Pathophysiology of congestive heart failure Flashcards
What is heart failure?
Occurs when the heart is unable to maintain an adequate circulation at normal filling pressures.
What are the determinants of cardiac output?
Preload
Afterload
Contractility
Heart rate
Distensibility
Synergy of contraction
What is preload?
the volume of blood that fills the heart during diastole
the stretching of the myocardial cells in a chamber during diastole, prior to the onset of contraction
the end-diastolic volume or end-diastolic pressure.
preload is equal to venous return plus the residual volume left in the cardiac chamber after the last contraction
Signs of left ventricular preload
pulmonary oedema as detected by crackles (if severe) or increased broncho-vesicular sounds (if mild or moderate) on pulmonary auscultation
hypoxemia/cyanosis
excessive right ventricular preload
Signs of right ventricular preload
jugular venous distention or distention of peripheral veins
positive hepato-jugular reflux test
pleural effusion as detected by increased/laboured respiration
hepatomegaly and/or splenomegaly
ascites (abdominal fluid)
subcutaneous edema
What is afterload?
Afterload refers to the arterial resistance the left ventricle encounters as it tries to eject blood.
Afterload is only conceptual and cannot be measured directly.
What is afterload affected by?
ventricular volume (size)
arterial vasomotor tone (arterial resistance)
ventricular wall thickness
What is afterload increased by?
increase in ventricular volume
increase in arterial vasomotor tone
decrease in ventricular wall thickness
Signs of a fall in cardiac output
cool extremities, fall in rectal temperature
weakness/syncope
shock
slow capillary refill time (>2 sec)
arrhythmias
reduced mentation/confusion
congestive failure signs usually coexist with a reduction in cardiac output
Compensatory mechanisms when the heart starts to fail
- Renin-Angiotensin-Aldosterone system (RAAS)
- Atrial natriuretic peptide (ANP) and BNP release
- Sympathetic nervous system
- Myocardial hypertrophy
Effects of RAAS activation
Na and water retnetion
Vasocontriction water retention
Atrial natriuretic peptide (ANP) and BNP release in heart failure
ANP is an antagonist to prevent volume overload.
ANP is released in response to atrial stretch and causes Na excretion.
It inhibits the RAAS and reduces tachycardia.
Stored and released from myocardium
Released when atria stretched
Natriuretics
Vasorelaxants
Attenuate aldosterone secretion
Inhibit sympathetic nervous system
Diagnostic markers
Sympathetic nervous sytem activation in heart failure
Noradrenaline is released in response to a fall in blood pressure or in response to exercise or excitement.
Acting via b-receptors, noradrenaline causes an increase in heart rate and contractility.
Acting via a-receptors, NA causes peripheral vasoconstriction to conserve blood flow to essential vascular beds (brain and heart) and also causes venoconstriction that increases venous return.
Respiratory sinus arrhythmia is abolished
Vagal restraint on the heart is reduced
Heart rate increases
§ Myocardial oxygen consumption increases
§ Diastole shortens and oxygen delivery to the myocardium is further decreased
Eccentric hypertrophy
Caused by volume overload
Increase in thickness and increase in radius
Leads to an overstretched ventricular myocardium so that myocytes are unable to interact and contract.
Concentric hypertrophy
Caused by pressure overload
Huge increase in thickness, and decrease in radius
Becomes so severe that MVO2 increases and the myocardium becomes hypoxic so dysrhythmias can occur. Eventually, fibrosis occurs and prevents the ventricles from relaxing, leading to diastolic failure.
Mechanisms of heart failure
Myocardial failure/pump failure
Volume overload
Pressure overload
Compliance (diastolic) failure
Abnormal heart rate/rhythm
Myocardial failure/pump failure
e.g. dilated cardiomyopathy.
This causes a failure in contractility and a decrease in forward stroke volume.
In DCM the myocardium is weak and dilated and cannot contract with sufficient force to eject the blood volume.
Volume overload
Increase in ventricular volume e.g. valve regurgitation and shunts such as PDA and ASD
The force of contraction increases to expel the extra blood.
The heart dilates due to the extra blood load and chamber enlargement is seen on radiographs and echocardiography.
Pressure overload
e.g. aortic stenosis, pulmonic stenosis or systemic hypertension.
Cause an increased afterload so the heart must work harder to maintain cardiac output and the heart muscle hypertrophies.
In the case of aortic stenosis, the left ventricular outflow tract is narrowed and the left ventricle must work harder to eject the blood.
The left ventricular muscle hypertrophies and prevents efficient chamber filling. The abnormally thick muscle is also prone to arrhythmias.
Compliance (diastolic) failure
prevents adequate ventricular relaxation, e.g. cardiac tamponade, myocardial diseases such as HCM and AV valve stenosis
These conditions all prevent adequate relaxation of the ventricles, therefore impeding filling.
In HCM the ventricular wall becomes so thick that the ventricular lumen is obliterated and cannot fill during diastole.
