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Supporting Life > Heart > Flashcards

Heart Flashcards

1
Q

What is heart failure

A

Inability to provide adequate output to support needs of the tissue

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2
Q

What are normal circulation values

A

Systemic veins: 5mmHg
Pulmonary artery: 30mmHg
Pulmonary veins: 8mmHg
Aorta: 100mmHg

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3
Q

What do baroreceptors do

A

In the aorta and bifurcation of the carotids - ensure aortic pressure is cosntant

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4
Q

What is right sided heart failure

A

Cannot pump blood effectively into pulmonary circulation. Blood backs up behind right ventricle. Only systemic venous pressure changes to 10mmHg as right ventricular end-diastolic pressure increases

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5
Q

What is left sided heart failrue

A

Impaired pumping causes CO to fall to 6mmHg. Blood backs up in to the left side of heart. Pulmonary venous pressure rises because left end-diastolic pressure is increased. Elevated venous pressure transmitted through lungs to increase pulmonary artery pressure

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6
Q

What is congestive heart failure

A

Failure of left side puts strain on the right. Increase of pulmonary vein pressure due to left side back up, increase of pulmonary artery pressure as lungs back up, increase of systemic veins as right side backs up

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7
Q

What pressure is kept constant

A

Aortic

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8
Q

What are the three causes of heart failure

A

Pressure overload, volume overload, contractile dysfunction

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9
Q

What are examples of pressure overload

A

Hypertension, aortic stenosis - obstruction in the outflow tract

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10
Q

What are examples of volume overload

A

Aortic or mitral valve regurgitation - ventricles have too much blood at the wrong time

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11
Q

What are examples of contractile dysfunction

A

Ischaemic heart disease, myocardial disease, pregnancy - changes to hormonal balance, congenital cardiomyopathies)

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12
Q

What is Laplace’s law

A

For a fixed wall stress, a small ventricle can generate high pressure than a large ventricle. When a heart gets bigger, for the heart to generate the same pressure it must either increase the amount of work done by the fibres or increase the wall thickness

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13
Q

What occurs to heart muscles during pressure overload

A

Increase in left ventricular pressure -> increase wall stress. Muscles have to work harder to muscles enter concentric hypertrophy (R becomes smaller) -> heart starts to dilate, which further increases wall stress

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14
Q

What occurs to heart muscles during volume overload

A

Valve regurgitation, increasing radius -> wall stress increases
Wall stress normalised by dilated hypertrophic myocardium -> eventually enters myocardial failure

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15
Q

What occurs to heart muscles during dilated cardiomyopathy

A

Hypertrophy equals degree of chamber enlargement -> excessive chamber enlarge and inadeqaute hypertrophy

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16
Q

What occurs to heart muscles in hypertrophic cardiomyopathy (normal relation between wall thickness and wall stress)

A

Development of dilation leads to myocardial failure

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17
Q

What is the normal weight of the heart

A

Less than 450g in males and less than 400g in females

Ratio of LV/body height should be less than 36

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18
Q

What happens in the cardiac compensatory mechanism

A

Acute overload -> myocyte growth - hypertrophy -> physiological hypertrophy (normal) or -> concentric hypertrophy (fatter) or eccentric hypertrophy (longer) - these both have increased expression of embryonic genes

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19
Q

What are the 3 phases of heart failrue

A 
Short term acute: functional reserves overwhelmed by overload
Compensated hypertrophy (can last up to 10 years): heart enlarges and adapts
Chronic failure: exhaustion, cell death and necrosis
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20
Q

Describe the steps of the neurohumoral compensatory mechanism

A

LV failure -> CO falls -> BP falls -> baroreceptor reflex sympathetic stimulation -> peripheral vasoconstriction and increased HR and contractility -> constriction of renal arteries to retain slat and water -> CO returns to normal and BP returns to normal

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21
Q

Describe the renal compensatory mechanism

A

Sympathetic stimulation -> renal artery vasoconstriction -> sodium and water retention -> RAAS pathway -> increased CVP -> increased end diastolic pressure

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22
Q

How does the RAAS pathway work

A

Renin secretion by juxtaglomerular cells kidney -> convert angiotensinogen to angiotensin I -> angiotensin II by ACE -> AGII causes vasoconstriction at tissues and raises blood pressure and releases aldosterone from adrenal lands -> slat and water retention

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23
Q

How do ANPs work

A

Rise in CNP cause release of ANP. Diuretic action - vasodilates and inhibits aldosterone secretion, noradrenaline release. ANP is an endogenous antagonist for AGII.

