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Medicine > CVS > Flashcards

CVS Flashcards

1
Q

What is the base of the heart called (furthest to the bottom)

A

Apex

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2
Q

What are coronary arteries?

A

Arteries that supply well oxygenated blood to the myocardium

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3
Q

What is the name given to the heart muscle?

A

Myocardium

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4
Q

What is the problem with the coronary arteries in terms of blood supply and risk of blockage?

A

They are end arteries with little anastomoses

This makes them prone to atheroma -> stenosis due to atheromatous plaque formation

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5
Q

What are the first 3 large arteries coming off the arch of the aorta?

A

1 - brachiocephalic
2 - right common carotid
3 - left subclavian artery

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6
Q

At what intercostal space is the apex of the heart found?

A

5th intercostal space

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7
Q

What vertical line is the apex of the heart found?

A

Mid-clavicular line

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8
Q

At what intercostal/costal space is the pulmonary trunk found?

A

2nd intercostal space

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9
Q

What is the cover for the heart called?

A

Pericardial sac

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10
Q

What are the two layers of the pericardium called?

A

Visceral and parietal layer
Visceral - inner
Parietal - outer

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11
Q

What is the parasympathetic innervation nerve that supplies the heart muscle?

A

L and R - Vagus nerve

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12
Q

What is the name of the space behind the aorta and pulmonary trunk?

A

Transverse pericardial sinus

Arteries in front of the veins

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13
Q

What two vessels lie anterior to the transverse pericardial sac?

A

Pulmonary trunk to the left

Aorta to the right

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14
Q

What is the oblique pericardial sinus?

A

The oblique sinus of the pericardial cavity is a blind ending passage posterior to the heart formed by the reflections of the visceral and parietal pericardium onto the vessels traversing the space

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15
Q

What is the name of the extended appendage of the right and left atria?

A

Right and left auricle

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16
Q

What are the main coronary arteries?

A

Right and left coronary arteries

Circumflex

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17
Q

What are the left coronary arteries branches?

A

LCA -> Circumflex branch -> Left marginal artery

LCA -> Anterior intraventricular (Left anterior descending) artery + diagonal artery

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18
Q

What are the right coronary artery branches?

A

RCA -> Right marginal artery (for right ventricle) + Atrioventricular nodal artery

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19
Q

Name the cardiac veins?

A

Right ventricle - Small cardiac vein -> coronary sinus
Left ventricle - Middle cardiac vein (posterior inter ventricular septum) + Great cardiac vein (anterior inter ventricular septum)
Posterior L atrium -> Oblique vein of left atrium
All drain into coronary sinus -> right atrium

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20
Q

What is the approximate pressure of blood in the right atrium?

A

SVC - 8-10mmHg / 0-8mmHg

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21
Q

What is the approximate pressure of blood in the right ventricle?

A

15-20mmHg / 0-8mmHg

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22
Q

What is the approximate pressure of blood in the pulmonary arteries?

A

15-25mmHg / 8-15mmHg

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23
Q

What is the approximate pressure of blood in the left atrium?

A

4-12mmHg

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24
Q

What is the approximate pressure of blood in the left ventricle?

A

110-130/ 4-12 mmHg

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25
Q

What is the approximate pressure of blood in the Aorta?

A

110-130 / 70-80 mmHg

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26
Q

What are the 3 layers of the arteries?

A

Tunica intima - epithelial layer + internal elastic lamina
Tunica media - muscular layer
Tunica externa - external elastic layer
Tunica adventitia - connective tissue layer

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27
Q

What is the difference between large, medium and small arteries in their function?

A

Large - elastic highest amount of pressure but also empties fastest therefore needs to rebound
Medium - distributing layer - muscle layer - controls where blood goes
Small (arterioles) - resistance vessels - control blood pressure

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28
Q

When looking at aortic pule pressure why is there a dichrotic notch?

A

Blood leaves ventricles - ventricular ejection
Blood pressure rises initially then starts to decrease as the blood leaving the heart starts to decrease in pressure. Then there is a second peak which is due to the aortic valves closing and the pressure caused by the blood pushing back

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29
Q

At rest what is roughly the normal stroke volume?

A

55-83ml/ blood

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30
Q

During exercise what is approximately the max stroke volume?

A

200ml

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31
Q

What are the 3 layers of the heart?

A

Epicardium - serous membrane smooth surface
Myocardium - middle layer of cardiac muscle
Endocardium - smooth inner surface of heart chambers

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32
Q

What is the name given to the muscular ridges in the auricles and right atrial wall?

A

Pectinate muscles

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33
Q

What is the name given to the muscular ridges and columns on inside walls of ventricles?

A

Trabeculae carnae

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34
Q

How many leaflets are found in the valves?

A

Tricuspid- 3 leaflets
Bicuspid/ Mitral - 2 leaflets
Aortic valve/ Pulmonary valve - 3 leaflets each

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35
Q

Why is erythrocyte sedimentation rate used and what is it a marker of?

A

It is used if there is a worry of increased blood viscosity
It is usually due to inflammatory reasons hence would have immune products inside it such as complement, CRP, Fibrinogen.

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36
Q

How does pressure change from the arteries to the vena cava?

A

Arteries - high pressure pulsating as per the BP
Large and medium arteries - pressure remains high due to the elasticity
Arterioles - pressure decreases rapidly
Capillaries - pressure the least as there is a huge cross-sectional space of blood vessels
Veins - very low pressure system but slightly higher pressures that capillaries as the vessels merge into larger veins

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37
Q

What is the pulse pressure calculation?

A

SBP - DBP

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38
Q

What is the mean arterial pressure calculation?

A

DBP + (1/3 of SBP-DBP)
Or DBP + 1/3 pulse pressure

OR cardiac output x total peripheral resistance

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39
Q

What do we feel when measuring the pulse?

A

The shock wave that arrives slightly before the blood itself

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40
Q

What is the total peripheral resistance calculation?

A

Mean aortic pressure - central venous pressure / Cardiac output

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41
Q

What are Karotkoff sounds?

A

The sounds heard when releasing a pressure cuff from limb when trying to obtain BP readings.
First sound is the sound of the SBP turbulent flow -> DBP - when the turbulent flow now becomes laminar and can’t be heard

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42
Q

Why are cardiac contractions longer than skeletal muscle?

A

To allow the muscle to fully contract which would allow most of the blood to be forced out.

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43
Q

How long is each single contraction of the heart?

A

280milliseconds

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44
Q

How do the valves stop from being forced in the opposite direction of the force of blood against it on ventricular contraction?

A

Cusp shaped

Chordae tendineae attach to papillary muscles which are attached to the cardiac muscle

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45
Q

Where are the pacemaker cells of the heart?

A

SA node

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46
Q

How long is the delay from AV node -> Perkinje fibres?

A

120ms

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47
Q

Which direction in the heart muscle does the electrical activity pass through?

A

From inner -> outer surface

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48
Q

What are the 7 phases of a cardiac cycle?

A 
1 - atrial contraction
2 - isovolumetric contraction
3 - rapid ejection
4 - reduced ejection
5 - isovolumetric relaxation
6 - rapid filling
7 - reduced filling
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49
Q

How long does the heart stay approximately in systole and diastole?

A

Diastole - 0.55seconds (61%)
Systole - 0.35seconds (39%)
Total 0.9seconds

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50
Q

What happens to atrial pressure, atrial volume, left ventricular pressure, left ventricular volume, ECG tracing and phonocardiogram during atrial contraction?

A 
AP = rises
AV = decreases
LVP = rises
LVV = rises
ECG = P wave
PCG = Pre-S1 i.e. no sound yet
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51
Q

What happens to atrial pressure, atrial volume, left ventricular pressure, left ventricular volume, ECG tracing and phonocardiogram during Isovolumetric contraction?

A 
AP = rises slightly due to closing of mitral valve putting pressure in atria
AV = decreased
LVP = Rapid rise
LVV = Isovolumetric therefore no change
ECG = QRS
PCG = S1 heart sound - mitral valve closing
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52
Q

What happens to atrial pressure, atrial volume, left ventricular pressure, left ventricular volume, ECG tracing and phonocardiogram during the first rapid ejection from the left ventricle?

A 
AP = decreases as the atrial base is pulled downwards as the ventricle contracts
AV = no change
LVP = rises but not as quickly as isovolumetric contraction
LVV = Rapidly declines as blood leaves into aorta
ECG = S-T segment
PCG = No heart sounds
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53
Q

What happens to atrial pressure, atrial volume, left ventricular pressure, left ventricular volume, ECG tracing and phonocardiogram during reduced ejection?

A 
AP = gradually rises due to continued venous return from lungs
AV = rises
LVP = Starts to decline as repolarisation of ventricles
LVV = Almost at the least pressure
ECG = T-wave
PCG = no sound
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54
Q

What happens to atrial pressure, atrial volume, left ventricular pressure, left ventricular volume, ECG tracing and phonocardiogram during isovolumetric relaxation?

