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Final FRCA SOE > Cardiac Physiology > Flashcards

Cardiac Physiology Flashcards

1
Q

Three features that optimise exchange of substances across capillaries

A
  1. low blood velocity
  2. large surface area
  3. Thin wall to minimise distance
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2
Q

Different types of capillaries

A
  1. Continuous - solute and water exchange paracellular diffusion, macromolecules trancytosis
  2. fenestrated - pores 20-100nm, allow water, solutes, peptides hormones to pass
  3. 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
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3
Q

Capillary flow mechanisms

A
  • precapillary sphincters contract, pulsatile.
  • increased by nitric oxide, H+, high temp, low PO2, high PCO2, lactic acid
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4
Q

Fluid shift across capillaries

A
  • 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
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5
Q

Causes of increased interstitial fluid volume

A
  1. Increased hydrostatic pressure e.g. fluid overload
  2. Reduced oncotic pressure e.g. malnutrition, hypoalbuminaemia
  3. Leaky capillaries - inflammation
  4. increased salt - fluid retention
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6
Q

Cardiac muscle structure

A
  • 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
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7
Q

Cardiac muscle contraction

A
  • 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
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8
Q

Cardiac Cycle 7 phases

A
  1. Atrial systole
  2. Isovolumetric contraction
  3. Rapid ejection
  4. Reduced ejection
  5. Isovolumetric relaxation
  6. Rapid filling
  7. Reduced filling
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9
Q

JVP

A

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

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10
Q

Myocardial action potential phases

A

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

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11
Q

SA node / pacemaker action potential phases

A

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

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12
Q

Autonomic innervation of heart

A
  • 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
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13
Q

Mechanisms regulating cardiac output

A
  1. Intrinsic rhythmicity SAN / AVN
  2. CVS receptor reflex - arterial baroreceptors
  3. Central factors - brainstem, cortex, hypothalamus
  4. Autonomic nervous system
  5. Biophysical properties - preload, after load, contractility
  6. Hormonal and metabolic
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14
Q

Baroreceptors

A

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

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15
Q

Autonomic regulation of cardiac function

A
  • 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
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16
Q

Hormones influencing autonomic control of cardiac function

A

Adrenal medulla –> Adr, NA
Post. pituitary –> Vasopressin
Thyroid –> T3/4
Hypothalamus –> dopamine
RAAS

17
Q

Metabolic factors affecting cardiac function

A

Electrolytes - Ca++ contractility, K+ (higher leads to slower conduction)
Acidosis - H+ competes with Ca++ leading to reduced contractility
Hypoxia - best inotrope
Temperature

18
Q

Stimulation of ADH release

A
  • SNS
  • AngII
  • Increased osmolality
  • Hypovolaemia
  • Hypotension
19
Q

ADH effects

A

V1 receptors - vasoconstriction
V2 receptors - renal H2O reabsorption, increasing blood volume

20
Q

RAAS

A
  • 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
21
Q

ANP / BNP

A

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

22
Q

Pressure-volume loops

A

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

23
Q

Frank-Starling Law

A

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

24
Q

LaPlace’s Law

A

P = 2Th/r
P= pressure
T = tension
h = thickness
r = radius

25
Q

Preload, afterload, contractility

A

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)

26
Q

Mean arterial pressure

A

Diastolic + 1/3(Systolic - Diastolic)

27
Q

Valsava maneouvre

A

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.

28
Q

Function of circulation

A
  • Exchange O2 / CO2
  • Distribute nutrients
  • Remove waste products
  • Temperature control
  • Distribute endocrine secretions
  • Fight infection
  • Prevent bleeding or thrombosis
29
Q

Layers of blood vessels

A

Tunica intima - innermost, squamous endothelium
Tunica media - elastic, connective tissue, smooth muscle
Tunica adventitia - outermost connective tissue, nerves

30
Q

Properties of vascular endothelium

A

Regulate vasomotor tone
- vasodilators - NO, prostacyclin
- vasoconstrictors - TXA2
Non-thrombogenic - Protein C / S
Smooth surface - laminar flow
Growth of surrounding tissue

31
Q

Flow

A

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

32
Q

Viscosity

A

internal friction of adjacent fluid layers. increased by
- high haematocrit
- lower temperature
- lower flow rate

Final FRCA SOE (11 decks)

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