Cardiovascular - Physiology

Question 1

Cardiac output & mean arterial pressure

• Cardiac output (CO)
  
  • Equations
  • Early vs. late stages of exercise
  • Diastole
• Mean arterial pressure (MAP) equations

Answer 1

• Cardiac output (CO)
  
  • Equations
    
    • CO = stroke volume (SV) × heart rate (HR).
    • CO = rate of O2 consumption / ( arterial O2 content - venous O2 content)
  • Early vs. late stages of exercise
    
    • During the early stages of exercise, CO is maintained by increased HR and increased SV.
    • During the late stages of exercise, CO is maintained by increased HR only (SV plateaus).
  • Diastole is preferentially shortened with increased HR
    
    • Less filling time –> decreased CO (e.g., ventricular tachycardia).
• Mean arterial pressure (MAP)
  
  • MAP = CO × TPR.
  • MAP = 2/3 diastolic pressure + 1/3 systolic pressure.

Question 2

Pulse pressure & stroke volume

• Pulse pressure
  
  • Equations
  • Increased in…
  • Decreased in…
• Stroke volume
  
  • Equation
  • Increased with…

Answer 2

• Pulse pressure
  
  • Pulse pressure = systolic pressure – diastolic pressure.
    
    • Pulse pressure is proportional to SV, inversely proportional to arterial compliance.
  • Increased in hyperthyroidism, aortic regurgitation, arteriosclerosis, obstructive sleep apnea (increased sympathetic tone), exercise (transient).
  • Decreased in aortic stenosis, cardiogenic shock, cardiac tamponade, and advanced heart failure.
• Stroke volume
  
  • SV = EDV - ESV
  • Increased with increased contractility, increased preload, or decreased afterload
    
    • Stroke Volume affected by Contractility, Afterload, and Preload
    • SV** **CAP

Question 3

Contractility

• Contractility (and SV) increase with:
• Contractility (and SV) decrease with:
• SV increases with:
• SV decreases with:
• Myocardial O2 demand is increased with:

Answer 3

• Contractility (and SV) increase with:
  
  • Catecholamines (increased activity of Ca2+ pump in sarcoplasmic reticulum).
  • Increased intracellular Ca2+.
  • Decreased extracellular Na+ (decreased activity of Na+/Ca2+ exchanger).
  • ƒƒDigitalis (blocks Na+/K+ pump –> increased intracellular Na+ –> decreased Na+/Ca2+ exchanger activity Ž–> increased intracellular Ca2+).
• Contractility (and SV) decrease with:
  
  • β1-blockade (decreased cAMP).
  • ƒƒHeart failure with systolic dysfunction.
  • Acidosis.
  • ƒƒHypoxia/hypercapnea (decreased Po2/ increased Pco2).
  • ƒƒNon-dihydropyridine Ca2+ channel blockers.
• SV increases with:
  
  • Anxiety
  • Exercise
  • Pregnancy.
• SV decreases with:
  
  • A failing heart (both decreased systolic and diastolic dysfunction).
• Myocardial O2 demand is increased with:
  
  • Increased afterload (∝ arterial pressure).
  • Increased contractility.
  • Increased HR.
  • Increased ventricular diameter (increased wall tension).

Question 4

Preload

Answer 4

• Preload approximated by ventricular EDV
• Depends on venous tone and circulating blood volume.
• VEnodilators (e.g., nitroglycerin) decrease prEload.
• ACE inhibitors and ARBs decrease both preload and afterload.

Question 5

Afterload

Answer 5

• Afterload approximated by MAP.
  
  • Chronic hypertension (increased MAP) Ž–> LV hypertrophy.
• Relation of LV size and afterload Ž–> Laplace’s law:
  
  • Wall tension = ( pressure × radius ) / ( 2 × wall thickness )
  • LV compensates for increased afterload by thickening (hypertrophy) to decrease wall tension.
• VAsodilators (e.g., hydrAl_a_zine) decrease Afterload (Arterial).
• ACE inhibitors and ARBs decrease both preload and afterload.

Question 6

Ejection fraction

Answer 6

• EF = SV / EDV = ( EDV - ESV ) / EDV
• Left ventricular EF is an index of ventricular contractility
  
  • Normal EF is ≥ 55%.
• EF decreases in systolic heart failure
  
  • EF is normal in diastolic heart failure.

