Session 11: Heart Failure

Question 1

define heart failure

Answer 1

a state in which the heart fails to maintain an adequate circulation for the needs of the body DESPITE an adequate filling pressure

Question 2

causes of systolic heart failure

Answer 2

IHD is primary cause of systolic HF

other causes: high output HF, pericardial disease, arrythmias, restrictive and hypertrophic cardiopathies, hypertension, dilated cardiomyopathies, valvular/congenital heart disease

Question 3

The starling curve in HF

Answer 3

the greater the HF, the lower the curve -> i.e. a lower the CO compared to the central venous pressure than normal

Question 4

progression of HF

Answer 4

Class I: no symptomatic limitation of phys. act.

Class II: no symptoms at rest, slight symptomatic limitation of phys. act., ordinary phys. act. leads to symptoms

Class III: no symptoms at rest, marked limitation of phys. act., less than ordinary phys. act. leads to symptoms

Class IV: can have symptoms at rest, inability to carry out phys. act. w/o symptoms, discomfort inc.s w/ any degree of phys. act.das

Question 5

clinical divisions of HF

Answer 5

l/sided, r/sided or biventricular/congestive HF

systolic/diastolic HF

Question 6

L/sided HF signs and symptoms

Answer 6

tachycardia

peripheral oedema

fatigue, SOB on exertion/lying flat/waking

cardiomegaly (enlarged heart displacing the apex beat)

3rd/4th heart sound making a ‘gallop’ rhythm

functional murmur of mitral regurgitation

basal pulmonary crackles

Question 7

R/sided HF causes and signs/symptoms

Answer 7

cause: most commonly found 2^o to L/sided HF directly causing chronic lung disease, pulm. embolism/hypertension, pulm./tricuspid valvular disease, L/->R/ shunts (A/VSD) or isolated r/ ventricular cardiomyopathy - these can also be due to something else

signs/symptoms: distension and fluid accumulation -> oedema in areas drained by systemic veins

dyspnoea (SOB), fatigue, anorexia, nausea, tender and smooth hepatic enlargement, inc. JVP, dependent pitting oedema (oedema leaves depressions in tissues), ascites (oedema in peritoneum), pleural effusion

Question 8

the two systems working in HF and their roles

Answer 8

SyNS: -acts on Beta-1 receptors in kidneys-> inc. renin release -> RAAS

• vasoconstriction of blood vessels by alpha-1 receptors -> inc BP -> inc. pre and after load
• act on beta-1 receptors in heart -> inc. chron- and inotropy

RAAS (Renin-Angiotensin-Aldosterone-System): SyNS and dec. BP stim.s renin release

• angiotensinogen is converted to angiotensin I by renin -> converted to angiotensin II by ACE
• > angiotensin II is a powerful vasoconstrictor (inc. BP etc) and promotes the release of aldosterone from zona glomerulosa in adrenal cortex (inc. Na⁺ and H₂O retention -> inc. BP etc)

Both of these systems end up agitating the situation by inc. CO so the struggling heart has to work even harder, also, by inc. HR, the vent.s fill less because of a smaller diastole, so the SV is smaller, leading to a vicious cycle

Question 9

Principles of and drugs for management of HF

Answer 9

Principles: correct the underlying cause, non pharmacological measures, pharmacological therapy (for symptomatic improvement, delaying the progression of HF, reducing mortality), treat complications/associated conditions/CVS risk factors eg arhythmias

Drugs: Beta-blockers eg atenolol, ACE-inhibitors eg anatipril, Ca2+ channel blockers, organic nitrates, cardiac glycosides (inhibits Na+/K+ ATPase -> NCX works other way round -> ICell. Ca2+ inc.s -> inc. contractility