What plasma K+ concentration constitutes hyperkalaemia?
And mild, moderate and severe hyperkalaemia?
What effect can hyperkalaemia have on the heart?
What are the treatments?
> 5.5mmol/L
Mild: 5.5-5.9mmol/L
Moderate: 6.0-6.4mmol/L
Severe: >6.5mmol/L (EMERGENCY)
- Membrane depolarises a bit.
- Increased number of inactivated Na+ channels means upstroke is slower - if sustained/severe can mean that threshold is not reached - ASYSTOLE
- May initially cause increased excitability - RMP is closer to threshold so more APs
TREATMENT:
- Calcium glauconite - Ca2+ makes heart less excitable
- Insulin + glucose - insulin promotes K+ moving into cells
How can heart failure lead to anaemia of chronic disease?
Reduced perfusion of kidneys leads to renal failure
This means less EPO is produced and so fewer new RBCs are made
Name an Angiotension II blocker. What is its mechanism of action?
Blocks AngII receptor type I
Prevents vasoconstriction and aldosterone-mediated Na+/H2O retention.
What is Eisenmenger’s syndrome?
Too much blood in pulmonary circulation due to e.g. Patent Ductus Arteriosus leads to pulmonary hypertension
This can lead to a reverse shunt R to L if there is a septal defect
What is patent ductus arteriosus? What does it lead to?
Communication between descending aorta and pulmonary artery persists after birth
Aorta has higher pressure so some oxygenated blood will flow into pulmonary artery and back to lungs –> increased pressure in lungs means they require more energy to inflate –> breathlessness
What happens in transposition of the great arteries? What needs to be present for an infant to be viable for life?
- Aorta arises from right ventricle and pulmonary trunk arises from left ventricle
- Likely due to incorrect formation of the aortic and pulmonary valves
- Blood returning to right side of the heart gets pumped back around body and oxygenated blood in left side gets pumped back to lungs
- Infant can only survive if there is a patent ductus arteriosus, atrial septal defect or ventricular septal defect.
What is coarctation of the aorta? How does it affect blood supply to the body?
Narrowing of the aorta in the region of the ligamentum arteriosum (former ductus arteriosus)
Increases afterload on LV –> LV hypertrophy
Vessels to head and limbs emerge proximal to coarctation - blood supply to them not compromised but leads to hypertension in arms and weak femoral pulses
Blood supply to rest of body reduced
What heart sound do you hear in aortic stenosis?
Crescendo-decrescendo murmur between S1 and S2
What heart sound would you hear in mitral valve stenosis?
Snap as valve opens followed by diastolic rumble
What causes aortic valve regurgitation? What are the consequences? What heart sounds would you hear?
CAUSES: Aortic root dilation, valve damage (endocarditis, rheumatic fever)
CONSEQUENCES: Blood flows back into LV during diastole - increases SV, increases systolic pressure, decreases diastolic pressure, bounding pulse (head bobbing and Quinke’s sign - cyclic change in nail bed colour)
SOUNDS: Early decrescendo diastolic murmur
Why does mitral valve regurgitation happen?
What are the consequences of this?
What sounds do you hear?
CAUSES:
- Chordae tendineae and papillary muscles normally prevent prolapse during systole - weakening of connective tissue e.g. Marfan’s syndrome, can weaken valve and cause it to prolapse.
- Damage to papillary muscles post-MI
- LSHF –> LV dilation –> stretched valve
- Rheumatic fever –> leaflet fibrosis
CONSEQUENCES:
As some blood leaks back into LA this increases preload as more blood then enters LV in subsequent cycles –> LV hypertrophy
SOUNDS: Holosystolic murmur (all of systole)
Which type of anaemia can result from aortic stenosis?
Microangiopathic haemolytic anaemia - due to shear stress on RBCs passing through the valve
