Cardiovascular - Physiology Flashcards
(48 cards)
1
Q
Cardiac output & mean arterial pressure
- Cardiac output (CO)
- Equations
- Early vs. late stages of exercise
- Diastole
- Mean arterial pressure (MAP) equations
A
- 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).
- Equations
- Mean arterial pressure (MAP)
- MAP = CO × TPR.
- MAP = 2/3 diastolic pressure + 1/3 systolic pressure.
2
Q
Pulse pressure & stroke volume
- Pulse pressure
- Equations
- Increased in…
- Decreased in…
- Stroke volume
- Equation
- Increased with…
A
- 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.
- Pulse pressure = systolic pressure – diastolic pressure.
- Stroke volume
- SV = EDV - ESV
- Increased with increased contractility, increased preload, or decreased afterload
- Stroke Volume affected by Contractility, Afterload, and Preload
- SV** **CAP
3
Q
Contractility
- Contractility (and SV) increase with:
- Contractility (and SV) decrease with:
- SV increases with:
- SV decreases with:
- Myocardial O2 demand is increased with:
A
- 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).
- Digitalis (blocks Na+/K+ pump –> increased intracellular Na+ –> decreased Na+/Ca2+ exchanger activity –> increased intracellular Ca2+).
- Contractility (and SV) decrease with:
- β1-blockade (decreased cAMP).
- Heart failure with systolic dysfunction.
- Acidosis.
- Hypoxia/hypercapnea (decreased Po2/ increased Pco2).
- Non-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).
4
Q
Preload
A
- 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.
5
Q
Afterload
A
- Afterload approximated by MAP.
- Chronic hypertension (increased MAP) –> LV hypertrophy.
- Relation of LV size and afterload –> 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.
6
Q
Ejection fraction
A
- 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.
7
Q
Starling curve
A
- 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.
8
Q
Resistance, pressure, flow
- Relationship
- Resistance
- Total resistance
- Viscosity
- Pressure
A
- 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 –> 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
- Hyperproteinemic states (e.g., multiple myeloma)
- Hereditary spherocytosis
- Viscosity decreases in anemia
- Viscosity increases in:
- Pressure gradient drives flow from high pressure to low pressure.
9
Q
Cardiac and vascular function curves (269)
- Intersection of curves
- Changes
- For each
- Effect
- Examples
- Inotropy
- Venous return
- Total peripheral resistance
A
- 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 –> fluid retention to increase preload to maintain CO)
- Inotropy
- Effect: Changes in contractility –> 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 –> 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 (-)
-
Effect: Changes in circulating volume or venous tone –> altered RA pressure for a given CO.
- Total peripheral resistance
-
Effect: Changes in TPR –> altered CO at a given RA pressure
- However, mean systemic pressure (x-intercept) is unchanged.
-
Examples:
- Vasopressors (+)
- Exercise, AV shunt (-)
-
Effect: Changes in TPR –> altered CO at a given RA pressure
10
Q
Pressure-volume loops and cardiac cycle:
Phases—left ventricle
- Isovolumetric contraction
- Systolic ejection
- Isovolumetric relaxation
- Rapid filling
- Reduced filling
A
- Isovolumetric contraction
- Period between mitral valve closing and aortic valve opening
- Period of highest O2 consumption
- Systolic ejection
- Period between aortic valve opening and closing
- Isovolumetric relaxation
- Period between aortic valve closing and mitral valve opening
- Rapid filling
- Period just after mitral valve opening
- Reduced filling
- Period just before mitral valve closing
11
Q
Pressure-volume loops and cardiac cycle:
Sounds
- S1
- S2
- S3
- S4
- Systolic heart sounds
- Diastolic heart sounds
A
- 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.
12
Q
Pressure-volume loops and cardiac cycle:
Jugular venous pulse (JVP)
- a wave
- c wave
- x descent
- v wave
- y descent
A
-
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.
13
Q
Normal splitting
A
- Inspiration
- –> drop in intrathoracic pressure
- –> increased venous return to the RV
- –> increased RV stroke volume
- –> increased RV ejection time
- –> 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.
14
Q
Wide splitting
A
- 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.
15
Q
Fixed splitting
A
- Seen in ASD.
- ASD
- –> left-to-right shunt
- –> increased RA and RV volumes
- –> increased flow through pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed.
16
Q
Paradoxical splitting
A
- 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.
17
Q
Auscultation of the heart:
Where to listen
- Aortic area
- Left sternal border
- Pulmonic area
- Tricuspid area
- Mitral area
A
- APT M
-
Aortic area
- Systolic murmur
- Aortic stenosis
- Flow murmur
- Aortic valve sclerosis
- Systolic murmur
- Left sternal border:
- Diastolic murmur
- Aortic regurgitation
- Pulmonic regurgitation
- Systolic murmur
- Hypertrophic cardiomyopathy
- Diastolic murmur
-
Pulmonic area:
- Systolic ejection murmur
- Pulmonic stenosis
- Flow murmur (e.g., physiologic murmur)
- Systolic ejection 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.
- Pansystolic murmur
-
Mitral area:
- Systolic murmur
- Mitral regurgitation
- Diastolic murmur
- Mitral stenosis
- Systolic murmur
18
Q
Auscultation of the heart:
Effects of these bedside maneuvers
- Inspiration
- Hand grip
- Valsalva (phase II, forcing exhalation against a closed airway), standing
- Rapid squatting
A
- 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
19
Q
Mitral/tricuspid regurgitation (MR/TR)
- Type of heart murmur
- Mitral characteristics
- Tricuspid characteristics
A
- 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.