A 
AP = rises slightly
AV = constant
LVP = rapid decline in pressure
LVV = remains constant all valves closed
ECG = End of T-wave 
PCG = S2 heart sound
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55
Q

What happens to atrial pressure, atrial volume, left ventricular pressure, left ventricular volume, ECG tracing and phonocardiogram during rapid filling?

A 
AP = fall in pressure
AV = decreases
LVP = intraventricular pressure
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56
Q

What happens to atrial pressure, atrial volume, left ventricular pressure, left ventricular volume, ECG tracing and phonocardiogram during reduced filling?

A 
AP = Flat - steady
AV = Flat - steady
LVP = Flat - steady
LVV = Flat steady - ventricles reach inherent relaxed volume. Further filling is driven by venous pressure.
ECG = Up to P wave
PCG = No heart sounds
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57
Q

What is the difference between stenosis and regurgitation?

A

Stenosis - pressure pushing blood through but narrowing makes it difficult
Regurgitation - back leakage when valve should be closed

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58
Q

What are 3 causes of aortic valve stenosis?

A

1 - degenerative (senile calcification/ fibrosis)
2 - congenital (bicuspid form of valve)
3 - chronic rheumatic fever - inflammation - commissural fusion - streptococcal infection - autoimmune response

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59
Q

What type of heart sound is heard in aortic valve stenosis?

A

Crescendo-decrescendo murmur

S1 merges into S2

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60
Q

What is a compensatory mechanism by the heart due to increased LV pressure?

A

LV hypertrophy

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61
Q

What is a side effect of left sided heart failure?

A

Syncope

Angina

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62
Q

What is a haematological problem due to aortic valve stenosis?

A

Shear stress -> microangiopathic haemolytic anaemia

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63
Q

What are 2 causes of aortic valve regurgitation?

A

Aortic root dilation - leaflets pulled apart

Valvular damage - endocarditis rheumatic fever

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64
Q

What is aortic valve regurgitation?

A

Blood flows back into the LV during diastole

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65
Q

What effects does aortic valve regurgitation have on stroke volume, SBP, DBP?

A

Stroke volume - increases
SBP - increases
DBP - decreases

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66
Q

What is a side effect on the myocardium of aortic valve regurgitation?

A

LV hypertrophy

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67
Q

What are the heart sounds of aortic valve regurgitation?

A

Early decrescendo diastolic murmur

S2 continuous decrescendo till S1

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68
Q

How is a aortic valve regurgitation pulse described as?

A

Bounding pulse

Can be seen in head bobbing or Quinke’s sign

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69
Q

What causes mitral valve regurgitation?

A

(1) Chordae tendineae and papillary muscle weaken due to myxomatous degeneration leading to tissue prolapse
(2) Damage to papillary muscle after heart attack
(3) Left sided heart failure leads to LV dilation which can stretch the valve
(4) Rheumatic fever can lead to leaflet fibrosis which disrupts seal formation

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70
Q

What type of murmur would a mitral valve regurgitation cause?

A

Holosystolic murmur

S1 to S2 constantly heard

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71
Q

What are the main causes of mitral valve stenosis?

A

99.9% - Rheumatic fever

Commissar also fusion of valve leaflets

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72
Q

What are the end results of mitral valve stenosis?

A

Increased left atrial pressure -> LA dilation -> (1) Atrial fibrillation -> thrombus formation
(2) Oesophagus compression -> dysphagia

Inc LA pressure -> Pulmonary oedema, dyspnoea, pulmonary HTN -> RV hypertrophy

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73
Q

What is the murmur heard if a patient has mitral valve stenosis?

A

Snap as valve opens - diastolic rumble

Murmur heard before the S1 HS and no more sounds till the next cardiac cycle

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74
Q

Define afterload

A

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

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75
Q

Define preload

A

The amount the ventricles are stretched (filled) in diastole - related to EDV or central venous pressure

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76
Q

What would happen to arterial and venous pressure if the total peripheral resistance fell and cardiac output was unchanged?

A

Arterial pressure will fall

Venous pressure will increase

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77
Q

What would happen to arterial and venous pressure if total peripheral resistance increased and cardiac output is unchanged?

A

Arterial pressure will increase

Venous pressure will fall

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78
Q

What would happen to arterial and venous pressure if total peripheral resistance unchanged and cardiac output is increased?

A

Arterial pressure will increase

Venous pressure will fall

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79
Q

What would happen to arterial and venous pressure if total peripheral resistance unchanged and cardiac output is decreases?

A

Arterial pressure decreases

Venous pressure increases

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80
Q

What changes occur in the vascular system in order to facilitate an increase in demand for blood in the tissues?

A

(1) Arterioles and precapillary sphincters dilate
(2) Peripheral resistance falls
(3) Heart pumps more so cardiac output rises
(4) Heart ‘sees’ changes in arterial blood pressure and central venous pressure
(5) Heart responds to changes in CVP and aBP by intrinsic and extrinsic mechanisms

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81
Q

What is the equation that leads to stroke volume?

A

End diastolic volume - end systolic volume

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82
Q

What function in the equation can be altered in order to increase stroke volume?

A

Increasing EDV or decreasing ESV

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83
Q

How does inc or dec cardiac compliance affect LV pressure?

A

Inc compliance - higher LV pressure

Dec compliance - lower LV pressure

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84
Q

What disease states would lead to a inc and dec cardiac compliance?

A

Inc - Hypertrophy or stiff heart

Dec - dilated cardiomyopathy

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85
Q

What is the Frank-Starling Law of the heart?

A

If stretch increases the harder the contraction
The more the heart fills -> the harder it contracts (up to a limit) -> the bigger the stroke volume.
As you increase venous return -> inc LVEDP and LVEDV (inc preload).

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86
Q

What is the intrinsic control mechanism of the heart?

A

Increased stroke volume with increased filing of the heart is the intrinsic control mechanism
It ensures that both sides of the heart pump maintain the same output

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87
Q

What is the extrinsic control mechanism of the heart?

A

Sympathetic stimulation and circulating adrenaline

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88
Q

How is contractility related to stroke volume?

A

Increase in contractility will lead to an increase in stroke volume as there is more force of contraction
This would mean Inc in contractility = inc force of contraction for a given LVEDP = inc stroke volume

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89
Q

What is the effect of increasing arterial pressure on stroke volume?

A

Afterload - pressure pumping against - pressure in aorta -> arterial (aortic) pressure increased when peripheral resistance is increased -> increased TPR also reduces venous pressure and therefore reduces filling of the heart -> Stroke volume decreases

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90
Q

What happens to systemic and GIT arterial and venous pressures after eating a meal?

A

GIT - decreased arterial pressure, inc venous pressure
Systemic - increased arterial pressure and decreased venous pressure
Due to inc cardiac output by in HR -> inc SV -> inc CO

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91
Q

What happens to arterial and venous pressures on standing up?

A

Dec venous pressure -> dec cardiac output -> dec arterial pressure
Intrinsic mechanisms the pressures can not control BP therefore extrinsic mechanism needs to regulate -> baroreceptor reflex and autonomic NS inc HR and inc TPR

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92
Q

What height of JVP is considered normal?

A

5-8cm H2O above the sternal angle

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93
Q

What 3 common conditions will increase JVP?

A

1 - right heart not pumping properly
2 - volume overload
3 - right heart impaired filling

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94
Q

At how many weeks of pregnancy does the heart start to form?

A

5th week of pregnancy

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95
Q

What two structures move together to form the circulatory structure?

A

Blood islands

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96
Q

What are the 6 structures of the primitive heart tube?

A

Sinus venosus -> Atrium -> Ventricle -> Bulbus cordis -> Trucus arteriosus -> Aortic roots

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97
Q

What structures of the primitive heart tube are found in the pericardial sac?

A

Ventricle, Bulbus cordis and trunks arteriosus

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98
Q

What is cardiac looping?

A

The primitive heart tube elongates -> runs out of room -> twists and folds up -> places inflow and outflow in the correct orientation

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99
Q

What is the transverse pericardial sinus?

A

The gap behind the arteries (aorta and pulmonary arteries) and in front of the veins (SVC, IVC)

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100
Q

How does the sinus venosus contribute to form the SVC and IVC?

A

Splits from one stem to the R + L sides.
Venous return shifts to R side, L sinus horn recedes to form the transverse sinus (blood flow back into the heart from the coronary vessels)
R sinus horn is absorbed by the enlarging right atrium

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101
Q

Why is the right atrium more trabecular and the left atrium is more smooth walled?

A

The right atrium came from the primitive atrium mostly and only a small amount from the SVC/ IVC
Most of the left atrium came from the sprouted pulmonary veins and only a little from primitive atrium -> hence mostly smooth walled

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102
Q

What is the oblique sinus?

A

Oblique pericardial sinus is formed as left atrium expands absorbing the pulmonary veins

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103
Q

What are the 3 foetal shunts that allow oxygenated blood to travel around the body in the foetus?

A

1 - ductus venosus - from umbilicus to the heart (around the liver)
2 - foramen ovale - RA -> LA
3 - ductus arteriosus - Pulmonary arteries -> aorta

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104
Q

How many aortic arches exist in human embryos?