Abnormal heart rate/rhythm
tachycardia can provoke a cardiomyopathy if sustained over a long enough period
A sustained tachycardia can result in a cardiomyopathy where the affected heart becomes dilated and hypocontractile.
Similarly, a profound bradycardia can cause low output failure.
Forward (low output) heart failure
Leads to a fall in systemic blood pressure.
Right-sided forward failure leads to a reduction in blood supply to the lungs.
Left sided failure leads to low output to the body.
Clinical signs of forward heart failure:
Exercise intolerance- Poor muscle perfusion
Pallor- Peripheral vasoconstriction
Tachycardia- Catecholamine release (sympathetic tone increase)
Weak femoral pulses- Poor contractility
Azotaemia- Poor renal perfusion
Increased thirst- Angiotensin II
Backward failure (congestive heart failure)
In contrast to forward failure, the clinical signs are different for left and right-sided failure.
Congestion occurs due to damming of the blood behind a failing heart.
The same basic processes occur that lead to pulmonary oedema (left-sided) or body cavity effusions (right-sided).
Clinical signs of left-sided backward failure:
Dyspnoea/tachypnoea
- Pulmonary oedema, pleural effusion in cats
Cough (especially in dogs)
- Left-sided cardiomegaly compressing left main-stem bronchus (harsh), pulmonary oedema (soft)
Respiratory crackles and wheezes
Absence of lung noise
- Pulmonary oedema, pulmonary effusion
Clinical signs of right-sided backward failure:
Jugular distension
- Increased RA pressure
Hepatomegaly
- Increased vena cava pressure
Ascites
- Venous congestion of liver
Positive hepatojugular reflex
- Blood displaced from liver to jugular
Pleural effusion (dogs)
- Increased pressure in azygous and bronchial veins
Peripheral oedema
- Increased systemic venous pressure and venoconstriction
New York Heart Association classification scheme for congestive heart failure
Class 1 No clinical signs but evidence of heart disease
Class 2 Exercise intolerance or dyspnoea after marked exercise
Class 3 Marked exercise intolerance, dyspnoea after mild exercise
Class 4 Cannot exercise, dyspnoea at rest
4 basic stages of myxomatous mitral valve degeneration
Stage A: patients at high risk
Stage B: patients with structural heart disease
B1: asymptomatic with no imaging evidence of structural change
B2: asymptomatic patients with haemodynamically significant valve regurgitation
Stage C: patients with past or current clinical signs
Stage D: patients with end-stage disease with clinical signs of heart failure caused by CVHD that are refractory to ‘‘standard therapy’’
Stage A of myxomatous mitral valve degeneration and failure
patients at high risk for developing chronic valvular heart disease (CVHD) but that currently have no identifiable structural disorder of the heart (eg, every Cavalier King Charles Spaniel without a heart murmur).
Stage B of myxomatous mitral valve degeneration and failure:
identifies patients with structural heart disease (eg, the typical murmur of mitral valve regurgitation is present), but that have never developed clinical signs caused by heart failure.
Because of important clinical implications for prognosis and treatment, the panel further subdivided Stage B into Stage B1 and B2.
Stage B1 of myxomatous mitral valve degeneration and failure:
asymptomatic patients that have no radiographic or echocardiographic evidence of cardiac remodelling in response to CVHD.
Stage B2 of myxomatous mitral valve degeneration and failure:
asymptomatic patients that have hemodynamically significant valve regurgitation, as evidenced by radiographic or echocardiographic findings of left-sided heart enlargement.
Stage C of myxomatous mitral valve degeneration and failure:
patients with past or current clinical signs of heart failure associated with structural heart disease.
Because of important treatment differences between dogs with acute heart failure requiring hospital care and those with heart failure that can be treated on an outpatient basis, these issues have been addressed separately by the panel.
Stage D of myxomatous mitral valve degeneration and failure:
patients with end-stage disease with clinical signs of heart failure caused by CVHD that are refractory to ‘‘standard therapy’’.
Such patients require advanced or specialized treatment strategies in order to remain clinically comfortable with their disease.
4 phases of diastole
Isovolumic relaxation
Rapid early mitral filling
Diastasis
Atrial contraction
Isovolumic relaxation
from closure of aortic valve to opening of the mitral valve
Rapid early mitral filling
Passive
Diastasis
a pause during which there is little change in ventricular volume or pressure
Atrial contraction
atrial systole and its contribution to ventricular filling
What is failure of relaxtion caused by?
Increased afterload
Ventricular hypertrophy
Abnormal calcium movement
Obstruction to ventricular filling
Increased chamber stiffness
Ventricular hypertophy causes
Hypertrophic cardiomyopathy
Aortic stenosis
Pulmonic stenosis
Heartworm disease
Systemic hypertension
Obstruction to ventricular filling causes
AV valve stenosis
Intracardiac neoplasia
Pericardial disease - causes tamponade
Increased chamber stiffness causes
Fibrosis
Ischaemia
Hypertrophy
§ HCM
§ Aortic/pulmonic stenosis
§ Heartworm
§ Hypertension
Tamponade
