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Primary FRCA > Physiology 6 > Flashcards

Physiology 6 Flashcards

1
Q

How does smooth muscle structure differ from skeletal muscle?

A
  • Irregular arrangement of actin and myosin filaments (so no striped appearance)
  • SM does not contain troponin
  • No Z lines but actin filaments bound to dense bodies instead
  • SM does not have t-tubules and has a poorly developed sarcoplasmic reticulum
  • SM contains few mitochondria and ATP is mainly produced through glycolysis
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2
Q

What are the types of smooth muscle?

A
  • Visceral (single unit)

- Multi-unit

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3
Q

How are APs passed from myocyte to myocyte in smooth muscle?

A
  • Visceral SM cells are connected by gap junctions, allowing APs to travel to connected cells.
  • Multi-unit SM cells are not connected via gap junctions. Each cell has its own nerve ending.
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4
Q

Outline the events leading to contraction of smooth muscle

A
  1. AP triggers opening of voltage-gated calcium channels on the myocyte surface, causing influx of calcium from extracellular fluid.
  2. Calcium binds intracellularly to calmodulin, activating calmodulin-dependent light chain kinase
  3. Light chain kinase catalyses phosphorylation of myosin head, activating myosin ATPase.
  4. Hydrolysis of ATP provides energy for formation of actin-myosin cross-bridges, producing SM contraction.
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5
Q

How does speed and length of contraction differ in smooth muscle from skeletal muscle?

A

Contraction and relaxation are slower in smooth muscle and last for longer.
Actin-myosin cross-bridges may remain attached for a period after Ca2+ levels fall, this is called the ‘latch-bridge mechanism’ and produces an energy-efficient sustained contraction.

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6
Q

How does a smooth muscle contraction end?

A

Relaxation occurs when calcium levels drop causing dissociation of the calcium-calmodulin complex. Myosin is dephosphorylated by myosin light chain phosphatase.

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7
Q

Outline the concept of smooth muscle plasticity

A

When stretched, smooth muscle tension initially increases, but beyond a point it decreases and may fall below the initial tension.

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8
Q

How does visceral smooth muscle membrane potential differ from other membrane potentials

A

The visceral SM membrane potential is unstable, with an average value of around -50 mV.
APs are generated spontaneously due to oscillations in the potential, independent of nerve supply.

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9
Q

How does increased parasympathetic tone affect visceral smooth muscle function?

A

ACh from parasympathetic nerve endings bind to M3 receptors. These G-protein coupled receptors act via phospholipase C activation and IP3 production to increase intracellular calcium.

GI: Increased motility, relaxation of sphincters, increased secretion

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10
Q

How does increased sympathetic tone affect visceral smooth muscle?

A

Mediated via alpha- and beta-receptors.

Alpha-receptors activate phospholipase C (PLC) via IP3 and diacylglycerol.

Beta receptors act via G-proteins to stimulate adenyl cyclase and increase IC cAMP

Both mechanisms decrease free intracellular calcium levels, inhibiting SM contraction.

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11
Q

Outline the effect of nitric oxide in vascular smooth muscle function

A

NO is produced by the vascular endolthelium by nitric oxide synthase (NOS) which is activated by increased intracellular calcium, eg. from ACh action or mechanical stretch.

NO then diffuses into adjacent smooth muscle activating guanylyl cyclase to produce cGMP from GTP.

cGMP activates protein kinases leading to reduced SM intracellular calcium and relaxation.

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12
Q

Define cardiac index

A

CO / BSA (m²)

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13
Q

What are the main factors regulating cardiac output?

A
  • cardiac intrinsic rhythmicity from SAN and AVN
  • cardiovascular receptor reflexes
  • Central control from brainstem, hypothalamus, cerebellum and cortex
  • autonomic nervous system
  • biophysical factors affecting CO
  • hormonal and metabolic factors
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14
Q

What is the initial membrane potential of sinoatrial node cells?

A

-50 to -70 mV

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15
Q

How are baroreceptors classified?

A

High and low pressure

High pressure: carotid sinus and aortic arch receptors

Low pressure: myelinated venoatrial receptors, non-myelinated receptors in atria, ventricles and pulmonary artery, coronary artery receptors

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16
Q

Describe the high pressure baroreceptor reflex arc

A

Baroreceptors in the carotid sinus and aortic arch send afferent fibres via the glossopharyngeal nerve (CN IX) and the vagus nerve (CN X) respectively to the nucleus tractus solitarius (NTS) in the dorsomedial medulla.
Efferent reflex innervation is via the sympathetic and parasympathetic nervous system

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17
Q

Outline the function of the myelinated venoatrial baroreceptors

A

To signal central blood volume.
An increase in central filling causes the seemingly paradoxical ‘Bainbridge reflex’ tachycardia which serves to move blood from a congested venous system to the arteries.

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18
Q

Outline the function of the non-myelinated baroreceptors

A

Found in the LV, atria and pulmonary artery, these receptors send a weak signal via vagal and sympathetic afferents and cause a reflex bradycardia and vasodilatatory response to cardiac distension.