Question 7

Starling curve

Answer 7

• Force of contraction is proportional to end-diastolic length of cardiac muscle fiber (preload).
• Increased contractility with catecholamines, digoxin.
• Decreased contractility with loss of myocardium (e.g., MI), β-blockers, calcium channel blockers, dilated cardiomyopathy.

Question 8

Resistance, pressure, flow

• Relationship
• Resistance
• Total resistance
• Viscosity
• Pressure

Answer 8

• ΔP = Q × R
  
  • Similar to Ohm’s law: ΔV = IR
• Resistance = driving pressure (ΔP) / flow (Q) = [8η (viscosity) × length] / πr4
  
  • Resistance is directly proportional to viscosity and vessel length and inversely proportional to the radius to the 4th power.
• Arterioles account for most of TPR Ž–> regulate capillary flow
  
  • Total resistance of vessels in series: TR = R1 + R2 + R3 . . .
  • Total resistance of vessels in parallel: 1/TR = (1/R1) + (1/R2) + (1/R3) . . .
• Viscosity depends mostly on hematocrit
  
  • Viscosity increases in:
    
    • Polycythemia
    • ƒƒHyperproteinemic states (e.g., multiple myeloma)
    • Hereditary spherocytosis
  • Viscosity decreases in anemia
• Pressure gradient drives flow from high pressure to low pressure.

Question 9

Cardiac and vascular function curves (269)

• Intersection of curves
• Changes
• For each
  
  • Effect
  • Examples
• Inotropy
• Venous return
• Total peripheral resistance

Answer 9

• Intersection of curves
  
  • Operating point of heart (i.e., venous return and CO are equal).
• Changes often occur in tandem, and may be either…
  
  • Reinforcing (exercise increases inotropy and decreases TPR to maximize CO)
  • Compensatory (heart failure decreases inotropy Ž–> fluid retention to increase preload to maintain CO)
• Inotropy
  
  • Effect: Changes in contractility Ž–> altered CO for a given RA pressure (preload).
  • Examples:
    
    • Catecholamines, digoxin (+)
    • Uncompensated heart failure, narcotic overdose (-)
• Venous return
  
  • Effect: Changes in circulating volume or venous tone –>Ž altered RA pressure for a given CO.
    
    • Mean systemic pressure (x-intercept) changes with volume/venous tone.
  • Examples:
    
    • Fluid infusion, sympathetic activity (+)
    • Acute hemorrhage, spinal anesthesia (-)
• Total peripheral resistance
  
  • Effect: Changes in TPR –>Ž altered CO at a given RA pressure
    
    • However, mean systemic pressure (x-intercept) is unchanged.
  • Examples:
    
    • Vasopressors (+)
    • Exercise, AV shunt (-)

Question 10

Pressure-volume loops and cardiac cycle:
Phases—left ventricle

1. Isovolumetric contraction
2. Systolic ejection
3. Isovolumetric relaxation
4. Rapid filling
5. Reduced filling

Answer 10

1. Isovolumetric contraction
   
   • Period between mitral valve closing and aortic valve opening
   • Period of highest O2 consumption
2. Systolic ejection
   
   • Period between aortic valve opening and closing
3. Isovolumetric relaxation
   
   • Period between aortic valve closing and mitral valve opening
4. Rapid filling
   
   • Period just after mitral valve opening
5. Reduced filling
   
   • Period just before mitral valve closing

Question 11

Pressure-volume loops and cardiac cycle:
Sounds

• S1
• S2
• S3
• S4
• Systolic heart sounds
• Diastolic heart sounds

Answer 11

• S1
  
  • Mitral and tricuspid valve closure.
  • Loudest at mitral area.
• S2
  
  • Aortic and pulmonary valve closure.
  • Loudest at left sternal border.
• S3
  
  • In early diastole during rapid ventricular filling phase.
  • Associated with increased filling pressures (e.g., mitral regurgitation, CHF)
  • More common in dilated ventricles (but normal in children and pregnant women).
• S4 (“atrial kick”)
  
  • In late diastole.
  • High atrial pressure.
  • Associated with ventricular hypertrophy.
  • Left atrium must push against stiff LV wall.
• Systolic heart sounds
  
  • Aortic/pulmonic stenosis, mitral/tricuspid regurgitation, ventricular septal defect.
• Diastolic heart sounds
  
  • Aortic/pulmonic regurgitation, mitral/tricuspid stenosis.

