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
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.
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
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
5
Q
Level of cardioaccelerator fibers
A
T1-T4
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
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
8
Q
CI=?
A
CO/BSA
9
Q
Parasympathetic receptors of heart
A
M2 cholinergic receptrs
10
Q
SV determinants
A
- Preload
- Afterload
- Contractility
- Wall motion abnormalities
- Valvular dysfunction
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
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
13
Q
Laplace’s Law
A
Wall tension or circumferential stress
T= Pr/2h
h= wall thickness
*increase thickness (hypertrophy) –> decrease tension
14
Q
SVR
A
SVR= 80 x (MAP-CVP)/CO
15
Q
Normal SVR
A
900-1500 dyn x s cm^-5
16
Q
PVR
A
PVR= 80 x (PAP-LAP)/CO
*usually PCWP ~ LAP
17
Q
Normal PVR
A
50-150 dyn x s cm^-5
18
Q
Vasodilatory metabolic by-products
A
K+ H+ CO2 adenosine lactate
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)
20
Q
Nitric Oxide
- synthesis
- mechanism of action
A
- synthesized from arginine by nitric oxide synthetase
- bind guanylate cyclase–>increases cGMP–>vasodilation
21
Q
Arginine Vasopressin (AVP) Receptors
A
V1: vasoconstriction
V2: antidiuretic effect (ADH)
22
Q
Right Coronary Artery
A
-supplies the RA, most of the RV, and a variable portion of the LV (inferior wall)
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
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)
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
