Cardiac Diseases Flashcards by Brendan Lewis

what is angina pectoris?

chest pain due to myocardial ischaemia
due to buildup of metabolites (lactate, K+)
ischaemia due to increased myocardial O2 demand which is not met

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describe stable angina

attacks predictable situations (exercise, stress)
caused by occlusive coronary artery disease (atherosclerosis)

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describe unstable angina

attacks unpredictable situations
coronay artery occlusion due to platelet adhesion to ruptured atherosclerotic plaque

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describe variant angina

attacks unpredictable situations
coronary artery occlusion caused by vasospasm

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what is coronary steal?

dangerous dilation of coronary arteries
vessel dilation sends more blood to well vascularised areas)

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what is the general solution to all angina types?

decreasing myocardial O2 demand

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how can myocardial O2 demand be reduced?

beta blockers (propranolol/atenolol)
lowering HR

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explain the mechanisms of ivabradine

anti anginal
blocks Na currents contributing to SA node depolarisation
decreases HR (not force)

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what is the effect of vasodilator drugs in arteries?

reduces myocardial work and O2 demand

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what are the effects of vasodilator drugs on veins?

reduces:
venous return
preload
ventricular/atrial stretch
contraction strength
myocardial work
myocardial O2 demand

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what is the bainbridge reflex and what does it do?

sympathetic reflex caused by increased blood in atria
causes SA node stimulation which stimulates baroreceptors in atria causing increased sympathetic stimulation

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what is GTN and how is it administered?

glycerol trinitrate is a nitrovasodilator
taken as sub-lingual tablet or spray as it inst orally active

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what are the uses of nitrovasodilators in angina?

prophylaxis in stable angina
rapid relief of ongoing angina

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describe pro-drugs and give an example

nitrovasodilators are pro drugs
lipophilic (enter smooth muscle cells and reduced to NO)
mimics action of endothelium derived NO

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what does NO do in the heart?

activates soluble guanylate cyclase (sGC) which is a cytoplasmic enzyme
NO binds to haem receptor increasing enzyme activation
this converts GMP to cGMP causing vasodilation

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what are the side effects of nitrovasodilators?

headache (cerebral artery dilation)
tolerance at prolongued use

describe L-type blockers and their mechanism of action, and give examples

dilates arteries (reduces TPR)
anti angilans as lowered TPR reduces afterload and CO (reduces myocardial O2 demand)

examples: verapamil, diltiazem, nifedipine

describe T-type (transient) channel blockers and give and example

ethosuxamide

present in pacemakers and smooth muscle
blocks Ca channels to thalamocortical (TC) neurons to treat absense seizures

describe K+ activators, give and example and state their advantages

nicorandil
venodilating properties
no tolerance built up over time and potent cardioprotective action

describe what heart failure is physiologically

inability of the heart to pump sufficient oxygenated blood to metabolising tissues despite adequate filling pressure

what are the causes of heart failure?

dysfunctional stenotic valve (most common)
genetics
congenital heart disease
endocrine dysfunction

what are the cardinal symptoms of heart failure?

breathlessness
ankle swelling
fatigue

what are the physical signs of heart failure?

sinus tachycardia
atrial fibrillation
BP changes
raised JVP
oedema
pleural effusion
displaced apex beat
murmurs

explain what can occur after myocardial remodelling

ventricular function and CO decrease causing overactivation of neurohormonal signalling pathways

what can neurohormonal signalling overactivation cause?

vasoconstriction, apoptoses, hypertrophy/fibroses increasing cardiac afterload or Na/water retention and increase in intravascular volume, increasing cardiac preload

what neurohormonal activations occur after a delay in the ventricular systolic function?

SNS through epinephrine and norepinephrine (a1, b1, b2) natriuretic peptide system through NPRs to neuropeptide receptors RAAS through angiotensin II to angiotensin II type 1 receptors

what does vasoconstriction by the SNS increase?

RAAS/vasopressin activity HR contractility

what does RAAS system cause and what does this increase?

causes vasoconstriction increases: BP sympathetic tone aldosterone hypertrophy fibrosis

what does the natriuretic peptide system cause and what does this decrease?

causes vasodilation decreases: BP sympathetic tone diuresis/natriuresis vasopressin/aldosterone activity hypertrophy fibrosis

name investigations in blood tests for heart failure

urate electrolytes liver function (LFT) thyroid function (TFT) creatine kinase (CK) iron BNPs (natriuretic function) full blood count (FBC)

name routine investigationd for heart failure and what it may show

chest x-ray, ECG, ECHO, cardiac MRI, endomyocardial biopsy can show wall dysfunction, valvular dysfunction or dilated chambers

what are the goals of heart failure treatment?

releive symptoms prevent premature death avoid admission/readmission

what are the common medications administered for heart failure and what do they do?

beta blockers (inhibit SNS) neprilysin inhibitors (inhibit natriuretic peptide system) ACE inhibitors (inhibit RAAS)

describe the mechanism of action of SGLT2 inhibitors

inhibit proximal tubular glucose reabsorption causes diuresis and natriuresis lowers BP and weight

what drugs aggrevate the symptoms of heart failure?

NSAIDs Ca antagonists anti-arrythmics tricyclic antidepressants corticosteroids

what do implantable cardioverter defibrillators (ICDs) do?

inserted into heart with a transvenous lead, chocking coils, pectoral device and endocardial sensor defibrillates heart in emergencies

describe the intra-aortic balloon pump

used for cardiogenic shock causes diastolic augmentation of aortic pressure increases coronary perfusion, reduces afterload anf improves CO

what is the function of an LVAD (LV assisting device)?

pumps blood for heart reducing cardiac work short temp VAds used to pump blood outside body before bringing it back in often used as bridge treatment in organ failure