Question 12

Pressure-volume loops and cardiac cycle:
Jugular venous pulse (JVP)

• a wave
• c wave
• x descent
• v wave
• y descent

Answer 12

• a wave
  
  • Atrial contraction.
• c wave
  
  • RV contraction (closed tricuspid valve bulging into atrium).
• x descent
  
  • Atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction.
  • Absent in tricuspid regurgitation.
• v wave
  
  • Increased right atrial pressure due to filling against closed tricuspid valve.
• y descent
  
  • Blood flow from RA to RV.

Question 13

Normal splitting

Answer 13

• Inspiration Ž
  
  • –> drop in intrathoracic pressure
  • –>Ž increased venous return to the RV Ž
  • –> increased RV stroke volume Ž
  • –> increased RV ejection time
  • Ž–> delayed closure of pulmonic valve. 
• Decreased pulmonary impedance (increased capacity of the pulmonary circulation)
  
  • Also occurs during inspiration
  • Contributes to delayed closure of pulmonic valve.

Question 14

Wide splitting

Answer 14

• Seen in conditions that delay RV emptying (pulmonic stenosis, right bundle branch block).
• Delay in RV emptying causes delayed pulmonic sound (regardless of breath).
• An exaggeration of normal splitting.

Question 15

Fixed splitting

Answer 15

• Seen in ASD.
• ASD
  
  • –>Ž left-to-right shunt
  • Ž–> increased RA and RV volumes Ž
  • –> increased flow through pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed.

Question 16

Paradoxical splitting

Answer 16

• Seen in conditions that delay LV emptying (aortic stenosis, left bundle branch block).
• Normal order of valve closure is reversed so that P2 sound occurs before delayed A2 sound.
• Therefore on inspiration, P2 closes later and moves closer to A2, thereby “paradoxically” eliminating the split.

Question 17

Auscultation of the heart:
Where to listen

• Aortic area
• Left sternal border
• Pulmonic area
• Tricuspid area
• Mitral area

Answer 17

• APT M
• Aortic area
  
  • Systolic murmur
    
    • Aortic stenosis
    • Flow murmur
    • Aortic valve sclerosis
• Left sternal border:
  
  • Diastolic murmur
    
    • Aortic regurgitation
    • Pulmonic regurgitation
  • Systolic murmur
    
    • Hypertrophic cardiomyopathy
• Pulmonic area:
  
  • Systolic ejection murmur
    
    • Pulmonic stenosis
    • Flow murmur (e.g., physiologic murmur)
• Tricuspid area:
  
  • Pansystolic murmur
    
    • Tricuspid regurgitation
    • Ventricular septal defect
  • Diastolic murmur
    
    • Tricuspid stenosis
    • Atrial septal defect
      
      • ASD commonly presents with a pulmonary flow murmur (increased flow through pulmonary valve) and a diastolic rumble (increased flow across tricuspid)
      • Blood flow across the actual ASD does not cause a murmur because there is no pressure gradient.
      • The murmur later progresses to a louder diastolic murmur of pulmonic regurgitation from dilatation of the pulmonary artery.
• Mitral area:
  
  • Systolic murmur
    
    • Mitral regurgitation
  • Diastolic murmur
    
    • Mitral stenosis

Question 18

Auscultation of the heart:
Effects of these bedside maneuvers

• Inspiration 
• Hand grip
• Valsalva (phase II, forcing exhalation against a closed airway), standing
• Rapid squatting

Answer 18

• Inspiration 
  
  • Increases intensity of right heart sounds
• Hand grip
  
  • Increases systemic vascular resistance
  • Increases intensity of MR, AR, VSD murmurs
  • Decreases intensity of AS, hypertrophic cardiomyopathy murmurs
  • MVP: increases murmur intensity, later onset of click/murmur
• Valsalva (phase II, forcing exhalation against a closed airway), standing
  
  • Decreases venous return
  • Decreases intensity of most murmurs (including AS)
  • Increases intensity of hypertrophic cardiomyopathy murmur
  • MVP: decreases murmur intensity, earlier onset of click/murmur
• Rapid squatting
  
