L19: Pathophysiology of heart failure Flashcards
What is heart failure?
Inability of the heart to meet the demands of the body
What do we mean by ‘demands of the body’?
Deliver a blood volume that allows body tissue to function as required
What is the official definition of heart failure?
Clinical syndrome of reduced cardiac output, tissue hypoperfusion, increased pulmonary pressure and tissue congestion
What enables the heart to work as an effective pump? What happens if these change?
Valves–> unidirectional, prevent backflow
Chamber size–> sufficient room for blood
Functioning muscle–> need muscle to contract to eject the blood
Changes can potentially lead to impaired cardaic function
What are the causes (aetiology) of heart disease?
1- Most common–> ischaemic heart disease (starvation of O2)
–> Myocardial dysfunction–> scarring–> fibrosis, remodelling of muscles
2- Hypertension ↑afterload–> pump against higher pressure, more difficult, and increased risk of athersclerosis
3- Arrhythmias–> heart contracting randomly, affects filling and emptying of chambers
4- Aortic stenosis–> difficult to pump blood out of the heart
5- Other valvular dysfunction or other myocardial structural diseases
6- Cardiomyopathies –> disease of the heart–> dilated, hypertrophic, restrictive
7- Pericardial disease–> disease of the pericardium –> prevents the heart from being able to relax and fill properly
8- Grossly elevated demand on CO–> severe anaemia, thyrotoxicosis, sepsis
Why is it important to identify the cause of heart failure?
Need to treat the cause
Prevent it happening again
How is cardiac function measured?
Cardiac output is measured CO= SV x HR CO--> volume delivered per minute SV--> volume ejected by ventricle each beat HR--> number of beats per minute
What is the ejection fraction? What does it show?
Percentage of blood ejected from the heart
Amount of blood ejected from ventricle each beat (SV)/ amount of blood in the ventricle at the end of diastole (EDV)
How well the heart is functioning
What influences the stroke volume?
Pre-load–> volume in the ventricles at the end of diastole–> stretch of the ventricles
After-load–> what the heart is having to pump against –> total peripheral resistance
Myocardial contractility–> ability of the heart to contract
What happens when the pre-load is increased in a normal healthy heart?
Increase the preload, increased the force of contraction
Frank-Starlings law –> more the heart fills= harder the heart contracts
Up to a point
More ventricular distension during diastole= greater volume ejected during systole
Why does an increase in pre-load result in an increase in contraction?
Increase pre-load, increase amount of blood in the heart
Means the myocardium is stretched- intrinsic property of myocytes
Actin and myosin aren’t as overlapped so have more area to overlap during contraction
This is up to a point–> over stretched–> actin and myosin don’t overlap at all–> reduced contraction
Other than stretch what can also influence Frank-Starling law of contraction?
Sympathetic input
Alters inotrophic state of the heart
Increase sympathetic activity increased CO for a given LVEDP (more volume is forced out)
Why is the cardiac output reduced in heart failure? Why?
Stroke volume is reduced
Reduced pre-load–> impaired filling of ventricles during diastole (rarely due to decreased venous return)
Reduced myocardial contractility–> muscle not able to produce same force of contraction for given volume
Increased afterload–> increased pressure to pump against e.g. increased TPR, valvular stenosis
In simple words what causes the heart to fail?
Filling problem - diastolic
Ejecting problem - systolic
What can cause the preload to decrease?
Impaired filling or space for filling reduced
- Ventricle chambers to stiff, not relaxing enough, less blood can enter
- Ventricle walls thickened (hypertrophic)–> taken up space in the chamber
What causes the systolic problems of heart failure?
Impaired ejection–> can’t pump with enough force
- Muscle wall thin/fibrosed–> fewer muscle cells for contraction
- Chambers enlarged (overstretched sarcomeres)–> actin and myosin don’t overlap so can’t interact
- Abnormal or uncoordinated myocardial contraction–> doesn’t contract as one so less blood ejected
What is the difference between sytolic and diastolic heart failure?
Systolic is a contraction (ejection) problem
Diastolic is a filling problem
How are the systolic and diastolic heart failures classified according to ejection fraction?