A

1-4 + 6 (5th doesn’t exist in humans)

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105
Q

From which aortic arches does the aorta come from?

A

4th Arch
R = proximal part of the R subclavian artery
L = arch of aorta

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106
Q

From which aortic arch does the pulmonary arch come from?

A 
R = R pulmonary artery
L = L pulmonary artery and ductus arteriosus
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107
Q

What is a problem with a patent ductus arteriosus?

A

Inc pressure in pulmonary trunk -> inc pressure in lungs -> inc back pressure into right ventricle -> RV hypertrophy

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108
Q

What is the function of septation?

A

Septation of the ventricular outflow tract - pulmonary trunk and aorta
Interatrial septation
Interventricular septation

Creates 4 chambers and achieve selective outflow

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109
Q

What is the first step of septation in the primitive heart?

A

Endocardial cushions - developing in the atrioventricular region divides the developing heart into right and left channels
Cushions develop dorsal to ventral separating L + R sides of the tube

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110
Q

What is the process of atrial septation?

A

1 - septum premium grows down towards the endocardial cushions
2 - ostium primum is the hole present before the septum primum fuses with endocardial cushions
3 - before ostium primum closes the second hole - ostium secundum appears in septum primum
4 - second crescent shaped septum, the septum secundum grows -> forms a hole in septum secundum -> foramen ovale

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111
Q

What is the adult remnant of the foramen ovale?

A

Fossa ovalis

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112
Q

What keeps a patent foramen ovale during embryonic and foetal development?

A

Pressure from RA > LA which keeps the septum primum open and away from the septum secundum

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113
Q

What are the atrial septal defects?

A

Ostium secundum defect - septum primum and septum secundum

Hypoplastic left heart syndrome

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114
Q

What is hypoplastic left heart syndrome?

A

Defect in development of mitral and aortic valves - resulting in atresia and therefore limited flow
Ostium secundum too small -> R to L inadequate flow in utero -> left heart underdeveloped -> ascending aorta very small -> right ventricle supports systemic circulation -> obligatory R->L shunt

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115
Q

How does ventricular septation occur?

A

Single ventricular chamber -> ventricular septum forms which has two components -> 1 - muscular 2 - membranous -> Muscular portion forms most of the septum and grows upwards towards the fused endocardial cushions

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116
Q

What causes the primary interventricular foramen to form in the embryo?

A

Muscular portion grows upwards towards the endocardial cushions leaving a small gap

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117
Q

What structure fills the primary interventricular foramen in embryo?

A

Membranous portion of the interventricular septum formed by the connective tissue derived from the endocardial cushions

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118
Q

What part of the ventricle in the embryo is most likely to lead to a VSD?

A

Membranous portion of the septum as growth is downwards and that might not occur

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119
Q

What structure is responsible for causing septation of the outflow tract in the embryological heart?

A

Endocardial cushions appear in the truncus arteriosus and as they grow towards each other they twist around and form a spiral septum

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120
Q

What 3 broad types of defects can occur in the formation of the heart?

A

Structural defect - chambers or vasculature
Obstruction - due to atresia
Communication between pulmonary and systemic circulations

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121
Q

What is transposition of the great arteries?

A

The pulmonary artery sends blood around the body and the aorta sends blood to the lungs. i.e. Pulmonary trunk from Left ventricle and Aorta from the Right ventricle

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122
Q

What is the result of transposition of the great arteries?

A

Cyanosis - depending on what other if any defects are present
Not viable unless two circuits communicate i.e. via atrial, ventricular or ductal shunts

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123
Q

What is tetralogy of fallow?

A

1 - Large ventricular septal defect
2 - overriding aorta
3 - right ventricular hypertrophy
4 - right ventricular outflow tract obstruction

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124
Q

What are the two main classifications of congenital heart defects?

A

1 - acynotic

2 - cyanotic

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125
Q

What are the acyanotic congenital heart defects?

A

1 - L->R shunts = ASD, VSD, PDA
2 - obstructive lesions: aortic stenosis, pulmonary stenosis (valve, outflow, branch), coarctation of the aorta, mitral stenosis

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126
Q

What are the cyanotic congenital heart defects?

A

1 - Tetralogy of fallot - VSD/ pulm stenosis/ RV hypertrophy/ overriding aorta
2 - Transposition of the great arteries
3 - Total anomalous pulmonary venous drainge
4 - Univentricular heart

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127
Q

What are the haemodynamic effects of atrial septal defects?

A

Increased pulmonary blood flow
RV volume overload
Pulmonary HTN - rare but possible
Eventual right heart failure

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128
Q

What are the haemodynamic effects of ventricular septal defects?

A

L->R shunt
LV volume overload therefore LV hypertrophy
Pulmonary venous congestion
Eventual pulmonary HTN

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129
Q

What is tricuspid atresia?

A

Malformation of the tricuspid valve
1 - no RV inlet
2 - R-L atrial shunt of entire venous return
3 - Blood flow to lungs via VSD or PDA

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130
Q

What two gradients force potassium into and out of the cell?

A

Electrical gradient - pushes potassium into the cells as more positive outside than inside
Chemical gradient - pushes potassium out of the cells as there is more potassium inside than outside cells

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131
Q

What is different in intracellular resting membrane potential of skeletal muscle compared to SA node in the heart?

A

-90mV in skeletal muscle and -60mV in SA node

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132
Q

What is different in action potential duration of skeletal muscle compared to SA node in the heart?

A

0.5ms skeletal muscle

100ms SA node

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133
Q

What ion is predominant in the cardiac action potential during phase 4 part of the cycle?

A

Sodium entering the cells via the voltage gated sodium channels

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134
Q

What ion is predominant in the cardiac action potential during phase 0 part of the cycle?

A

Sodium is rushing into the cells via the voltage gated sodium channels - cell becomes depolarised

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135
Q

What ion is predominant in the cardiac action potential during phase 1 part of the cycle?

A

Transient outward potassium current + reversal of NCX hence repolarisation

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136
Q

What ion is predominant in the cardiac action potential during phase 2 part of the cycle?

A

Opening of voltage gated calcium channels (some K channels also open)

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137
Q

What ion is predominant in the cardiac action potential during phase 3 part of the cycle?

A

Calcium channels inactivate and voltage gated potassium channels open

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138
Q

What occurs in the cardiac cycle at each stage in terms of ions?

A

0 - RMP due to background K channels
1 - Upstroke due to opening of voltage gated sodium channels - influx of sodium
2 - initial repolarisation due to transient outward K channels
3 - Plateau due to opening of VGCC (L-type) - influx of calcium - balanced with K efflux
4 - repolarisation due to efflux of K through voltage gated K channels

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139
Q

What causes the SA node action potential to be the way it is and allow automaticity?

A

1 (-60mV) - initial incline - spontaneous depolarisation - due to pacemaker potential, If (funny current), influx of Na. Permeable to Na and K
2 (-50mV to +15mV) - Opening of VGCC causes the steep incline - depolarisation
3 (+15mV to -60mV) - Repolarisation due to opening of VGKC and turning off Ca channels
HCN start the spontaneous depolarisation at -50mV

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140
Q

What does HCN stand for in terms of ion channels and where is it found?

A

Hyperpolarisation-activated, Cyclic Nucleotide-gated channels

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141
Q

What 2 calcium channels are found in the heart that allow the SA node to repolarise?

A

T-type (transient) and L-type channels

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142
Q

In the SA node what ion is responsible for causing upstroke of the action potential?

A

Opening of voltage-gated calcium channels

Calcium influx into the cell

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143
Q

In the SA node what ion is responsible for causing downstroke of the action potential?

A

Opening of voltage gated K channels

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144
Q

What is the effect of hyperkalaemia on the heart?

A

Increased extracellular K+ levels -> Less K+ leaves the cells -> RMP would become decreased (i.e. more positive) + membrane becomes partially depolarised -> inc membrane excitability -> inactivates some VGNC -> slows upstroke.
Downstroke in stage 2 of the cardiac cycle becomes quicker and more abrupt rather than a smooth decline.

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145
Q

What is the effect of hypokalaemia on the heart?

A

RMP is inc -> both AP and refractory periods are prolonged

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146
Q

What ECG changes will be seen in hyperkalaemia?

A

Tall Tented T waves, Shortened QT interval, Prolonged PR interval, Flattened P waves, Widened QRS complex
In the end stage - ST segment merges with T wave - to give sine wave pattern

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147
Q

What ECG changes will be seen in hypokalaemia?

A

Flattened T waves, Peaked P waves, Lengthened QRS complex, ST depression, appearance of a U wave

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148
Q

What are the risks with hyperkalaemia?

A

Asystole

Initially increase in excitability due to repolarisation not being as significant

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149
Q

How do you treat hyperkalaemia?

A

Insulin + dextrose
Calcium gluconate - divalent ion shields the membrane and decreases excitability
Magnesium protects the If

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150
Q

What are the problems with hypokalaemia?

A

Longer AP can lead to early after depolarisations - leads to oscillating membrane potential
Can result in VF

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151
Q

What happens to the cardiac myocyte once it has been excited?

