Failure Flashcards
Define heart failure
Pathophysiological state in which the heart is incapable of pumping sufficient supply of blood to meet the metabolic requirement of the body, or requires elevated ventricular pressures to achieve the same.
Failing heart may still maintain perfusion via frank starling mechanisms- low filling volume hypoperfusion indicates pump-priming probe distinct from cardiac disease
Briefly define diastolic and systolic heart failure
Systolic failure is defined as failure with EF >40%
Diastolic failure or EF preserved failure is a pathological condtiion with normal or near normal EF with failure of ventricular relaxation and consequent high filling pressure.
Discuss the 4 categories of heart failure as per the ASA
1) patients at risk of developing failure
2) asymptomatic LV dysfunction
3) symptomatic HF
4) refractory HF
List predisposing factors to the development of Heart failure
HTN, atherosclerosis, DM, tobacco use, dyslipidaemia, obesity cocaine
Discuss frank starling mechanisms
Within physiological limits force of ventricular contraction is directly related to end disatolic length of the myofibril
Discuss factors affecting heart contractility
Physiological depressants
- acidosis
- hypercarbia
- hypoxia
- ishcaemia
Pharmacological agents
- B blockade
- CA blocker
- antiarythmic agents
Discuss preload
The amount of force stretching the myofibril before contraction
Optimal preload stretches the myofibrils to the fullest and leads to the most forceful contraciotn
The risk of pulmonary oedema increases when LV end diastolic pressure rises significantly above normal ranges
Discuss afterload
Pressure against which the heart must pump to eject blood.
Afterload represent the mural tensions on myocardial cells during contraction and is determined by the TPVR and the cardiac chamber size
BP is determined by the product of CO and SVR
HTN is a major contributor to heart failure. Those in failure tend to maintain their blood pressure through peripheral vasoconstriction mediated mainly by endogenous catecholamines and teh RAAS
Failing ventricles have difficulty overcoming increases in peripheral resistance instead dilating further increasing end diastolci volume to maintain SV even with decreasing EF –they are therfore extremely afterload dependant and modest vasodilation can dramatically increase cardiac ouptut
Discuss cardiac output
CO = HR *SV
CO increase to a heart rate of about 160 above this diastolic filling time is compromised leading to decreased cardaic output and coronary artery perfusion.
Discuss increase in SV, SVR and development of cardiac
Increase in SV occurs in response to increase in preload it i prompt and effective in improving CO in response to acute demands. Its response is limited however because myofibril stretch to a sarcomere length beyond 2.2um does not increase stroke output and may reduce it
Increase in SVR results in redistribution of a subnormal CO away from skin and skeletal muscle and kidneys to maintain normal blood flow to the brain and heart
Discuss cardiac hypertrophy as a compensatory mechanisms
LV remodeling describes the changes in ventricular mass volume, shape and composition in response to mechanical stress and systemic neurohormonal activity.
Development of cardiac hypertrophy is the primary chronic adaptation of the heart to compensate for pump failure.
Hypertrophy predominates increasing the number of myofibrils per cell as the heart has a very limited abilities to produce new cells. New myofibrils arrange in series in response to an increase in chamber volume (leading to dilation) and in parallel when responding to higher pressures ( leading to increase in wall thickness). Mitochondrial mass also expands leading to an increase in availablility of ATP- mitochondrial dysfunciton is well recongnised in failure.
Initially these changes lead to improved function of each cell but at a higher energy cost.
Discuss the cardiac neurohormonal response
Increase in myocardial wall stretch activate and release cardiac natriuretic peptides. These including c type and b type natriuretic peptide.
These peptides promote water and sodium excretion increase peripheral vasodilation and inhibit the RAAS. In early failure they play a key role in compensation for LV dysfucntion. Attenuation of renal response to these peptides occur as failure progresses
Discuss the CNS and ANS neurohormonal response to failure
The heart and great vessels contain sensory receptors that detect changes in perfusion.
ADH is release from the pituitary gland in response to decreases in perfusion – this increases intravascular volume and decrease osmolality
Failure in general leads to activation of the sympathetic and inactivation of the parasympthetic systems
Chronically a decrease in the number and affinity of surface catecholamines occur in the myocardial tissues reducing responsiveness to norad and adrenaline - elevated catecholamine’s adversly affect myocardial perfusion leading to progressive cardiac cell death and fibrosis
Discuss renal neurohormonal response
Decreased glomerular perfusion results in reducced renal excreation of sodium causing renal arteriolar and adrenergic receptors to stimulate renin release and active RAS +aldosterone
Renal adaptation to hypoperfusion occurs mainly through production of vasodilatory hormones such as prostacyclin along with PGI2 and PGE2 – Nsaids inhibit this by interfering with COX therefore except for there useful antiplatlet effect they should be avoided in patient with chronic heart failure
Discuss vascular endothelial neurohormonal response
Endothelial function locally regulates vasomotor tone. Endothelins are produced by endothelial and smooth muscle cells as well as neural renal pulmonary and inflammatory cells.
This occurs in response to HD stress, hypoxia, catecholamines, angiotensin 2 and many inflammatory cytokines.
NO is almost universally produced by all tissues. Reduced synthesis or increased degradation at the endothelial level is detrimental to heart failure.
