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.
  • Some Risky Meds Can Prolong QT:
    
    • Sotalol
    • Risperidone (antipsychotics)
    • Macrolides
    • Chloroquine
    • Protease inhibitors (-navir)
    • Quinidine (class Ia; also class III)
    • Thiazides

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