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
Hormones influencing autonomic control of cardiac function
Adrenal medulla –> Adr, NA
Post. pituitary –> Vasopressin
Thyroid –> T3/4
Hypothalamus –> dopamine
RAAS
Metabolic factors affecting cardiac function
Electrolytes - Ca++ contractility, K+ (higher leads to slower conduction)
Acidosis - H+ competes with Ca++ leading to reduced contractility
Hypoxia - best inotrope
Temperature
Stimulation of ADH release
- SNS
- AngII
- Increased osmolality
- Hypovolaemia
- Hypotension
ADH effects
V1 receptors - vasoconstriction
V2 receptors - renal H2O reabsorption, increasing blood volume
RAAS
- Renin release due to reduced tubular pressure, reduced tubular Na, increased SNS (hypovolaemia)
- AngII effects
1. Vasoconstriction
2. ADH release
3. SNS increased
4. Aldosterone - Na/H2O retention
ANP / BNP
ANP = atrial BNP = ventricular
released in response to stress
reduce preload by excretion of Na and H2O
reduce after load by relaxation of smooth muscle
Pressure-volume loops
EDPVR
- LV Elastance (change in pressure per unit change in volume).
- Normal LV low Elastance (wide range of volume, minimal change in pressure)
- For given volume, pressure increased in stiff ventricle (curve up and left). Increased pressure may be transmitted to LA, lungs
ESPVR
- End-systolic pressure - left behind at end of systole. Max pressure generated by LV for given volume
- ESPVR - different pressure at different volumes. Linear.
- Vaguely represents contractility
- Slope of ESPVR - increased gradient with increased contractility (higher pressure for given volume)
Effective arterial Elastance (eEa)
- As LV ejects in aorta, LV stroke volume enters artery. As it receives SV, arterial pressure increases. The relationship of increase in pressure to volume is Ea
- Increased Ea = steeper curve. Increased LVESP and reduced SV
- Representation of after load
Frank-Starling Law
Contractile force of cardiac muscle is proportional to initial fibre length
x axis = index of resting fibre length e.g. LVEDV
y axis = index of contractility e.g. SV
LaPlace’s Law
P = 2Th/r
P= pressure
T = tension
h = thickness
r = radius
Preload, afterload, contractility
Preload = myocardial sarcomere length just prior to contraction. Best approximation is EDV
Contractility = power of ventricle for given preload and after load
Afterload = resistance to ventricular ejection
- myocardial wall stress (intracardiac)
- input impedance (extracardiac)
Mean arterial pressure
Diastolic + 1/3(Systolic - Diastolic)
Valsava maneouvre
Respiratory effort against a closed glottis, generates Intrathoracic pressure of 40mmHg for 15 seconds
Phase 1 - increased Intrathoracic pressure, reduced venous return. Increased BP due to reduced afterload and increased LV preload (displacement of blood). Reduced HR - Baroreflex
Early phase 2 - decreased CO due to sustained Intrathoracic pressure reducing LV preload. Increased HR due to low BP
Late phase 2 - restored CO by tachycardia, restored BP by SNS from Baroreflex increasing SVR
Phase 3 - release of Intrathoracic pressure (opening glottis). Increased RV preload and reduced afterload due to reduced Intrathoracic pressure. Decrease LV preload, increased LV afterload. Decreased BP, baroreceptor mediated increased HR
Phase 4 - Restored LV preload, transient increase in BP as increased preload, high SVR. HR decreases - baroreceptor response to higher BP.
Function of circulation
- Exchange O2 / CO2
- Distribute nutrients
- Remove waste products
- Temperature control
- Distribute endocrine secretions
- Fight infection
- Prevent bleeding or thrombosis
Layers of blood vessels
Tunica intima - innermost, squamous endothelium
Tunica media - elastic, connective tissue, smooth muscle
Tunica adventitia - outermost connective tissue, nerves
Properties of vascular endothelium
Regulate vasomotor tone
- vasodilators - NO, prostacyclin
- vasoconstrictors - TXA2
Non-thrombogenic - Protein C / S
Smooth surface - laminar flow
Growth of surrounding tissue
Flow
Volume of blood moving per unit time
Hagan-Poiseuilles equation PDTTr4 / 8nl
Resistance inverse
Laminar = smooth layers parallel to vessel wall, central highest veolicyty
Re < 2000
Turbulence increases energy required to drive flow
Viscosity
internal friction of adjacent fluid layers. increased by
- high haematocrit
- lower temperature
- lower flow rate