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24
Q

Why do the beneficial effects of ANP not dominate

A

Increase in ANP overwhelmed by vasoconstriction and slat and water retention induced by activation of RAAS. ANP secretion becomes down regulated and vascular ANP receptors desensitised

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25
Q

What are the treatments for heart failure

A

Beta blockers for sympathetic activation
ACE inhibitors for RAAS
Spironolactone for aldosterone secretion

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26
Q

What are the consequences of cardiac hypertrophy

A

Increases susceptibility to ischaemia, incidence of arrhythmias, sudden wall.
Increased wall stress -> increased O2 consumption but there is a capillary inadequacy impaired vascular reserve -> O2 imbalance energy crisis -> focal fibrosis, ischaemia, and collagen depo -> decreased contractility and increased stiffness -> LV dilatation -> LV failure

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27
Q

What is the fluid movement on the arterial side of normal capillary

A

Hydrostatic pressure > colloidal pressure -> loss of fluid into the lymph. Gradient is reversed at distal end and fluid moves back into the vessels. No net loss of fluid movment

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28
Q

What is fluid movement of normal pulmonary circulation

A

Colloidal > hydrostatic throughout. Net loss of fluid from the lung. Not a problem as we are constantly breathing in humidified air

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29
Q

What is the fluid movement in heart failure

A

High pulmonary circulation pressure, gradient is reversed. Hydrostatic pressure is higher on the arterial side of the capillary. Net gain of fluid into the lungs

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30
Q

What happens as a result of mild fluid accumulation in the lungs

A 
Dyspnoea
Pleural effusion (fluid accumulation in interstitium and pleural spaces). Lungs stiffer, more difficult to breath. Increase pulmonary vascular resistance. Increase PA pressure
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31
Q

What happens as a result of severe fluid accumulation in the lungs

A 
Dyspnoea
Pulmonary oedema (fluid accumulation in the alveoli). Reduced volume for gas exchanged. Severe pulmonary congestion. Increase PA pressure increase RA pressure, right heart side heart failure, systemic venous pressure increase
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32
Q

What are the symptoms of angina of effort

A

Tightness, squeezing, crushing sensation in the chest.

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33
Q

What causes angina of effort

A

Increased O2 demand with restricted blood flow (particularly in left ventricle due to fixed stenosis)
Decrease O2 in cardiac tissue -> release of proton, bradykinin -> activation of TRPV1 of sensory nerves -> pain, also release of substance P (not enough to overcome effects of stenosis) -> coronary vasodilation

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34
Q

What is bradykinin

A

Inflammatory mediator, causes blood vessels to dilate and BP to fall. ACE inhibitors increase bradykinin

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35
Q

What is substance P

A

Involved in vasodilation, inflammation, pain, mood, vomiting, and cell growth

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36
Q

How does heparin work

A

Activates antithrombin II (AT). AT inactivates thrombin and Xa. LMWH has 4x longer half life.

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37
Q

How does warfarin work

A

Blocks vitamin K epoxide reductase. Inhibits factors II, VII, IX, and X

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38
Q

What is mixed angina

A

Unpredictable, develops at different levels of exercise

Probably due to stenosis + vasospasm

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39
Q

What is vasospastic angina

A

Decreased O2 supply due to spasm of coronary artery, occurs at rest

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40
Q

What is microvascular angina

A

Chest pain, normally coronary angiogram, positive exercise test, endothelial dysfunction, microvasculature is constricted. More common in women

