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)
What is Torsades de Pointes?
A distinctive polymorphic ventricular tachycardia in which QRS amplitude varies and QRS complexes appear to twist around the baseline.
Usually not sustained and terminates spontaneously, but can develop into VF
Caused by long QT syndrome (congenital or acquired)
Management of cardiac arrest
Basic life support: chest compression and external ventilation
Advanced life support: defibrillation by electrical current delivery to heart which depolarises all the cells (puts them all into the refractory period) then allows coordinated electrical activity to restart. Shockable rhythms are VT and VF, non shockable are asystole and PEA
Adrenaline: enhances myocardial function. Acts on alpha 1 receptors on peripheral vasculature to increase TPR, this increases BP and helps blood flow to the heart
Define haemodynamic shock
An acute condition of inadequate blood flow throughout the body. A catastrophic fall in arterial BP leads to circulatory shock.
It can be due to:
-fall in cardiac output (mechanical failure, pump failure, loss of blood volume)
-fall in TPR beyond the capacity of the heart to cope (excessive vasodilation)
Cardiogenic shock (pump failure)
Acute failure of the heart to maintain cardiac output. May be due to MI (damaged LV), serious arrhythmias or acute worsening of heart failure
Heart fills but fails to pump effectively as ventricle cannot empty properly
- CVP may be normal or raised
- dramatic fall in arterial BP
Consequences:
- coronary arteries poorly perfused so exacerbates problem
- kidneys poorly perfused so reduced urine production (oliguria)
- brain not perfused properly so may lose consciousness
How might mechanical shock (obstructive issue meaning ventricle cannot fill properly) be caused?
- CARDIAC TAMPONADE
- blood/fluid in pericardial space so restricts filling limiting EDV; affects left and right sides as heart trapped by fibrous pericardium so can’t contract properly
- high CVP is hallmark (see raised JVP)
- low arterial blood pressure
- heart attempts to beat: continued electrical activity - MASSIVE PULMONARY EMBOLISM
- embolus occludes a large pulmonary artery, so PA pressure is high
- RV cannot empty; CVP high
- reduced return of blood to left heart so limits filling of left heart, so left atrial pressure is low
- arterial pressure low–>shock
- other symptoms-chest pain, dyspnoea
How much blood is lost for hypovolaemic shock to occur?
Causes of hypovolaemic shock?
Haemorrhage:
- Venous pressure falls, so CO falls (Starling’s law)
- Arterial pressure falls-detected by baroreceptors
Severe burns
Severe diarrhoea/vomiting and loss of Na+
Compensatory mechanisms activated by baroreceptors in hypovolaemia?
Increased sympathetic stimulation:
- tachycardia
- increased force of contraction (increased myocyte contractility, so steeper Starling curve)
- peripheral vasoconstriction (will increase TPR so help maintain BP)
- venoconstriction (help to maintain venous pressure and return blood to heart)
Internal transfusion:
- increased TPR reduces the capillary hydrostatic pressure
- net movement of fluid into the capillaries
- helps to boost blood volume to help to maintain blood pressure
Signs of hypovolaemic shock
Tachycardia
Weak thready pulse (as SV reduced)
Pale skin
Cold, clammy extremities
Decompensation in hypovolaemic shock?
Peripheral vasoconstriction impairs tissue perfusion:
- tissue damage due to hypoxia
- release of vasodilators
- TPR falls
- BP falls dramatically
- vital organs can no longer be perfused
- multi system failure
Longer term responses to restore blood volume?
RAAS
ADH
20% volume loss restored in about 3 days if salt and water intake are adequate
What is distributive shock?
Low-resistance shock (normovolaemic) i.e. normal CO but decreased TPR due to excess peripheral vasodilation (volume of circulation increased even though blood volume constant)
- toxic shock
- anaphylactic shock
Toxic shock i.e. septicaemia
Cause: endotoxins released by circulating bacteria:
- cause profound vasodialtion so dramatic drop in TPR and arterial BP
- impaired perfusion of vital organs
- capillaries become leaky causing reduced blood volume over time
Response: baroreceptors detect fall in arterial BP, increased sympathetic output so HR and SV increase but vasoconstrictor effect overriden by mediators of vasodilation
Signs: tachycardia, warm red extremities (vasodilation). Later stages vasoconstriction
Anaphylactic shock
A severe allergic reaction which causes:
- release of histamine from mast cells
- powerful vasodilation so fall in TPR
- dramatic drop in arterial BP. Increased sympathetic response increases CO but can’t overcome vasodilation
- impaired perfusion of vital organs
- mediators also cause bronchoconstriction and laryngeal oedema: difficulty breathing
Signs: difficulty breathing, collapse, tachycardia, red warm extremities
Acutely life threatening
Treatmnet: adrenaline. Vasoconstriction via action at alpha 1 adrenoceptors
Hypertension
Sustained increase in arteria BP ( > 140/90 mmHg)
BP regulated by kidneys (volume-alters SV), heart (CO-alters rate and force of contraction) and vasculature (regulates TPR)
Consequences: left ventricular hypertrophy, risk of heart failure. Risk of arterial disease: coronary arteries (MI/angina), cerebrovascular system (stroke), renal vasculature (kidney failure), retina, aorta
Treatment:
- non pharmacalogical ie weight loss, exercise, reduced salt
- pharmacological: diuretics, vasodilators, ACE inhibitors