  • Increases venous return
  • Increases preload
  • Increases afterload with prolonged squatting
  • Decreases intensity of hypertrophic cardiomyopathy murmur
  • Increases intensity of AS murmur
  • MVP: increases murmur intensity, later onset of click/murmur

Question 19

Mitral/tricuspid regurgitation (MR/TR)

• Type of heart murmur
• Mitral characteristics
• Tricuspid characteristics

Answer 19

• Systolic heart murmur
  
  • Holosystolic, high-pitched “blowing murmur.”
• Mitral characteristics
  
  • Loudest at apex and radiates toward axilla.
  • Enhanced by maneuvers that increase TPR (e.g., squatting, hand grip).
  • MR is often due to ischemic heart disease, MVP, or LV dilation.
• Tricuspid characteristics
  
  • Loudest at tricuspid area and radiates to right sternal border.
  • Enhanced by maneuvers that increase RA return (e.g., inspiration).
  • TR commonly caused by RV dilation.
  • Rheumatic fever and infective endocarditis can cause either MR or TR.

Question 20

Aortic stenosis (AS)

• Type of heart murmur
• Characteristics

Answer 20

• Systolic heart murmur
  
  • Crescendo-decrescendo systolic ejection murmur.
• Characteristics
  
  • LV >> aortic pressure during systole.
  • Loudest at heart base; radiates to carotids.
  • “Pulsus parvus et tardus”—pulses are weak with a delayed peak.
  • Can lead to Syncope, Angina, and Dyspnea on exertion (SAD).
  • Often due to age-related calcific aortic stenosis or bicuspid aortic valve.

Question 21

VSD

• Type of heart murmur
• Characteristics

Answer 21

• Systolic heart murmur
  
  • Holosystolic, harsh-sounding murmur.
• Characteristics
  
  • Loudest at tricuspid area, accentuated with hand grip maneuver due to increased afterload.

Question 22

Mitral valve prolapse (MVP)

• Type of heart murmur
• Characteristics

Answer 22

• Systolic heart murmur
  
  • Late systolic crescendo murmur with midsystolic click (MC; due to sudden tensing of chordae tendineae).
• Characteristics
  
  • Most frequent valvular lesion.
  • Best heard over apex.
  • Loudest just before S2.
  • Usually benign.
  • Can predispose to infective endocarditis.
  • Can be caused by myxomatous degeneration, rheumatic fever, or chordae rupture.
  • Occurs earlier with maneuvers that decrease venous return (e.g., standing or Valsalva).

Question 23

Aortic regurgitation (AR)

• Type of heart murmur
• Characteristics

Answer 23

• Diastolic heart murmur
  
  • High-pitched “blowing” early diastolic decrescendo murmur.
• Characteristics
  
  • Wide pulse pressure when chronic
  • Can present with bounding pulses and head bobbing.
  • Often due to aortic root dilation, bicuspid aortic valve, endocarditis, or rheumatic fever.
  • Increased murmur during hand grip.
  • Vasodilators decrease intensity of murmur.

Question 24

Mitral stenosis (MS)

• Type of heart murmur
• Characteristics

Answer 24

• Diastolic heart murmur
  
  • Delayed rumbling late diastolic murmur
• Characteristics
  
  • Follows opening snap (OS)
    
    • Due to abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips.
  • Decreased interval between S2 and OS correlates with increased severity.
  • LA >> LV pressure during diastole.
  • Often occurs 2° to rheumatic fever.
  • Chronic MS can result in LA dilation.
  • Enhanced by maneuvers that increase LA return (e.g., expiration).

Question 25

PDA * Type of heart murmur * Characteristics

Answer 25

* Continuous heart murmur * Continuous machine-like murmur. * Characteristics * Loudest at S2. * Often due to congenital rubella or prematurity. * Best heard at left infraclavicular area.

Question 26

Ventricular action potential: Phases * Phase 0 * Phase 1 * Phase 2 * Phase 3 * Phase 4

Answer 26

* Phase 0 * Rapid upstroke and depolarization * Voltage-gated Na+ channels open. * Phase 1 * Initial repolarization * Inactivation of voltage-gated Na+ channels. * Voltage-gated K+ channels begin to open. * Phase 2 * Plateau * Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflux. * Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction. * Phase 3 * Rapid repolarization * Massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca2+ channels. * Phase 4 * Resting potential * High K+ permeability through K+ channels.

