Week 12: Pathophysiology of Heart Failure Flashcards
Why does heart failure occur?
An insufficiency of cardiac output to meet the metabolic demands of the tissue
What are the 2 variables determining Heart rate and the 3 determining stroke volume?
Those that effect heart rate
Sympathetic tone
Parasympathetic tone
Those that effect stroke volume
Contractility (Is the ability of the myocardial cells to generate force. A decline in contractility is the most common cause of heart failure)
Preload (the degree of stretch of myocardial fibres prior to contraction)
Afterload (the load against which the myocardial fibres shorten during contraction)
What are the 3 things which ventricular wall stress is dependent on?
Ventricular pressure (P)
Ventricular radius (r)
Ventricular thickness (h)
For a failing heart, any increase in ventricular pressure (due to rise in arterial blood pressure) or ventricular radius (ventricular radius increases causing volume overload) will result in an _____
An increase in wall thickness wall stress
increased wall stress
reduces
the greater the wall stress, the greater the _____ demand of the ventricle wall (as more energy is required to oppose the force)
oxygen
What is cardiac reserve?
the difference between resting cardiac output and maximum cardiac output
What are the two main classifications for heart failure?
Acute (Sudden onset which requires hospitalizations and urgent therapy. E.g. as with the reduced cardiac output during a myocardial infarction)
Chronic (Symptoms are continuous, CO slowly decreases, It is progressive in nature and does not improve over time. Majority of heart failure cases are this type)
What are the 3 common causes for heart failure?
Coronary artery disease (65%)
Is the most common cause as it usually results in a myocardial infarction
Contractile myocytes are then lost, decreasing the contractility of the heart
The remaining myocytes will remodel and try to take over, but eventually as they are working far beyond their scope they will fail
Hypertension (30%)
Dilated cardiomyopathy (5 – 10%)
Is a condition characterised by the hearts reduced ability to pump blood
This is caused by myocardial defects (could be from congenital defects or drug and alcohol abuse)
What are the 2 dysfunctions that heart failure cause?
Systolic dysfunction (reduced systolic performance)
Diastolic dysfunction (reduced diastolic performance)
What are 3 pathophysiological factors which typically cause heart failure? and which are the cause of systolic dysfunction and diastolic dysfunction?
Impaired ventricular contractility (like in MI or chronic volume overload)
Increased afterload (chronic hypertension forcing the myocytes to do more work causing deuteriation)
If 1 or 2 – these will cause systolic dysfunction
Impaired ventricular relaxation and filling (ageing causing fibrosis, restrictive cardiomyopathy – causes diastolic dysfunction
What is the ejection fraction?
Is the fraction of end diastolic volume (EDV) that is ejected during one systole
The ejection fraction is basically the ratio between Stroke Volume : End Diastolic Volume
Stroke volume is the amount of blood ejected, that is the difference between End Diastolic Volume and End Systolic Volume
End Diastolic Volume is the amount of blood within the chambers after ventricular filling
If a patient has diastolic dysfunction, will the ejection fraction be increased or reduced or normal?
will be normal
If a patient has systolic dysfunction will the ejection fraction be increased or reduced or normal?
reduced
What is systolic dysfunction?
Is when there is an issue with the myocardial contraction causing significantly diminished cardiac output and ejection fraction
basically from the inability of the cardiac muscle to contract (reduced inotropy)
The ventricles are still getting filled, but the force of contraction is less, reducing the stroke volume which in turn obviously reduces the cardiac output
what are the causes for systolic dysfunction and what do they lead to (in terms of myocyte health)
Myocardial Infarction
Coronary Artery Disease
Any other coronary disorder (e.g. valvular disorders, chronic hypertension etc.)
these lead to:
loss of myocytes, abnormal myocyte function, reduced ATP production or down regulation of sympathetic receptors (beta1) by overstimulation
What morphological and functional changes will occur due to systolic dysfunction?
The most clear and obvious change will be a reduced ejection fraction (below 40%)
Other changes include;
- Increased end systolic volume Because the heart is not able to contract well enough to eject the entire ventricular volume)
- Increased end diastolic volume As not all the blood is ejected from the ventricle, the filling causes increased end diastolic volume
- Decreased end systolic pressure As the myocytes are not able to generate as much force
- Increased left ventricular cavity size This is caused by chronic volume overload
- Decreased ventricular wall thickness This increasers the wall tension
- A prominent S3 sound will be heard As there is excess turbulence when new diastolic blood is mixed with the blood left over from the previous contraction
what is diastolic dysfunction?
