Ischaemic heart disease problems Flashcards
Give a classic prinzmetals angina scenario
Nocturnal chest pain accompanied by transient ST-segment elevation, an one episode of polymorphic ventricular tachycardia, coronary angiogram showed normal coronary arteries.
infusion of acetylcholine induced multifocal hyperactive vasoconstriction in some coronary segments but some vasodilatation elsewhere. Spasm resolved by intracoronary infusion of nitroglycerine
Prinzmetals angina: why nocturnal chest discomfort?
anginal pain and work of breathing increase, therefore pulmonary congestion?
PNS active at rest and at night –> Ach –> vsospasam
Symptoms worse when lying since
- Increased venous return leads to increased RV and LV filling
- Greater LV filling –> greater LV load and increased O2 demand
- Imparied LV function –> greater pulmonary congestion
Prinzmetals angina: why did the woman faint when she tried to get up?
Postural hypotension
- venous return reduced when standing (gravity, distends veins)
- reduced preload
- Reduced CO
- Leads to reduced MAP
- Leads to reduced cerebral perfusion (faint)
Give a possible reason as to why acheylcholine provoked vasospasm in some coronary segments and explain why this was reversed by nitroglycerine
Endothelial lining of BV’s responds to shear stress of Ach (via M3 receptors), by releasing NO which diffuses to the smooth muscle that is just outside the endothelial layer, and causes into relax.
But in this case we have Ach causing vasoconstriction not vasodilation with poorly functioning/ damaged endothelium Ach now acting directly on smooth muscle causing contraction
Give a possible reason why Ach provoked vasospasm in some coronary segments and explain why this is reversed by nitroglycerine
Nitroglycerin increases NO levels - act directly on VSM
Explain the ST segment elevation of her ECG during her angina attacks
Action potential magnitude and duration reduced in ischaemic region
Reflected in ST segment elevation leads “addressing” that region
- Current flowing in the tissue region when it shouldn’t be, either during systole or diastolie, region of the tissue thats ischaemic, normally in the plateau of the AP of the ventricular myocytes, there is no difference in potential anywhere in the myocardium, so isoelectric period normally zero on ECG, but because of ischaemic patch you cave current flowing where there shouldn’t be.
The mechanisms for ST segment elevation on an ECG
ST segment elevation occurs because when the ventricle is at rest and therefore repolarized, the depolarized ischemic region generates electrical currents that are traveling away from the recording electrode; therefore, the baseline voltage prior to the QRS complex is depressed (red line before R wave). When the ventricle becomes depolarized, all the muscle is depolarized during the ST segment so that zero voltage is recorded by the electrode (red line after R wave). When the ventricle is completely repolarized after the T wave, the baseline is once again negative as in the resting state. Therefore, the net effect of the depressed baseline voltage is that the ST segment appears to be elevated relative to the baseline.
Explain what is meant by the term polymorphic ventricular tachycardia
Abnormal QRS complexes that are changing shape throughout the tachycardia
Reentrant tachycardia requires?
trigger - delayed after depolarisations
unidirectional prorogation
relatively short wavelength (refractory period*conduciton velocity)
Why are the reentrant tachycardia requirements more probable in ischaemia?
Reduced ATP and thus Ca2+ ATPase activity –> Increased [Ca2+]i –> DADs
Spatial inhomogeneities in electrical properties
Shortened action potential duration as a result of hyperkalemia and activation of I(kATP) slow prorogation due to partial depolarisation (hyperkalemia), inactivation of sodium channels and gap junction uncoupling.
Why is the tachycardia polymorphic?
polymorphic VT reflects the fact that the reentrant circuit is not anchored on any anatomic structure (as is the case with head MI) but moves around within the ischaemic region.
How does nifedipine help a prinzmetals angina patient?
Ca2+ channel blocker - inhibits Ca2+ influx into cardiac and smooth muscle
2 mechanisms for pinzmetals angina
- Relaxation and prevention of coronary artery spasm
Dilates the main coronary arteries and arterioles, in normal and ischaemic regions
Is a potent inhibitor of coronary artery spasm, thus increasing myocardial O2 delivery in patients with coronary artery spasm
- Reuction of oxygen utilisation
Reduced arterial pressure at rest and at any given level of exercise
By dilating arterioles and reducing the TPR
This unloading of the heart reduces myocardial energy and O2 requirements
Why not use nitroglycerine in management of prinzmetals angina?
very short acting (half life 1-4 minuets, rapidly metabolised in live ray hepatic enzymes)
Tolerance issues
why is there elevated cardiac output and heart rate at rest during anaemia?
The only way we can meet oxygen demand is by Increasing Cardiac output,
Total peripheral resistance reduced
- local control (vasodilator mediated)
- Low viscosity (anaemia)
Increased ANS activity (to maintain BP and flow)
- Increase HR and inotropic state
- Increase CO
Why would an anaemic patient have large pulse pressure?
As a result of peripheral vasodilation (lowered total peripheral resistance) - leading to rapid runoff and lowered diastolic pressure
