Cardiovascular - Physiology Flashcards
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
Q
PDA
- Type of heart murmur
- Characteristics
A
- 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
Q
Ventricular action potential:
Phases
- Phase 0
- Phase 1
- Phase 2
- Phase 3
- Phase 4
A
- 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
Q
Ventricular action potential
- Also occurs in…
- In contrast to skeletal muscle:
A
- 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.
- Cardiac muscle action potential has a plateau, which is due to Ca2+ influx and K+ efflux
28
Q
Pacemaker action potential
- Occurs in…
- Key differences from the ventricular action potential include:
- Phase 0
- Phase 1
- Phase 2
- Phase 3
- Phase 4
A
- 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.
- Membrane potential spontaneously depolarizes as Na+ conductance increases
- 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.
- Slow diastolic depolarization
- Phase 0
29
Q
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
A
- 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.
- P wave
- 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
Q
Torsades de pointes
- Definition
- Caused by…
A
- 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
32
Q
Wolff-Parkinson-White syndrome
A
- 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
Q
ECG tracings:
Atrial fibrillation
- Definition
- Treatment
A
- 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
Q
ECG tracings:
Atrial flutter
- Definition
- Treatment
A
- 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
Q
ECG tracings:
Ventricular fibrillation
- Definition
- Treatment
A
- Definition
- A completely erratic rhythm with no identifiable waves.
- Treatment
- Fatal arrhythmia without immediate CPR and defibrillation.
36
Q
ECG tracings:
1st degree AV block
A
- The PR interval is prolonged (> 200 msec).
- Benign and asymptomatic.
- No treatment required.
37
Q
ECG tracings:
Mobitz type I (Wenckebach) 2nd degree AV block
A
- Progressive lengthening of the PR interval until a beat is “dropped” (a P wave not followed by a QRS complex).
- Usually asymptomatic.
38
Q
ECG tracings:
Mobitz type II 2nd degree AV block
A
- 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
Q
ECG tracings:
3rd degree AV block
A
- 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.
42
Q
Baroreceptors and chemoreceptors
- Receptors:
- Aortic arch
- Carotid sinus
- Chemoreceptors:
- Peripheral
- Central
A
- 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.
- Aortic arch
- 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.
- Peripheral
43
Q
Baroreceptors and chemoreceptors
- Baroreceptors
- Hypotension
- Carotid massage
- Cushing reaction
A
- 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.
- Decreased arterial pressure
- 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.
- Hypotension
45
Q
Normal pressures
- Pulmonary capillary wedge pressure (PCWP)
- Normal pressures
- RA
- RV
- PA
- LA
- LV
- AA
A
- 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
Q
Capillary fluid exchange
- Starling forces
- Pc
- Pi
- πc
- πi
- Net filtration pressure (Pnet)
- Kf
- Jv
A
- 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).
48
Q
Edema
- Definition
- Capillary pressure
- Plasma proteins
- Capillary permeability
- Interstitial fluid colloid osmotic pressure
A
- 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
