Cardiac Physiology Flashcards
Three features that optimise exchange of substances across capillaries
- low blood velocity
- large surface area
- Thin wall to minimise distance
Different types of capillaries
- Continuous - solute and water exchange paracellular diffusion, macromolecules trancytosis
- fenestrated - pores 20-100nm, allow water, solutes, peptides hormones to pass
- sinusoidal - larger molecules and cells can pass through
+ specialised
a. blood-brain barrier - continuous, tight junctions, gaps very small, specialised transport mechanisms e.g. GLUT1. Small lipid soluble molecules pass - CO2, O2, ammonia, steroids. Leaky if inflamed.
b. Glomerular - fenestrated 70-90nm pores. 4nm free filter, 8nm + excluded
Capillary flow mechanisms
- precapillary sphincters contract, pulsatile.
- increased by nitric oxide, H+, high temp, low PO2, high PCO2, lactic acid
Fluid shift across capillaries
- hydrostatic pressure drives fluid out
- oncotic pressure due to non-diffusible molecules albumin, globulin retains fluid
- starlings forces. alterations e.g. increased hydrostatic, reduced oncotic, leads to fluid leak
Causes of increased interstitial fluid volume
- Increased hydrostatic pressure e.g. fluid overload
- Reduced oncotic pressure e.g. malnutrition, hypoalbuminaemia
- Leaky capillaries - inflammation
- increased salt - fluid retention
Cardiac muscle structure
- Sarcomere = basic contractile unit, composed of thick filaments and thin filaments
- Sarcolemma = cardiomyocyte membrane. Deep invaginations T tubules enables rapid depolarisation
- Sarcoplasmic reticulum stores and releases calcium via RYR2 receptor
- Membrane receptors - myocytes respond to extracellular signalling - adrenergic, muscarnic
Cardiac muscle contraction
- Thick filaments = 200+ myosin
- Thin filaments surround thick = actin, troponin, tropomyosin
- Tropomyosin overlays myosin binding site on actin, locked into position by TnI and TnT
- Calcium release from SR due to membrane depolarisation, bind to TnC, causes tropomyosin to unbind from actin, allowing myosin head to bind to actin
- Myosin head pulls actin towards centre of sarcomere
Cardiac Cycle 7 phases
- Atrial systole
- Isovolumetric contraction
- Rapid ejection
- Reduced ejection
- Isovolumetric relaxation
- Rapid filling
- Reduced filling
JVP
Waves a-c-v
Descent x-y
a= atrial contraction
c = cusps of AV valves bulge back into atria
x = drop in atrial pressure due to relaxation
v = in ventricular systole, passive atrial filling
y = AV valves open and blood flows into ventricle
Myocardial action potential phases
0 = Na+ in
1 = K+ out
2 = Ca++ in (prolong refractory period)
3 = K+ out with Ca++ closed
4 = RMP Na+/K+ ATPase maintain potential -85mV
SA node / pacemaker action potential phases
4 = funny currents, slow leakage of Na+ into cell until -50mV. iCaT (transient) further inflow Ca++ to -40mV. Then iCaL (long) - sustained Ca++ in
0 = continued flow of Ca++. slow upstroke, no plateau
3 = Ca++ close, K+ open with outflow
Autonomic innervation of heart
- Sympathetic nervous system - activation leads to Adr / NA circulating, stimulated B1 receptors. In SA node increased Na and Ca permeability
- Parasympathetic - muscarinic ACh from vagus directly SAN and AVN. K+ leaks out causing hyper polarisation
Mechanisms regulating cardiac output
- Intrinsic rhythmicity SAN / AVN
- CVS receptor reflex - arterial baroreceptors
- Central factors - brainstem, cortex, hypothalamus
- Autonomic nervous system
- Biophysical properties - preload, after load, contractility
- Hormonal and metabolic
Baroreceptors
Mechanoreceptors that respond to stretch - reflex arc to maintain MAP
1. High pressure - aortic arch, carotid sinus. Increased MAP –> increased baroreceptor via IX and X to Nucleus Tractus Solitarius –> inhibition of SNS (rostral ventrolateral medulla) and activation of PNS (Nucleus Amibguus) to reduce MAP. Vice versa.
2. Low pressure e.g. vino-atrial (monitor blood volume), pulmonary artery, coronary artery
Autonomic regulation of cardiac function
- PNS inhibition of intrinsic pacemaker predominates at rest
- SNS - T1-T5 cardiac acceleratory fibres.
- chronotropic - SAN Na+ and Ca permeability
- inotropic - increase Ca++ release from SR, increased actin-myosin interaction
- lusitropic - shorten duration of contraction and increased relaxation
- PNS - long preganglionic fibres originate from vagal motor nuclei of brainstem. Short postganglionic effect SA / AVN