Heart failure

Question 1

Heart failure

intro and causes

Answer 1

• when can’t supply adequate O2 without increasing filling pressure
  o get SOBOE to rest and pulmonary/systemic oedema
• usually LVF
• RVF usually secondary to LVF but sometimes found alone or secondary to pulmonary disease
• Causes -
  o Intrinsic
• CAD
• Decreased blood flow, hypoxia, dysfunction
• MI – non infarcted areas must compensate
• Valvular disease
• Congenital defects
• Cardiomyopathy
• intrinsic disease of myocardium, lose inotropy
• bacterial, viral, alcohol, idiopathic
• infective or non infective myocarditis – inflame of myocardium
• chronic arrhythmias

o extrinsic

• increased afterload – hypertension
• increased stroke volume – aterial venous shunts
• increased demand – high output failure in thyrotoxicosis and pregnancy

Question 2

systolic vs diastolic

Answer 2

o Systolic
• Changes in cellular signal transduction and excitation contraction coupling – lose inotropy
• Shifts frank starling curve down – decreased stroke volume and increased preload (LVEDP or V or pulmonary capillary wedge pressure). Need the increased preload or SV would be lower image 94 (or 31)
• decreases slope of ESPVR (inotropy) so at any volume less pressure can be generated in systole so less volume ejected so increased ESV and then in turn EDV to a lesser degree, so increased stroke volume
• Decreased EF as EDV increase and SV decrease

o Diastolic
• Impaired filling from decreased compliance (hypertrophy) or impaired relaxation (decreased lusitropy)
• Reduced compliance shifts EDPVR curve up and to left
• Decreased EDV, increased EDP(normally 10mmHg, can get up to 30mmHg, decreased SV
• EF may not change depending on relative decreased SV and EDV so EF only useful in systolic failure
• Raised EDP can raise LAP and pulmonary capillary pressure, if pulmonary capillary wedge pressure >20mmHg (normally 6-13mmHg) can get pulmonary oedema (or peripheral oedema and ascities if right sided)

o Systolic and diastolic
• Dramatic decrease in SV as ESV increased and EDV decreased, high EDP, pulmonary oedema

Question 3

compensation mechansisms in heart failure

Answer 3

o Decreased SV so decreased CO → decreased MAP and CVP
o Activates neurohormonal mechanisms
• Decreased baroreceptor firing
• Sympathetic to heart and vasculature →
• Renin – angiotensin II-aldosterone →
• Vasopressin (even though RAP high, prob stimulated in heart failure by sympathetic and ANII)
• So vaso/venoconstriction and fluid retention →both further increase venous pressure and preload and stroke volume
• High RAP releases ANP to counterregulate renin-angiotensin-aldosteron
• Above things can also make heart failure worse by increasing afterload and increasing preload to point of pulmonary/systemic congestion

Question 4

exercise limitation in heart failure

Answer 4

• Compensation mechanisms may keep CO and BP normal at rest in early stages
• But generally decreased SV and CO and therefore MAP at rest, and an increased HR.
• At rest normal whole body O2 consumption but increased arterial venous O2 difference because more O2 extracted as organ blood flow reduced
• Exercise – unable to increase SV and therefore CO by as much or increase HR (because chronic activatation of B1 downregulates them) by as much. Then drop MAP as SVR drops in exercise. Reduced O2 consumption cos reduced perfusion and O2 delivary to muscles
• Chronic increase in sympathetic activity at rest means less chronotropic and inotropic response to activation in exercise. This and circulating vasoconstrictors means can’t vasodilate muscle vessels. Limits O2 delivary, increased O2 extraction (and a-v difference), more lactic acid and fatigue sooner
• Less reserve to increase preload in exercise cos already done

Question 5

treatment in heart failure

Answer 5

• Aim to
• reduce oedema and SOB
• Enhance organ perfusion
• Increase exercise capcity
• 4 approaches
• Decrease CVP to decrease oedema and SOB
o Diuretics and ACE inhibitor to get rid of volume
o Doesn’t decrease SV if LVEDP stays

• Reduce afterload
o To increase SV, will decrease LVEDV and preload. Doesn’t cause drop in MAP cos CO increased
o Vasodilators like ACE inhib and ARB

• Stimulate inotropy
o Digoxin inhibits Na+/K+ pump, increses intracellular Ca. Doesn’t reduce mortality
o If acute or end state use Dobutamine – (stimulate B1) or Milrinone (inhibit cAMP dependent phosphodiesterase), deleterious long term

• BB to stop long term sympathetic activation
o Even tho seems counterintuitive
o Reduced ventricular hypertrophy and dilation
o Reduce mortality