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41
Q

What is unstable decrease O2 supply angina

A

Due to transient formation of non-occlusive thrombus, an acute coronary symptom

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42
Q

What is the treatment for immediate relief

A

Short acting nitrate

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43
Q

What is prophylaxis for angina

A
  1. Beta blocker or CCB
  2. Beta blocker + vascular selective CCB
  3. Beta blocker + vascular selective CCB + long acting nitrate or ivabradine, nicroandil, ranolazine
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44
Q

How do you diagnose angina

A

Myocardial perfusion scan, MRI, Echo, US

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45
Q

How do nitrates work

A

Decrease CVP through dilating veins - reduces size of heart, decreasing wall tension
Release NO
Activates ATP driven Ca2+ pumps. Ca2+ densitization also occurs

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46
Q

How does NO work

A

Works through cyclic GMP second messenger system. Opens K+ channels, hyperpolarises cells. Prevents membrane depolarisation and blocks L-gated Ca2+ channels

47
Q

What is GTN used for

A

Taken sublingually has very rapid effect - cut short impending angina attack

48
Q

What is isosorbide

dinitrate

A

Long acting organic nitrate - taken as ongoing treatment

49
Q

What are the major actions of nitrates

A

Relax venules + veins. So decreased CVP and thus decreased cardiac wall tension. Decreased cardiac O2 demand

50
Q

What are the minor actions of nitrates

A

Dilate larger coronary arteries, increasing blood flow through coronary collaterals. Decreased TPR and afterload, therefore decreased O2 demand

51
Q

What are the side effects of nitrates

A

Headache, facial flushing, decreased BP, reflex increase in HR

52
Q

How does GTN work

A

GTN->MtALDH-2->Guanylate cyclase->vasodilation
But MtALDH-2->superoxide->endothelin-1->increases responsiveness to vasoconstrictors->decreases arterial dilatation
Superoixde inhibits cGMP and prevents vasodilation

53
Q

How is tolerance to GTN developed

A

Superoxide very reactive with NO to form peroxynitrate, which inhibits MtALDH2 - responsible for tolerance

54
Q

What are the effects of ivabradine

A

Blocks If by entering the open channel from inside the cell, gets trapped when
the channel shuts. Slows heart rate, allows longer time for left ventricle to be perfused by reducing phase forward depolarisation.

55
Q

What is the funny current

A

Activated by hyperpolarisation and is a mixed Na+/K+ current. Involved in SAN pacemaking

56
Q

What are the haemodynamic effects of ivabradine

A

Decrease HR allows time for blood to perfuse myocardium, reduces ischaemia.
Reduces HR -> reduced afterload -> decreased O2 demand

57
Q

How do beta blockers work

A

On SAN, reduces HR and reduces heart contractility.

Inhibit sympathetic stimulation of heart

58
Q

Why are beta blockers contraindicated in vasospastic angina

A

Adrenaline dilates coronary arteries. Beta blockers cause coronary restriction. Causes damage to endothlieum

59
Q

What else are beta blockers used for

A

Decrease risk of chronic heart failure post MI

60
Q

What are examples of CCBs

A

Amlodipine (DHP), verapamil, diltiazem

61
Q

What is the best CCB for vasodilatation

A

DHPs>diltiazem>verapamil

62
Q

What is the best CCB for negative inotropy

A

verapamil>diltiazem>DHPs

63
Q

How do DHPs work

A

Vasodilatation -> reducing afterload and therefore cardiac work

64
Q

How dooes verapamil work

A

Direct negative inotropic effect, with some reudction in afterload

65
Q

What are beneficial effets of CCBs

A

Dilate coronary arteries - useful in coronary vasoconstriction angina
Decreased reperfusion injury
Decreased atheroma progression
Reduction of left ventricular hypertrophy

66
Q

How does Ranolazine work

A

Decreases wall tension

Inhibits late Na current in myocytes, which occurs in hypoxia of myocardium, reperfusion, ischaemia

67
Q

How does late Na current cause damage

A

Causes cells to generate more superoxide speices -> more Na+ current in myocytes -> prolongation of AP -> cause of arrythmia
Increase intracellular Na+, so cytoplasm Ca2+ increases -> myocardial stunning and diastolic stiffness

