Physiology Flashcards
Cardiac Output =
Stroke Volume * Heart Rate
Fick Principle
Cardiac Output = rate of O2 consumption/(arterial O2 content - venous O2 content)
Mean arterial pressure (MAP)
Cardiac Output * Total Peripheral Resistance
OR
2/3 diastolic pressure + 1/3 systolic pressure
Pulse pressure
systolic pressure - diastolic pressure
Pulse pressure is proportionate to stroke volume
Stroke volume
CO/HR
or
EDV - ESV
In exercise how is CO maintained
Early
Late
What if HR gets too high?
Early: Increased HR and increase SV
Late: Increased HR only (SV plateaus)
If HR is too high, diastolic filling is incomplete and CO decreased (VT)
What effects stroke volume?
Increased stroke volume when…
Contractility, Afterload, Preload (SV CAP)
Increased stroke volume when increased preload, decreased afterload, or increased contractility
Contractility increased with
- Catecholamines (Increased activity of Ca2+ pump in sarcoplasmic reticulum)
- Increased intracellular Ca2+
- Decreased extracellular Na+ (decreased Na+/Ca+ exchanger)
- Digitalis (blocks Na+/K+ pump -> increased intracellular Na+ -> decreased Na+/Ca+)
Contractility decreased with
- Beta-blockade (decreased cAMP)
- Heart failure (systolic dysfunction)
- Acidosis
- Hypoxia/hypercapnea (decrease PO2/increased PCO2)
- Non-dihydropyridine Ca2+ channel blockers
Stroke volume increased in these conditions
anxiety, exercise, pregnancy
Stroke volume decreases in this condition
Heart failure
Myocardial O2 demand is increased by
Increase afterload
Increase contractility
Increase HR
Increased heart size (increase wall tension)
Preload =
ventricular EDV
Afterload =
mean arterial pressure (proportional to peripheral resistance)
Venodilators do what to preload
Decrease preload (nitroglycerin)
Vasodilators do what to afterload
Decreased afterload (hydralazine)
Preload increases with
Exercise (slightly)
Increased blood volume (overtransfusion)
Excitement (increased SNS)
Force of contraction is proportional to what
End diastolic length of cardiac muscle fiber (preload)
Starling curve axis
Slope of curve decreases with
X axis = ventricular EDV (preload)
Y axis = CO or Stroke Volume
Slope decreases with CHF + digoxin, CHF
Slope increases with exercise (sympathetic nerve impulses)
Ejection fraction =
What is it an index for?
Normal percent?
Stroke Volume/End Diastolic Volume or EDV - ESV/EDV Index for ventricular contractility Normally greater/equal to 55% (decreases in systolic HF)
Driving pressure =
Flow * Resistance (Q*R) (similar to Ohm’s of change in V = IR)
Resistance =
driving pressure/flow (deltaP/Q)
or
8n (viscosity) * length/ pi*r^4
Total resistance in vessels in series =
R1 + R2 + R3….
Total resistance in vessels in parallel =
1/R1 + 1/R2 + 1/R3…
Viscosity depends on…
Viscosity increases in…
Viscosity decreases in…
Depends on hematocrit
Increases polycythemia, hyperproteinemic states (multiple myeloma), hereditary spherocytosis
Decreases in anemia
Pressure gradient drives flow to what direction?
High pressure to low pressure
Resistance is proportional and inversely proportional to
Directly proportional to viscosity and vessel length
Inversely proportional to radius to the 4th power
Most peripheral resistance comes from these vessels…
arterioles (regulate capillary flow)
Phases of cardiac cycle in LV: isovolumetric contraction
period between mitral valve closure and aortic valve opening; period of highest O2 consumption
Phases of cardiac cycle in LV: systolic ejection
period between aortic valve opening and closing
Phases of cardiac cycle in LV: isovolumetric relaxation
period between aortic valve closing and mitral valve opening
Phases of cardiac cycle in LV: rapid filling
Period just after mitral valve opening
Phases of cardiac cycle in LV: reduced filling
Period just before mitral valve closure
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 (MR, CHF) and more common in dilated ventricles (but normal in pregnant and children)
To hear: https://www.youtube.com/watch?v=xbLMC0kPQ-E&list=UUkiESbCo0zbmPwovRiXC8VQ&index=14
S4
Atrial kick - in late diastole. High atrial pressure. Associated with ventricular hypertroph. Left atrium must push against stiff LV wall.