A

1- Depolarisation opens L-type Ca channels in T-tubule system
2 - Localised Ca entry opens Calcium-induced calcium release channels in the SR
3 - Close link between L-type channels and Ca release channels
4 - 25% enters across sarcolemma and 75% released from SR

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152
Q

What happens to cause the cardiac myocyte to become relaxed again ready for the next depolarisation?

A

Ca levels must return to resting levels
Most pumped back into the SER via SERCA = sarcoplasmic endoplasmic reticulum Ca- ATPase
Some exits across the cell membrane via the NCX channel

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153
Q

How does the smooth muscle in the vasculature constrict in terms of the intrinsic mechanism?

A

VGCC allow Ca to enter the cell or Adrenaline attaches to A1 receptors on the vascular wall. A1 = Gq receptor.
Gq => PLC -> PIP3 -> IP3 and DAG
IP3 causes inc in intracellular calcium by release from SR
Ca from SER and VGCC => Attaches to calmodulin -> activates MLCK which causes ATP-> ADP and activates a myosin II head -> contracts as the myosin head moves along the actin filament.
MLCP inactivates the myosin head by removing the phosphate group from the myosin.
DAG cause PKC to be produced which then phosphorylates MLCP causing its inhibition to allow a sustained contraction

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154
Q

What is the difference in calcium binding from a cardiac myocyte compared to smooth muscle?

A

Cardiac myocyte - Ca binds to the troponin-C which moves out of the way for myosin to attach to actin
SM - Ca binds to calmodulin which activates MLCK -> phsphorylates myosin light chain

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155
Q

What receptor is acted on by the sympathetic NS and what is the effect on the heart?

A

B1 receptor - adrenaline/ noradrenaline

Positively chronotripic and inotropic

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156
Q

What receptor is acted on by the parasympathetic NS and what is the cause on the heart?

A

M2 receptor - acetylcholine
Negatively chronotropic
Dec AV node conduction velocity and SA node conduction velocity

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157
Q

At rest what is the heart mostly under the influence of in terms of HR?

A

PNS - Vagal influence - Vagus nerve

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158
Q

Where in the brain is the cardiovascular centre?

A

Medulla oblongata

159
Q

Where are baroreceptors found?

A

Arch of the aorta

Just distal to the bifurcation of the carotid arteries on the internal carotid artery - carotid sinus

160
Q

What is the ANS effects on the vasculature?

A

Most vessels -> sympathetic innervation (except erectile tissue)
Have alpha-1 receptors and some have B2 receptors

161
Q

Why is vasomotor tone important?

A

Gives the vessel the ability to allow vasodilation and vasoconstriction to occur
At maximal vasodilation there would be no room to allow expansion if blood volume increased or BP needed to be reduced.

162
Q

What is the benefit of having B2 and A1 receptors on the vessel wall?

A

B2 => Vasodilation - Inc cAMP -> PKA -> opens potassium channels + inhibits MLCK -> relaxation of smooth muscle
A1 => Vasoconstriction
Stimulates IP3 production from PIP3 (+DAG) -> Inc Ca release from SER and influx of Ca from extracellularly -> contraction of smooth muscle

163
Q

What is the effect of B2 receptor innervation on the vascular smooth muscle?

A

Vasodilation - Inc cAMP -> PKA -> opens potassium channels + inhibits MLCK -> relaxation of smooth muscle

164
Q

What is the effect of A1 receptor innervation on the vascular smooth muscle?

A

Vasoconstriction
Stimulates IP3 production from PIP3 (+DAG) -> Inc Ca release from SER and influx of Ca from extracellularly -> contraction of smooth muscle

165
Q

What local metabolites would have an effect on the vasculature?

A

Adenosine
Potassium
H+
Increase in pCO2

166
Q

What effect would local metabolites have on the vasculature?

A

Vasodilation as they indicate an increase in metabolic demand of the tissues and so would need to increase blood flow to that region

167
Q

Apart from baroreceptors where else are receptors located that help detect changes in BP?

A

Atria in the low pressure system

168
Q

What is good and bad about the baroreceptor reflex?

A

Good - quick changes in BP can be responded to quickly and does not require thinking as it is a reflex
Bad - Prolonged raised BP can cause the baroreceptors to re-set at higher BP levels which would mean there is a generalised increased BP

169
Q

What are sympathomimetic drugs and what is their function on the heart?

A

Act on the sympathetic NS
CV uses - adrenaline to restore function in cardiac arrest
B1 agonist - dobutamine given in cariogenic shock - acute heart failure

170
Q

What are adrenoceptor antagonists and what is their function on the heart and vasculature?

A

Alpha-adrenoceptor antagonists and beta-adrenoceptor antagonists
A1- doxazosin and prazosin - anti-HTN, inhibits NA action on vascular smooth muscle - vasodilation
B1/B2 - propranolol= nonselective -ve chronotropic and inotropic effects
atenolol = selective B1 (cardio-selective) less risk of bronchoconstriction

171
Q

What cholinergics would be used in the cardiovascular system and for what effect?

A

Muscarinic antagonist = Atropine/ tropicamide = increases heart rate, bronchial dilation

172
Q

What is a normal/ ideal BP range?

A

90/60 - 120/80mmHg

173
Q

How is HTN classified?

A

Stage 1 -> 2 -> Severe

174
Q

What BP is classified as stage 1 HTN?

A

Clinic BP = ≥140/90mmHg

ABPM/HBPM = ≥ 135/85mmHg

175
Q

What BP is classified as stage 2 HTN?

A

Clinic BP= ≥160/100mmHg

ABPM/HBPM= ≥150/95mmHg

176
Q

What BP is classified as severe HTN?

A

Clinic BP= ≥180 SBP or ≥110DBP

177
Q

What are the causes of HTN?

A

Primary/ essential = unknown cause

Secondary = defined cause - Renvascular disease, Chronic renal disease, Hyperaldosteronism, Cushings syndrome

178
Q

Why is it important to treat HTN?

A

Silent killer

Leads to Heart and vascular problems: HF, MI, Stroke, Renal failure, Retinopathy

179
Q

What are the 4 neurohumoral pathways to controlling circulating volume and hence BP?

A

1 - RAAS
2 - Sympathetic NS
3 - ADH
4 - ANP

180
Q

Why do ACE-I cause respiratory problems?

A

Cough is a side effect
ACE converts Bradykinin to Peptide fragments and if this does not occur then the patient will have a build up of bradykinin and hence a cough.

181
Q

What cause ANP to be released?

A

ANP promotes Na+ excretion
Synthesised and stored in atrial myocytes
Release from atria in response to stretch
Low pressure volume sensors in the atria
Reduced effective circulating volume inhibits release go ANP

182
Q

How do atrial natriuretic peptides affect BP?

A

Vasodilation of afferent arteriole in kidneys -> increased Na+ delivery to tubules and hence to JGA cells -> less renin produced -> decreased BP.
Inhibits Na+ reabsorption along nephron

183
Q

How do prostaglandins affect BP?

A

Act as vasodilators
Long acting prostaglandins PGE2 enhance GFR and reduce Na+ reabsorption
Act as a buffer to excess vasoconstriction produced by SNS and RAAS hence important when Ang2 levels are high

184
Q

Where is dopamine made and how does it affect BP?

A

Formed in the kidney from circulating L-dopa
Dopamine receptors are present on renal blood vessels and cells of the PCT and TAL
DA causes vasodilation and increases renal blood flow
DA reduces reabsorption of NaCl - inhibits NH exchanger and Na/K ATPase in principal cells of PCT and TAL

185
Q

How does renovascular disease cause HTN?

A

Occlusion of renal artery -> reduced renal perfusion -> inc renin production -> activation of RAAS -> vasoconstriction and Na+ retention at other kidney (affected kidney doesn’t get an increase in RBF due to stenosis)

186
Q

How does renal parenchymal disease cause HTN?

A

Earlier stage may be a loss of vasodilator substances

In later stage Na and water retention due to inadequate GFR - volume dependent HTN

187
Q

What is Conns syndrome and how does it affect BP?

A

Aldosterone secreting adenoma

Hypertension and hypokalaemia

188
Q

How does Cushings syndrome cause HTN?

A

Excess secretion of cortisol - high concs acts on aldosterone receptors -> sodium and water retention

189
Q

How does phaeochromocytoma cause HTN?

A

Secretes catecholamines - adrenaline and norad

190
Q

How do L-type calcium channel inhibitors work to reduce HTN?

A

Verapamil/ diltiazem

Reduce Ca entry into vascular smooth muscle -> relaxation of smooth muscle -> vasodilation

191
Q

How do Alpha-blockers treat HTN?

A

Reduce sympathetic tone -> hypotension

Can cause postural hypotension

192
Q

What is the fibrous ring of the heart and what is the function of it?

A

Dense connective tissue that forms four rings in the plane between the atria and ventricles
It is an electrical insulator that allows the atria to contract separately from the ventricles
There is a small passageway between the ventricles and atria that allows the bundle of His to flow through it

193
Q

What structure is the only conducting pathway from the atria to the ventricles?

A

Bundle of His

194
Q

Why is there a flat line on an ECG?