Heart Failure reduced Ejection fraction (HFrEF)–> systolic heart failure - contractility problem
Heart Failure preserved Ejection fraction (HFpEF)–> diastolic heart failure - filling problem
What is a normal ejection fraction? What ejection fraction would suggest heart failure?
Normal >50% (typically 60%)
Abnormal <40%
How is the ejection fraction measured?
Echocardiogram
Amount of blood pumped out the ventricle (SV)/ total amount of blood in ventricle (EDV)
Is it possible to maintain the EF but still be in heart failure? If so, how?
Yes it is
Filling problem - Diastolic heart failure
Less blood in the ventricle but still same amount (proportion) pumped out so ejection fraction the same but volume different
How are heart failures classified according to the ventricles involved?
Left ventricle failure–> most common
Right ventricle failure–> usually a result of LV failure, can occur in isolation or as a result of chronic lung disease
Involvement of both ventricles –> congestive heart failure–> biventricular failure
What happens when the pre-load is increased in a failing heart?
Little increase in CO
Big increase in LVEDV (pre-load)–> falling of CO and development of pulmonary congestion
What physiological mechanisms normally act to correct the decrease in CO?
Neuro-hormonal activation –> Increased sympathetic drive
Activate renin-angiotensin-aldosterone system–> increase BP/BV and sympathetic activity
What happens when the physiological mechanisms are activated in heart failure?
Neuro-hormonal activation
Baroreceptors detect decrease in BP–> Increase sympathetic drive–> Increases heart rate and increase total peripheral resistance (increase afterload)
Decreased BP–> decreased renal perfusion–> activation of renin-angiotensin-aldoterone system (RAAS)–> increase aldosterone (Na+ and H2O retention), increase ADH (decrease water loss) both act to increase preload–> RAAS increase vasoconstriction and enhances sympathetic activity increases afterload
However both increase demand on heart
Heart is failing results in more heart failure
What are the clinical signs and symptoms of heart failure?
Fatigue/ lethargy
Breathlessness
+/- oedema - leg swelling
How is tissue fluid normally developed?
Gradient between hydrostatic pressure and oncotic pressure
Higher pressure in the arterial circulation–> hydrostatic pressure» oncotic pressure so fluid moves out
Lower pressure in the venous circulation–> Hydrostatic pressure«_space;oncotic pressure so fluid moves in
Why do you get oedema in heart failure?
Increased capillary hydrostatic pressure prevents as much fluid being drawn back into the capillaries
Venous circulation–> hydrostatic pressure is increased due to backpressure from the heart–> means the gradient between hydrostatic and oncotic not as steep/ less favourable for fluid returning to capillary–> fluid remains in interstitium and builds up
Which oedema is associated with each type of heart failure? Why?
Peripheral oedema associated with Right ventricular heart failure–> due to back pressure from right side of heart into venous circulation
Pulmonary oedema associated with left ventricular heart failure–> back pressure from left side of heart into the pulmonary circulation
What symptoms are associated with left ventricular heart failure?
Lethargy/ fatigue
Breathlessness (exertional)
Orthopnoea–> breathlessness when lying flat
Paroxysmal nocturnal dyspnoea–> waking up in the night gasping for breath and having to sit up to relieve it
Basal pulmonary crackles
Cardiomegaly (displaced apex beat- indicates englarged LV)
What are the symptoms associated with right ventricular heart failure?
Fatigue/ lethargy Breatlessness Peripheral oedema (pitting) Raised jugular venous pressure Tender, smooth enlarged liver (liver congestion)
Why do you get orthopnoea and Paroxysmal nocturnal dyspnoea?
Breathlessness worse lying flat
1- Pulmonary oedema usually at base of lung when standing (gravity)- spreads out over lungs when lying down
2- Peripheral oedema is resolved on lying down (less pooling of blood due to gravity- more blood in system)
3- Vasodilation of capillaries at top of lung that are usually constricted due to gravity (negative pressure) so more blood in system
What causes Basal pulmonary crackles?
Fluid in the lungs
What does the jugular venous pressure show?
The pressure in the right side of the heart
Raised jugular venous pressure means that the pulse appears higher in the neck than normal
Indicates higher pressure in the right side
Normal height <3cm
Raised JVP >3cm
