280
Q

What other diuretucis are there, that done have an effect on the distal tubule directly?

A

Aldosterone antagonist

281
Q

Fluid collected from clotted blood is known as what

A

Serum

282
Q

Fluid collected from unclotted blood is what?

A

Plasma

283
Q

What is serum?

A

Plasma with clotting factors (in particular fibrinogen)

284
Q

What is the most common cause of increased plasma viscosity

A

Multiple myeloma

285
Q

What is an increase in RBC known as?

A

Polycythaemia

286
Q

What is an increase in platelets known as?

A

Thrombocythaemia

287
Q

What is an increase in white cells known as

A

Leukaemia

288
Q

Polycythaemia, thrombocythaemia and leukaemia all result in what?

A

Increase whole blood viscosity

289
Q

What is the effect on blood viscosity of raised levels f acute phase plasma proteins?

A

Minor changes in plasma viscosity

290
Q

Name some acute phase plasma proteins

A

Fibrinogen
Complement
CRP

291
Q

Raised acute phase plasma proteins are usually due to what?

A

Acute inflammation

292
Q

A minor change in viscostiy of plasma can be a measure of what?

A

Inflammation

293
Q

What marker is used to primarily measure inflammation ?

A

CRP

294
Q

What is laminar flow?

A

Streamline flow with layers staying the same distance apart

295
Q

What is happening to viscosity in laminar flow

A

Parabolic profile- the velocity of blood in the centre is greater than on the edges

296
Q

What is turbulent flow?

A

When blood is continually mixing in the vessel

297
Q

When can turbulent flow occur?

A 
When flow is too great
When it passes an obstruction
Whe it makes a sharp turn
When it passes over a rough surface
When there is increased resistance to flow
298
Q

What is the equation for pulse pressure?

A

Peak systolic pressure-end diastolic pressure

299
Q

If our BP is 120/80 what is our pulse pressure?

A

40

300
Q

What are the 4 stages of pulse pressure

A

Systolic uptake
Peak systolic pressire
Decline with diacrotic notch
Diacrotic run off

301
Q

How is MAP estimated

A

Diastolic+ 1//3 of pulse pressure
E.g 120/80
80+ (1/3 of 40)= 93

302
Q

A MAP below what level is dangerous and why?

A

Below 70

Organ perfusion is low

303
Q

If peripheral resistance is high what can occur?

A

Retrograde flow

304
Q

What 2 things can determine the feel of a pulse

A

The force that the left ventricle is able to eject blood at

The pulse pressure

305
Q

In pulse strength what kind of things can alter the strength due to changing the left ventricle contraction force

A

LV failure
Aortic stenosis
Hypovolaemia

306
Q

What is a strong pulse described as?

A

Bounding

307
Q

What can bradycardia do to the feel of a pulse?

A

Widens pulse pressure leading to bounding pulse

308
Q

What effect does low peripheral resitance have on diastolic pressure?

A

Low diastolic pressure

309
Q

Vasodilation causes what in terms of resistance and diastolic pressure

A

Low resistance, low pressure

310
Q

High peripheral resistance does what to diastolic pressure?

A

High diastolic pressure

311
Q

Hot bath, exercise, pregnancy can all do what to peripheral resistance?

A

Lowers TPR

312
Q

Lowering diastolic pressure eg exercise does what to pulse pressure

A

Increases it

313
Q

What 4 systems can present with chest pain

A

Resp
Cardiac
GI
Msk

314
Q

What are some examples of respiratory conditions that may present similar to an MI

A

Pneumonia

PE

315
Q

What are some differences that a pneumonia presents with compared to an MI

A

Pain often slightly off to side

Can come with cough, temp and breathlessness

316
Q

What differences would a patient who has a PE have to differentiate from MI

A

Pain sharp and well localised
Often worse with inspiration
Likely breathless

317
Q

What are some examples of MSK pains that could be confused with MI?

A

Costochondiritis

Rib Fracture

318
Q

What are some differences with having costochondiritis compared to an MI

A

Sharp well localised pain

Painful to palpate

319
Q

What upper GI condition can present similar to an MI?

A

Reflux

320
Q

How is reflux often described

A

Burning central pain

Worse on lying/ certain food

321
Q

What 2 causes of chest pain related to the cardiac system are there?

