03-09-22 - Pathophysiology of Cardiac Failure Flashcards
Learning outcomes
- To define heart failure in terms of systolic/diastolic function and severity.
- To describe the pathological impact of heart failure on the systemic and pulmonary circulations.
- To explain the issues with the compensatory mechanisms that are initiated to deal with low cardiac output and predict how these may worsen the underlying issue in heart failure.
What is the New York Heart Association Classification of Heart Failure?
What is the New York Heart Association Classification of Heart Failure?
What is the ejection fraction?
How does ejection fraction differ in systolic vs diastolic ventricular dysfunction?
What is impaired in diastolic dysfunction?
- The ejection fraction is a measurement, expressed as a % of how much blood is pumped out of the ventricle with each contraction
- In systolic ventricular dysfunction, there is impaired cardiac contractility, meaning the ejection fraction decreases (from the normal 50-65% to less than 40%)
- In diastolic ventricular dysfunction, the ejection fraction is normal, but there is impaired ventricular relaxation and decreased filling, leading to a decreases in stroke volume (SV) and therefore cardiac output (CO)
What 3 factors that, when affected, typically lead to systolic dysfunction?
What conditions might affect these factors?
What 3 things does systolic dysfunction lead to?
- 3 factors that, when affected, typically lead to systolic dysfunction:
1) Contractility – affected In IHD and cardiomyopathy
2) Volume and or pressure overload – affected in valvular stenosis and hypertension - Due to a decrease in ejection fraction, systolic dysfunction leads to:
1) Greater EDV
2) Increased Ventricular dilation
3) Increased ventricular wall tension
Is systolic or diastolic dysfunction more common?
What 4 factors that, when affected, typically lead to diastolic dysfunction?
What conditions might affect these factors?
- Diastolic dysfunction is less common than systolic dysfunction
- 4 factors that, when affected, typically lead to diastolic dysfunction:
1) Impedance (resistance) of ventricular expansion – affected in constrictive pericarditis
2) Increased wall thickness – affected by hypertrophy
3) Delayed diastolic relaxation – affected in aging and ischaemia
4) Increased heart rate
What is classification of ventricular dysfunction?
What side is more likely to lead to what?
What does long-term heart failure usually involve?
What is the difference between oedema and ascites?
What is the difference between PND and orthopnoea?
- Classification of ventricular dysfunction is according to the side of the heart that is primarily affected
- We are unlikely to find something that affects both sides immediately at the same time
- We are more likely to see left sided heart failure lead to right sided heart failure
- Long term heart failure usually involves both sides
- Ascites is fluid build-up in the abdomen while oedema is the swelling and puffiness in the different parts of the body
- PND and orthopnoea are both caused by fluid build-up in the lungs, but PND can take a few hours to occur
What are the 4 causes of right ventricular dysfunction?
- Causes of right ventricular dysfunction:
1) Conditions that impede blood flow into the lungs
* Pulmonary hypertension
* Low oxygen supply (such as high altitudes) lead to there being no need to perfuse inactive regions of the lung
* A large constriction of vessels can lead to increased resistances to flow and pulmonary hypertension
* Valve damage/stenosis/incompetence
2) Decreased pumping ability of the right ventricle
* Cardiomyopathy
* Infarction
3) Left ventricular failure
4) Congenital heart defects
What are 4 causes of Left Ventricular Dysfunction?
- 4 causes of Left Ventricular Dysfunction:
1) Hypertension (↑TPR)
2) Acute myocardial infarction
3) Aortic or mitral valve stenosis or regurgitation
4) Increase in pulmonary pressure can lead to right ventricular failure
What are compensatory mechanisms used for in heart failure?
Where else are these compensatory mechanisms seen?
Why is this?
Long term, what do these compensatory mechanisms lead to?
