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.
Discuss maladapative changes in heart failure
Ventricular remodeling includes cardiac dilation, reactive hypertrophy, progressive fibrosis and changes in wall conformation.
Reverse remodeling is a concept in which progressive LV dysfunction is not simply arrested but also partially reversed
Various antihypertensive therapies inclduing B blockade, ACE, ARBs and alodseterone antaognist allow regression of LV hypertrophy and reducen the rate of sudden death.,
List Aetiology of reduced ejection failure
- Ischaemic heart disease – dominant cause of HF in developed countries
- Valvular disease - aortic stenosis
- Cardiomyopathy (alcoholic, thyroidtoxic, HOCM)
- HTN
- Arrhythmuias and conduction system disease
Discuss mechanisms that lead to diastolic or EF preserved dysfunction List Aetiology of EF preserved failure
1) imparied ventricular relaxation
2) increased ventricular wall thickness
3) accumulation of myocardial interstitial collagen
Impaired lusitropy of the myocardium leads to higher ventricular filling pressure reuslting in congetive symptoms. Relaxation is an active energy requiring process.
DDX of HFpEF
Cardiomyopathies with preserved EF
- Restrictive
—– familial ( amyloidosis, fabry disease, familial causes of iron overload)
—– nonfamilial ( Systemic sclerosis, carcinoid heart disease, metastatic cancer, radiation)
- Hypertrophic
—–Familial
Vavular heart disease
- Mitral stenosis or regurg
- aortic regurg
Right heart failure
- pulmonary HTN
- Right ventricular infarct
- ARVD
Pericardial dsiase
- cardiac tamponade
- constrictive pericardtiis
- effusive constrictive pericardial disease
Obstructive lesion in heart or great vessel
- atrial myxoma
- pulmonary vein stenosis
Highoutput heart failrue
Discuss right vs left failure
somewhat artificial term and unless failure is of acute aetiology (MI) will happen in concert.
Part of the same circuit and output of the two sides must be equal. Also share a ventricular wall failure in one side leads to bowing of the septum to the other ventricle leading to reduced filling and reduced CO
Discuss high output failure vs low output failure
High output refers to a hyperdynamic state with supernormal cardiac output, lowered PVR and low AV o2 difference (decreased o2 extraction ratio) -results in borderline preserved or depressed systemic arterial blood pressure and elevated cardiac filling pressures - this leads to activation of RAS and increase in salt and water retention – chronci volume overload leads to ventricular enlargement and failure
Aetiology
-Increased preload (sodium retention or excess mineralocorticoids)
-reduced SVR (pregnancy, av fistula, chirrhosis, severe anaemia, thyrotoxicosis, pagets disease)
- increased sympathetic activity
- persistent tachycardia
Myocardial and reduced vascular effect
- sepsis
- beriberi
- acromegaly
Recognition of these states early allows for treatment of undelrying cause and may prevent development of heart failrue
Persistence of a hyper dynamic state leads to cardiac damage
Low output states is the classical heart failure
List common precipitating causes of acute heart failure
- Sodium or volume excess
- PE
- MI
- HTN
- Systemic infection
- dysrhthmias
- pregnancny
- anaemia
- thyrotoxicosis
- acute mycocarditis
- valvular pathology
- sympathomimeitic or acohol excess
- excessive exertion or truama
- pharm
Discuss clinical features of heart failure
- dyspnoea
- chest pain
- previous heart disease
- catheterization
- current meds and adherance to the same
- PND is caused from pulmonary congestion precipitated by plasm volume expansion that occurs during recumbencey because intersitial oedema is reabsorbed into the circulation
- Orthopnoea occurs via the same mechanisms
Most patient with ACPE are dipahoretic because of intense sympathetic activation.
Clinical finding
- wheeze
- creps
- positive response to bronchodilator therapy does not exclude heart failure
- raised JVP
- S3 gallop
- peripheral oedema
Discuss DDX of cardiac failrue
Normal present with respiratory copromise -non cardiac APO -PE -Pneumonia -COPD - pneumothorax 0 cardiac tamponade - anaphylaxis
Discuss IX
Bloods - FBC - anaemia , U&E for electrolytes, renal function, BNP, TNI
CXR - exlude multiple DDX
Bedside ultrasound