247 Heart failure Flashcards
What is heart failure?
Heart failure = abnormality of the heart where patients demonstrate clinical signs because of an inability to sustain cardiac output.
- Forward failure = inadequate cardiac output with normal filling pressures
- Backward or CHF = Clinical signs as a consequence of excessive cardiac filling pressures but normal cardiac output
What are the signs consistent with presence of heart failure?
- Tachypnoea, dyspnea, or respiratory distress
- Exercise intolerance
- Cyanosis
- Weakness and lethargy
What PE findings indicate heart failure?
- Heart murmur +/- Arrhythmia
- Increased RR and effort with audible pulmonary crackles
- Abdominal distension with fluid wave - jugular venous distension and/or hepatojugular reflux
- Pallor and cold periphery
What diagnostic findings indicate cardiac disease?
- X-Ray -> cardiomegaly with pulmonary venous congestion ad alveolar/interstitial pattern of lung parenchyma
- > pleural effusion
- > hepatic venous congestion on US or RSHF or pericardial effusion
- > Hypotension
What is preload and how is it managed?
= the left ventricular end-diastolic pressure, which is the amount of ventricular stretch at the end of diastole. It is determined by the pressure which blood returns to heart from venous circulation and influences by size of ventricle.
- The adaptive mechanisms leads to fluid retention, causing an increase in filling venous circulation (i.e. preload).
Management = drugs reducing circulation volume (diuretics) and dilate veins (venodilators)
What is afterload and how is it managed?
= the force resisting contraction of the myocardium.
- Main determinant of afterload is resistance in vascular bed which the ventricle is ejecting
- increased afterload -> inhibit ventricular ejection, reduce CO, increase myocardial work, and -> result in signs of poor perfusion.
Management = Vasodilators reduce systemic or pulmonary vascular resistance
How would impaired myocardial contractility cause heart failure?
- impairment would cause signs of inadequate cardiac output
- positive inotropic drugs lead to increased contractility
How do abnormalities (heart rate, myocardial disease) to cardiac filling cause heart disease?
- The heart must have enough time and be flexible to allow adequate venous return to enter the ventricles during diastole
- Diseases causing myocardium stiffness, impair relaxation (impair lusitropy), of insufficient time or space to fill compromise filling.
- Lusiotropic drugs -> sympathomimetic agents and calcium channel blockers
- Filling improved directly by modifying heart rate and rhythm so more time for ventricular relaxation and filling.
How would abnormality of heart rate and rhythm result in heart failure?
- bradycardia -> drop CO due to drop in heart rate
- tachycardia -> drop CO due to insufficient time to ventricles to fill and in some cases loss of normal coordinated patter of ventricular contraction (ventricular dyssynchrony)
What is the MOA of diuretics?
- Result in excretion of sodium and reduce patients EFV.
- This lowers circulating fluid volume and reduction in preload.
What are the loop diuretics? MOA? Site of action? Max fractional excretion of sodium achieved?
= Furosemide and toresmide
MOA= blockade of Na/K/2Cl- carrier.
Action site= Loop of Henle
- up to 25% excreted
What are the thiazides? MOA? Site of action? Max fractional excretion of sodium achieved?
= hydrochlorothiazide
MOA= blockade of Na+/Cl- carrier
Action site = distal tubule and connecting segment
- 5% maximum fraction excretion
What is a potassium sparing diuretic? MOA? Site in nephron? Max fractional excretion?
= Spironolactone
MOA= blockade of aldosterone receptors
Site= cortical collecting tubule
- max fractional excretion 2%
What are complications of diuretic treatment?
- volume depletion and reduced cardiac output=>result in hypotension and/or azotemia.
- electrolyte abnormalities : RAAS and increased aldosterone in response to diuretic treatment result in attempting to retain sodium and increasing potassium loss => hypokalemia
- hypotension - stimulates vasopressin release-> free water retention lead to expansion of circulating fluid and reduction of sodium concentration. => hypokalemia
- signs of volume depletion and electrolyte abnormalities occur 10-14 days following diuretic regime. Check urea, creatinine, sodium, potassium, and chloride concentrations 10-14 day after initiation or alteration.
What do venodilators do?
= dilate vessels.
- This is used where preload reduction is required acutely.
- Nitroglycerin administered cutaneously in an ointment .
- N.B. Method of administration and development of tachyphylaxis (tolerance and rapid loss of efficacy) limit use of nitroglycerin to short periods of administration in hospitalised patients
