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Anesthesia > Basic Cardiovascular Physiology > Flashcards

Basic Cardiovascular Physiology Flashcards

1
Q

Impact on cardiac muscle contraction:

  • quantity of intracellular Ca2+ available
  • its rate of delivery
  • its rate of removal determine
A
  • quantity of intracellular Ca2+ available->maximum tension developed
  • its rate of delivery->rate of contraction
  • its rate of removal determine->rate of relaxation
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2
Q

Effect of sympathetic stimulation

A

Sympathetic stimulation increases the force of contraction by raising intracellular Ca2+ concentration via a β1-adrenergic receptor-mediated increase in intracellular cyclic adenosine monophosphate (cAMP) through the action of a stimulatory G protein. The increase in cAMP recruits additional open calcium channels.

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3
Q

Effect of parasympathetic stimulation

A

Release of acetylcholine following vagal stimulation depresses contractility through increased cyclic guanosine monophosphate (cGMP) levels and inhibition of adenylyl cyclase
–>mediated by an inhibitory G protein

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4
Q

Effect of volatile anesthetics on cardiac contractility

*potentiated by what?

A

Depress cardiac contractility by decreasing the entry of Ca2+ into cells during depolarization (affecting T- and L-type calcium channels), altering the kinetics of its release and uptake into the sarcoplasmic reticulum, and decreasing the sensitivity of contractile proteins to Ca2+
*Anesthetic-induced cardiac depression is potentiated by hypocalcemia, β-adrenergic blockade, and calcium channel blockers

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5
Q

Level of cardioaccelerator fibers

A

T1-T4

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6
Q

Cardiac autonomic innervation

A
  • cardiac sympathetic fibers originate in spinal cord T1-T4
  • travel to heart through cervical (stellate) ganglia
  • sidedness: right sympathetic and vagus nerves primarily affect SA node, whereas left sympathetic and vagus nerves principally affect the AV node
  • vagal effects frequently have a very rapid onset and resolution, whereas sympathetic influences generally have a more gradual onset and dissipation
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7
Q

Three waves on atrial pressure tracings (JVP)

A
  • a wave- due to atrial systole
  • c wave- coincides with ventricular contraction and is said to be caused by bulging of the AV valve into the atrium
  • v wave- the result of pressure buildup from venous return before the AV valve opens again
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8
Q

CI=?

A

CO/BSA

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9
Q

Parasympathetic receptors of heart

A

M2 cholinergic receptrs

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10
Q

SV determinants

A
  • Preload
  • Afterload
  • Contractility
  • Wall motion abnormalities
  • Valvular dysfunction
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11
Q

Factors affecting ventricular preload

A
  • Blood volume
  • Distribution of blood volume (posture, intrathoracic pressure, pericardial pressure, venous tone)
  • Rhythm (atrial contraction)
  • Heart rate
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12
Q

Factors affecting ventricular compliance

A
  • Rate of relaxation (early diastolic compliance)
  • ->hypertrophy, ischemia, and asynchrony
  • Passive stiffness of ventricles (late diastolic compliance)
  • ->hypertrophy and fibrosis
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13
Q

Laplace’s Law

A

Wall tension or circumferential stress

T= Pr/2h

h= wall thickness
*increase thickness (hypertrophy) –> decrease tension

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14
Q

SVR

A

SVR= 80 x (MAP-CVP)/CO

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15
Q

Normal SVR

A

900-1500 dyn x s cm^-5

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16
Q

PVR

A

PVR= 80 x (PAP-LAP)/CO

*usually PCWP ~ LAP

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17
Q

Normal PVR

A

50-150 dyn x s cm^-5

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18
Q

Vasodilatory metabolic by-products

A 
K+
H+
CO2
adenosine
lactate
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19
Q

Endothelium-Derived Factors

  • Vasodilators
  • Vasoconstrictors
  • Anticoagulants
  • Fibrinolytics
  • Platelet Aggregation Inhibitors
A
  • Vasodilators: nitric oxide, prostacyclin (PGI2)
  • Vasoconstrictors: endothelins, thromboxane A2
  • Anticoagulants: thrombomodulin, protein C
  • Fibrinolytics: TPA
  • Platelet Aggregation Inhibitors: nitric oxide, prostacyclin (PGI2)
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20
Q

Nitric Oxide

  • synthesis
  • mechanism of action
A
  • synthesized from arginine by nitric oxide synthetase

- bind guanylate cyclase–>increases cGMP–>vasodilation

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21
Q

Arginine Vasopressin (AVP) Receptors

A

V1: vasoconstriction
V2: antidiuretic effect (ADH)

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22
Q

Right Coronary Artery

A

-supplies the RA, most of the RV, and a variable portion of the LV (inferior wall)