A

Ischaemia

Pericarditis

322
Q

What would an ischaemic cardiac pain present with?

A

Dull retrosternal pain/ heaviness
May be worse on exertion
May radiate to jaw, neck, shoulder, arm l>r

323
Q

A patient with pericarditis would present with what symptoms?

A

Sharp retrosternal pain.
Can change with position (eased leaning forwards, worse lying flat)
Can worsen with deep breath/cough

324
Q

Somatic cardiac pain refers to what structures?

A

Pleural sac, pericardial sac

325
Q

How is somatic chest pain usually described?

A

Sharp, well localised, worse with cough/inspiration

326
Q

What would visceral chest pain likely have as its source?

A

Heart or lung

327
Q

Visceral pain is generally described how?

A

Dull, poorly localised and worse with exertion

328
Q

What is pericarditis?

A

Inflammation of pericardium

329
Q

Pericarditis is usually secondary to what?

A

Viral illness

330
Q

What is the pathophysiological route of ischaemic heart disease

A

Atherosclerosis of coronary arteries

331
Q

What are some non modifiable risk factors of IHD

A

Gender (male)
Age
Family history

332
Q

What are some modifiable atherosclerosis risk factors?

A

Smoking, HTN, high cholesterol, diabetes, obesity, sedentary life

333
Q

Is stable angina part of acute coronary syndrome?

A

No

334
Q

What is stable angina?

A

Heart tissue ischaemia only occurs when metabolic demand of the cardiac muscle is greater than what can be delivered by coronary arteries.

335
Q

What is essential for stable angina?

A

Relationship between rest and ease of symptoms

336
Q

When is GTN spray able to relieve symptoms?

A

In stable angina

337
Q

What does acute coronary syndrome encapsulate

A

UNstable angina

Myocardial infarction- STEMI/ NSTEMI

338
Q

What is unstable angina?

A

When a stable angina plaque ruptures

339
Q

If you have unstable angina and the plaque has ruptured, what will follow?

A

Platelet aggregation and thrombus formation leading to either partial or complete occlusion

340
Q

What does an NSTEMI represent at a vessel level?

A

Partial occlusion of the vessel

341
Q

Are there detectable enzymes with plaque rupture?

A

No, only once infarct is present

342
Q

What is the main difference in history of a patient with acute coronary syndrome

A

Similar to stable angina but more intense and pain lasting longer

343
Q

What clinical signs might differntiate stable angina from acute coronary syndrome?

A

Look unwell

Increased autonomic output- pale, nausea, sweating

344
Q

Do you get heart murmurs with STEMI/NStemi

A

You can but not always

345
Q

What are some key diagnostic tests when differentiating whether acute coronary syndrome is occurring

A

ECG

Blood test- troponin

346
Q

What would you look at in an ECG when looking for acute cornonary syndrome

A

ST segment
T waves
Q wave

347
Q

On an ecg what would you see with a STEMI

A

ST segment elevation

Hyperacute T waves

348
Q

In unstable angina and NSTEMI what would you see on ECG

A

Patterns of ischaemia, ST depression, T wave flattened or inverted

349
Q

What does a STEMI represent at a vessel level?

A

Complete occlusion of a vessel

350
Q

How would you determine if the diagnosis was unstable angina or NSTEMI?

A

?

351
Q

What is heart failure defined as

A

A state in which the heart fails to maintain adequate circulation the body needs despite adequate filling pressures.

352
Q

Heart failure has a characteristic pattern of what?

A

Haemodynamic, renal, neural and hormonal responses

353
Q

What is the primary cause of systolic heart failure?

A

IHD

354
Q

What causes of non ischaemic heart disease can lead to heart failure?

A 
HTN
dilated cardiomyopathy 
Valvular issues 
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
355
Q

How is heart failure classed?

A

1-4

356
Q

What is class 1 heart failure

A

No symptoms

357
Q

What is class 2 heart failure?

A

Slightly limited physically but normal at rest

358
Q

What is class 3 heart failure

A

Marked physical limitation but no symptoms at rest

359
Q

What is class 4 heart failure.

A

Inability to carry out physical activity and may have symptoms at rest

360
Q

What is the average cardiac output

A

5L/min

361
Q

What is an average LV end systolic volume

A

75ml

362
Q

What is an average LV end diastolic volume?

