Heart Flashcards
What is heart failure
Inability to provide adequate output to support needs of the tissue
What are normal circulation values
Systemic veins: 5mmHg
Pulmonary artery: 30mmHg
Pulmonary veins: 8mmHg
Aorta: 100mmHg
What do baroreceptors do
In the aorta and bifurcation of the carotids - ensure aortic pressure is cosntant
What is right sided heart failure
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
What is left sided heart failrue
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
What is congestive heart failure
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
What pressure is kept constant
Aortic
What are the three causes of heart failure
Pressure overload, volume overload, contractile dysfunction
What are examples of pressure overload
Hypertension, aortic stenosis - obstruction in the outflow tract
What are examples of volume overload
Aortic or mitral valve regurgitation - ventricles have too much blood at the wrong time
What are examples of contractile dysfunction
Ischaemic heart disease, myocardial disease, pregnancy - changes to hormonal balance, congenital cardiomyopathies)
What is Laplace’s law
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
What occurs to heart muscles during pressure overload
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
What occurs to heart muscles during volume overload
Valve regurgitation, increasing radius -> wall stress increases
Wall stress normalised by dilated hypertrophic myocardium -> eventually enters myocardial failure
What occurs to heart muscles during dilated cardiomyopathy
Hypertrophy equals degree of chamber enlargement -> excessive chamber enlarge and inadeqaute hypertrophy
What occurs to heart muscles in hypertrophic cardiomyopathy (normal relation between wall thickness and wall stress)
Development of dilation leads to myocardial failure
What is the normal weight of the heart
Less than 450g in males and less than 400g in females
Ratio of LV/body height should be less than 36
What happens in the cardiac compensatory mechanism
Acute overload -> myocyte growth - hypertrophy -> physiological hypertrophy (normal) or -> concentric hypertrophy (fatter) or eccentric hypertrophy (longer) - these both have increased expression of embryonic genes
What are the 3 phases of heart failrue
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
Describe the steps of the neurohumoral compensatory mechanism
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
Describe the renal compensatory mechanism
Sympathetic stimulation -> renal artery vasoconstriction -> sodium and water retention -> RAAS pathway -> increased CVP -> increased end diastolic pressure
How does the RAAS pathway work
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
How do ANPs work
Rise in CNP cause release of ANP. Diuretic action - vasodilates and inhibits aldosterone secretion, noradrenaline release. ANP is an endogenous antagonist for AGII.
Why do the beneficial effects of ANP not dominate
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
What are the treatments for heart failure
Beta blockers for sympathetic activation
ACE inhibitors for RAAS
Spironolactone for aldosterone secretion
What are the consequences of cardiac hypertrophy
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
What is the fluid movement on the arterial side of normal capillary
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
What is fluid movement of normal pulmonary circulation
Colloidal > hydrostatic throughout. Net loss of fluid from the lung. Not a problem as we are constantly breathing in humidified air
What is the fluid movement in heart failure
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
What happens as a result of mild fluid accumulation in the lungs
Dyspnoea Pleural effusion (fluid accumulation in interstitium and pleural spaces). Lungs stiffer, more difficult to breath. Increase pulmonary vascular resistance. Increase PA pressure
What happens as a result of severe fluid accumulation in the lungs
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
What are the symptoms of angina of effort
Tightness, squeezing, crushing sensation in the chest.
What causes angina of effort
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
What is bradykinin
Inflammatory mediator, causes blood vessels to dilate and BP to fall. ACE inhibitors increase bradykinin
What is substance P
Involved in vasodilation, inflammation, pain, mood, vomiting, and cell growth
How does heparin work
Activates antithrombin II (AT). AT inactivates thrombin and Xa. LMWH has 4x longer half life.
