Cardiovascular physiology Flashcards
Turbulent flow
Reynold’s number = (velocity x diameter x viscosity)/density
Enables formation of of vortexes which provide the sound of murmurs/bruits
Laplace’s law and implications
Wall tension = (transmural pressure x radius)/(wall thickness x2)
As radius increases so does wall tension (pressure is constant in vasculature) and so aneurysms are more common in large arteries and are less stable as they grow.
As pressure increases in the heart chambers (e.g. LV), wall tension increases. To compensate, walls hypertrophy. If unable to compensate (e.g. post-MI, cardiomyopathy) then walls dilate
Vascular neurotransmitters
Noradrenaline - mainly acts on alpha-receptors. A1 = constrict, A2 = pre-synaptic inhibition.
Adrenaline - mainly acts on beta-receptors. B1 = heart, B2 = bronchial/smooth muscle wall constriction
Inotropes
Increase cardiac contractility in order to increase cardiac output (CO) e.g. in cardiac arrest, cardiogenic shock.
Adrenaline - beta-1 = increases contractility and HR. 0.05mcg/kg/min
Dobutamine - in doses of 5- 10mcg/kg/min
Isoprenaline
Vasopressors
Induce vasoconstriction in order to increase PVR e.g. sepsis, hypovolaemia
Noradrenaline - alpha-1 = vasoconstriction. Risk of reflex bradycardia and peripheral ischaemia. 0.05mcg/kg/min
Vasopressin - VR1 = vasoconstriction.
Phenylephrine
Reason for arterial and venous pressures
Transferring blood through the circulatory system affects pressures according to compliance. Veins are very compliant, arteries much less.
Cardiac output equation
CO = (ABP-RAP) / TPR
Preload
The initial stretching of the cardiomyocytes prior to contraction. Estimated as the end-diastolic volume
Determined by the ventricular filling pressure + ventricular wall compliance
Increases with venous return, slower HR (longer time to fill), atrial contraction, afterload.
MR/TR reduce preload due to decreased forward flow of blood
Afterload
The force against which the heart contracts to eject blood
Determined by myocardial wall stress (intra-cardiac) and input impedance (extra-cardiac)
Increases with outflow tract stenosis, peripheral HTN, chamber dilatation (increases transmural pressure)
Frank-Starling mechanism
LV stroke volume increases in proportion to the preload - increased preload = more myocyte stretch = more forceful contraction
The quality of this mechanism is dependent on the heart function and PVR.
The Bowditch effect
Increasing heart rate increases the force of myocardial contraction
Increased HR -> great Ca2+ influx + less time to efflux -> stronger contraction
Venous return
VR = (MSFP-RAP) / RvR
Resting vascular tone
Tonic action of postganglionic NA on alpha-1-adrenoceptors in the vasculature
- Has a resting tone so that inhibition can reduce this and cause vasodilation
- Postganglionic means that spinal cord damage above T1 can stop these signals and cause circulatory collapse
Heart rate
Basal activity via If in SAN/AVN/myocytes
PNS signals via [X] act on M2 receptors in the nodes to reduce HR
SNS signals act via systemic NA/Adr on beta-1-adrenoceptors in the nodes and myocyte tissue to increase HR
Coronary circulation
The coronary arteries originate under the coronary cusps of the aortic valve
Two main branches
- LCA -> LAD + LCX
- RCA
Dominance:
- Determined by which artery produces the posterior descending, supplying the apex
- 80% RCA, 20% LCX
LAD
- Supplies anterior LV and septum
- Subdivides into a number of perforating branches
- Proximal occlusion can affect a large area of the heart
