pathophysiology of cardiac failure tom grant ([email protected]) sammy case...
TRANSCRIPT
Define Cardiac Failure
Inability of the heart to pump blood forward at a sufficient rate to meet metabolic demands
Or
the ability to do so only when filling (diastolic) pressures are abnormally high
It’s a syndrome not a disease! The cause of the failure always needs to be determined!
What is pre-load, contractility and afterload?
Pre-load = Initial stretching of the cardiac myocytes prior to contraction
Contractility = force of contraction of the myocardium. Directly controls stroke volume by influencing end systolic volume.
Afterload = The tension or stress developed in the wall of the left ventricle during ejection
Fill in the table!
What’s the difference between left and right sided cardiac failure?
Left ventricular failure leads to pulmonary congestion as blood cannot be pumped forwards and so backs up into the lungs. This causes symptoms such as dyspnoea, paroxysmal nocturnal dyspnoea and orthopnoea (THINK! Cardiac history taking).
Right ventricular failure leads to systemic congestion as blood cannot be pumped forwards and so fluid accumulation generates in the body. This causes symptoms such as ascites, sacral and ankle oedema and nocturia.
What are the four stages of cardiac failure?
Class I - no limitation of physical activity, Ordinary physical activity doesn't cause undue breathlessness, fatigue or palpitations
Class II - slight limitation of physical activity. Comfortable at rest but ordinary activity causes undue breathlessness and fatigue.
Class III - marked limitation of physical activity. Comfortable at rest but less than ordinary activity causes undue breathlessness and fatigue.
Class IV - unable to carry on any physical activity without discomfort. Symptoms may be present at rest.
Ventricular Remodelling Chronic volume overload = ventricular
dilation.
Chronic pressure overload = hypertrophy
Initial remodelling phase results in repair -> beneficial (improvement in or maintenance of LV function and cardiac output)
Over time, however, as the heart undergoes ongoing remodelling, it becomes more spherical. Ventricular mass and volume increase = cardiac function. Eventually, diastolic function may become impaired, further causing decline.
A patient presents to A&E with dyspnoea, ascites, a raised JVP and ankle oedema. An on call doctor examines the patient and diagnoses them with heart failure. What sided heart failure would present in this way?
- Right
What is another name for pulmonary heart disease?
- Cor Pulmonale
What are the first line treatment options for this?
- Oxygen, diuretics (furosemide), methylxanthine bronchodilators (theophylline), inotropic drugs (digoxin), IV vasodilator (nitrate)
What is a possible complication to the liver that can occur?
- Nutmeg liver
Consider the definition of heart failure:
1. Metabolic demands have been increased
2. The heart output has been decreased
There are two reasons the heart might not be meeting metabolic demands:
Inability of the heart to pump blood forward at a sufficient rate to meet metabolic demands Orthe ability to do so only when filling (diastolic) pressures are abnormally high
A professional and dedicated stamp licker, Brintha Nanthakumar, 36, enters the clinic. She has a known history of anaemia and thyrotoxicosis. She complains that recently she has been getting short of breath, tired and that her shoes don’t seem to fit her anymore. She wonders if this is because of the anaemia, and is surprised when you assess her for heart failure. Why do you want to assess her for heart failure? (3)Anaemia and thyrotoxicosis are both causes of high output cardiac failure
Anaemia = less RBC/haemoglobin = less oxygen in blood = increased cardiac output in order to adequately perfuse tissues -> cardiac compensation
Thyrotoxicosis = increased metabolic demands of body = increased cardiac output in order to meet increased metabolic demands -> cardiac compensation
Compensatory mechanisms
Remember! Heart failure is the inability of the heart to pump blood forward at a sufficient rate to meet metabolic demands
This results in low blood pressure systemically which is detected by the body. Compensatory mechanisms are initiated to counteract this.