A

Isoelectric point - no current flowing from the outside to inside of the cell

195
Q

In what direction does repolarisation occur of the ventricles?

A

Backwards direction to the depolarisation travel

196
Q

How does ECG wave amplitude alter with direct and indirect travel of the depolarisation?

A

Direct > indirect amplitude

197
Q

What causes a P wave on the ECG?

A

Atrial depolarisation
Spread through the atria from the SVC junction to the AV node
Indirect depolarisation hence only a small wave seen on ECG
Lasts 80-100ms

198
Q

What ECG line is seen during the delay at the AV node?

A

Isoelectric = flat line

199
Q

What subsections of the bundle of His and perkinje fibres are there?

A

Left bundle branch and Right bundle branch

200
Q

What is the normal duration from start of atrial depolarisation to the start of ventricular muscle depolarisation?

A

120-200ms

201
Q

Why is the Q wave a downward deflection when the ventricles are depolarising?

A

The depolarisation occur obliquely away along the

ventricle from the left ventricle side to the right ventricle. It is depolarisation of the interventricular septum

202
Q

If there is a large Q wave would could this be a sign of?

A

Previous MI

Always pathological

203
Q

What causes the R wave on an ECG?

A

Large upward deflection due to depolarisation at the apex and free ventricular wall
Upward deflection as depolarisation moves directly towards the electrode
Large deflection because of large muscle mass hence more electrical activity

204
Q

What would a larger R wave be sign of?

A

Hypertrophic left ventricle

205
Q

What causes the S wave on an ECG?

A

Depolarisation spreads upwards to the base of the ventricles which produces a small downward deflection
Downwards = moves away from the electrode but a small peak as it is not directly away

206
Q

How long should the QRS complex normally be?

A

80-120ms

207
Q

What causes the T wave on an ECG?

A

Begins on epicardial surface
Spreads in the opposite direction to depolarisation
Produces a medium upward deflection - T wave
Upward because it is a wave of repolarisation moving away from the electrode

208
Q

What are the limb leads?

A

I, II, III, aVR, aVF, aVL

6 views in the vertical plane

209
Q

What would the aVR lead look like?

A

Upside down to an ECG normally known as. Mirror image

It looks at it from the opposite direction to lead II which is the main one seen and compared against

210
Q

What would the aVL lead look like?

A

No P wave

Small QRS complex seen as it an oblique view of the heart

211
Q

What would the aVF lead look like?

A

Similar to a normal ECG in lead II however there is less tall QRS complex

212
Q

What would a lead I ECG look like?

A

Same as lead II but less tall QRS complex and less deep S wave
Oblique view of the heart

213
Q

What would a lead III ECG look like?

A

Much smaller version of Lead II in all aspects.

P wave and T waves are barely seen.

214
Q

What are the horizontal planes of an ECG?

A

6 chest leads V1-V6

Look at different views of the anterior portion of the heart

215
Q

What region of the heart is seen in leads V1 to V4?

A

Antero-septal leads

216
Q

What region of the heart is seen in leads V1 to V2?

A

RV and septum

217
Q

What region of the heart is seen in leads V3 to V4?

A

Apex of heart and anterior wall of RV and LV

218
Q

What region of the heart is seen in leads V5 to V6?

A

LV (lateral leads)

219
Q

What limb leads would be best to see if there is muscle necrosis on the lateral LV?

A

Leads 1 and aVL

220
Q

What limb leads would be best to see if there is muscle necrosis on the anterior surface of the heart?

A

II, III, aVF

221
Q

What limb leads would be best to see if there is muscle necrosis on the septum and anterior surface of the ventricles of the heart?

A

V1, V2, V3, V4
V1,V2 - RV and septum
V3,V4 - Apex and anterior surface of ventricles

222
Q

What limb leads would be best to see if there is muscle necrosis on the lateral surface of the heart?

A

Lead 1, aVL, V5, V6

223
Q

What would a normal ECG look like in leads V1 and V2?

A

No Q waves
Small R wave
Large S wave

224
Q

What would a normal ECG look like in leads V3 and V4?

A

Large R wave

Smaller S wave

225
Q

What would a normal ECG look like in leads V5 and V6?

A

Q waves present
Large R wave
Small S wave

226
Q

On ECG paper how many seconds does a small and large square represent?

A 
Large = 200 millisecond
Small = 40 milliseconds
227
Q

On ECG paper how many seconds would represent 1 minute?

A

300 big squares

228
Q

On ECG paper how many seconds would represent 1 second?

A

5 large squares

25 small squares

229
Q

How would you easily calculate heart rate on an ECG?

A

R-R interval number of seconds

230
Q

On an ECG what would be classified as one heart beat?

A

Beginning of one P wave to the beginning of the next P wave

231
Q

What is a normal P-R interval?

A

120-200ms

232
Q

What would be classified as a prolonged P-R interval?

A

> 1 large box = >200ms

233
Q

What does a prolonged PR interval indicate?

A

Delayed conduction through AV need and bundle of His

234
Q

What is a normal QRS interval?

A

<120 milliseconds

235
Q

What is classed as a prolonged QRS interval?

A

> 120 milliseconds

236
Q

What could be a cause for a widened QRS interval?

A

Depolarisation arising in ventricle and not spreading via the rapid conducting His-Perkinje system hence takes more time

237
Q

What is defined as the QT interval?

A

From the beginning of the Q wave to the end of the T wave
Time taken for depolarisation and repolarisation of the ventricle
Varies with heart rate
Calculation to correct for HR

238
Q

Why is QT interval corrected?

A

QT changes with varying HR - depolarisation of ventricles varies
QTc takes this into account and allows for easier comparison
QT interval shortens when HR increases

239
Q

What HR’s would be classed as tachycardia or bradycardia?

A

Bradycardia < 60bpm - 100bpm < tachycardia

240
Q

What is a heart block?

A

Conduction problem from the atria to ventricles

241
Q

What types of heart block are there?

A

1st degree
2nd degree- Mobitz type 1 and Mobitz type 2
3rd degree

242
Q

What can be causes of heart block?

A

Acute MI

Degenerative changes e.g. pacemaker

243
Q

What is first degree heart block characterised by on an ECG?

A

PR interval prolongation - regular intervals

>200milliseconds

244
Q

What is second degree mobitz type 1 heart block characterised by on an ECG?

A

PR interval prolongation till a QRS is dropped then cycle restarts
AKA Wenkebach type

245
Q

What is second degree mobitz type 2 heart block characterised by on an ECG?

A

Sudden drop of a QRS complex without a change in PR interval - can lead to complete heart block

246
Q

What is third degree heart block characterised by on an ECG and why?

A

Complete heart block
No impulses from atria -> ventricles
No regular PR interval
P - P wave regular AND R - R wave is regular but not related rhythms
P-P interval will be much quicker than the R-R interval
Wide QRS complex
Ventricular rate is 30-40BPM which is insufficient to maintain BP - urgent pacemaker insertion required

247
Q

What is a bundle branch block?

A

Delayed conduction in the branches of the bundle of His
Could be either RBBB or LBBB
P wave and PR interval are normal though
Wide QRS complex - since ventricular depolarisation takes longer (because going through myocytes

248
Q

What lead would indicate a RBBB and what would the ECG look like?

A

V6 - looks at left ventricular lateral wall
Lead 2 may show a STEMI but V6 may show no signs of that just a RBBB
Lead I = wide S wave
Lead V1 = triphasic QRS complex - RSR wave

249
Q

Where can abnormal impulses arise from and what are they called?

A

SA node
Atrium
AV node
All above are called supraventricular rhythms

Ventricle - ventricular rhythms (more dangerous than supraventricular)

250
Q

What would an ECG show in a supraventricular rhythm?

A

Normal or narrowed QRS complex

Tachycardia

251
Q

What would an ECG show in an abnormal ventricular arrhythmia?

A

VT would just look like a sine wave with wide QRS complexes

252
Q

What type of arrhythmia is atrial fibrillation and what causes it?

A

Supraventricular rhythm - irregularly irregular pattern on ECG
Rhythm arises from multiple atrial foci - causing a re-entrant rhythm
Impulses reach AV node at rapid irregular rate - not all are conducted through because AV node refractory period

253
Q

What does an AF ECG show?

A

No P wave
Just wavy baseline
Narrow QRS complex with IRREGULAR R-R intervals

254
Q

What would a ventricular ectopic beat look like on ECG and what causes it?

A

Ectopic focus in ventricle muscle
Impulse does not spread via the fast His-Perkinje system therefore much slow depolarisation of ventricle muscle therefore wide QRS complex, different in shape to usual QRS

255
Q

What occurs in VT and what is the ECG tracing?

A

Run of ≥3 consecutive ventricular ectopics is defined as VT
VT is a broad complex tachycardia
Persistent VT is a dangerous rhythm needing urgent treatment that if untreated will lead to ventricular fibrillation

256
Q

What is ventricular fibrillation?

