Pathophysiology of heart failure Flashcards
HEART FAILURE
i) what is it? can you get HF even if the heart is not implicated?
ii) what is the ejection fraction status in systolic and diastolic HF?
iii) name five things that can lead to HF
i) clinical syndrome where the cardiac output doesnt meet systemic requirements/demands
ii) systolic (LV doesnt contract completely) = reduced E
- diastolic (LV doesnt fill properly) = preserved EF
iii) ischaemia, hypertension, arrhythmia (AF), cardiomyopathy, valvular disease (eg incompetence)
RIGHT SIDED HF
i) what is it most commonly due to? what can this lead to?
ii) what is isolated RHF called? what is this most commonly caused by?
iii) name five symptoms
i) most commonly due to left heart failure > congestive cardiac failure
ii) isol RHF = cor pulmonale > caused by chronic lung conditions eg fibrosis > pulm hypertension
- increased pressure in lung vasculature > back pressure on RV
iii) inc peripheral venous pressure, enlarged liver/spleen, distended jugular veins, weight gain, dependent oedema, ascites
LEFT SIDED HF
i) what colour may sputum be?
ii) is pitting oedema common?
iii) name four other symptoms
i) may be blood stained > frothy pink
ii) pitting oedema more common in RHF
iii) PND, orthopnea, dyspnoea, pulm congestion (crackles), cyanosis, fatigue
PATHOPHYSIOLOGY OF HEART FAILURE
i) what is arterial pressure determined by? (2)
ii) what happens to aterial and venous pressuire if CO falls and TPR stays constant? what happens physiologically to compensate?
iii) what happens to art/venous pressure if CO increases and TPR stays constant?
iv) what happens to vessels in septic shock? what happens to TPR? what needs to increase for BP to be maintained? how does the body do this?
i) arterial pressure is determined by CO and TPR
ii) CO falls, TPR constant > art pressure decreases and venous pressure increases as blood pools in the veins
- physiol - body increases TPR > vconstriction to increase arterial pressure
iii) if CO increases but TPR stays the same - art pressure increase and venous press decrease
iv) septic shock > periph vasodilation > drops TPR
- CO needs to increase to maintain BP
- heart pumps more blood (inc SV)
CO = SV x HR
STROKE VOLUME AND STARLING CURVE
i) what is SV? what two things is it the difference between?
ii) how does end dias volume affect stroke volume?
iii) how does mild and moderate heart failure impact on SV in relation to ventricular filling?
iv) what is end systolic volume? what two things does it depend on?
i) SV = volume of blood pumped out of the heart in each beat
- diff between end dias volume and end systolic volume
ii) increase in EDV > increase in SV
iii) for a given volume of filling - there is a lower SV with heart failure
iv) end sys volume = amount left after a heart beat
- depends on contractility and resistance to flow out of the heart
CONTROL OF HR
i) what is autonomic outflow of the heart controlled by? where are messages sent to?
ii) how is HR increased?
iii) how is contractility increased?
i) autonomic outflow is controlled by signals from baroreceptors in carotid sinus > send signals to the medulla
ii) inc in HR > reducing psym or increasing symp activity
iii) inc contractility by increasing symp activity
RENIN ANGIOTENSIN ALDO SYSTEM
i) what does low arterial pressure in the afferent arteriole in renal glom cause release of? from which cells? which receptors are implicated?
ii) which cells in which tubule sense conc of sodium and chloride ions in the tubular fluid? what happens if this is low?
iii) what is angiotensinogen converted to?
i) low art pressure > juxtaglomerular cells release renin
- beta adrenoergic receptors on JG cells respond to symp stim > renin
ii) macula densa cells in teh DT sense Na and Cl > if its low then renin is released from JG cells
iii) angiotensinogen > AG I by renin
ANGIOTENSIN II
i) what effect does it have on blood vessels? what two things does this lead to?
ii) what effect does it have on sodium transport in renal tubules?
iii) what does it do at the adrenal glands? what does this lead to
iv) what does it cause to be released from the post pit?
v) does it increase or decrease symp activity?
vi) what effect does it have on the heart muscle?
i) arterial vasconstriction > increases TPR and arterial pressure
ii) stim sodium reabs > inc sodium and water retention
iii) adrenals > release aldo > acts at kidneys to increase sodium and water retention
iv) vasopressin (ADH) release from post pit > increases sodiuma nd water retention
v) increases symp activity
vi) stim cardiac hypertrophy
HF MEDICATION AND RAAS
i) which type of HF can be treated with ACEi, BB and mineralocorticoid R antagonists? does this have reduced or preserved EF?
ii) which type of HF can only really be treated with diuretics? why?
i) treat systolic HF with ACEi etc (disease modifying)
- reduced ejection fraction
ii) diastolic HF (preserved EF) - only solution is diuretics
- need to take volume out of the system as ventricles are stiff > cant fill properly so get overload
NATRIURETIC PEPTIDES
i) what is ANP released from? in response to what? (3)
ii) where is BNP released from?
iii) what do both ANP and BNP cause in relation to the veins? (2)
iv) what action do they have on the kidneys? what does this lead to?
v) do they complement or counteract the RAAS?
i) ANP released from atrial myocytes in response to atrial distenion, AG II and symp stimulation
ii) BNP released by the ventricles (used as a marker of HF in the community)
iii) both cause venous dilatation (inc venous compliance) and reduce venous return and preload
iv) act on kidneys to increase GFR, increasing sodium and water excretion
v) counter regulatory system to RAAS
MECHANISMS OF HF
i) which two systems are upregulated in HF?
ii) what does reduced CO due to HF cause? which drugs can therefore be useful?
i) increase in RAAS and sympathetic system
ii) HF > reduced CO > reduced BP > kidneys respond by releasing renin etc > inc sodium retention - ACEi block this
- baroRs detect low BP > increase in symp acitivity > beta blockers block this (decrease heart rate to increase filling and stop the inefficient system)