Question 27

Ventricular action potential * Also occurs in... * In contrast to skeletal muscle:

Answer 27

* Also occurs in bundle of His and Purkinje fibers. * In contrast to skeletal muscle: * Cardiac muscle action potential has a plateau, which is due to Ca2+ influx and K+ efflux * Myocyte contraction occurs due to Ca2+-induced Ca2+ release from the sarcoplasmic reticulum. * Cardiac nodal cells spontaneously depolarize during diastole, resulting in automaticity due to I_f channels * I_f = “funny current” channels responsible for a slow, mixed Na+/K+ inward current. * Cardiac myocytes are electrically coupled to each other by gap junctions.

Question 28

Pacemaker action potential * Occurs in... * Key differences from the ventricular action potential include: * Phase 0 * Phase 1 * Phase 2 * Phase 3 * Phase 4

Answer 28

* Occurs in the SA and AV nodes. * Key differences from the ventricular action potential include: * Phase 0 * Upstroke—opening of voltage-gated Ca2+ channels. * Fast voltage-gated Na+ channels are permanently inactivated because of the less negative resting voltage of these cells. * Results in a slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles. * Phase 1 * No differences. * Phase 2 * Absent. * Phase 3 * Inactivation of the Ca2+ channels and increased activation of K+ channels --\>Ž increased K+ efflux. * Phase 4 * Slow diastolic depolarization * Membrane potential spontaneously depolarizes as Na+ conductance increases * I_f different from I_Na in phase 0 of ventricular action potential. * Accounts for automaticity of SA and AV nodes. * The slope of phase 4 in the SA node determines HR. * ACh/adenosine decreases the rate of diastolic depolarization and decreases HR * Catecholamines increase depolarization and increase HR. * Sympathetic stimulation increases the chance that I_f channels are open and thus increases HR.

Question 29

Electrocardiogram * Components * P wave * PR interval * QRS complex * QT interval * T wave * ST segment * U wave * Speed of conduction * Pacemakers * Conduction pathway * SA node “pacemaker” * AV node—100-msec delay

Answer 29

* Components * P wave * Atrial depolarization. * Atrial repolarization is masked by QRS complex. * PR interval * Conduction delay through AV node (normally \< 200 msec). * QRS complex * Ventricular depolarization (normally \< 120 msec). * QT interval * Mechanical contraction of the ventricles. * T wave * Ventricular repolarization. * T-wave inversion may indicate recent MI. * ST segment * Isoelectric, ventricles depolarized. * U wave * Caused by hypokalemia, bradycardia. * Speed of conduction * Purkinje \> atria \> ventricles \> AV node. * Pacemakers * SA \> AV \> bundle of His/Purkinje/ventricles. * Conduction pathway * SA node Ž--\> atria Ž--\> AV node Ž--\> common bundle Ž--\> bundle branches --\> Purkinje fibers --\>Ž ventricles. * SA node “pacemaker” * Inherent dominance with slow phase of upstroke. * AV node—100-msec delay * Atrioventricular delay that allows time for ventricular filling.

Question 30

Torsades de pointes * Definition * Caused by...

Answer 30

* Definition * Polymorphic ventricular tachycardia, characterized by shifting sinusoidal waveforms on ECG * Can progress to ventricular fibrillation. * Treatment includes magnesium sulfate. * Caused by... * Long QT interval predisposes to torsades de pointes. * Caused by drugs, decreased K+, decreased Mg2+, other abnormalities. * ****_S_**ome **_R_**isky **_M_**eds **_C_**an **_P_**rolong _QT_:** * **_S_**otalol * **_R_**isperidone (antipsychotics) * **_M_**acrolides * **_C_**hloroquine * **_P_**rotease inhibitors (-navir) * **_Q_**uinidine (class Ia; also class III) * **_T_**hiazides

Question 31

Congenital long QT syndrome * Definition * Romano-Ward syndrome * Jervell and Lange-Nielsen syndrome

Answer 31

* Definition * Inherited disorder of myocardial repolarization * Typically due to ion channel defects * Increased risk of sudden cardiac death due to torsades de pointes * **Romano-Ward syndrome** * Autosomal dominant * Pure cardiac phenotype (no deafness). * **Jervell and Lange-Nielsen syndrome** * Autosomal recessive * Sensorineural deafness.