A
  • Abnormal, chaotic, fast, ventricular depolarisation
  • Impulses from numerous ectopic sites in ventricular muscle
  • No coordinated contraction - ventricles quiver like in AF
  • No cardiac output possible therefore cardiac arrest
257
Q

What does ventricular fibrillation look like on an ECG?

A

Very rapid, irregular heart rhythm could be seen in lead 2 or 3

258
Q

What ECG leads would inform if coronary artery has occluded?

A

Need to look at all 12 leads for PQRST waves

259
Q

What ECG leads would inform of a right coronary artery occlusion?

A

II, III, aVF

260
Q

What ECG leads to inform of a LAD occlusion?

A

V1-V4

261
Q

What ECG leads would inform of a circumflex artery occlusion?

A

I, aVL, V5, V6

262
Q

In myocardial ischaemia is there is muscle necrosis?

A

No

263
Q

Is there a blood test that will indicate cardiac myocyte necrosis?

A

Yes cardiac troponins

These will only be seen during infarction and tissue necrosis

264
Q

How could you tell the difference between myocardial infarction and myocardial ischaemia?

A

Cardiac troponin release into the bloods will occur if there is cardiac necrosis and hence infarction

265
Q

What would cause a STEMI?

A

Complete occlusion of a coronary artery by a thrombus

Full thickness of the myocardium is involved

266
Q

Why is the ST segment elevation in a myocardial infarction?

A

The heart behaves as if there is an abnormal current coming towards injured epicardium during repolarisation

267
Q

What 3 things change in an ECG trace hours after a STEMI?

A

ST elevation continues
Depressed R wave
Pathological Q wave begins

268
Q

What 2 things change in an ECG trace 1-2 days after a STEMI?

A

T wave inversion

Q wave becomes deeper

269
Q

What 2 things change in an ECG trace many days after a STEMI?

A

ST normalises

T wave inverted

270
Q

What 2 things change in an ECG trace weeks after a STEMI?

A

ST and T normal

Q wave persists

271
Q

Why can Q waves be seen post STEMI?

A

The area of heart that has been damaged doesn’t produce action potentials. It acts if there was window in that location and so the electrocardiograph picks up the electrical activity in tissues on the other side of the window

272
Q

What ECG changes can be seen in an NSTEMI/ unstable angina?

A

Acutely = T wave inversion OR ST depression OR both ST depression and T inversion
Weeks later = ST and T normal, No Q waves (no muscle necrosis)

273
Q

What happens to an ECG trace in stable angina?

A

ECG is normal at rest BUT then during exercise there is ST depression
This is found out on an exercise treadmill
Changes are reversible at rest after about 5-10minutes

274
Q

What are the causes of tachyarrhythmias?

A
  • Ectopic pacemaker activity
  • Afterdepolarisations
  • Atrial flutter/ atrial fibrillation
  • Re-entry loop
275
Q

What are 2 causes of ectopic pacemaker activity in the heart causing tachyarrhythmias?

A

1 - damaged area of myocardium becomes depolarised and spontaneously active
2 - latent pacemaker region activated due to ischaemia - dominates over SA node

276
Q

What causes afterdepolarisations that lead to tachyarrhythmias?

A

Abnormal depolarisations following the action potential (triggered activity)

277
Q

What are 2 causes of a bradyarrhythmia?

A
  • Sinus bradycardia

- Conduction block

278
Q

What are causes of sinus bradycardia?

A
  • Sick sinus syndrome - intrinsic SA node dysfunction

- Extrinsic factors such as drugs (beta blockers and some CCBs)

279
Q

What are 2 causes of a conduction block causing a bradyarrhythmia?

A
  • Problems at AV node or bundle of His

- Slow conduction at AV node due to extrinsic factors (beta blockers and some CCBs)

280
Q

What are two triggered activities on the heart that cause incorrect timing of depolarisations?

A

1 - delayed after-depolarisations

2 - early after-depolarisations

281
Q

What is a delayed after-depolarisation?

A

A depolarisation occurring in a cardiac myocyte that causes a second wave of small activity.
Usually occurs in late stage 3 or 4.
Usually seen in excess cardiac calcium concentration when the myocytes are excessively excited causing a small contraction, commonly seen in digoxin toxicity.

282
Q

What is an early after-depolarisation?

A

Leads to oscillations in the tracer.
Occur in late phase 2 or phase 3.
Occurs when action potentials durations are increased leading to multiple action potentials successively or a prolonged series of action potentials.

283
Q

What happens at AV nodal re-entry?

A

Fast and slow pathways in the AV node create a re-entry loop - atrial premature beat

284
Q

What happens in ventricular pre-excitation that ends up being a problem?

A

An accessory pathway between atria and ventricles creates a re-entry loop such as in Wolff-Parkinson-White syndrome

285
Q

What are the basic classes of anti-arrhythmic drugs?

A 
4 classes
1 - drugs that block voltage-sensitive Na channels
2 - Beta-adrenoceptor antagonists
3 - Potassium channel blocker
4 - Calcium channel blocker
286
Q

How do sodium channel blockers treat arrhythmias?

A

Use dependent blockade
Only blocks VGNC in open or inactive states - therefore preferentially blocks damaged depolarised tissues. Damaged tissues have more Na channels open.
Little effect in normal cardiac tissue because it dissociates rapidly.
Blocks during depolarisation but dissociates in time for next AP

287
Q

How do beta-adrenoceptor antagonists treat arrhythmias?

A

Block sympathetic action on b1 receptors

Decrease slope of pacemaker potential in SA node and slows conduction at AV node

288
Q

What can beta-blockers be used for?

A

Prevention of supraventricular tachycardia
- Beta-blockers slow conduction in AV node
- slows ventricular rate in patients with AF
Used following MI
- post MI inc in sympathetic activity leads to arrhythmias - block this and reduced chance
Also reduces O2 demand - reduces myocardial ischaemia which is more beneficial post MI

289
Q

What effect do potassium channel blockers have on the heart?

A

Prolong APs - blocking K channels
Lengthens absolute refractory period
In theory would prevent another AP occurring too soon
Can become pro arrhythmic though and prolong QT interval

290
Q

Why is amiodarone used even though it can be pro-arrhythmic in its potassium channel blockade?

A

Also has effects on Na channels so not just K channels

291
Q

What channel does amiodarone work on?

A

Potassium channels

292
Q

What can amiodarone be used for?

A

Tachycardia associated with Wolff-Parkinson-White syndrome (re-entry loop)
Suppression of ventricular arrhythmias post MI

293
Q

What effect do CCB’s have on the heart?

A

Decreases slope of AP at SA node
Decreases AV nodal conduction
Decreases force of contraction (negative inotropy)

Dihydropyridine CCB’s not effective in preventing arrhythmias

294
Q

What CCB’s would be used for cardiac arrhythmias?

A

Non-dihydropyridine CCBs

295
Q

How does adenosine affect the heart?

A

Acts on A1 receptors at the AV node but has a very short half life
Enhances K conductance - hyper polarises cells of conducting tissue therefore heart momentarily stops
Its anti-arrhythmic effects occur because they stop the heart and allow termination of re-entrant SVT’s

296
Q

How do positive inotropes work on the heart and give examples?

A

Increase contractility and thus CO
Cardiac glycoside - digoxin
Beta-agonists - dobutamine

297
Q

How does digoxin work?

A

Blocks Na/K ATPase
Stops setting up of the electrochemical gradient - leading to a rise in intracellular sodium and this then prevents sodium to be released by the NCX.
Inc intracellular Ca2+ -> inc force of contraction
Also acts to increase vagal activity via the CNS -> slows AV conduction and slows HR - used in HF when there is an arrhythmia

298
Q

What is the principal in managing HF?

A

Cardiac glycosides will relieve symptoms by making heart contract harder but won’t improve mortality.
Better to reduce workload -> ACE-I/ ARB’s + Beta-blockers.

299
Q

What system does nitric oxide work on best and why?

A

Venous. Potent vasodilator on veins more so than arteries.
Due to less endogenous nitric oxide in veins.
NO increase granulate cyclase -> inc GTP to cGMP production -> PKG rises -> decreases intracellular calcium -> relaxation of smooth muscle

300
Q

What is the mechanism by which GTN helps relieve symptoms?

A

Venodilation -> lowers preload -> reduces workload of heart -> heart fills less therefore force of contraction reduced -> lowers O2 demand
Secondary action -> on coronary collateral arteries improves O2 delivery to ischaemic myocardium

301
Q

What are the two lung circulations?

A

Bronchial circulation - part of systemic circulation - meets metabolic requirements of the lungs.
Pulmonary circulation - blood supply to alveoli - required for gas exchange

302
Q

What features allows the pulmonary circulations to have low resistance?

A

Short, wide vessels
Lots of capillaries - many parallel elements
Arterioles have relatively little smooth muscle

303
Q

What maintains the pulmonary ventilation/perfusion ratio?

A

Hypoxic pulmonary vasoconstriction
Normally if a tissues is becoming hypoxic the arterioles will dilate to allow more blood flow.
In the lungs -> vasoconstriction to ensure perfusion matches ventilation
Poorly ventilated areas are less well perfused

304
Q

Why influences the pulmonary circulation as a a low pressure system to maintain perfusion?