- In the early stages of heart failure, compensatory mechanisms maintain cardiac output
- These compensatory mechanisms are also seen in hypovolaemia (decrease in blood volume due to blood loss)
- The body does not sense the drop in volume from hypovolaemia or drop in cardiac output from cardiac failure, only the drop in MABP which is sensed by arterial baroreceptors in both cases
- This leads to the same compensatory mechanisms being used for hypovolaemia and heart failure
- Long term, these compensatory mechanisms lead to the worsening of the condition
What are the 3 compensatory mechanisms seen during cardiac failure?
- 3 compensatory mechanisms seen during cardiac failure:
1) Frank-Starling mechanism
2) Sympathetic activity
3) RAAS system – Renin-angiotensin-aldosterone system
How is the Frank Starling triggered?
What are problems with the Frank Starling mechanisms as compensatory mechanism in cardiac failure?
What can occur if the heart stretches too far?
- The Frank Starling mechanism is triggered by an increase in vascular return
- This leads to an increase in EDV, which triggers an increase in muscle stretch and O2 consumption
- This triggers an increase in contractility through a greater overlap between actin and myosin in the sarcomeres
- Problems with the Frank Starling mechanisms as compensatory mechanism in cardiac failure:
- When EDV starts to become too high, this can stretch the overlap of actin and myosin too far, decreasing the ability of the ventricle to generate force, causing ventricular dysfunction
- This will mean the Frank Starling mechanism won’t contribute a huge amount of ability towards heart contraction
- If the heart stretches too far, this can lead to dilated cardiomyopathies,
What is the problem of the Frank Starling mechanism as a compensatory mechanism in systolic dysfunction?
- Problem of the Frank Starling mechanism as a compensatory mechanism in systolic dysfunction:
- In systolic dysfunction, there is impaired contractility
- If the contractility of the heart has been impaired, then the impact of the Frank Starling mechanism can be significantly muted
- The contribution of the FSM gets worse as heart failure gets worse
Why is long term sympathetic activity as a compensatory mechanism in heart failure not useful in the long term?
What 5 effects does sympathetic innervation have on the body?
What changes in receptor sensitivity do we see?
How does this contribute to the worsening of heart failure?
- Initially, sympathetic activity can be helpful as a compensatory mechanism in heart failure, long-term it is not:
- Sympathetic innervation leads to:
1) Tachycardia,
2) Vasoconstriction,
3) ↓ perfusion of tissues,
4) Cardiac arrhythmias,
5) Renin release (increases MABP) - Sympathetic innervation will cause the Desensitisation of β but not α receptors
- With β-receptor desensitisation, this decreases the ability of the sympathetics to increase HR and contractility
- With the α receptor sensitivity staying the same, sympathetic mediated vasoconstriction can still stay in place, meaning resistance in the vessels will stay high
- These changes will all ↑ the workload of the heart, leading to ischaemia, damage to myocytes, and ↓ contractility, leading to worsening of heart failure
Summary of compensatory mechanisms so far
Summary of compensatory mechanisms so far
What triggers renin release?
What does the increase in renin stimulate the formation/release of?
What are the 3 roles of angiotensin 2?
What are angiotensin 2 and aldosterone involved in?
How does this change the function of the heart?
- Renin released is triggered by decreased arterial pressure, and decreased renal blood flow
- An increase in renin leads to great angiotensin 2 formation
- Role of angiotensin 2:
1) Vasoconstriction
* Angiotensin causes vasoconstriction of renal arteries, which increases total peripheral resistance and constricts blood flow via the kidneys
2) Release of aldosterone
* Angiotensin 2 causes the release of aldosterone from the zona glomerulosa (outermost region) of the adrenal glands, which decreases the volume of water excreted from the kidney by increasing Na+ and water reabsorption
3) Stimulation of release of ADH (vasopressin) form the pituitary
* ADH increases blood volume by increasing water permeability in the renal collecting ducts, which decreases urine production
* Angiotensin II and aldosterone are also involved inflammatory responses leading to deposition of fibroblasts and collagen in the ventricles
* This leads to an increase in stiffness, and a decrease in contractility of the heart, leading to myocardial remodelling and progressing dysfunction