A

150

363
Q

What is an average stroke volume

A

75ml

364
Q

A normal ejection fracture is what?

A

50% upwards

365
Q

What’s the normal weight of a heart?

A

330g

366
Q

What 4 things does cardiac output depend upon?

A

Heart rate
Venous capacity (LV preload)
Aortic and peripheral impendence (afterload)
Myocardial contractility

367
Q

What occurs in ventricular remodelling following acute infarction?

A

Initial infarct spreads. Cardiac tissue remodels and scars.
Wall thins to increase capacity
(Decreases cardiac output)

368
Q

In heart failure what systems are activated

A 
Neuro-hormonal:
Sympathetic nervous system 
RAAS
Natriuretic hormones
ADH
Endothelin
Prostaglandins
369
Q

What is the early compensatory response of the sympathetic nervous system to heart failure?

A

Increase contractility, vasoconstriction and tachycardia

370
Q

What is the long term change of the sympathetic nervous system in response to heart failure?

A

Down regulation of beta andergenic receptors
Noradrenaline induces cardiac hypertrophy.
Up regulation of RAAS

371
Q

What component of the RAAS causes organ damage in response to heart failure?

A

Angiotensin 2

372
Q

What organs are damaged from the upregulation of RAAS in heart failure by angiotensin 2?

A

Heart- LV hypertrophy, fibrosis and remodelling
Vascular- atherosclerosis, vascular hypertrophy
Kidney- decrease in glomerular filtration rate and increase in proteinuria leading to renal failure

373
Q

What are sensitive markers for heart failure?

A

Natriuretic hormones

374
Q

How do natriuretic hormones respond to up-regulation of RAAS in heart failure?

A

Atrial stretch causes release of ANP/BNP
Constriction of afferent arterioles to kidneys.
Decreases NA reabsorbtion and inhibits RAAS

375
Q

What happens to sodium levels in heart failure? Why?

A

Excess NA retention due to RAAS up regulation

376
Q

Why is RAAS activated in heart failure?

A

Reduced renal blood flow

SNS induction of renin from macula densa

377
Q

What peptides act to balance the effects of RAAS in heart failure (NA+ and H20 balance as well as vascular tone)

A

Natriuretic peptides

378
Q

Why do we get hyponatraemia in heart failure?

A

Excess H20 retention due to excess NA retention

379
Q

Normally what would hyponatraemia do to ADH (vasopressin) what happens in heart failure? What’s the outcome?

A

Normally it would inhibit ADH release
In heart failure its stimulated
Causes more H20 retention and increased systemic resistance

380
Q

What is a poor prognostic sign in heart failure? Why is it being secreted?

A

Endothelin

Secreted as a renal vasoconstrictor

381
Q

Why does heart failure lead to oedema?

A

Increased capillary hydrostatic pressure

382
Q

What is oedema?

A

Excessive fluid within tissues interstitium/ intracellular

383
Q

Why does vascular endothelium have increased arterial resistance in heart failure?

A

Due to SNS
RAAS
Reduced NO
Increased endothelin

384
Q

What does increased arterial resistance in heart failure result in systemically?

A

Cachexia
Renal failure
Anaemia (due to less EPO from kidneys)

385
Q

What is used to treat anaemia associated with heart failure?

A

EPO (less produced by kidneys)

386
Q

Heart failure with normal LV function is known as what?

A

Heart failure with a preserved ejection fracture

387
Q

What is the issue with heart failure with a preserved ejection fraction?

A

Diagnosis is more difficult but mortality is similar

388
Q

What are some clincal signs of right sided heart failure?

A 
Raised JVP
Dyspnoea 
Hepatic enlargement
Ascites
Pleural effusion
389
Q

What are some signs of left sided heart failure?

A

Fatigue, exertional dysponoae, Orthopnea, gallop rhythm.

390
Q

What are signs of chronic heart failure?

A

Pulmonary congestion, venous congestion, dependent oedema

391
Q

What are some symptoms of chronic heart failure?

A

Dyspnoea, lethargy, Orthopnea

392
Q

Where is JVP visualised?