A

In upright position (orthostasis) there is greater hydrostatic pressure on vessels in the lower part of the lung
This is due to gravity.

305
Q

What happens to the vessels in the lungs during diastole?

A

Vessels at the apex - collaspe
Level of heart - vessels continuously patent
Base - Vessels distended (inc hydrostatic pressure)

306
Q

What is the effect of exercise on the apical blood vessels of the lungs?

A

They remain open as the pulmonary arterial pressure rises slightly to increase O2 uptake by the lungs

307
Q

How does a low pressure system help maintain a short diffusion distance in gas exchange?

A

Prevents lung lymph fluid formation as there is a reduced hydrostatic force compared plasma oncotic pressures

308
Q

Why does LV failure/ mitral valve stenosis lead to pulmonary oedema?

A

Left atrial pressure would be raised
Increase pressure at end of systole and increase resistance for blood. Therefore increased hydrostatic pressure -> pulmonary lymph fluid accumulates -> pulmonary oedema

309
Q

How is blood supply to the brain secured in the event there is a problem?

A

Structurally - lots of anastomoses between basilar and internal carotid arteries
Functionally - myogenic auto regulation maintains perfusion during hypotension. Metabolic factors affect blood flow. Brainstem regulates other circulations and prioritises brain first.

310
Q

Why is a diastolic BP of ≤50mmHg incompatible with life?

A

The brain perfusion fails at this amount.
The myogenic response can maintain BP and cerebral blood flow to the brain however anything below 50mmHg the myogenic response can’t work and fails.

311
Q

What is the Cushing’s reflex?

A

Rigid cranium protect brain - does not allow for volume expansion
Inc in intracranial pressure impairs cerebral blood flow
Impaired blood flow to vasomotor control regions of the brainstem increase sympathetic vasomotor activity

312
Q

Why is coronary artery perfusion mainly during diastole?

A

Aortic valves prevent blood going into the coronary arteries

Pressure from contracting heart prevents blood flow into the capillaries of the heart during systole

313
Q

Production of what substance allow a high basal blood flow into the coronary capillaries?

A

Nitric oxide

314
Q

Why are coronary arteries prone to atheroma?

A

Few arterio-aterial anastomoses

Narrowed coronary arteries -> increased risk of deposition of cholesterol

315
Q

Why does narrowed coronary arteries lead to angina on exercise?

A

Increase O2 demand -> blood flow mostly during diastole -> reduces as HR increases -> stress and cold can also cause sympathetic coronary vasoconstriction and angina -> sudden obstruction by thrombus causes MI

316
Q

What chemical mediators cause vasodilation of muscle capillaries?

A

Inc K+, Osmolarity, Inorganic phosphates, Adenosine, H+

317
Q

What is the function of the cutaneous blood circulation?

A

Special role in temperature regulation
Core temp is maintained around 37 degrees
Skin is main heat dissipating surface
Role in BP maintenance - peripheral vasoconstriction in cutaneous circulation alters BP

318
Q

What is the purpose of arteriovenous anastomoses in the skin?

A

Skin has high surface area to volume ratio
AVAs under neuronal control - sympathetic vasoconstrictor fibres
Decreased core temp -> inc sympathetic tone in AVAs -> dec blood flow to apical skin -> inc core temp.

319
Q

What does SQITARS stand for?

A 
Site
Quality
Intensity
Aggravating factors
Relieving factors
Secondary symptoms
320
Q

What two subtypes of check pain that is cardiac could be described?

A

Ischaemic chest pain - cardiac in nature

Pleuritic chest pain - pleural/ pericardial

321
Q

Describe the type of pain felt in visceral cardiac pain?

A

Dull
Poorly localised
Worsened with exertion

322
Q

Describe the type of pain felt in somatic cardiac pain?

A

Sharp pain, well localised

Worse with inspiration, coughing or positional movement

323
Q

Name 4 non-cardiac causes of chest pain

A

Respiratory - pneumonia/ pleurisy/ PE
GI - reflux, peptic ulcer disease
MSK - costochondritis, rib fracture
Aortic dissection

324
Q

What causes chest pain in stable angina?

A

Heart tissue ischaemia occurs only when metabolic demands of cardiac muscle are greater than what can be delivered via coronary arteries e.g. on exertion.
Relieved on rest.

325
Q

What are the acute coronary syndromes?

A

Unstable angina
MI
STEMI
NSTEMI

326
Q

What causes ACS chest pain?

A

Acute myocardial ischaemia caused by atherosclerotic coronary artery disease
Atheromatous plaques rupture with thrombus formation causing an acute increased occlusion (in an already partially occluded lumen) leading to ischaemia and potentially infarction (myocardial tissue necrosis)

327
Q

What diagnostic tests would be done in suspected ACS?

A

1 - ECG - changes suggestive of ischaemia/ infarction
2 - Blood tests - troponin I
3 - chest x-ray, potential complications identification

328
Q

What lead would a LBBB be best seen in and what is the ECG pattern?

A

Lead I = Deep R wave

Lead V1 = Large QS (R wave)

329
Q

What would a STEMI present with in ECG changes in an infarct?

A

ST elevation

hyper acute T waves

330
Q

What ECG changes would be seen in UA and NSTEMI?

A

Patterns of ischaemia-
ST segment depression
T wave flattening or inversion

331
Q

What is a type 1 MI?

A

Atherosclerotic plaque rupture, ulceration, fissure, erosion or dissection with resulting intraluminal thrombus in one or more coronary arteries leading to decreased myocardial blood flow and/or distal embolisation and subsequent myocardial necrosis

332
Q

What is a type 2 MI and what are some of its causes?

A

A condition other than coronary plaque instability contributes to an imbalance between myocardial oxygen supply and demand.
Causes: coronary artery spasm, coronary endothelial dysfunction, tachyarrhythmia, bradyarrhythmia, anaemia, rest failure, hypotension, severe hypertension, critically ill patients, HF, PE, Tako-tsubo cardiomyopathy, aortic dissection

333
Q

What is a type 3 MI?

A

MI resulting in death when biomarkers not available

334
Q

What is a type 4 MI?

A

MI related to PCI

335
Q

What is a type 5 MI?

A

MI related to coronary artery bypass surgery

336
Q

What can ST depression in the anterior leads sometimes be indicative of?

A

Posterior MI = sudden occlusion of a vessel at the back of the heart

337
Q

Where are the chest leads placed to obtain an ECG trace?

A

V1 - 4th right intercostal space, parasternal
V2 - 4th left intercostal space, parasternal
V3 - midway between V2 and V4
V4 - 5th intercostal space in mid clavicular line
V5 - 5th intercostal space in anterior axillary line
V6 - 5th intercostal space in mid axillary line

338
Q

What troponins would be measured and how long do they remain elevated for in a N/STEMI?

A

Troponin T and I - high sensitivity
Raised within 3 hours of cardiac damage, peaks at 24-48hours
Remains elevated for 2 weeks

339
Q

Apart from a N/STEMI why else would cardiac troponins also be raised?

A 
Renal failure
PE
Severe pulmonary HTN
Sepsis
Burns
Extreme exertion
Amyloidosis
340
Q

What is heart failure?

A

Inability of the heart to meet the demands of the body - i.e. deliver blood to tissues
It is a clinical syndrome of reduced cardiac output, tissue perfusion, increased pulmonary pressures and tissue congestion.

341
Q

What is the most common cause of HF?

A

IHD - myocardial dysfunction

342
Q

Apart from IHD what are the causes of HF?

A

HTN, Aortic stenosis, Cardiomyopathies, Arrhythmias, Other valvular or myocardial structural diseases, Pericardial diseases
Rarely = Sepsis, severe anaemia, thyrotoxicosis

343
Q

What is a normal cardiac ejection fraction?

A

> 55%

344
Q

How does increased inotropy affect cardiac output at a given LVEDP?

A

> CO for a given LVDEP

345
Q

Why is cardiac output reduced in HF?

A

Stroke volume reduced due to:
Reduced preload (reduced EDV) due to impaired filling
Reduced myocardial contractility - not able to produce same force of contraction
Increased afterload = increased pressure due to aortic stenosis, chronic severe HTN for example

346
Q

What is the basic problem in systolic heart failure?

A

Inability to pump - contractility problem - ejection. LV capacity to fill is larger but not able to empty

347
Q

What is the basic problem in diastolic heart failure?

A

Filling problem - possibly post MI - concentric remodelling of ventricle/ stiff

348
Q

How is HF classified?

A

HF with reduced ejection fraction

HF with preserved ejection fraction

349
Q

What is HF with reduced ejection fraction?

A

Systolic dysfunction that is a contractility problem

Most common type

350
Q

What is HF with preserved ejection fraction?

A

Diastolic dysfunction - filling problem

351
Q

What is a normal ejection fraction?

A

> 50% typically 60% +

352
Q

What would be classed as a reduced ejection fraction?

A

<40%

353
Q

Explain why there is still HF even if the ejection fraction is preserved?

