Basic Cardiovascular Physiology Flashcards
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
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.
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
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
Level of cardioaccelerator fibers
T1-T4
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
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
CI=?
CO/BSA
Parasympathetic receptors of heart
M2 cholinergic receptrs
SV determinants
- Preload
- Afterload
- Contractility
- Wall motion abnormalities
- Valvular dysfunction
Factors affecting ventricular preload
- Blood volume
- Distribution of blood volume (posture, intrathoracic pressure, pericardial pressure, venous tone)
- Rhythm (atrial contraction)
- Heart rate
Factors affecting ventricular compliance
- Rate of relaxation (early diastolic compliance)
- ->hypertrophy, ischemia, and asynchrony
- Passive stiffness of ventricles (late diastolic compliance)
- ->hypertrophy and fibrosis
Laplace’s Law
Wall tension or circumferential stress
T= Pr/2h
h= wall thickness
*increase thickness (hypertrophy) –> decrease tension
SVR
SVR= 80 x (MAP-CVP)/CO
Normal SVR
900-1500 dyn x s cm^-5
PVR
PVR= 80 x (PAP-LAP)/CO
*usually PCWP ~ LAP
Normal PVR
50-150 dyn x s cm^-5
Vasodilatory metabolic by-products
K+ H+ CO2 adenosine lactate
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)
Nitric Oxide
- synthesis
- mechanism of action
- synthesized from arginine by nitric oxide synthetase
- bind guanylate cyclase–>increases cGMP–>vasodilation
Arginine Vasopressin (AVP) Receptors
V1: vasoconstriction
V2: antidiuretic effect (ADH)
Right Coronary Artery
-supplies the RA, most of the RV, and a variable portion of the LV (inferior wall)
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
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)
Blood Supply
- SA node
- AV node
SA node: RCA (60%) or LAD (40%)
AV node: RCA (85%) or CX (15%)
Effect of heart rate on coronary perfusion
Increases in heart rate decrease coronary perfusion *disproportionately greater reduction in diastolic time as heart rate increases
Coronary Blood Flow (ml/min)
250 ml/min
Myocardium oxygen extraction %
65% (25% most other tissues)
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
Sympathetic innervation to the heart
T2-T4–>stellate ganglion–>cardiac nerves the join and course w/LMCA
S3
- early diastole
- atrial blood reverberating against a stiff ventricle
- strongly associated w/MACE (Major Adverse Cardiac Events)
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
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
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
Normal coronary sinus Hb sat
30%
MVsat (SvO2) v ScvO2
MVsat is 2-5 points lower than ScvO2
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
Largest component of myocardial oxygen demand
Wall tension
Poiseuille’s Law
Describes laminar flow through a tube
Q = (πPr^4)/(8nl)
Q is flow rate, n is viscosity, l is length
Boyle’s Law
P1V1 = P2V2
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
Nitroglycerin v Nitroprusside
- Nitroglycerin increases venous capacitance and decreases preload
- Nitroprusside, in addition to venodilation, decreases afterload
Heart rate at which CI is maximized in normal people
120 (~150 for toddlers)
*above 120, decreases in SV outweigh increases in HR
Normal CI and maximal CI
Normal: 3.5 l/min/m2
Maximal (HR @120): 5.5 l/min/m2
Cardiac Output Per Organ
High:
- liver 19%
- muscle 19%
- heart and lungs 19%
- kidney 16%
Medium:
- brain 10%
- intestines 6%
Low:
-skin
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
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
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
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
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
Beta-2 Agonism
Beta-2 Receptor–>cAMP–>uptake of Ca back into SR–>decreased contraction
Nitric Oxide Mechanism
NO–>guanylate cyclase–>cGMP–>decreased contraction
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
What increases PVR?
Hypoxia
Hypercarbia
Acidemia
Elective surgery after balloon angioplasty
14 days
*continue ASA throughout perioperative period
ACE-I and perioperative outcomes
Increased intraoperative hypotension but no increase or reduction in MI, stroke, or mortality
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)
Normal Values:
- CVP
- Wedge
- CO
- SV
- CVP: 6 mm Hg
- Wedge: 10 mm Hg
- CO: 5.0 L/min
- SV: 70 cc
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
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
Activation of cAMP
- chemicals/drugs
- effect on VSM
- beta2, adenosine, prostacyclin
- vasodilation
What activates gaunylate cyclase?
Nitric oxide
-leads to increased cGMP and vasodilation