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19
Q

Explain the role of the nucleus tractus solitarius in coordinating the response to changes in cardiovascular status

A

NTS receives baroreceptor afferents and is the main relay centre for nervous cardiac control.

In response to falling MAP, the NTS activates the rostral ventral lateral medulla (RVLM) which in turn activates the sympathetic nervous system to increase MA

In response to increasing MAP, the NTS activates the nucleus ambiguus (NA) which increases vagal parasympathetic tone, reducing MAP. The NTS also relays via the caudal ventrolateral medulla (CVLM) which decreases RVLM activity.

The NTS also receives input from the cortex, hypothalamus and medulla, modulating response

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20
Q

What role does the periaqueductal grey matter (PAG) play in cardiovascular control?

A

Lateral areas are involved in vasoconstriction and hypertension and ventrolateral areas are involved in vasodilation and hypotension

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21
Q

How does stress affect cardiac function?

A

Stress causes the hypothalamus to activate the RVLM, causing increased sympathetic tone.
Strong emotions eg fear activate the limbic system which further enhances the hypothalamic response.
The cerebral cortex may modulate these responses further.

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22
Q

How does increased sympathetic tone affect cardiac chronotropy?

A

Increased permeability of SAN cells to calcium and sodium, thus decreasing the length of phase 4 decay due to a more positive starting potential - increasing heart rate.

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23
Q

How does increased sympathetic tone affect cardiac inotropy?

A

Increases permeability to calcium ions, especially during phase 2 of cardiac AP.
Increases Ca2+ in sarcoplasmic reticulum.

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24
Q

How does increased sympathetic tone affect cardiac lusitropy?

A

Decreases length of contraction and increases speed of relaxation to preserve diastolic filling.

25
Q

How does increased parasympathetic tone affect cardiac chronotropy?

A

Increased K+ permeability of SAN and AVN, causing membrane hyperpolarisation and thus a longer decay to threshold, reducing heart rate

26
Q

How does increased parasympathetic tone affect cardiac inotropy?

A

Less effect than sympathetic system.

Parasympathetic stimulation may decrease contractility by 20-30%

27
Q

List the key hormones affecting cardiac function

A 
Adrenal: Adrenaline, noradrenaline
Hypothalamic: Dopamine
Posterior pituitary: Vasopressin
Thyroid: T3, T4
RAAS: Rennin, angiotensin, aldosterone
Cardiac: ANP, BNP
28
Q

What are the key metabolic factors affecting cardiac function?

A

Electrolytes
Acid-base balance
Oxygen
Temperature

29
Q

Outline the action of catecholamines in regulation of cardiac function

A

Adrenaline and noradrenaline are released from the adrenal medulla in a 4:1 ratio.

They exert their CVS effects through α- and β-adrenoreceptors.

α1: Cause IP3-mediated increase in IC Ca2+ causing vascular smooth muscle contraction, especially in skin, splanchnic bed, arteries and veins. Norad has greater potency than adrenaline. Causes increased SBP and DBP, causing reflex brady.

β1: Cause increased HR and myocardial contractility, increasing CO and O2 demand.

β2: Cause cAMP-mediated smooth muscle relaxation, particularly in skeletal vascular bed. Adrenaline has greater potency than norad.

Dopamine also exerts positive α- and β- effects.

30
Q

Discuss dopamine’s role in cardiovascular regulation

A

A catecholamine released from the hypothalamus. Precursor of noradrenaline.
Agonist at α- and β-adrenoceptors and DA receptors DA1 and DA2.

DA1R: mediate vasodilatation of renal, mesenteric and cerebral circulation.

DA2R: Presynaptically inhibit noradrenaline release.

31
Q

Discuss vasopressin and its role in CVS regulation

A

aka. ADH, a peptide hormone released from posterior pituitary in response to increased plasma omsolality, hypovolaemia, angiotensin II, pain, stress and exercise. Its two main effects are:
1. Water retention and volume expansion: via V2 receptors in the renal collecting ducts increasing aquaporin 2 expression. Increases cardiac preload.
2. Arteriolar constriction: via V1 receptors which increase intracellular calcium. Increases arterial pressure and afterload.

32
Q

Discuss the thyroid hormones and their role in CVS regulation

A

T3 and T4 regulate metabolism and influence cardiac function via a positive chronotropic and inotropic effect.

33
Q

Discuss the RAAS pathway and its role in CVS regulation

A

The RAAS pathway regulates fluid balance and BP, thus affecting preload and afterload.

Sympathetic stimulation or reduced renal tubular pressure / sodium content causes renin release from juxtaglomerular apparatus.

Renin cleaves angiotensinogen to angiotensin I, which is converted to angiotensin II by ACE in the lungs.

Angiotensin II is a direct vasoconstrictor but also acts to:

  1. Increase aldosterone levels, causing increased renal sodium reabsorption
  2. Increase ADH (vasopressin) secretion by posterior pituitary
  3. Increase thirst via hypothalamus
  4. Increase sympathetic activity
34
Q

Discuss ANP and BNP and their role in CVS regulation

A

Cardiac hormones, ANP and BNP are produced by the cardiac atria and ventricles respectively in response to stretch/distension.