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23
Q

Right or Left Dominance

A

Right- 85%: RCA gives rise to PDA which supplies the superior-posterior inter ventricular septum and inferior wall

Left- 15%: LCA gives rise to PDA

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24
Q

LCA

  • supply
  • branches
A
  • supplies LA, most of interventricular septum, and LV (septal, anterior, and lateral walls)
  • bifurcates into LAD and CX
  • LAD: septum and anterior wall
  • CX: lateral wall
  • wraps around the AV groove and continues down as the PDA (posterior septum and inferior wall)
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25
Q

Blood Supply

  • SA node
  • AV node
A

SA node: RCA (60%) or LAD (40%)

AV node: RCA (85%) or CX (15%)

26
Q

Effect of heart rate on coronary perfusion

A

Increases in heart rate decrease coronary perfusion *disproportionately greater reduction in diastolic time as heart rate increases

27
Q

Coronary Blood Flow (ml/min)

A

250 ml/min

28
Q

Myocardium oxygen extraction %

A

65% (25% most other tissues)

29
Q

Parasympathetic innervation to the heart

A
  • arise from the dorsal vagal nucleus and nucleus ambiguous and carried by the vagus nerve
  • gives rise to two plexuses: dorsal and ventral cardiopulmonary plexuses, located between the aortic arch and the tracheal bifurcation
  • greatest concentration of nicotinic AchR at SA node, then AV node, then heart chambers
30
Q

Sympathetic innervation to the heart

A

T2-T4–>stellate ganglion–>cardiac nerves the join and course w/LMCA

31
Q

S3

A
  • early diastole
  • atrial blood reverberating against a stiff ventricle
  • strongly associated w/MACE (Major Adverse Cardiac Events)
32
Q

Spontaneous Respiration- changes during inspiration

A

Negative intrathoracic and pleural pressures–>increased venous return–>increased RV preload–>pulmonic valve closure delayed–>split S2 (physiologic)

Increased pulmonary venous capacitance–>decreased LV preload–>decrease in ABP

Negative intrathoracic and pleural pressures–>increased LV afterload–>decrease in ABP

Inhibition of vagal tone (respiratory sinus arrhythmia)–>increase in HR

33
Q

MI Patterns

  • LCx
  • LAD
  • LMCA
  • RCA
A

LCx: lateral left ventricle–>I, aVL, V5, V6

LAD: septal and or anterior LV–>V1-V4 classic, V5-6 as well

LMCA: LAD and LCx

RCA: inferior MI–>II, III, aVF

34
Q

S4

A
  • due to atrial contraction ejecting blood into a noncompliant ventricle, aka gallop
  • associated w/LV concentric hypertrophy (HTN, AS)
  • just after p wave (atrial contraction) and during ‘a’ wave on cvp
35
Q

Normal coronary sinus Hb sat

A

30%

36
Q

MVsat (SvO2) v ScvO2

A

MVsat is 2-5 points lower than ScvO2

37
Q

Amiodarone

  • class of antiarrhythmic and MOA
  • pharmacodynamics
  • pharmacokinetics
  • dosing
  • side effects
A
  • Class III antiarrhythmic: potassium-blocking agent
  • therefore, delays phase 3 repolarization
  • Slows conduction, acts as an AV nodal blocker (like BBs), and is generally effective for both atrial and ventricular arrhythmias
  • less depressant effects on BP than BBs or CCBs
  • long half-life, very fat soluble (high V of D)
  • loading doses require 10 g over a few days
  • single bolus ineffective after a couple hours–>need gtt

Side effects:

  • lungs: pulmonary fibrosis (RLD, decreased DLCO)
  • liver: transaminitis and jaundice (cirrhosis if continued)
  • limbs: peripheral neuropathies
  • thyroid: hypothyroidism, less often hyperthyroidism
38
Q

Largest component of myocardial oxygen demand

A

Wall tension

39
Q

Poiseuille’s Law

A

Describes laminar flow through a tube

Q = (πPr^4)/(8nl)

Q is flow rate, n is viscosity, l is length

40
Q

Boyle’s Law

A

P1V1 = P2V2

41
Q

Beta Blocker Effects

A
  • antiarrhythmics, decrease sympathetic input to SA and AV node, increase refractory period
  • bronchospasm (beta 2 antagonism)
  • anti-nociception
  • decrease glycogenolysis and glucagon secretion leading to hypoglycemia
  • decrease aqueous humor secretion from ciliary epithelium (beta 2 antagonism)
  • decrease release of aldosterone (beta 1 antagonism reduces renin production, leading to less to less angiotensin and thus less angiotensin II and thus less aldosterone)
  • decreases peripheral conversion of T4 to T3
42
Q

