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Flashcards in Basic Cardiovascular Physiology Deck (62):
1

Impact on cardiac muscle contraction:
-quantity of intracellular Ca2+ available
-its rate of delivery
-its rate of removal determine

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

2

Effect of sympathetic stimulation

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.

3

Effect of parasympathetic stimulation

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

4

Effect of volatile anesthetics on cardiac contractility
*potentiated by what?

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

5

Level of cardioaccelerator fibers

T1-T4

6

Cardiac autonomic innervation

-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

7

Three waves on atrial pressure tracings (JVP)

-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

8

CI=?

CO/BSA

9

Parasympathetic receptors of heart

M2 cholinergic receptrs

10

SV determinants

-Preload
-Afterload
-Contractility
-Wall motion abnormalities
-Valvular dysfunction

11

Factors affecting ventricular preload

-Blood volume
-Distribution of blood volume (posture, intrathoracic pressure, pericardial pressure, venous tone)
-Rhythm (atrial contraction)
-Heart rate

12

Factors affecting ventricular compliance

-Rate of relaxation (early diastolic compliance)
-->hypertrophy, ischemia, and asynchrony

-Passive stiffness of ventricles (late diastolic compliance)
-->hypertrophy and fibrosis

13

Laplace's Law

Wall tension or circumferential stress

T= Pr/2h

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

14

SVR

SVR= 80 x (MAP-CVP)/CO

15

Normal SVR

900-1500 dyn x s cm^-5

16

PVR

PVR= 80 x (PAP-LAP)/CO

*usually PCWP ~ LAP

17

Normal PVR

50-150 dyn x s cm^-5

18

Vasodilatory metabolic by-products

K+
H+
CO2
adenosine
lactate

19

Endothelium-Derived Factors
-Vasodilators
-Vasoconstrictors
-Anticoagulants
-Fibrinolytics
-Platelet Aggregation Inhibitors

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

20

Nitric Oxide
-synthesis
-mechanism of action

-synthesized from arginine by nitric oxide synthetase
-bind guanylate cyclase-->increases cGMP-->vasodilation

21

Arginine Vasopressin (AVP) Receptors

V1: vasoconstriction
V2: antidiuretic effect (ADH)

22

Right Coronary Artery

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

23

Right or Left Dominance

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

24

LCA
-supply
-branches

-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)

25

Blood Supply
-SA node
-AV node

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

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

26

Effect of heart rate on coronary perfusion

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

27

Coronary Blood Flow (ml/min)

250 ml/min

28

Myocardium oxygen extraction %

65% (25% most other tissues)

29

Parasympathetic innervation to the heart

-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

Sympathetic innervation to the heart

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

31

S3

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

32

Spontaneous Respiration- changes during inspiration

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

MI Patterns
-LCx
-LAD
-LMCA
-RCA

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

S4

-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

Normal coronary sinus Hb sat

30%

36

MVsat (SvO2) v ScvO2

MVsat is 2-5 points lower than ScvO2

37

Amiodarone
-class of antiarrhythmic and MOA
-pharmacodynamics
-pharmacokinetics
-dosing
-side effects

-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

Largest component of myocardial oxygen demand

Wall tension

39

Poiseuille's Law

Describes laminar flow through a tube

Q = (πPr^4)/(8nl)

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

40

Boyle's Law

P1V1 = P2V2

41

Beta Blocker Effects

-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

Nitroglycerin v Nitroprusside

-Nitroglycerin increases venous capacitance and decreases preload
-Nitroprusside, in addition to venodilation, decreases afterload

43

Heart rate at which CI is maximized in normal people

120 (~150 for toddlers)

*above 120, decreases in SV outweigh increases in HR

44

Normal CI and maximal CI

Normal: 3.5 l/min/m2

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

45

Cardiac Output Per Organ

High:
-liver 19%
-muscle 19%
-heart and lungs 19%
-kidney 16%

Medium:
-brain 10%
-intestines 6%

Low:
-skin

46

von Bezold-Jarisch reflex

-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

Bainbridge Atrial Reflex

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

Baroreceptor Reflex

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

Chemoreceptor Reflex in carotid and aortic bodies

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

Alpha-1 Mediated Vasoconstriction

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

51

Beta-2 Agonism

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

52

Nitric Oxide Mechanism

NO-->guanylate cyclase-->cGMP-->decreased contraction

53

Stimuli for ADH release

Inhibition of ADH release

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

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

54

What increases PVR?

Hypoxia
Hypercarbia
Acidemia

55

Elective surgery after balloon angioplasty

14 days
*continue ASA throughout perioperative period

56

ACE-I and perioperative outcomes

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

57

Starling Equation

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

Normal Values:
-CVP
-Wedge
-CO
-SV

-CVP: 6 mm Hg
-Wedge: 10 mm Hg
-CO: 5.0 L/min
-SV: 70 cc

59

Role of cAMP
-heart
-blood vessels

Metabolism of cAMP

Heart: cAMP leads to increased contractility

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

Hydrolysis by phosphodiesterase inhibitors

60

Role of cGMP

-effect of PDE
-effect of PDE 5 inhibitors (sildenafil)

Relaxes smooth muscle and leads to vasodilation

-PDE hydrolyzes cBMP
-PDE5Is prevent degradation, increasing/prolonging effect

61

Activation of cAMP
-chemicals/drugs
-effect on VSM

-beta2, adenosine, prostacyclin
-vasodilation

62

What activates gaunylate cyclase?

Nitric oxide
-leads to increased cGMP and vasodilation