Deck 4 Flashcards Preview

Cardio - pathology > Deck 4 > Flashcards

Flashcards in Deck 4 Deck (13)
Loading flashcards...

Q. Describe the two main types of heart failure (HF)?

A. LVSD (left ventricular systolic dysfunction): heart failure due to left ventricular systolic dysfunction, the LV muscles are worn out and unable to pump blood efficiently <55%

B. HFPEF (heart failure with preserved ejection fraction): heart failure with preserved ejection fraction, heart muscles are too stiff to fill fully, muscles can still pump >55%


What is neuro-humoral response in HF?

A. Compensatory mechanisms that occur in heart failure
B. Activation of sympathetic NS and RAAS system, increased vasopressin and ANP
C. Net effect: produce arterial vasoconstriction to help maintain arterial pressure, venous constriction and increased blood volume
D. In order to increase ventricular filling
E. These responses can aggravate heart failure by increasing ventricular afterload


Q. Describe the treatment steps for HF

A. ACE inhibitors and Beta-blockers: slow up titration
B. Aldosterone antagonists: reduce water and sodium retention
C. Angiotensin II receptor blockers (ARBs): if ACE inhibitors contraindicated or not tolerated (e.g. chronic dry cough)
D. ACE-1 and ARB intolerant: hydralazine/nitrate combination (peripheral vasodilators)
E. Diuretics: reduction of congestion – symptom treatment


Q. What are cardiac natriuretic peptides (CNPs)? When are they released?

A. Atrial natriuretic peptide – hormone released from atria
B. N-natriuretic peptide (BNP) – horomone released from ventricles
C. Released by stretching of atrial/ventricular muscle cells, raised atrial/ventricular pressure, volume overload


Q. What are the main effects of CNPs?

A. Main effects on the kidney:
B. Increased renal excretion of sodium (natriuresis) and water (diuresis)
C. Relax vascular smooth muscle (except efferent arterioles of renal glomeruli)
D. Increased vascular permeability
E. Inhibit release of: Aldosterone, angiotensin II, endothelin, ADH
F. Counter-regulatory system to renin-angiotensin system


Q. What metabolises CNPs?

A. Neutral endopeptidase (NEP, neprilysin)


Q. How can CNPs be pharmalogically targeted?

A. Sacubitril: Neutral endopeptidase inhibitor
B. (Valsartan – angiotensin II blocker)
C. Entresto: combination sacubitril and valsartan = novel therapy for HF


Q. How can nitrates treat HF? Name an example

A. Arterial and venous dilators
B. Reduction of preload and afterload – reducing pressure against which the heart has to contract
C. Lower BP
D. GTN spray/tablet – s/l


Q. Name an adverse effect of nitrates

A. Headache – pounding
B. Syncope – fainting due to low BP


Q. Describe treatment steps for chronic stable angina

A. First-line regular treatment: Beta blockers/CCB (prophylaxis)
If intolerant: switch if not controlled: combine
B. Sublingual glyceryl trinitrate (GTN): rapid relief
C. Long-acting nitrate: nicorandil/ivabradine/ranolazine if BB and CCB are contraindicated or not tolerated
D. Secondary prevention: Antiplatelet therapy: aspirin (clopidogrel if aspirin intolerant), ACE inhibitor for stable angina/diabetes mellitus
E. Lipid lowering therapy: Statins (simvastatin etc)


Q. Describe treatment steps for acute coronary syndromes – NSTEMI/STEMI\

A. Pain relief: GTN spray (nitrates), diamorphine (opiates)
B. Dual antiplatelet therapy: Aspirin + ticagrelor/prasugrel/clopidogrel
C. Anti-thrombin therapy: Fondaparinux
D. High risk cases: consider glycoprotein IIb IIIa inhibitor: tirofiban/eptifibatide/abciximab
E. Background angina therapy: ACE-I/BB?aldosterone antagonist
F. Invasive: PCI/angioplasty/CABG


Q. What class of drugs may be used in cases of AF and severe HF? What is the mechanism?

A. Antiarrhythmic drugs: Digoxin (is a cardiac glycoside)
B. Inhibit Na/K pump
C. Effects on the heart: Bradycardia, slowing of ATN conduction, increased contractility (inotropic)
D. Narrow therapeutic range


Q. Describe the classifications of antiarrhythmic agent (Vaughan Williams)

I. Fast sodium channel blockers
Ia - Quinidine, procainamide, disopyramide (depress phase 0, prolonging repolarization)
Ib - Lidocaine, phenytoin, mexiletine (depress phase 0 selectively in abnormal/ischemic tissue, shorten repolarization)
Ic - Flecainide, propafenone, moricizine (markedly depress phase 0, minimal effect on repolarization)
II. Beta blockers
e.g. propranolol, bisoprolol

III. Potassium channel blockers
e.g. Amiodarone, sotalol

IV. Calcium channel blockers
e.g. verapamil, diltiazem

V. Variable mechanism
Adenosine, digoxin, magnesium sulfate