CVS session 12: review, cardiac arrest and shock Flashcards
Where can poor perfusion occur?
Regional: e.g. limbs, heart, kidney, brain. Due to arterial occlusion (peripheral or coronary artery disease) or venous congestion (varicose veins or deep vein thrombosis)
Generalised: insufficient cardiac output to meet all the body’s needs. Affects kidneys and brain more
What is pressure the product of?
Flow and resistance
What is mean arterial blood pressure the product of?
heart rate x stroke volume x total peripheral resistance
i.e.
CARDIAC OUTPUT X TPR
Arterial occlusion causing peripheral vascular disease
Most common in lower limbs-same risk factors as for CHD. Due to partial occlusion of arteries by an atheromatous plaque: if radius becomes half of normal, flow is reduced to 1/16 (due to Pouiselle’s law regarding r ^4)
Pain with exercise will develop to pain at rest-intermittent claudication
Structural features of veins
Capacitance vessels:
- thin walls
- low pressure
- valves
- external compression by skeletal muscles (musculovenous pump)
Superficial vessels drain into deep vessles by perforating veins
Deep veins often run as venae comitantes along with the arteries
Veins contain ~70% of blood volume at any one time
Peripheral vascular disease due to venous problems
VARICOSE VEINS
- dilated, torturous superficial veins
- can be asymptomatic or cause venous ulcers
- often occur over the medial malleolus as the great saphenous vein passes anterior to this
DEEP VEIN THROMBOSIS
- major risk factor is stasis
- calf, popliteal, femoral and iliac veins
- causes tender, swollen calves/area where thrombus is
- risk of pulmonary embolism: chest pain and breathlessness
Coronary artery disease
Atheromatous plaque partially occludes a coronary artery. These are functional end arteries with few anastomoses, so leads to ischaemia:
- > 70% occlusion: compromised blood flow when O2 demand increases, diastole shortened in exercise so blood flow through LCA is reduced (so symptoms when exercise)
- 90% occlusion: ischaemia at rest
Stable angina
Brought on by exercise or stress, relieved by rest
Diagnosis:
- used to use exercise stress test: ECG, HR and BP monitored whilst exercise level gradually increased. Positive if symptoms or ECG changes
- or pharmacological stress test with increasing doses of beta-adrenoceptor agonist e.g. dobutamine
- ECG change is ST depression in leads affected
Treatment:
- nitrates (release NO for venodilation-not arterioles!). GTN spray for acute episodes, or a longer-acting. Reduce venous pressure returning heart so reduced preload so heart pumps less
- Beta blockers
- Ca2+ channel antagonists
Acute coronary syndromes?
Unstable angina
NSTEMI
STEMI
Unstable angina
Rapid onset pain at rest: severe central, may radiate less than an MI
Caused by disruption of an atherosclerotic plaque and thrombus formation, with limited duration and extent of obstruction. No detectable necrosis (troponin and cardiac enzymes not elevated)
ECG: ST depression and/or T wave inversion
Myocardial infarction
Symptoms: acute central chest pain radiating to neck, left shoulder and arm that is not relieved by rest (though some patients don’t get pain, especially diabetics), sense of doom, pallor (symp. vasoconstriction which increases TPR to try to maintain BP), sweating (circulating adrenaline and symp. release ACh)
Cause: rupture of atheromatous plaque forming a thrombus. It detaches or propagates along coronary artery and blocks it, causing myocardial necrosis
NSTEMI: necrosis more limited. ST depression and inverted T waves
STEMI: necrosis of full thickness of myocardial wall. ECG typically shows ST elevation, pathological Q waves and T wave inversion; most obvious in leads viewing the damaged myocardium
Describe the progression of ECG changes in an ST-elevated myocardial infarction
Acute: ST elevation
Hours: ST elevation, smaller R wave, pathological Q waves
Day 1-2: T wave inversion, Q wave deeper
Days later: ST normalises, T wave inverted
Weeks later: ST and T normal, pathological Q wave persists because part of the myocardium is dead
Describe the markers for an MI
Cardiac specific isoforms of troponins I and T: takes a while to increase beyond threshold for MI, so may not detect if arrive in hospital very quickly. Signal reaches maximum 18-36 hours following MI then takes about 6 days to tail off to pre-MI levels so can still detect if arrive late
CK-MB also used to be used
Define cardiac arrest
Unresponsiveness associated with a lack of pulse: heart has stopped or ceased to pump effectively
Describe the 3 types of cardiac arrest
ASYSTOLE: loss of electrical and mechanical activity
PULSELESS ELECTICAL ACTIVITY (PEA): dissociation between electrical and mechanical activity. Can be caused by severe hypoxia or a toxin that prevents the contraction mechanism occurring
VENTRICULAR FIBRILLATION
- most common
- fibrillating ventricle will not pump therefore no pulse due to depolarised damaged area of heart
- often following an MI, or due to electrolyte imbalance or arrhythmia (e.g. long QT and Torsades de Pointes)