A

Between 2 heads of Sternocleidomastoid

393
Q

What is CRT (sacubitril)

A

Drug that delivers 2 active molecules in salt complex.
One enhances vasorelaxation
One inhibits AT1 receptors

394
Q

In the viscous circle of heart failure, what is the overlapping cause

A

A decrease in cardiac output and stroke volume

395
Q

In the viscous circle of heart failure. Once you have decreased cardiac output and stroke volume. What 2 (main things occur) how are they linked?

A

There is neurohormonal activation
There is decreased renal perfusion
Decreased renal perfusion additionally increases neurohormoal activation

396
Q

IN the viscous circle of heart failure, when you have decreased renal perfusion following a decrease in cardiac output and stroke volume, how does that perpetuate a further fall in CO and SV?

A

There is an increase in sodium and water retention (due to decreased perfusion) this increases blood volume and therefore preload on the heart. This leads to further ventricular dilation and wall stress

397
Q

In the viscous cycle of heart failure, once you have decreased CO and SV that leads to neurohormoal activation. What primary effects occur and how does that perpetuate further decreases in CO and SV

A

Increased neurohormoal activation increases systemic vascular resistance. Increased outflow resistance further impairs the LV function thus decreaseing CO and SV

398
Q

What underpins the treatment of heart failure?

A

Overactivation of RAAS and SNS

399
Q

What is prescribed to mange the overactivation of the SNS in heart failure

A

Beta blockers

400
Q

What is prescribed to manage the overactivation of RAAS in heart failure

A

RAAS inhibitors- ACE, ARB, MRA

401
Q

In what direction to ventricles depolarise

A

Endocardium to epicardium

402
Q

What node has the fastest rhythm, what is it?

A

SA node 60-100

403
Q

What is the AV node continuous with

A

Bundle of HIs

404
Q

How can depolarisation reach the ventricles

A

Only through the bundle of HIS

405
Q

Where do the right and left bundle branches lie?

A

Sub endochrondrially in the IV septum

406
Q

What is the purkinje fibres role?

A

Allow rapid spread of depolarisation through ventricular myocardium
4 meters per second

407
Q

If depolarising waves are heading towards a lead. What will happen?

A

Positive complex

408
Q

If depolarising waves are heading away from a lead, what will happen?

A

Negative complex

409
Q

If repolarisation waves are heading towards a lead what will be seen?

A

Negative complex

410
Q

If repolarising waves are heading away from a lead, what will be seen?

A

Positive complex

411
Q

What can change the size of complex on ECG ?

A

Size of signal, direction (if straight at electrode larger deflection)

412
Q

When can you see SA node depolarisation on an ECG

A

You cant see it as its too small, but assume its directly before start of P wave

413
Q

What does the P wave represent

A

The spread of depolarisation across the atria

414
Q

What happens on an ECG as the depol reaches the AV node

A

There is an isoeletric flat line where no activity is detected

415
Q

Other than the AV node delay, what else contributes to the isoelectric flat line following a P wave

A

The spread through the fibrous ring and bundle of HIS

416
Q

What direction is the Q wave seen in lead 2 and why?

A

Downward deflection due to oblique depolarisation in the septum

417
Q

What does the R wave represent?

A

Depol spreading towards the apex

418
Q

What can give a larger R wave

A

Cardiac hypertrophy

419
Q

What is the S wave caused by

A

Depolarisation away from lead 2 to base of heart

420
Q

How is repolarisation seen on ECG

A

As a t wave, upwards as it is moving away

421
Q

How many views of the heart does an ECG give you

A

12

422
Q

How many chest leads?

A

6

423
Q

How many limb views? What are they

A

AVR, AVL, 1,2,AVF, 3

424
Q

What views look at the inferior heart?

A

2,3,AVF

425
Q

What leads look at the left side of the heart

A

1 AVL

426
Q

What do V1/2 chest leads look at?

A

Right ventricle and septum

427
Q

What do v3/4 chest leads look at

A

Apex and anterior wall of ventricles

428
Q

What do V5/6 chest leads look at

A

Left ventricle

429
Q

What is one second on ECG paper

A

5 large squares, 25 small ones

430
Q

1 large square is how many seconds

A

0.2

431
Q

1 small square is how many seconds

A

0.04

432
Q

How many boxes is the pr interval

A

3-5

433
Q

How many boxes is the QRS

A

3

434
Q

Abnormal rhythms on ECG are due to what (2)

A

Abnormal impulse formation

Abnormal conduction

435
Q

Supraventricular rhythms can arise from where?

