Haemodynamics Flashcards
control of arterial blood pressure
and the formulas
control CO and peripheral resistance
- mean arterial BP = CO x TPR
- CO = SV x HR
- mean arterial BP= SV x HR x TPR
- maBP = diastolic pressure + 1/3 pulse pressure
haemodynamic shock and the formula that goes with it
- acute condition of inadequate blood flow throughout the body
- catastrophic fall in arterial blood pressure leads to circulatory shock
- mabp = co x TPR
- so CO must fall or TPR fall beyond the heart can cope for
what can cause decrease in MAP adn cause shock
decrease CO
- mechanical - pump cant fill (so cant meet bodies 9demands) (mechanical shock)
- pump failure (cardiogenic shock)
- loss of blood volume (hypovolaemic shock)
fall in peripheral resistance
- excessive vasodilation
shock due to decrease in cardiac output
- cardiogenic shock (due to pump failure) ventricles dont empty properly
- mechanical shock( obstructive) ventricles cant fill properly
- hypovolaemic shock : reduced blood volume leads to poor venous return
cardiogenic shock
- failure of ventricles to empty properly
- so cant maintain cardiac output
- causes:
- mi (damage to left ventricle, fibrosis so muscles dont contract)
- serious arrythmias (heart block too slow or tachycardia)
- acute worsening heart failure
- central venous pressure CVP may be normal or raised
- dramatic drop of arterial BP
- tissues poory perfused;
- coronary arteries may be porrly perfused causes worsening problems
- kidney not well perfused so dark small amounts of urine
mechanical shock
- cardiac tamponade
- blood or fluid build up in pericardial spcae restricts fillings of the heart limiting end diastolic volume, affects left and right side of heart
- patients has high central venous pressure so have raised jugular
- low arterial bp because heart cant fill
what can also cause mechanical shock
pulomnary embolism by increaseing pulomnary pressure so high pulmonary artery pressure, RV cant empty, central venous pressure high, reduced reutn of volume of b to left, so reduce stroke volume be less blood can be umped out by the left
so chestpain and angina
how does embolus reach the lungs and types of PE
deep vein thrombosis
portion of embolism breaks off
travels in venous system to right side of heart
pumped out via pulmonary artery to lungs adn can cause occlusion depening on how big it is
saddle embolism
- massive pe; >60% reduction in blood flow, rapidly fatal (saddle embolism especially can be more fatal)
- major pe; medium sized vessels are blocked, patients are short of breath +/- cough and blood stained sputum
- minor pe ; small peripheral pulmonary arteries blocked. asymptomatic or minor shortness of breath (recurrent minor PE can cause pulomnary hypertension)
hypovolaemic shock
- reduced blood volume
- most commonyl due to haemmorrhage
- <20% of blood loss is not going to cause shock
- 20-30% some signs of shock
- 30-40% substantial decrease in mean aBP and serious shock
- shock is dependent on speed of blood loss and amount of blood loss
what are the reasons for hypovolaemic shock and how does body cope with this?
haemmorhage
- venous pressure drops
- CO failure (starlings law, the ventricles arent being stretched much so heart not contracting as much)
- arterial bp drops
- detected by baroreceptors
- COMPENSATORY RESPONSE
- increased sympateric stimulation so tachycardia
- increased force of contraction
- peripheral vasoconstriction
- venoconstriction
what changes in capilaries occurs in hypovolaemic shock
- reversed due to decrease in venous pressure so decreased hydrostatic pressure and theres vasoconstriction for compensatory response to keep arterial blood pressure maintained (this though causes the pressure downstream in the veins to be low)
- so now instead of fluid moving out, the pressure gradients favour the movement of fluid into the capillaries wc is called internal transfusion
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how does a patient with hypovolaemic shock present and what are ‘minor’ ways to get hypovolaemic shock
- tachycardia (due to the sympathetic nervous system)
- weak pulse
- pale skin (due decreased blood volume)
- cold clamy extermities (due to sYMP)
- low cvp (centralvenous pressure
severe burns/ severe diarrhoae or vomitting an dloss of NA+
what is a complicaiton of long term (not too long term) hypovolaemic shock dangerous and how do you treat?
-
DANGER OF DECOMPENSATION (compensation failure over long period time)
- peripheral vasoconstriction (shutdown) impairs tissue perfusion
- tissue damage to hypoxia
- release chemical mediators - vasdoidlators
- these vasodilators are working against the compensatory mechanisms of the body (symp) and so vasodilation overcomes vasoconsitrcion so TPR fails
- blood pressure fails dramatically
- vital organs can no longer be perfused
- multi system failure
fluids and ADH adn RAAS agonists
what are wsys to restore blood volume
- RAAS and ADH and fluids
- 20% blood volume loss takes 3 days restoration
cardiac arrest what is it and how to treat?
unresponsiveness assocaiated with lack of pulse
heart has stoppped or has ceased to pump effectively
asysyole (loss of electrical activity adn mechanical activity)
pulseless electrical activity
ventricular fibrillation
-
basic life support (chest compression
- advanced life support (defib to depolarise whole heart at once putting it into refractory period and to restart it) BUT YOU GIVE ADRENALINE AT THE SAME TIME (to enhance mycocardial function adn it alos acts on a1 receptors on vessels to increase blood pressure )
