Transcript Congestive Heart Failure Pathophysiology and other relations

Congestive Heart Failure
Pathophysiology and other relations
Summary of mainly Robbins and Cotran (relevant material from chapter 12)
Congestive Heart Failure –CHF
Definition: When the heart is unable to pump blood at
a rate sufficient to meet the metabolic demands of
the tissues or can do so only at an elevated filling
pressure.
CHF can develop over different time periods:
• Chronic work overload (valve disease, HTN or post
MI)  CHF developing insidiously
• Acute hemodynamic stress (fluid overload, acute
valvular dysfunction or acute MI)  acute CHF
Compensatory Mechanisms during CHFCardiac
• Frank-Starling mechanism Normally moderate ventricular
dilation during diastole
increases the extent of
sarcomere shortening and
hence inotropy via Frank
Starling law… but with further
dilation, effective overlap of
actin/ myosin filaments is
reduced and force of
contraction decreases sharply.
• Ventricular dilation or
hypertrophy - starts off as a
compensatory response to
increased mechanical work but
leads to increased cardiac
dysfunction.
Compensatory Mechanisms during CHFAutonomic Nerves
• Increased sympathetic adrenergic activity
which increases TPR, HR and inotropy
• Reduced vagal activity to heart (athletes
have increased vagal tone)
Compensatory Mechanisms during CHFHormones
• Renin-angiotensin-aldosterone system to
increase/ adjust filling volumes and
pressures
• Natriuretic peptides (ANP/ BNP) to reduce/
adjust filling volumes and pressures
Pathophysiology of CHF – systolic
dysfunction
Broadly, there are two paths that lead to CHF; the more
common one is that of systolic dysfunction (pump
failure), where progressive myocardial contractile
dysfunction is attributable to:
• Ischemic injury, which replaces viable myocytes with
fibrous scar tissue.
• Pressure - overload (afterload)/ volume – overload
(preload) due to valvular (esp. aortic) insufficiency or
HTN with resultant hypertrophy.
• Dilated cardiomyopathy, with decreased cardiac output
related to a weakened and enlarged heart wall.
• Drugs causing intracellular damage and oxidative stress.
• Defective signal transduction mechanisms eg.
Abnormalities in distribution of gap junctions and defects
in their proteins may contribute to arrhythmia and heart
failure
Pathophysiology of CHF – systolic
dysfunction
Ventricular end-diastolic pressure and
volume increases due to reduced stroke
volume  transmitted to the atria;
• left side  congested pulmonary
vasculature and oedema.
• right side  systemic venous
hypertension and oedema.
Pathophysiology of CHF – diastolic
dysfunction
Sometimes however, CHF results from an inability of
ventricles to expand when filling with blood during
diastole – can’t enrol help of Frank-Starling mechanism.
Diastolic dysfunction can occur as a consequence of
gross left ventricular hypertrophy, myocardial fibrosis,
deposition of amyloid or constrictive pericarditis and
normal stiffening with age.
The stiffer ventricular wall is unable to allow adequate
diastolic filling thus reducing the end diastolic volume
which reduces stroke volume and the cardiac output
goes down – causing identical symptoms of pulmonary
congestion and oedema on the left side and portal
hypertension and peripheral oedema on the right;
although if systolic function is preserved, diastolic
dysfunction may not manifest itself except in physiologic
extremes.
Cardiac Hypertrophy and
progression to failure
The response to increased mechanical work due to
pressure or volume overload and other trophic signals
cause myocytes to increase in size – producing an
increase in the size and weight of the heart.
• Increased ventricular systolic pressures (afterload) 
Concentric hypertrophy (thick wall due to new
sarcomeres positioned in parallel with existing ones)
• Volume overload (preload) caused by the regurgitant
fractions Excentric hypertrophy (dilation due to new
sarcomeres positioned in series with existing ones)
Cardiac Hypertrophy and
progression to failure
Increase in myocyte size and hence metabolic
demand is not met with a proportional increase
in capillary numbers  weak oxygen and
nutrient supply causing an hypoxic state, which
is especially bad new in systolic dysfunction.
This situation means that the hypertrophied
heart is vulnerable to decompensation  death.
So, the compensatory changes in hypertrophied
hearts that initially serve to maintain function
actually serve to promote heart failure.
Left-sided Heart Failure (LHF)
LHF is most often caused by IHD, HTN,
aortic and mitral valvular disease and
unusual restrictive cardiomyopathies.
Morphology and clinical features of LHF
are primarily due to pulmonary circulation
congestion, stasis of blood on left side of
heart, and lack of perfusion to tissues (eg.
Kidneys) leading to organ dysfunction.
LHF Morphology
• Myocyte hypertrophy and variable interstitial
fibrosis microscopically
• Myocardial infarction
• Left atrial dilation  increase risk of AF and
hence thrombosis
• Perivascular/ interstitial oedema  Kerley B
lines on x-ray
• Widening alveolar septa
• Hemosiderin-laden macrophages (HF cells) due
to extravasation of RBC’s
LHF Clinical features
• Cough
• Dyspnea (at rest when condition
decompensates)
• Orthopnea
• CNS  hypoxic encephalopathy  coma
• AF  stroke
LHF signs
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Tachypea and increased work of breathing
Rales/ Crackles in lung bases
Cyanosis due to severe hypoxia
Laterally placed apical beat
Additional HS (S4 is caused by the atria contracting
forcefully in an effort to overcome an abnormally stiff or
hypertrophic ventricle causing abnormal turbulent flow)
• Murmurs (regurg or stenosis may be cause or result of
CHF – soft pan-systolic normally mitral regurgitation
during systole – pt should be placed in left lateral
position etc)
LHF signs
• Decreased CO causes reduction in renal perfusion
causing triggering of RAAS – eventually increasing
interstitial and intravascular fluid volumes and TPR; this
increases organ perfusion and venous return but also
exacerbates pulmonary oedema. If renal hypoperfusion
worsens  azotemia (prerenal).
• Left sided Diastolic failure (stiff LV) disables the heart to
increase CO in response to increased peripheral
demand which exhibits itself most commonly as
exertional dyspnea, moreover, increased filling pressures
are immediately transmitted back to the pulmonary
circulation causing flash pulmonary oedema.
Hypertensive females are the most likely to get diastolic
LV dysfunction.
Right-sided Heart Failure (RHF)
• RHF is most commonly caused by LHF since
increase pulmonary pressure is eventually
transmitted to the right ventricle. Thus all the
causes of LHF are indirect causes of RHF too.
• When it does happen though, pure RHF
develops from pathology of lungs hence cor
pulmonale (heart pathology from lungs). Cor
pulmonale usually arises secondary to Interstitial
Lung Disease (eg. SLE, RA, TB, sarcoidosis,
PCP) but can also arise from pulmonary
vasculature disease (PE, pulmonary HTN) or
hypoxia-induced pulmonary vasoconstriction.
RHF Morphology and clinical
features
• Right atrial and ventricular hypertrophy
• Portal HTN and associated hepatosplenomegaly
and cirrhosis
• Pleural, Pericardial and Peritoneal effusions 
ascites
• Peripheral oedema (pitting) and JVPE
• More marked azotemia than LHF
• CNS  hypoxic encephalopathy  coma
• Parasternal heave due to right sided
hypertrophy
Only indirectly related…