A

Sinus node
Atrium
Av node

436
Q

Ventricular rhthms arise from where?

A

Ventricle only

437
Q

Supraventricular rhythms will always have normal what?

A

Normal ventricular depolarisation

Normal narrow QRS complex

438
Q

Ventricular rhythms demonstrate what changes?

A

Longer depolarisation

Wide and bizarre QRS complexes (dependent on foci)

439
Q

What are 3 ventricular rhythms

A

Ventricular premature beats
VT
VF

440
Q

What ECG changes are seen with an atrial beat

A

The p wave doesnt have perfect round shape

441
Q

What ECG changes are seen in an AV junctional beat? What different AV junction beats are there?

A

The P wave becomes inverted (depol heading upwards)

High, middle or low AV junctiona beats

442
Q

The shape of a ventricular rhythm will dependent on what?

A

The foci of the beat

443
Q

What is lead 2 usually best for looking at?

A

P waves

Rhythm

444
Q

What are some key ECG changes with AF

A

No p waves just wavy baseline
Impulses arrive at AV node rapidly and irregularly
Some are conducted to ventricles and form normal QRS

445
Q

In AF what is the pulse and heart rate described as

A

Irregularly irregular

446
Q

What is the reason fo AF

A

Multiple atrial foci chaotically impulsing

447
Q

What does the atria do in AF

A

Quiver rather than contracts

448
Q

What is an AV conduction block (both its lay name and what it is)

A

Heart block

A delay or failure of conduction of impulse from atrium to ventricles via AV node or bundle of HIS

449
Q

What are causes of AV conduction blocks

A

acute MI

Degenerative

450
Q

What different types of heart block are there

A

First degree
Second degree: mobitz type 1 and type 2
Third degree aka complete heart block

451
Q

What rhythm develops in complete heart block

A

Ventricular escape rhythm

452
Q

What ECG changes are seen in first degree heart block

A

PR interval prolonged over 5 small squares

Normal QRS

453
Q

What’s happening in first degree heart block

A

Slow conduction in av node and bundle HIS

454
Q

What is 2nd degree mobitz type 1? What phenomenon is happening

A

Wenkebach phenomenon

There is progressive lengthening of the PR interval until one P is no conducted.

455
Q

What is seen on the ECG of 2nd degree type 2 heart block?

A

Sudden non-conduction of a beat (dropped QRS), normal PR interval

456
Q

What is the risk of 2.2 heart block

A

High risk of progressing to CHB

457
Q

What is happening in 3rd degree heart block?

A

The impulses from the atria cant reach the ventricle. Results in ventricular pace maker taking over

458
Q

What is seen on ECG of 3rd degree heart block

A

Dissociation of P- QRS

Very slow QRS complex that are usually wide

459
Q

What rate does a ventricular escape rhythm normally run at

A

30-40bom

460
Q

What are the clincal implications of 3rd degree heart block

A

HR often too slow to maintain BP

Urgent pacemaker needed

461
Q

What is seen on ECG with a ventricular ectopic beat?

A

Wide QRS in a different shape

462
Q

Why is the QRS wider in ventricular ectopics

A

Slower depolarisation

463
Q

What’s ventricular tachycardia defined as?

A

Run of 3+ ventricular ectopics

464
Q

What is VT described as?

A

A broad complex tachycardia

465
Q

What’s dangerous about VT

A

Persistent VT at high risk of VF

466
Q

What’s occurring in VF

A

Abnormal chaotic, fast chaotic ventricular depol

Impulses from numerous ectopic sites

467
Q

What’s the clincal outcomes of VF

A

There’s no coordinated contraction, no cardiac output and therefore cardiac arrest

468
Q

Where are changes of ischaemia or MI seen

A

In the leads that are facing the area

469
Q

I want to look at the inferior aspect of the heart, what leads should i look at

A

2,3, AVF

470
Q

I want to look at the lateral aspect of the heart, what leads should i look at

A

1, AVL, V5, V6

471
Q

I want to look at the septum, what leads should i look at

A

V1, V2

472
Q

I want to look at the anterior heart, what leads should i look at

A

V3,4

473
Q

What heart muscle is the most vulnerable

A

Sub-endocardial (furthest away from coronary )

474
Q

When is ‘flow’

A

Diastole

475
Q

Why does exercise decrease myocardial perfusion

A

Diastole is shorter with rapid heart rate, there is less time for blood flow.

