Pathophysiology of Heart Failure Flashcards
What is Starling’s Law?
As ventricular end diastolic volume increases, cardiac muscle fibes are subject to increased stretch. The more they stretch, the higher their contractility and therefore the higher the stroke volume.
- This occurs up to a certain point, after which there is a decline in contractility despite increased cardiac myocyte stretch.
What increases contractility?
- Exercise
- Positive inotropes
- Sympathetic stimulation:
- Increases heart rate, contractility, rate force development and rest.
What factors affect stroke volume?
How is stroke volume calculated?
Stroke volume = EDV - ESV
Define net filtration pressure
Hydrostatic pressure - osmotic force
What facilitates filtration in the capillaries?
What facilitates absorption?
Positive net filtration pressure (hydrostatic pressure > osmotic force) facilitates filtration
Negative net filtration pressure (hydrostatic pressure < osmotic force) facilitates absorption
Loss from plasma in filtration should equal gain from plasma in absorption
What is the clinical definition of heart failure?
Clinically defined as a syndrome in which patients have classical symptoms (breathlessness, ankle swelling and fatigue) and signs (raised JVP, pulmonary crackles and displaced apex beat) resulting from abnormal cardiac structure or function.
What is the pathological definition of heart failure?
An abnormality of the cardiac structure or function leading to failure of the heart to deliver oxygen at a rate which is commensurate with the requirements of the metabolising tissues.
Name some common causes of heart failure
- Hypertension (systemic and pulmonary)
- Dilated, restrictive or hypetrophic cardiomyopathy
- Intrinsic myocardial disease
How is heart failure classified?
HFrEF: Heart failure with reduced ejection fraction
- Failure indicated by inabiity of the left ventricle to eject enough stroke volume to provide required oxygen to tissues.
HFpEF: Heart failure with preserved ejection fraction
- Preserved ejection fraction, inefficiency of heart
- Often caused by HTN
How is HFrEF diagnosed?
Must have all 3 symptoms of:
- Typical symptoms of HF
- Typical signs of HF
- Reduced LVEF
How is HFpEF diagnosed?
Must have all 4 of:
- Typical symptoms of HF
- Typical signs of HF
- Normal or mildly reduced LVEF, no LV dilation
- Relevant structural heart disease (LV hypertrophy/LA enlargement and/or diastolic dysfunction)
In a failing heart, what will be the effect of increasing end diastolic volume? How does this compare to a normal heart?
In a normal heart, increasing the end diastolic volume will increase the stroke volume as it will increase ventricular contractility.
In a failing heart, increasing end diastolic volume will reduce the contractility and therefore stroke volume which reduces the ejection fraction.
What are echocardiograms used for?
What are the pros and cons?
What alternative imaging can be used?
To determine cardiac structure and function
Pros: cheap and robust
Cons: very subjective
CMR and nuclear can be used
What can cause HFrEF?
What can HFrEF lead to?
Can be caused by:
- Regional damage (MI)
- Global (cardiomyopathy)
Can lead to:
- Myocardial injury
- Myocardial overload (increased preload or afterload)
What is the effect of long term remodelling on the stroke volume and end diastolic volume?
As end diastolic volume increases, stroke volume increases very little and begins to decline earlier than in a normal heart.
What occurs in ventricular remodelling?
Chronic pressure overload = hypertrophy
Myocardial injury or chronic volume overload = ventricular dilation
Describe the process of ventricular remodelling following an acute MI
Initial cardiac muscle infarction
Cardiac infarction spreads (over hours to days)
Global remodelling (days to months):
- The remaining healthy myocardium compensates but cannot compensate completely
- The ejection fraction reduces
- Increased pressure on the left ventricle due to increased volume causes eventual dilation
- This has additional complications such as stretching of the chordae tendinae.
Describe the process of ventricular remodelling in diastolic and systolic heart failure
- Hypertrophy caused by chronic hypertension leading to preserved ejection fraction heart failure.
- Hypertrophied muscle compensates initially but eventually fails due to lack of extra vascularisation to cope with extra muscle mass.
- This results in ischeamias and fibrosis of cardiac muscle.
- Ventricle dilates.
Describe the microscopic features of ventricular remodelling
Myocyte changes:
- Cell thinning and lengthening
- Hypertrophy
- Necrosis
- Apoptosis
Disorganised muscle fibre orientation
Extracellular matrix alterations and inflammatory changes
Describe the macropscopic features of ventricular remodelling
Loss of muscle mass
Alteration in chamber size (dilation/hypertrophy)
Dys-synchronous contractions
Describe the intracellular features of ventricular remodelling
Contractile protein structural and functional derangements
Disorganised cytoskeleton
Impaired cell-cell communication
Altered energy metabolism
Deranged excitation
What are the signs and symptoms associated with left ventricular failure?
What are these caused by?
Decreased cardiac output causes:
- Intolerance to exercise
- Signs of poor tissue perfusion
Pulmonary congestion causes:
- Pulmonary oedema leading to frothy sputum, orthopnoea, paroxysmal nocturnal dyspnoea.
- Impaired gas exchange → cyanosis and signs of hypoxia
What are the signs and symptoms associated with right ventricular failure?
What is the cause of these?
Right heart failure causes increase in venous pressure and congestion of peripheral tissues. This causes:
- Liver congestion → impaired liver function, hepatomegaly
- Reduced metabolism of certain hormones e.g. aldosterone → more sodium retention → increased intravascular volume
- Gi tract congestion → anorexia, GI distress, weight loss
- Dependent oedema and ascites
How does acute heart failure present?
- Dilated pupils (sympathetic)
- Skin pale, grey or cyanotic
- Dyspnoea
- Orthopnoea
- Crackles, wheeze
- Cough (+/- frothy white sputum)
- Low BP
- Nausea and vomiting (decreased peristalsis)
- Ascites
- Dependent, pitting oedema in legs/sacrum
- Anxiety
- Low O2 sats
- Confusion (decreased cerebral perfusion)
- Raised JVP
- Third heart sound (gallop)
- Enlarged spleen and liver
- Decreased urine output
- Weak pulse
- Cool, moist skin
Why does oedema occur in heart failure?
Increased hydrostatic pressure causes filtration to exceed absorption therefore there is a net loss from plasma (loss from plasma does not equal gain from plasma) and fluid is retained in the extracellular space.
Describe the compensatory mechanisms in heart failure
Fall in blood pressure from left ventricular failure leads to:
- Activation of the sympathetic nervous system (vasoconstriction, increased heart rate and contractility)
- SNS activates RAAS system
- Decreased renal perfusion
- Which activates RAAS system
RAAS system:
- Aldosterone:
- Increases sodium and water retention
- Circulating volume increases, eventually inhibiting renin release from kidneys.
- Causes myocardial fibrosis
- Coronary vasculopathy
- Angiotensin II causes:
- Vasoconstriction
- Which increases wall stress
- Myocardial fibrosis
- Increases sodium and water retention
Hepatic congestion results in reduced metabolism of aldosterone therefore extra aldosterone is present so its effects are increased.
How is acute decompensated heart failure treated?
Oxygen
Loop diuretics (fast acting)
- E.g. furosemide, bumetanide
GTN (spray/infusion)
cPAP if necessary
Inotropes