Question 32

Wolff-Parkinson-White syndrome

Answer 32

* Most common type of ventricular pre-excitation syndrome. * Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses the rate-slowing AV node. * As a result, ventricles begin to partially depolarize earlier, giving rise to characteristic delta wave with shortened PR interval on ECG. * May result in reentry circuit --\>Ž supraventricular tachycardia.

Question 33

ECG tracings: Atrial fibrillation * Definition * Treatment

Answer 33

* Definition * Chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between irregularly spaced QRS complexes. * Can result in atrial stasis and lead to thromboembolic stroke. * Treatment * Includes rate control, anticoagulation, and possible pharmacological or electrical cardioversion.

Question 34

ECG tracings: Atrial flutter * Definition * Treatment

Answer 34

* Definition * A rapid succession of identical, back-to-back atrial depolarization waves. * The identical appearance accounts for the “sawtooth” appearance of the flutter waves. * Treatment * Pharmacologic conversion to sinus rhythm: class IA, IC, or III antiarrhythmics. * Rate control: β-blocker or calcium channel blocker. * Definitive treatment is catheter ablation.

Question 35

ECG tracings: Ventricular fibrillation * Definition * Treatment

Answer 35

* Definition * A completely erratic rhythm with no identifiable waves. * Treatment * Fatal arrhythmia without immediate CPR and defibrillation.

Question 36

ECG tracings: 1st degree AV block

Answer 36

* The PR interval is prolonged (\> 200 msec). * Benign and asymptomatic. * No treatment required.

Question 37

ECG tracings: Mobitz type I (Wenckebach) 2nd degree AV block

Answer 37

* Progressive lengthening of the PR interval until a beat is “dropped” (a P wave not followed by a QRS complex). * Usually asymptomatic.

Question 38

ECG tracings: Mobitz type II 2nd degree AV block

Answer 38

* Dropped beats that are not preceded by a change in the length of the PR interval (as in type I). * It is often found as 2:1 block, where there are 2 or more P waves to 1 QRS response. * May progress to 3rd-degree block. * Often treated with pacemaker.

Question 39

ECG tracings: 3rd degree AV block

Answer 39

* AKA complete AV block * The atria and ventricles beat independently of each other. * Both P waves and QRS complexes are present, although the P waves bear no relation to the QRS complexes. * The atrial rate is faster than the ventricular rate. * Usually treated with pacemaker. * Lyme disease can result in 3rd-degree heart block.

Question 40

Atrial natriuretic peptide

Answer 40

* Released from **atrial myocytes** in response to increased blood volume and atrial pressure. * Causes vasodilation and decreased Na+ reabsorption at the renal collecting tubule. * Constricts efferent renal arterioles and dilates afferent arterioles via cGMP, promoting diuresis and contributing to “aldosterone escape” mechanism.

Question 41

B-type natriuretic peptide

Answer 41

* AKA B-type (brain) natriuretic peptide * Released from **ventricular myocytes** in response to increased tension. * Similar physiologic action to atrial natriuretic peptide (ANP), with longer half-life. * BNP blood test used for diagnosing heart failure (very good negative predictive value). * Available in recombinant form (nesiritide) for treatment of heart failure.

Question 42

Baroreceptors and chemoreceptors * Receptors: * Aortic arch * Carotid sinus * Chemoreceptors: * Peripheral * Central

Answer 42

* Receptors: * Aortic arch * Transmits via vagus nerve to solitary nucleus of medulla * **Responds only** to increased BP. * Carotid sinus * Dilated region at carotid bifurcation * Transmits via glossopharyngeal nerve to solitary nucleus of medulla * Responds to decreases and increases in BP. * Chemoreceptors: * Peripheral * Carotid and aortic bodies are stimulated by decreassed Po2 (\< 60 mmHg), increased Pco2, and decreased pH of blood. * Central * Stimulated by changes in pH and Pco2 of brain interstitial fluid, which in turn are influenced by arterial CO2. * Do not directly respond to Po2.