Both act to increase the transglomerular filtration pressure (increasing GFR) and decrease sodium resorption in the collecting ducts. This reduces preload.

ANP also reduces preload by inhibiting renin and aldosterone release. This then causes a secondary vasodilatation, also reducing afterload.

35
Q

Describe and explain the effect of deranged Ca2+ homeostasis on cardiac function

A

Hypocalcaemia: Reduces contractility and causes peripheral vasodilatation, reducing CO and MAP. Prolongs QT interval, increasing risk of dysrhythmias

Hypercalcaemia: Increases contractility and irritability. Hypertension, reduced QT interval and bundle branch blocks may occur.

36
Q

Describe and explain the effect of deranged K+ homeostasis on cardiac function

A

Hyperkalaemia reduces the cardiac resting membrane potential and intensity of the cardiac AP. Nodal conduction is delayed, PR prolonged and bradycardia and asystole may occur. Hyperkalaemia is associated with a dilated and flaccid myocardium.

37
Q

Describe and explain the effect of acidosis on cardiac function

A

Intracellular acidosis leads to reduction in myocardial contractility and CO due to competition with IC Ca+
Vasodilatation and reduced MAP occur via the same mechanism.

38
Q

Describe and explain the effect of temperature on cardiac function

A

Intrinsic cardiac pacemaker rate is affected by temperature with a 10 bpm change in HR for every 1°C change in temperature.

Myocardial contractility increases transiently with a moderate increase in temperature.

39
Q

What factors combine to provide effective cardiopulmonary function?

A

Delivered O2 (DO2) and perfusion pressure (PP)

40
Q

What factors determine DO2?

A

Arterial oxygen content (CaO2) and cardiac output (CO)

41
Q

What factors determine perfusion pressure?

A

Cardiac output (CO) and peripheral vascular resistance (PVR)

42
Q

What factors determine Cardiac Output (CO)?

A

HR x SV

43
Q

What factors determine stroke volume?

A

Preload
Contractility
Afterload

44
Q

List the key points in the ventricular P-V loop

A
  1. End diastolic point (EDP)
  2. Isovolumetric contraction
  3. Ejection phase
  4. Isovolumetric relaxation
  5. Ventricular filling
45
Q

How can the ventricular P-V loop be used to calculate stroke volume?

A

SV = EDV - ESV

46
Q

How can the ventricular P-V loop be used to calculate stroke work?

A

Stroke work = area inside the loop (ΔP x ΔV)

47
Q

What is the end diastolic pressure-volume relationship (EDPVR)?

A

EDPVR refers to the change in EDP in a given ventricle at different volumes. This can be plotted graphically as a line, the gradient of which represents the elastance of a ventricle.
The steeper the gradient, the less compliant the ventricle.

48
Q

What is the end systolic pressure-volume relationship (ESPVR)?

A

ESPVR refers to the change in ESP in a given ventricle at different volumes. This can be plotted graphically as a line, the gradient of which represents the contractility of a ventricle.

The steeper the gradient the more contractile the ventricle and vice versa.

49
Q

What is the Frank-Starling Law?

A

“The contractile force of a cardiac muscle fibre is proportional to the initial fibre length”

50
Q

How may a Frank-Starling curve (ventricular function curve) be plotted?

A

Index of resting fibre length on the x-axis (eg. CVP, LV/RV EDP/EDV) and an index of contractility on the y-axis (eg. SV, SW, LV/RV ESP).

51
Q

Define and explain Laplace’s Law

A

Laplace’s Law relates wall stress (ie. myocardial fibre tension) to internal pressure.

P = 2Th / R

Where:
P = Intraventricular pressure
T = Tension (wall stress)
h = Wall thickness
r = Radius of sphere
52
Q

How is cardiac preload ‘measured’ in practice?

A

Presystolic fibre length cannot be measured in clinical situations so a surrogate marker is used - EDP

This is estimated using pulmonary capillary wedge pressure or pulmonary artery diastolic pressure for the LV and CVP for the RV

53
Q

How is cardiac afterload ‘measured’ in practice?

A

Muscle fibre tension during contraction cannot be measured in clinical situations so a surrogate marker is used - ESVP

ESVP is estimated using SVR and MAP.

54
Q

How is SVR calculated?

A

SVR = (MAP-CVP)x80 / CO

55
Q

What is the Anrep effect?

A

The Anrep effect describes the increase in myocardial contractility (and SV) seen with an increase in afterload, due to the Frank-Starling law

56
Q

What is the Treppe / Bowditch effect?

A

The Treppe/Bowditch effect is the increase in myocardial contractility seen at increased heart rates (between 40-140 bpm). This is due to the reduced diastolic time resulting in more intracellular calcium for excitation-contraction coupling.

57
Q

How does the cardiac P-V curve relate to ventriculo-arterial coupling?

A

The end-systolic point (ESP) of the P-V curve represents the equilibrium between the opposing elastance of the LV and arterial system.

58
Q

When does optimal ventriculoarterial coupling occur?

A

When Ees = 2 x Ea

59
Q

How is the gradient Ea (arterial elastance) calculated?

A

Drawing a line between the EDV and ESP

Primary FRCA (34 decks)

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