How does warfarin work
Blocks vitamin K epoxide reductase. Inhibits factors II, VII, IX, and X
What is mixed angina
Unpredictable, develops at different levels of exercise
Probably due to stenosis + vasospasm
What is vasospastic angina
Decreased O2 supply due to spasm of coronary artery, occurs at rest
What is microvascular angina
Chest pain, normally coronary angiogram, positive exercise test, endothelial dysfunction, microvasculature is constricted. More common in women
What is unstable decrease O2 supply angina
Due to transient formation of non-occlusive thrombus, an acute coronary symptom
What is the treatment for immediate relief
Short acting nitrate
What is prophylaxis for angina
- Beta blocker or CCB
- Beta blocker + vascular selective CCB
- Beta blocker + vascular selective CCB + long acting nitrate or ivabradine, nicroandil, ranolazine
How do you diagnose angina
Myocardial perfusion scan, MRI, Echo, US
How do nitrates work
Decrease CVP through dilating veins - reduces size of heart, decreasing wall tension
Release NO
Activates ATP driven Ca2+ pumps. Ca2+ densitization also occurs
How does NO work
Works through cyclic GMP second messenger system. Opens K+ channels, hyperpolarises cells. Prevents membrane depolarisation and blocks L-gated Ca2+ channels
What is GTN used for
Taken sublingually has very rapid effect - cut short impending angina attack
What is isosorbide
dinitrate
Long acting organic nitrate - taken as ongoing treatment
What are the major actions of nitrates
Relax venules + veins. So decreased CVP and thus decreased cardiac wall tension. Decreased cardiac O2 demand
What are the minor actions of nitrates
Dilate larger coronary arteries, increasing blood flow through coronary collaterals. Decreased TPR and afterload, therefore decreased O2 demand
What are the side effects of nitrates
Headache, facial flushing, decreased BP, reflex increase in HR
How does GTN work
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
How is tolerance to GTN developed
Superoxide very reactive with NO to form peroxynitrate, which inhibits MtALDH2 - responsible for tolerance
What are the effects of ivabradine
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.
What is the funny current
Activated by hyperpolarisation and is a mixed Na+/K+ current. Involved in SAN pacemaking
What are the haemodynamic effects of ivabradine
Decrease HR allows time for blood to perfuse myocardium, reduces ischaemia.
Reduces HR -> reduced afterload -> decreased O2 demand
How do beta blockers work
On SAN, reduces HR and reduces heart contractility.
Inhibit sympathetic stimulation of heart
Why are beta blockers contraindicated in vasospastic angina
Adrenaline dilates coronary arteries. Beta blockers cause coronary restriction. Causes damage to endothlieum
What else are beta blockers used for
Decrease risk of chronic heart failure post MI
What are examples of CCBs
Amlodipine (DHP), verapamil, diltiazem
What is the best CCB for vasodilatation
DHPs>diltiazem>verapamil
What is the best CCB for negative inotropy
verapamil>diltiazem>DHPs
How do DHPs work
Vasodilatation -> reducing afterload and therefore cardiac work
How dooes verapamil work
Direct negative inotropic effect, with some reudction in afterload
What are beneficial effets of CCBs
Dilate coronary arteries - useful in coronary vasoconstriction angina
Decreased reperfusion injury
Decreased atheroma progression
Reduction of left ventricular hypertrophy
How does Ranolazine work
Decreases wall tension
Inhibits late Na current in myocytes, which occurs in hypoxia of myocardium, reperfusion, ischaemia
How does late Na current cause damage
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
What is the dual action of K+ channel activators (Nicorandil)
Opens ATP sensitive K+ channels in vascular SM cells
Stimulate guanylate cyclase -> icnrease vascular smooth cell cGMP
What are the effects of K+ channel activators
Relaxation of vascular smooth muscle through multiple mechanism: hyperpolarisation, removal of Ca2+ from cytoplasm, Ca2+ desensitisation -> decreased preload and afterload
How does statins work
Block rate limiting enzyme in production of cholesterol. Lower LDL, which brings cholesterol to the tisseu
What are surgical options for angina
Percutaneous coronary intervention -> catheter through coronary
Coronary artery bypass (CABG) -> use piece of saphenous vein or diverted internal mammary artery
What is cardiogenic shock
Ventricular myocardium damaged in infarction - ejection fraction of the heart decrease. Px may require inotropic support and/or intra-aortic balloon pump
What is chronic heart failure
If px survives acute phase, ventricular myocardium dysfunction resulting in chorinc heart failure. Loop diuretics such as furosemide will decrease fluid overload.