Nitroglycerin v Nitroprusside

A
  • Nitroglycerin increases venous capacitance and decreases preload
  • Nitroprusside, in addition to venodilation, decreases afterload
43
Q

Heart rate at which CI is maximized in normal people

A

120 (~150 for toddlers)

*above 120, decreases in SV outweigh increases in HR

44
Q

Normal CI and maximal CI

A

Normal: 3.5 l/min/m2

Maximal (HR @120): 5.5 l/min/m2

45
Q

Cardiac Output Per Organ

A

High:

  • liver 19%
  • muscle 19%
  • heart and lungs 19%
  • kidney 16%

Medium:

  • brain 10%
  • intestines 6%

Low:
-skin

46
Q

von Bezold-Jarisch reflex

A
  • Receptors in LV (both mechano and chemo) that fire with very low pressures (low preload)
  • oops- receptors are wired to vagal afferents–>paradoxical bradycardia and hypotension
  • also leads to coronary vasodilation, perhaps why it exists
  • situations you see it
    1. hypovolemic patient w/sudden further decrease in preload (eg. orthostatic or spinal anesthesia)
    2. MI or coronary reperfusion
47
Q

Bainbridge Atrial Reflex

A

Paradoxical tachycardia in response to fluid bolus

  • decreased vagal tone (from fluid or hypervolemia)–>increased HR through neural input into medulla as well as SA node stretching and increased automaticity
  • well-described in dogs, less so in humans
48
Q

Baroreceptor Reflex

A

Baroreceptors in carotid sinus response to increased blood pressured–>afferents by glossopharyngeal (Hering n) to CV centers in medulla–>inhibition of sympathetic activity and increased parasympathetic outflow

  • responsible for second to second maintenance of BP
  • depressed by anesthetics
49
Q

Chemoreceptor Reflex in carotid and aortic bodies

A

Low oxygen tension and acidemia–>outflow through Herring nerve (CN 9, GPN)–>increase ventilation and secondary increase in BP

*even more sensitive to anesthetics (esp volatiles) than baroreceptor reflex in carotid sinus

50
Q

Alpha-1 Mediated Vasoconstriction

A

Alpha-1 Receptor (G protein receptor–>activation of PLC–>IP3 formation–>calcium release from SR into cytosol–>increased contraction smooth muscle

51
Q

Beta-2 Agonism

A

Beta-2 Receptor–>cAMP–>uptake of Ca back into SR–>decreased contraction

52
Q

Nitric Oxide Mechanism

A

NO–>guanylate cyclase–>cGMP–>decreased contraction

53
Q

Stimuli for ADH release

Inhibition of ADH release

A

Stimuli: hypovolemia, increased plasma osmolality, ATII, cholecystokinin, pain, nicotine

Inhibition: hypervolemia from ANP (atrial natriuretic peptide), EtOH

54
Q

What increases PVR?

A

Hypoxia
Hypercarbia
Acidemia

55
Q

Elective surgery after balloon angioplasty

A

14 days

*continue ASA throughout perioperative period

56
Q

ACE-I and perioperative outcomes

A

Increased intraoperative hypotension but no increase or reduction in MI, stroke, or mortality

57
Q

Starling Equation

A

Q = kA X [(Pc – Pi) + σ(πi-πc)]

Q: net fluid filtration; k: capillary filtration coefficient (of water); A: area of the membrane; σ: reflection coefficient (of albumin). Pc: capillary hydrostatic pressure; Pi: interstitial hydrostatic pressure; πi: interstitial colloid osmotic pressure; πc: capillary colloid os- motic pressure.

  • low k–>more impermeable to water
  • low σ–>protein crosses membrane easily (e.g. ARDS)
58
Q

Normal Values:

  • CVP
  • Wedge
  • CO
  • SV
A
  • CVP: 6 mm Hg
  • Wedge: 10 mm Hg
  • CO: 5.0 L/min
  • SV: 70 cc
59
Q

Role of cAMP

  • heart
  • blood vessels

Metabolism of cAMP

A

Heart: cAMP leads to increased contractility

Blood vessels: cAMP leads to reduced contractility (smooth muscle) and vasodilation

Hydrolysis by phosphodiesterase inhibitors

60
Q

Role of cGMP

  • effect of PDE
  • effect of PDE 5 inhibitors (sildenafil)
A

Relaxes smooth muscle and leads to vasodilation

  • PDE hydrolyzes cBMP
  • PDE5Is prevent degradation, increasing/prolonging effect
61
Q

Activation of cAMP

  • chemicals/drugs
  • effect on VSM
A
  • beta2, adenosine, prostacyclin

- vasodilation

62
Q

What activates gaunylate cyclase?

A

Nitric oxide

-leads to increased cGMP and vasodilation

Anesthesia (16 decks)

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