476
Q

What do leads facing an area of reduced myocardial perfusion show?

A

ST segment depression and T wave inversion

477
Q

When are ischaemic changes seen on ECG

A

May only be during exercise but with severe lumen reduction seen at rest

478
Q

What is reduced myocardial perfusion caused by

A

Coronary atherosclerosis

479
Q

What is seen acutely in the ECG of unstable angin/ NSTEMI

A

T wave inversion or

ST depression

480
Q

What is seen weeks after unstable angina or NSTEMI on ecg

A

St and t waves normal

No Q waves

481
Q

If a muscle injury extends the full thickness from endocardium to epicardium, what is the result?

A

STEMI

482
Q

What is a STEMI due to?

A

Complete occlusion of lumen by thrombus

483
Q

What is seen on ECG of a STEMI

A

ST segment elevation in leads facing area

484
Q

What happens in a stemi if perfusion is not re-established?

A

Muscle necrosis

485
Q

In the days that follow a STEMI, what ECG changes are seen

A

T wave inverts, Q wave deepens.

After weeks it normalises other than the deep Q wave

486
Q

What does a pathological q wave look like

A

Over 1 small square wide

A depth more than 1/4 of the r wave

487
Q

What do pathological q waves indicate

A

Necrosis

488
Q

What happens to the resting membrane potential in hyperkalaemia

A

Less negative

489
Q

What happpens to the RMP in hypokalaemia

A

More negative

490
Q

What ECG changes are seen in early hyperkalaemia (7)

A

High t waves

491
Q

What ecg changes are seen with a serum potassium of 10

A

VF

492
Q

What ecg changes are seen in hyperkalaemia with a serum potassium of 8

A

Prolonged PR interval
Depressed ST segment
High T wave

493
Q

What ecg changes could be seen with a serum potassium of 3.5

A

Low t waves

494
Q

What ecg changes could be seen with a serum potassium of 2.5

A

Low t wave, low st segment

495
Q

The overall direction of spread of the ventricular depolarisation is called what

A

Cardiac axis

496
Q

Where is the normal cardiac axis

A

Down to the left

-30 to +90

497
Q

What is a left axis (less than -30) deviation associated with

A

Conduction block of anterior branch left bundle
Inferior MI
LVH

498
Q

What is a right axis deviation (+90) associated with

A

RVH

499
Q

Cardiovascular drugs can alter what? (Some drugs alter more than one of these aspects)

A

Circulating blood volume
Peripheral resistance and blood flow
Force the heart contracts at
Rate and rhythm of the heart

500
Q

What is Atrial flutter?

A

Atrial chambers beat too fast and are out of sync with the ventricles- usually due to circular organised motion
The difference between flutter and fibrilation is that flutter is regular

501
Q

What is atrial fibrilation

A

Disorganised contactions of the atria, irregularly irregular

502
Q

What are the two types of tachycardia?

A

Supraventricular and ventricular

503
Q

What are some potential causes of tachycardia?

A

Ectopic pacemaker activity
Afterdepolarisations
AF/AFL
Re-entry loops

504
Q

What are 2 causes of ectopic pacemaker activity?

A

1, damaged myocardium that depolarises spontaneously

2, latent pacemaker region activated due to ischaemia that dominates over the SA node

505
Q

What do afterdepolarisations cause?

A

Tachycardia following triggered activity

506
Q

What is sick sinus syndrome

A

Sinus bradycardia due to an intrinsic issue to the SA node causing slow depolarisation

507
Q

Other than sick sinus syndrome what else can cause a sinus bradycardia?

A

Beta blockers and calcium channel blockers

Conduction block at AV node or bundle of HIS

508
Q

What is triggered activity?

A

Delayed after depolarisation

Early after depolarisation

509
Q

What is a delayed after repolarisation and when is it more likely to happen?

A

Action potential straight after RMP has resumed

More likely to happen if intracellular calcium is too high

510
Q

What is early after depolarisation? When is it more likely to occur?

A

As the cell is returning to RMP another action potential occurs potentially leading to oscillation
More likely to happen when action potential is prolonged

511
Q

Do re-entrant mechanisms occur in the normal heart? Do they occur when a complete block of conduction has occurred?