68
Q

What is the dual action of K+ channel activators (Nicorandil)

A

Opens ATP sensitive K+ channels in vascular SM cells

Stimulate guanylate cyclase -> icnrease vascular smooth cell cGMP

69
Q

What are the effects of K+ channel activators

A

Relaxation of vascular smooth muscle through multiple mechanism: hyperpolarisation, removal of Ca2+ from cytoplasm, Ca2+ desensitisation -> decreased preload and afterload

70
Q

How does statins work

A

Block rate limiting enzyme in production of cholesterol. Lower LDL, which brings cholesterol to the tisseu

71
Q

What are surgical options for angina

A

Percutaneous coronary intervention -> catheter through coronary
Coronary artery bypass (CABG) -> use piece of saphenous vein or diverted internal mammary artery

72
Q

What is cardiogenic shock

A

Ventricular myocardium damaged in infarction - ejection fraction of the heart decrease. Px may require inotropic support and/or intra-aortic balloon pump

73
Q

What is chronic heart failure

A

If px survives acute phase, ventricular myocardium dysfunction resulting in chorinc heart failure. Loop diuretics such as furosemide will decrease fluid overload.

74
Q

What causes tachyarrythmias

A

VF

75
Q

What causes bradyarrythmias

A

AV block following inferior MI

76
Q

What is pericarditis

A

Most common in the first 48 hours following a transmural MI. Pain is worse on lying lap. Pericardial rub may be heard. Pericardial effusion demonstrated on echo

77
Q

What is Dressler’s syndrome

A

2-6 weeks following MI. Autoimmune reaction following antigenic proteins formed as myocardium recovers. Combination of fever, pleuritic pain, pericardial effusion and a raised ESR. Treated with NSAIDS

78
Q

What is left ventricular aneurysm

A

Ischaemic damage sustained may weaken the mycaordium - aneurysm formation. Associated with persistent ST elevation and left ventricular failure. Thrombus may form. Anticoagulation required.

79
Q

What is left ventricular free wall rupture

A

1-2 weeks after MI. Acute heart failure secodmary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds)

80
Q

What is acute mitral regurg

A

Common with infero-posterior infarcation. May be due to ischaemia or rupture of the papillary muscle. Early-to-mid systolic murmur typically heard.

81
Q

What causes loud S1

A

Mitral stenosis
Left to right shunts
Short PR interval

82
Q

What causes quiet S1

A

Mitral regurgitation

83
Q

What causes loud S2

A

hypertension: systemic (loud A2) or pulmonary (loud P2)
hyperdynamic states
atrial septal defect without pulmonary hypertension

84
Q

What causes quiet S2

A

Aortic stenosis

85
Q

What causes S3

A

caused by diastolic filling of the ventricle
considered normal if < 30 years old (may persist in women up to 50 years old)
heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock) and mitral regurgitation

86
Q

What causes S4

A

may be heard in aortic stenosis, HOCM, hypertension
caused by atrial contraction against a stiff ventricle
in HOCM a double apical impulse may be felt as a result of a palpable S4

87
Q

What is giant cell arteritis

A

systemic immune-mediated vasculitis affecting medium sized and large sized arteries. Sudden and potentially bilateral vision loss in the arteries.
Symptoms:

88
Q

What is ABPI

A

The ankle-brachial pressure index (ABPI) or ankle-brachial index (ABI) is the ratio of the blood pressure at the ankle to the blood pressure in the upper arm (brachium)
below 0.9 is suggestive of arterial disease and below 0.5 is suggestive of severe arterial disease. Percutaneous transluminal angioplasty is the first line of surgical intervention

89
Q

What is arrhythmia

A

Disturbance of the normal rhythmic beating of the heart - usually due to an ectopic pacemaker. SA node no longer driving heart

90
Q

What are the symptoms of arrhythmia

A

palpitations, breathlessness, dizziness, faintness, syncope

91
Q

What is bradyarrhythmia

A

Bradyarrhythmia (<60 bpm):

impulse from SAN is blocked, slower distal pacemaker takes over

92
Q

What is tachyarrhythmia

A

(>100bpm):
Disorders of impulse generation
Disorders of impulse conduction - re-entry (main cause)