A

Filling problem
Ventricles eject less volume in a heart beat as there is less volume to begin with
Fraction of what is available to eject is still >50%
Hence Ejection fraction is preserved

354
Q

Why is biventricular HF congestive?

A

There is reduced blood flowing out of the LV but also RV. There would be a inc pressure in the pulmonary circulation due to reduced pre-load into the LV and so more blood in pulmonary circulation -> inc hydrostatic pressure -> fluid pushed out of the capillaries

355
Q

What are clinical signs and symptoms of heart failure?

A

Symptoms - fatigue/ lethargy, breathlessness, +/- leg swelling
Signs - due to increased oedema - pulmonary oedema and peripheral oedema

356
Q

What are the symptoms in left ventricular heart failure?

A 
Fatigue/ lethargy
Breathlessness (exertional)
Orthopnoea 
Paroxysmal nocturnal dyspnoea
Basal pulmonary crackles
Cardiomegaly (displaced apex beat indicating enlarged LV)
357
Q

Why do patients get orthopnoea in LV heart failure?

A

Breathlessness when lying fat

Blood redistributes when lying flat -> fluid accumulates in lungs

358
Q

Why do patients get paroxysmal nocturnal dyspnoea?

A

Suddenly waking up at night gasping for air because there is blood redistributing from the peripheries to the lungs and the ventricle can’t handle this excess causing congestion in the lungs

359
Q

What are symptoms of right ventricular heart failure?

A 
Fatigue/ lethargy
Breathlessness
Peripheral oedema (pitting)
Raised JVP
Tender, smooth enlarged liver (liver congestion)
360
Q

Why does Frank-Starling Curve dip down at a certain point in ventricular end diastolic volume?

A

The sarcomere length increases to a point when it can no longer contract which results in LV dysfunction

361
Q

What is the NYHA functional HF classification?

A

Class 1 - No symptomatic limitation of physical activity
Class 2 - Slight limitation of physical activity. No symptoms at rest. Ordinary physical activity results in symptoms
Class 3 - Marked limitation of physical activity. Less than ordinary physical activity results in symptoms. No symptoms at rest
Class 4 - Inability to carry out any physical activity without symptoms. May have symptoms at rest. Discomfort increases with any degree of physical activity

362
Q

What drugs can be used to improve the prognosis of HF?

A

ACE/ARB, Beta-blockers, Spironolactone, Sacubitril valsartan

Ivabradine, hydralazine, nitrates, IV iron

363
Q

What is the problem with using beta-blockers in acute HF?

A

They can make things worse by negative inotropic effects which doesn’t help treat the HF and fluid overload which requires a strong beat

364
Q

What would be seen in a HF patient’s CXR?

A 
Cardiomegaly
Upper lobe diversion
Fluid in the fissures
Pleural effusions
Kerley B lines
365
Q

What is the most important blood test for HF and why?

A

NTpro-BNP
Hormone released in response to atrial/ventricular stretch due to fluid overload
Afib can tripple NTpro-BNP

366
Q

What are long-term deleterious effects of excess activation of the SNS in heart failure?

A

Beta-adrenergic receptors are down-regulated/ uncoupled
Norad induces cardiac hypertrophy/ myocyte apoptosis and necrosis via a-receptors
Induce up-regulation of RAAS

367
Q

Why are aldosterone antagonists good in HF?

A

Aldosterone escape is controlled.

Aldosterone concentration returns to normal in spite of ACE-I and ARB therapy.

368
Q

What are the arteries from which blood moves from the superficial veins to the deep veins?

A

Perforating veins

369
Q

What is the cause and result of peripheral venous disease?

A

Varicose veins - valves ineffective and blood movement is slow or even reversed - saphenous veins are common site of pathology
Walls are weak -> varicosities develop and valve cusps separate becoming incompetent.

370
Q

What are the symptoms of peripheral vascular disease?

A

Heaviness, aching, muscle cramps and throbbing thin itchy skin

371
Q

What are the complications of chronic venous insufficiency associated with venous HTN?

A 
Varicose veins
Skin pigmentation - haemosiderin staining
Lipodermatosclerosis
Venous ulceration
Oedema
Haemorrhage 
Thrombophlebitis
372
Q

What is venous eczema and ulceration of the lower limb?

A

Venous eczema - chronic, itchy red and swollen tight feeling that can lead to lipodermatosclerosis - hard to the touch and other fatty tissues above or below
Venous ulceration - chronic painful and often develop around hard nodular areas typically medial malleolus
Result of venous HTN

373
Q

Why do patients get venous HTN and calf muscle pump failure?

A

Calf muscle doesn’t pump then the blood can’t be squeezed up to the heart - blood pools there -> deep vein becomes incompetent -> retrograde flow to superficial veins

374
Q

How do you treat varicose veins?

A

Stripping and ligation which prevents the back pressure of blood into the superficial veins

375
Q

What is peripheral arterial disease?

A

Leading cause of both acute and chronic limb ischaemia
Atheroma or blockage of a major vessel causes collateral vessels to be formed around this stenosis/ occlusion but in doing so it bypasses some tissues in the area thet require blood flow to it

376
Q

What is acute limb ischaemia?

A

Occlusion occurs acutely - minutes to days - no collateral circulation can develop to overcome this. Trauma and embolisation are most common causes - AF/ abdominal aortic aneurysm.

377
Q

What are the symptoms of acute limb ischaemia?

A 
6P's:
Pain
Pallor
Perishing with cold
Pulseless
Paraesthesia
Paralysis or reduced power
378
Q

What is chronic peripheral arterial disease?

A

Intermittent claudication of the lower limb caused by atherosclerosis which is exercise induced
Pain goes away on rest

379
Q

What is critical ischaemia in peripheral artery disease?

A

Rest pain - blood supply so poor there is pain at rest

Untreated leads to ulceration and gangrene

380
Q

What measuring technique is used to identify blood flow in the limbs for peripheral arterial disease?

A

Doppler ultrasound

381
Q

What is haemodynamic shock?

A

Acute condition of inadequate blood flow throughout the body
A catastrophic fall in arterial blood pressure - circulatory shock
Fall in CO or TPR

382
Q

What are the 3 main types of haemodynamic shock?

A

Mechanical
Cardiogenic
Hypovolaemic

383
Q

What is cardiogenic shock?

A

Pump failure - ventricles cannot empty properly
Causes: post-MI, Serious arrhythmias, acute worsening of HF
Central venous pressure is normal or raised but dramatic drop in arterial BP

384
Q

What is mechanical shock?

A

Obstructive - ventricles cannot fill properly
Massive PE can cause this
Pulmonary artery pressure is high, right ventricles cannot empty, central venous pressure is high
Reduced return of blood to left heart
Left atrial pressure is low and arterial blood pressure is low -> shock

385
Q

What is hypovolaemic shock?

A

Reduced blood volume leads to poor venous return
20-30% of blood loss can cause shock response
30-40% substantial decrease in mean aBP and serious shock response.
Severity of shock is related to amount and speed of blood loss

386
Q

What is a cardiac arrest?

A

Unresponsiveness associated with lack of pulse
Heart has stopped or has ceased to pump effectively
Asystole - loss of electrical and mechanical activity
Pulseless Electrical Activity
Ventricular fibrillation - most common form of cardiac arrest - often following MI
Requires defibrillation to treat it and adrenaline to get the heart pumping again

387
Q

What is cardiac tamponade?

A

Blood/ fluid in the pericardial space - restricts filling of the heart - limits EDV on L and R heart
- High central venous pressure
- Low arterial blood pressure
Heart still attempts to beat

388
Q

Why does a massive PE cause mechanical shock of the heart?

A

Pulmonary artery pressure is high, right ventricles cannot empty, central venous pressure is high
Reduced return of blood to left heart
Left atrial pressure is low and arterial blood pressure is low -> shock

389
Q

What are symptoms of hypovolaemic shock?

A 
Tachycardia
Weak pulse
Pale skin
Cold, clammy extremeties
Low central venous pressure
390
Q

What is the danger of decompensation in hypovolaemic shock?

A

Peripheral vasoconstriction impaires tissue perfusion

Tissue damage due to hypoxia -> multi system failure

391
Q

What is distributive shock?

A

Low resistance shock - normovolaemic
Profound peripheral vasodilation -> dec TPR
Toxic shock or anaphylactic shock could be causes

392
Q

What is toxic shock?

A

Endotoxins released by circulating bacteria -> profound vasodilation -> fall in TPR and arterial pressure -> capillaries become leaky and so also reduced blood volume
Inc coagulation and localised hypo-perfusion

393
Q

What is septic shock?

A

Persisting hypotension requiring treatment to maintain blood pressure despite fluid resuscitation
Decreased arterial pressure -> HR and SV increases
Patient has tachycardia and warm extremities initially but later stages -> vasoconstriction -> localised hypo-perfusion.

394
Q

Why does anaphylaxis cause anaphylactic shock?

A

Severe allergic reaction - anaphylaxis.
Release of histamine a potent vasodilator -> fall in TPR -> dramatic drop in arterial pressure
Impaired organ perfusion
Mediators cause bronchoconstriction and laryngeal oedema

Medicine (15 decks)

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