A

No, No

Re-entrant depolarisations occur when there is incomplete unidirectional damage

512
Q

What is a re-entrant loop? What can it cause?

A

When a circular loop occurs of action potential that isn’t being stopped by cells in refractory period
Can cause:
AF in atria
Av nodal re-entry
Accessory pathway between atria and ventricles, wolf Parkinson white syndrome

513
Q

What are the 5 basic methods/classes of drugs used to treat arrythmias?

A
  1. Drugs that block voltage sensitive sodium channels
  2. Antagonists of beta adrenoreceptors
  3. Drugs that block K channels
  4. Drugs that block calcium channels
  5. Adenosine (not 1-4)
514
Q

What is an example of a drug that is used to treat arythmia that blocks voltage sensitive Na channels?
How does it stop arythmia?
When is it used clinically?

A

Lidocaine
Blocks Na channels in open or inactive state- preferentially damaged depolarised tissue as these fire automatically.
Used post MI if patient has signs of VT

515
Q

What drug in antiarythmia treatment is a beta blocker?
How does it have its affect?
What does it treat?
When is it used?

A

Propranolol
Blocks beta 1 decreasing sympathetic input by decreasing the slope of pacemaker potential in SA node.
Prevents supraventricular tachycardia, slows rate in AF
Also used following MI to decrease work of heart
Also prevents ventricular arythmia
Also used in myocardial ischaemia

516
Q

Potassium channel blockers are generally not used to treat arythmia due to arythmia causing effect, what drug is the exception and when is it used?

A

Amioderone, treatment on Wolff Parkinson white and can also suppress ventricular arythmia post MI

517
Q

What drug treats arythmia by blocking calcium channels?

How does it work?

A

Veramipril

Decreases slow of AP at SA node, decreasing AV nodal conduction and decreasing force of contraction

518
Q

What is Adenosines mode of action? How can it be used in short spells of time?

A

Acts on A1 receptors at AV node enhancing K conduction and hyperpolarising cells to terminate re-entrant SVT
Has a short half life

519
Q

What are the two drug methods in treating heart failure, which one is predominantly used?

A
  1. Using positive inotropy to increase cardiac output

2. Drugs that reduce the work of heart (predominant use)

520
Q

What is DIgoxin an example of?
How does it work? (Channel change and nerve change)
What’s the result?
When would it be used in Heart failure?

A

Cardiac glycoside
Channel- blocks Na/K atpase, leading to increase Na inctracelluar, which leads to less Na/Ca out of cell. Ca stores increase within the cells increasing force of contraction
INcrease vagal nerve activity- slowing AV conduction
Decrease HR and INcrease contraction force

Used when arrythmias like AF are also present in HF

521
Q

What is Dobutamine and when is it used?

A

Beta adrenonergic agonist used in cardiogenic shock or acute but reversible heart failure

522
Q

What 3 drug classes are predominantly used in heart failure treatment

A

ACE inhibitor
Beta blocker
Diuretics

523
Q

What effect does anACE initiator have i reference to decreasing work load for a heart failure patient?

A

Decrease vasomotor tone thus decreasing afterload

Decrease blood volume which reduces preload

524
Q

When does angina occur?
What is it due to?
How do you want to treat it ? Generally

A

When oxygen supply doesnt meet demand of heart (no myocytes death)
Due to narrowing of coronary arteries
Reduce the work load of heart and improve blood supply

525
Q

Briefly explain how the following drug classes will help with myocardial ischaemia
Beta blocker
Calcium channel antagonist
Glycerol trinitrate

A

Beta blocker- decreased work by decreases sympathetic
Calcium channel antagonist- decrease AV node conduction and chronotropy
Glyceryl nitrate- venodialtion , collateral coronary dilation

526
Q

How do organic nitrates cause dilation of vessels?

A

React with thiols in smooth muscle to give NO release

NO activate gunylate cyclase which increases cGMP which lowers inreacellular calcium causing relaxation

527
Q

What heart conditions come with an increased risk of thrombus

A

AF
Acute MI
Mechanical prosthetic heart valves

528
Q

What are some anticoagulants? And general site of action

A

Heparin inhibits thrombin
Warfarin inhibits vitamin K
Digabatran-oral thrombin inhibitor
Aspirin- antiplatelte

529
Q

What is HTN associated with?