93
Q

What is the cause of tacharrythmia

A

Rapid HR caused by re-entry
Pulse is delayed in one region of the heart
Adjacent tissue finishes depolarises and is no longer refractory
Delayed impulse then re-enters the adjacent tissue and then spreads throughout the heart. This can occur once, creating a premature beat or indefinitely, generating a sustained tachycardia
Can occur whenever adjacent areas of the myocardium have different conduction rates and refractoriness (ischaemia, myocardial scarring). Often triggered from triggered automaticity

94
Q

What is AF

A

Chaotic atrial rhythm with rapid and irregularly irregular ventricular rhythm

95
Q

What are the causes and risk factors for AF

A

Cause: ectopic focus located in the cardiac muscle surrounding a pulmonary vein. RF: atrial dilatation, heart failure, hypertension, excessive alcohol intake

96
Q

What are the effects of AF

A

Effect on cardiac rhythm: no organised atrial beating. Ventricular excitation occurs when atrial depolarisation are sufficient to be conducted through the AVN
Symptoms: palpitations, breathlessness, dizziness, syncope

97
Q

What are class 1 anti arrhythmic drugs

A

Na+ channel blockers - suppress conduction e.g. flecainide

98
Q

What are class 2 anti arrhythmic drugs

A

beta receptor blockers - reduce excitability, inhibit AVN conduction e..g bisoprolol

99
Q

What are class 3 anti arrhythmic drugs

A

prolong AP and refractory period e.g. amiodarone

100
Q

What are class 4 anti arrhythmic drugs

A

Ca2+ channel blockers - inhibit AVN conduction e.g. verapamil

101
Q

What does adenosoine do

A

slows AV nodal conduction

102
Q

What does digoxin do

A

stimulates vagus, slows AV nodal conduction

103
Q

What is the rate control method of anti-arrhthmia control

A

Reduce proportion of impulses conducted through the AV node = rate control
Atrial tachycardia continues, but the ventricles slow down, improving CO
Class 2, 4, adenosine, digoxin

104
Q

What is the rhythm control method of anti-arrhythmia

A

Target source of arrhythmia or the conduction of the impulse away from the source by blocking the re-entrant pathway = rhythm control
Class 3 or 1: suppress re-entry
Anti-coagulant therapy to prevent stroke is required for AF

105
Q

What is radiofrequency catheter ablation

A

Transvenous catheter is threaded into heart, placed against endocardium and radio-frequency energy is delivered to the tip.

106
Q

What is ventricular tachycardia

A

Run of rapid (120-200) successive ventricular beats caused by an ectopic site in one of the ventricles

107
Q

What are the causes and effects of VT

A

Cause: cardiac scarring after MI or dilated cardiomyopathy. Almost always due to re-entry
Effects: tachycardia. Rhythm may be regular (monomorphic) or irregular (polymorphic)
Symptoms: chest pain, SOB, syncope

108
Q

What is the prognosis of VT

A

if persistent, may comprise cardiac pumping leading to heart failure and death
Can deteriorate into ventricular fibrillation -> sudden death

109
Q

What is the ECG sign for VT

A

broad (QRS complex is slower) complex rapid rhythm. Atria usually beat more slowly and independently of the ventricles.

110
Q

What are the treatments for VT

A

Class 1 or 3. inhibit conduction in the conduction system or cardiac muscle or increase refractory period
Class 2: reduce excitability
Implanted defib: connected to electrodes in the right ventricles and SVC

111
Q

What is VF

A

chaotic and disorganised electrical activity of the heart

112
Q

What are the causes and effects of VF

A

Cause: usually MI< ischaemic heart disease, cardiomyopathy
Effect: no organised ventricular beat so no CO

113
Q

What is used to treat VF

A

Defib:
Used to terminate VF
Momentary discharge of large current across charge at sternum and RV apex
Applied at onset of QRS complex
Stops the heart, allows SAN to reassert itself

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