Is characterised by an inability of the ventricles to relax, causing a diminished ventricular filling
the heart failure caused by inadequate ventricular filling, due to inability of the cardiac muscle to relax (reduced lusitrophy) usually caused by fibrosis (or due to lesions that reduce inflow)
This obviously decreases the preload of the myocytes, the stroke volume and inevitably the cardiac output
What is systolic dysfunction associated with and the causes for it?
increased stiffness (from myocardial fibrosis), ischemia (reduced ATP which facilitates relaxation), external force (pericardial disease),
Commonly results due to chronic hypertension, ageing, ischemic heart disease etc
What are the morphological and functional changes that arise due to diastolic dysfunction?
The most obvious is a normal ejection fraction
Other changes include;
Decrease in End Diastolic Volume As it can’t relax meaning filling time is reduced
Elevated left atrial volume Caused by high pressure in ventricle during diastole, forcing blood back into the atria (high intraventricular pressure)
Increased wall thickness
aggravated by increased heart rate as it further reduces diastolic time
S4 heart sound is common
Late diastole, as the atrial contraction forces blood into a non-compliant left ventricle This causes increased turbulence
What are the 3 compensatory mechanisms for chronic heart failure?
- Rise in sympathetic nervous system activity
- Increase in the preload via neurohormonal responses (mainly RAAS)
- Myocardial Hypertrophy and Remodelling
- Eventually these compensatory responses will further decline the heart function, causing a decompensated failure
Describe the mechanism for the compensatory mechanism of the rise in sympathetic nervous system activity and what complication does this create for the heart?
- Heart failure results in decreased cardiac output which causes a drop-in blood pressure
- The baroreceptors within the aortic arch and carotid sinus artery sense this drop and signal the CNS to increase SNS tone and decrease PNS tone in order to resist the change to homeostasis
- This increases the heart rate, increases the contractility (which raises the CO back to normal)
- At the same time, this SNS also increases the peripheral vascular resistance through vascular constriction (by alpha1 receptors)
- Whilst these changes do help to maintain homeostasis, they also increase afterload and oxygen demand which causes further deterioration (as the heart is made to do more work)
Differentiate between the 2 types of myocardial hypertrophy in heart failure
- Concentric hypertrophy
- Is caused by the chronic pressure overload caused by diastolic dysfunction
- This increases the stress on the myocytes during systole, causing the replication of sarcomeres parallel (to make the force of contraction stronger)
- This causes the ventricle lumen to decrease in size as the wall gets thicker so that more systolic force can be generated - Eccentric hypertrophy
- Is caused by the chronic volume overload caused by systolic dysfunction
- This increases the stress on the myocytes to be increased, causing the replication of sarcomeres in series (next to each other) so the ventricle can accommodate more blood
- This causes the ventricle to widen, causing abnormal lengthening and dilation
- The walls are therefore thin, and disproportionate
What is the one compensatory mechanism that will not lead to any detrimental effect over time and is good?
and explain the mechanism
- With heart failure, there will be an increase in ANP and BNP
- The mechanism of ANP and BNP is as follows;
- ANP is secreted by the right atria and is stimulated by stretch (when the atria stretches)
- When there is heart failure, volume overload and fluid retention cause the atria to stretch
- This releases ANP
- As the ventricles are stressed as well, they start to produce and secrete BNP
- Both ANP and BNP cause diuresis (more sodium and water excretion) which is caused by decreased ADH, decreased renin, decreased aldosterone, increased GFR and decreased blood pressure
- To some extent, this mechanism does help the patient, however it is not good enough to completely balance out the other 3 compensatory mechanisms
- It is important to note that BNP is not detected in normal hearts and so is a useful marker for ventricular myocardium stress
- Whilst the administration of synthetic natriuretic peptides like nesiritide produces a beneficial haemodynamic effect in acute heart failure, It has since been associated with an increased risk of death (we don’t know the reason)
Explain how pulmonary oedema is caused?
Left ventricle will have an increase accumulation of blood as it is unable to remove it.
- The pressure of the LV therefore rises, eventually causing the left atrium to be unable to empty its blood into the LV
- Blood therefore starts accumulating in the left atrium which eventually increases the pulmonary venous pressure
- This eventually causes pulmonary congestion, and increased pulmonary hydrostatic pressure, forcing fluid out and making it accumulate in the lung interstitial (causing pulmonary oedema)
- Thus it can be said, pulmonary oedema is caused by the backward failure effect of left sided heart failure
How does peripheral oedema occur?
- Right ventricle failure causes increased RV preload (from accumulation) and thus increased RA pressure, causing systemic venous congestion
- As the blood builds up in the systemic circulation peripheral oedema occurs (as blood cannot drain into inferior vena cava)
Draw a curve of frank starling law for a normal heart and failing heart