What are some resultant drugs used for this?

A

Increased blood volume (due to Na and water retention) or increased TPR
ACE inhibitor- lower blood volume, and TPR
Calcium channel blocker- selective for smooth muscle
Diuretic

Beta blocker and alpha 1 antagonist not routinely used

530
Q

What is pericardiocentesis?

A

Procedure to remove blood/fluid from pericardial sac

531
Q

What heart sound would you hear with pericarditis?

A

Friction rub

Later effusion would result in soft distant heart sound

532
Q

What’s the physiological range for CVP

A

3-8mmHg

533
Q

What mechanism maintains the right and left eject the same volume over a minute?

A

Frank starling mechanism

534
Q

What does ASKME refer to in relation to JVP pressure?

A 
The JVP pulse pressure changes
Atrial contraction
Systole
Klosed tricuspid
Max atrial filling
Emptying of atria
535
Q

What is coarction of the aorta?

A

Narrowing of the aorta where the ductus arteriosis was

Decreased peripheral pulses as a result

536
Q

What makes up the tetralogy of fallot

A

Overriding aorta
Pulmonic stenosis
VSD
RVH

537
Q

What cardiac issues is down syndrome associated with?

A

VSD and ASD

538
Q

What heart sound is heard with a patent ductus arteriosus?

A

Long crescendo following S2

539
Q

What would the physiological effects of poisoning by using a acetylcholinesterease inhibitor be?

A

AUtonomic- increased saliva and pancreatic juices, decrease HR and BP, pupil constrict
NMJ- paralysis due to NMJ blockade
Brain- initial increase with convulsions followed by depression

540
Q

What’s an acetylcholinesterase?

A

Breaks down Ach in cleft of NMJ

541
Q

What would be the most life threatening aspect of Achestersase inhibitor??

A

Paralysis of resp muscles (requires ventilation)

542
Q

What is the treatment for ACh-esterase inhibitors poison?

A

Atropine- muscarinic receptor agonist

543
Q

2 sites of baroreceptors

A

Carotid sinus

Aortic arch

544
Q

Sympathetic stimulation does what to HR and TPR

A

Increase x2

545
Q

In cardiac tamponade what happens to CVP?
Pulm pressure?
LA pressure?
CO?

A

CVP increases as heart cant fill causing back fill
Pulm pressure increases as blood cant enter LA
LA pressure increases due to compression
CO falls

546
Q

If a 70kg man loses 1.25L of blood what is the loss?

What will be the sequence of events in falling pressures

A 
25% loss
Decreased venous return
Decreased EDV
Decreased SV
Decreased CO
Decreased BP
547
Q

How can circulating volume be increased after haemorrhage

A
  1. Blood

2. Crystalloid fluid

548
Q

Fluid resuscitation uses what?

A

Crystalloid fluid

549
Q

What are some mediators of anaphylaxis

A 
Histamine
Lekotrines
Prostaglandins
Cytokines
Kinins
550
Q

In anaphylaxis what will the hands and pulse feel like?

A

Warm hands, strong bounding pulse

551
Q

In haemorrhage what will the hands and pulse feel like

A

Cold and thready

552
Q

Why does someone with COPD or asbestosis often have creamy secretions? Why do they change with infection

A

Constant prescence of neutrophils/macrophages due to chronic inflection change in colour with infection as new cell types enter

553
Q

Why is nausea associated with cor pulmonale

A

Hepatomegally compressing stomach

554
Q

An increase in HB in hypoxia due to cor pulmonale is good and bad why

A

Increased O2 capacity

Increased viscosity

555
Q

In MI what would happen to blood Co2 levels as CO is increased

A

Initial decrease due to high RR

Then an increase as gas exchange impaired

556
Q

Why give aspirin post MI

A

Decreased risk of further clots

557
Q

What is a recommended treatment for STEMI (under 12 h)

A

Percutaneous coronary intervention to reurfuse

558
Q

What is unstable angina?

A

Thrombosis on top of atheromatous plaque that doesnt completely occlude vessel but causes iscaemia

559
Q

What would a loud systolic murmur and strong apex beat likely be?

A

Aortic stenosis with LVH

ESA 2 (10 decks)

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