20
Q
Aortic stenosis (AS)
- Type of heart murmur
- Characteristics
A
- 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.
21
Q
VSD
- Type of heart murmur
- Characteristics
A
- Systolic heart murmur
- Holosystolic, harsh-sounding murmur.
- Characteristics
- Loudest at tricuspid area, accentuated with hand grip maneuver due to increased afterload.
22
Q
Mitral valve prolapse (MVP)
- Type of heart murmur
- Characteristics
A
- 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).
23
Q
Aortic regurgitation (AR)
- Type of heart murmur
- Characteristics
A
- 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.
24
Q
Mitral stenosis (MS)
- Type of heart murmur
- Characteristics
A
- 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).
- Follows opening snap (OS)
25
PDA
* Type of heart murmur
* Characteristics
* Continuous heart murmur
* Continuous machine-like murmur.
* Characteristics
* Loudest at S2.
* Often due to congenital rubella or prematurity.
* Best heard at left infraclavicular area.
26
Ventricular action potential:
Phases
* Phase 0
* Phase 1
* Phase 2
* Phase 3
* Phase 4
* 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.
27
Ventricular action potential
* Also occurs in...
* In contrast to skeletal muscle:
* 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 If channels
* If = “funny current” channels responsible for a slow, mixed Na+/K+ inward current.
* Cardiac myocytes are electrically coupled to each other by gap junctions.
28
Pacemaker action potential
* Occurs in...
* Key differences from the ventricular action potential include:
* Phase 0
* Phase 1
* Phase 2
* Phase 3
* Phase 4
* 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 --\> increased K+ efflux.
* Phase 4
* Slow diastolic depolarization
* Membrane potential spontaneously depolarizes as Na+ conductance increases
* If different from INa 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 If channels are open and thus increases HR.
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
* 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 --\> atria --\> AV node --\> common bundle --\> bundle branches --\> Purkinje fibers --\> ventricles.
* SA node “pacemaker”
* Inherent dominance with slow phase of upstroke.
* AV node—100-msec delay
* Atrioventricular delay that allows time for ventricular filling.
30
Torsades de pointes
* Definition
* Caused by...
* 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
31
Congenital long QT syndrome
* Definition
* Romano-Ward syndrome
* Jervell and Lange-Nielsen syndrome
* 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.
32
Wolff-Parkinson-White syndrome
* 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 --\> supraventricular tachycardia.
33
ECG tracings:
Atrial fibrillation
* Definition
* Treatment
* 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.
34
ECG tracings:
Atrial flutter
* Definition
* Treatment
* 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.
35
ECG tracings:
Ventricular fibrillation
* Definition
* Treatment
* Definition
* A completely erratic rhythm with no identifiable waves.
* Treatment
* Fatal arrhythmia without immediate CPR and defibrillation.
36
ECG tracings:
1st degree AV block
* The PR interval is prolonged (\> 200 msec).
* Benign and asymptomatic.
* No treatment required.
37
ECG tracings:
Mobitz type I (Wenckebach) 2nd degree AV block
* Progressive lengthening of the PR interval until a beat is “dropped” (a P wave not followed by a QRS complex).
* Usually asymptomatic.
38
ECG tracings:
Mobitz type II 2nd degree AV block
* 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.
39
ECG tracings:
3rd degree AV block
* 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.
40
Atrial natriuretic peptide
* 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.
41
B-type natriuretic peptide
* 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.
42
Baroreceptors and chemoreceptors
* Receptors:
* Aortic arch
* Carotid sinus
* Chemoreceptors:
* Peripheral
* Central
* 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.
43
Baroreceptors and chemoreceptors
* Baroreceptors
* Hypotension
* Carotid massage
* Cushing reaction
* Baroreceptors:
* Hypotension
* Decreased arterial pressure
* --\> decreased stretch
* --\> decreased afferent baroreceptor firing
* --\> increased efferent sympathetic firing and decreased efferent parasympathetic stimulation
* --\> vasoconstriction, increased HR, increased contractility, increased BP.
* Important in the response to severe hemorrhage.
* Carotid massage
* Increased pressure on carotid sinus
* --\> 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
* --\> cerebral ischemia and reflex sympathetic increases in perfusion pressure (hypertension)
* --\> increased stretch
* --\> reflex baroreceptor induced–bradycardia.
44
Circulation through organs
* Lung
* Liver
* Kidney
* Heart
* 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.
45
Normal pressures
* Pulmonary capillary wedge pressure (PCWP)
* Normal pressures
* RA
* RV
* PA
* LA
* LV
* AA
* 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
46
Capillary fluid exchange
* Starling forces
* Pc
* Pi
* πc
* πi
* Net filtration pressure (Pnet)
* Kf
* Jv
* 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).
47
Autoregulation
* Definition
* Factors determining autoregulation in these organs
* Heart
* Brain
* Kidneys
* Lungs
* Skeletal muscle
* Skin
* Hypoxia: lungs vs. other organs
* 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.
48
Edema
* Definition
* Capillary pressure
* Plasma proteins
* Capillary permeability
* Interstitial fluid colloid osmotic pressure
* 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