How can the heart compensate when it is failing to meet metabolic demands? (4)
1. Ventricular hypertrophy
2. Neuronal (sympathetic) stimulation (activated by low BP/stretch on baroreceptors in aortic arch/carotid sinus)
1. ↑HR
2. ↑Contractility
3. Venous constriction -> ↑Preload -> Frank Starling Mechanism*
4. ↑Arteriolar constriction
3. Hormonal stimulation (RAAS) (activated by reduced renal perfusion (due to initial low BP))
1. ↑Fluid retention -> ↑Preload -> Frank Starling Mechanism*
2. ↑Arteriolar constriction
4. Frank Starling Mechanism** (due to increased end diastolic pressure)
*Increased venous return following hormonal and neuronal stimulation leads to increased cardiac output due to the Frank Starling mechanism.
**Both systolic and diastolic dysfunction result in a higher ventricular end-diastolic pressure, which serves as a compensatory mechanism by utilizing the Frank-Starling mechanism to augment stroke volume
Frank Starling Mechanism
Stroke volume of the heart increases in response to an increase in the volume of blood filling the heart when all other factors remain constant.
This allows cardiac output to be synchronized with venous return and arterial blood supply without depending upon external regulation.
Makes its biggest contribution to increasing stroke volume at lower work rates.
Neurohormonal activation
BP = CO * SVR
Neurohormonal activation increases BP:
- Sympathetic NS activation = tachycardia and vasoconstriction
- RAAS = vasoconstriction and salt/water retention
- ADH = salt/water retention
BUT
Atrial natriuretic peptide and brain natriuretic peptide counteract these mechanisms. They are released in response to atrial or ventricular stretch. Elevated ANP/BNP is an early indicator of heart failure.
A 40 year old man, Dan Waite, enters your clinic. He has a history of aortic valve stenosis, caused by rheumatic fever as a child. He says that recently when he has been chewing on his toenails he has been getting short of breath, and that this activity tires him out much faster than it usually does.
Symptoms are in keeping with this diagnosis
Aortic valve stenosis -> Increased afterload -> Increased functional demand on the heart -> Compensation
You suspect heart failure. Why? (2)
Pulmonary oedema (due to increased pulmonary venous pressure)
Why is the patient short of breath? (1)
Why does he find that sleeping with more pillows has been helpful? (1) Increased drainage of pulmonary vessels with gravity (reduced
hydrostatic pressure)
You ask Dan if you can take his blood pressure. He says yes, and takes off his shirt before you can stop him. This confuses you slightly, but he does appear to be quite a strange fellow. You take his BP. It is 160/94.
Initially reduced CO -> Reduced kidney perfusion -> Activation of RAAS system -> Fluid retention (increasing preload) and vasoconstriction (further increase in afterload) -> Increased blood pressure
Initially reduced CO -> Initial BP reduction -> Activation of baroreceptors (aortic arch and carotid sinus) -> Increased sympathetic stimulation -> Increased HR and vasoconstriction -> Increased blood pressure
Why might this patient’s BP be elevated? (4)
Left ventricular hypertrophy *NOT hyperplasia
An echocardiogram is performed on the patient, which reveals enlargement of the left ventricle.
What term is given to this? (1)
Why have the myocytes undergone hypertrophy? (1) In response to increased functional demand (contracting against
increased afterload) – this is pathological hyperplasia
As left ventricular hypertrophy progresses, will the heart continue to pump blood out at a greater rate? (1)
No – As ventricle walls grow thicker, they lose elasticity and fail to pump with as much force as that of a healthy heart
When might LVH not be pathological? (1) LVH can occur due to aerobic exercise and strength training (due to
increased metabolic demands of the body) – This type of physiological hypertrophy is reversible and non-pathological
Displacement of the apex beat
What might we look for on clinical examination to assess left ventricular hypertrophy? (1)
Where is the apex beat normally found on a patient?
a) Mid-axillary line, 5th ICS, left hand side
b) Mid-axillary line, 4th ICS, left hand side
c) 4th-5th ICS, parasternal, left hand side
d) Mid-clavicular line, 5th ICS, left hand side
e) Mid-clavicular line, 4th ICS, left hand side
Mid-clavicular line, 5th ICS, left hand side
SV/EDV=EF
50/140= 0.357 = 36%
Dan’s ESV is 90ml and his EDV is 140ml. What is his ejection fraction? (1)
What does this mean? (1)
In systole the heart pumps out 36% of the blood from the ventricles
At what ejection fraction do we diagnose systolic heart failure? (1) <40%
What ejection fraction is considered normal? (1)
55-75% (depends on source)