Question 43

Baroreceptors and chemoreceptors * Baroreceptors * Hypotension * Carotid massage * Cushing reaction

Answer 43

* Baroreceptors: * ƒƒHypotension * Decreased arterial pressure * --\> decreased stretch * --\>Ž decreased afferent baroreceptor firing * --\>Ž increased efferent sympathetic firing and decreased efferent parasympathetic stimulation * Ž--\> vasoconstriction, increased HR, increased contractility, increased BP. * Important in the response to severe hemorrhage. * Carotid massage * Increased pressure on carotid sinus * Ž--\> increased stretch * --\> increased afferent baroreceptor firing * --\> increased AV node refractory period * --\> decreased HR. * Contributes to Cushing reaction * Triad of hypertension, bradycardia, and respiratory depression * Increased intracranial pressure constricts arterioles * Ž--\> cerebral ischemia and reflex sympathetic increases in perfusion pressure (hypertension) Ž * --\> increased stretch * --\>Ž reflex baroreceptor induced–bradycardia.

Question 44

Circulation through organs * Lung * Liver * Kidney * Heart

Answer 44

* Lung * Organ with largest blood flow (100% of cardiac output). * Liver * Largest share of systemic cardiac output. * Kidney * Highest blood flow per gram of tissue. * Heart * Largest arteriovenous O2 difference because O2 extraction is ∼ 80%. * Therefore increased O2 demand is met by increased coronary blood flow, not by increased extraction of O2.

Question 45

Normal pressures * Pulmonary capillary wedge pressure (PCWP) * Normal pressures * RA * RV * PA * LA * LV * AA

Answer 45

* Pulmonary capillary wedge pressure (PCWP) * Measured in mmHg with pulmonary artery catheter (Swan-Ganz catheter). * A good approximation of left atrial pressure. * In mitral stenosis, PCWP \> LV diastolic pressure. * Normal pressures * RA \< 5 * RV = 25/5 * PA = 25/10 * LA \< 12 * LV = 130/10 * AA = 130/90

Question 46

Capillary fluid exchange * Starling forces * Pc * Pi * πc * πi * Net filtration pressure (Pnet) * Kf * Jv

Answer 46

* Starling forces determine fluid movement through capillary membranes: * Pc = capillary pressure—pushes fluid out of capillary * Pi = interstitial fluid pressure—pushes fluid into capillary * πc = plasma colloid osmotic pressure—pulls fluid into capillary * πi = interstitial fluid colloid osmotic pressure—pulls fluid out of capillary * Net filtration pressure (Pnet) = [(Pc - Pi) - (πc - πi)]. * Kf = filtration constant (capillary permeability). * Jv = net fluid flow = (Kf)(Pnet).

Question 47

Autoregulation * Definition * Factors determining autoregulation in these organs * Heart * Brain * Kidneys * Lungs * Skeletal muscle * Skin * Hypoxia: lungs vs. other organs

Answer 47

* Definition * How blood flow to an organ remains constant over a wide range of perfusion pressures. * Factors determining autoregulation in these organs * Heart * Local metabolites (vasodilatory)–CO2, adenosine, NO * Brain * Local metabolites (vasodilatory)–CO2 (pH) * Kidneys * Myogenic and tubuloglomerular feedback * Lungs * Hypoxia causes vasoconstriction * Skeletal muscle * Local metabolites—lactate, adenosine, K+, H+, CO2 * Skin * Sympathetic stimulation most important mechanism—temperature control * Hypoxia: lungs vs. other organs * The pulmonary vasculature is unique in that hypoxia causes vasoconstriction so that only well-ventilated areas are perfused. * In other organs, hypoxia causes vasodilation.

Question 48

Edema * Definition * Capillary pressure * Plasma proteins * Capillary permeability * Interstitial fluid colloid osmotic pressure

Answer 48

* Definition * Excess fluid outflow into interstitium commonly caused by: * Increased capillary pressure * Increased Pc * Heart failure * Decreased plasma proteins * Decreased πc * Nephrotic syndrome, liver failure * Increased capillary permeability * Increased Kf * Toxins, infections, burns * Increased interstitial fluid colloid osmotic pressure * Increased πi * Lymphatic blockage