What causes tachyarrythmias
VF
What causes bradyarrythmias
AV block following inferior MI
What is pericarditis
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
What is Dressler’s syndrome
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
What is left ventricular aneurysm
Ischaemic damage sustained may weaken the mycaordium - aneurysm formation. Associated with persistent ST elevation and left ventricular failure. Thrombus may form. Anticoagulation required.
What is left ventricular free wall rupture
1-2 weeks after MI. Acute heart failure secodmary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds)
What is acute mitral regurg
Common with infero-posterior infarcation. May be due to ischaemia or rupture of the papillary muscle. Early-to-mid systolic murmur typically heard.
What causes loud S1
Mitral stenosis
Left to right shunts
Short PR interval
What causes quiet S1
Mitral regurgitation
What causes loud S2
hypertension: systemic (loud A2) or pulmonary (loud P2)
hyperdynamic states
atrial septal defect without pulmonary hypertension
What causes quiet S2
Aortic stenosis
What causes S3
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
What causes S4
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
What is giant cell arteritis
systemic immune-mediated vasculitis affecting medium sized and large sized arteries. Sudden and potentially bilateral vision loss in the arteries.
Symptoms:
What is ABPI
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
What is arrhythmia
Disturbance of the normal rhythmic beating of the heart - usually due to an ectopic pacemaker. SA node no longer driving heart
What are the symptoms of arrhythmia
palpitations, breathlessness, dizziness, faintness, syncope
What is bradyarrhythmia
Bradyarrhythmia (<60 bpm):
impulse from SAN is blocked, slower distal pacemaker takes over
What is tachyarrhythmia
(>100bpm):
Disorders of impulse generation
Disorders of impulse conduction - re-entry (main cause)
What is the cause of tacharrythmia
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
What is AF
Chaotic atrial rhythm with rapid and irregularly irregular ventricular rhythm
What are the causes and risk factors for AF
Cause: ectopic focus located in the cardiac muscle surrounding a pulmonary vein. RF: atrial dilatation, heart failure, hypertension, excessive alcohol intake
What are the effects of AF
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
What are class 1 anti arrhythmic drugs
Na+ channel blockers - suppress conduction e.g. flecainide
What are class 2 anti arrhythmic drugs
beta receptor blockers - reduce excitability, inhibit AVN conduction e..g bisoprolol
What are class 3 anti arrhythmic drugs
prolong AP and refractory period e.g. amiodarone
What are class 4 anti arrhythmic drugs
Ca2+ channel blockers - inhibit AVN conduction e.g. verapamil
What does adenosoine do
slows AV nodal conduction
What does digoxin do
stimulates vagus, slows AV nodal conduction
What is the rate control method of anti-arrhthmia control
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
What is the rhythm control method of anti-arrhythmia
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
What is radiofrequency catheter ablation
Transvenous catheter is threaded into heart, placed against endocardium and radio-frequency energy is delivered to the tip.
What is ventricular tachycardia
Run of rapid (120-200) successive ventricular beats caused by an ectopic site in one of the ventricles
What are the causes and effects of VT
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
What is the prognosis of VT
if persistent, may comprise cardiac pumping leading to heart failure and death
Can deteriorate into ventricular fibrillation -> sudden death
What is the ECG sign for VT
broad (QRS complex is slower) complex rapid rhythm. Atria usually beat more slowly and independently of the ventricles.
What are the treatments for VT
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
What is VF
chaotic and disorganised electrical activity of the heart
What are the causes and effects of VF
Cause: usually MI< ischaemic heart disease, cardiomyopathy
Effect: no organised ventricular beat so no CO
What is used to treat VF
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