Systole includes
Isovolumetric contraction
Rapid ejection
Reduced ejection
Jugular venous pulse
a wave - atrial contraction
c wave - RV contraction (closed tricuspid bulging into atrium)
x descent - atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction
v wave - increased R atrial pressure due to filling against closed tricuspid valve
y descent - blood flow from RA to RV
Normal splitting
Inspiration –> drop in intrathoracic pressure –> increase venous return to the RV –> increased RV stroke volume –> increased RV ejection time –> delayed closure of pulmonic valve (also due to decreased pulmonary impedance during inspiration)
Wide splitting
Conditions that delay RV emptying (pulm stenosis, right bundle branch block)
Delay in RV emptying causes delayed pulmonic sound (regardless of breath) –> exaggeration of normal splitting
to hear: https://www.youtube.com/watch?v=5tBk1XuEyuM&list=UUkiESbCo0zbmPwovRiXC8VQ
Fixed splitting
Seen in ASD. ASD –> left-to-right shunt –> increased right atrial and right ventricular volumes –> increased flow through pulmonic valve such that (regardless of breath) pulmonic closure is greatly delayed
to hear: https://www.youtube.com/watch?v=5tBk1XuEyuM&list=UUkiESbCo0zbmPwovRiXC8VQ
Paradoxical splitting
Seen in conditions that delay LV emptying (aortic stenosis, left BBB)
Normal order of valve closure is reversed so that P2 sounds occur before delayed A2 sound so on inspiration P2 closes later and moves closer to A2 (paradoxically eliminating the split)
to hear: https://www.youtube.com/watch?v=5tBk1XuEyuM&list=UUkiESbCo0zbmPwovRiXC8VQ
Aortic ascultation
Right sternal border
Systolic murmur = aortic stenosis, flow murmur, aortic valve sclerosis
MR SAS (Mitral regur, Systolic, Aortic Stenosis)
Left sternal border ascultation
Left sternal border
Diastolic murmur = aortic regurgitation, pulmonic regurgitation
Systolic murmur = hypertrophic cardiomyopathy
MS DAR (mitral sten, diastolic, aortic regur)
Pulmonic ascultation
Systolic ejection murmur
Pulmonic stenosis, flow murmur (ASD, PDA)
Tricuspid ascultation
Pansystolic murmur =Tricuspid regurgitation, VSD
Diastolic murmur = tricuspid stenosis, ASD
Mitral ascultation
Systolic murmur = mitral regrug
Diastolic murmur = mitral stenosis
Machine-like murmur of PDA is best appreciated in this location
Left infraclavicular region
ASD presents with this kind of murmur - early and late
pulmonary flow murmur (increase flow through pulmonary valve) and a diastolic rumble (increased flow across tricuspid)
later progresses to louder diastolic murmur of pulmonic regurg from dilatation of pulmonary artery
Increase intensity of right heart sounds by
inspiration
Increase intensity of left heard sound by
expiration
Increase intensity of MR, AR, VSD, MVP murmurs
Decrease intensity of AS, hypertrophic cardiomyopathy murmur
Hand grip (increase systemic vascular resistance)
Decrease intensity of most murmur
Increase intensity of MVP, hypertrophic cardiomyopathy murmur
Valsalva (decrease venous return)
Decrease intensity of MPV, hypertrophic cardiomyopathy murmur
Rapid squatting (increase venous return, increase preload, increase afterload with prolonged squatting)
Systolic heart sounds
aortic/pulmonic stenosis, mitral/tricuspid regurg, VSD
To hear normal: https://www.youtube.com/watch?v=xS3jX1FYG-M&list=UUkiESbCo0zbmPwovRiXC8VQ
Diastolic heart sound
aortic/pulmonic regurg, mitral/tricuspid stenosis
To hear normal: https://www.youtube.com/watch?v=xS3jX1FYG-M&list=UUkiESbCo0zbmPwovRiXC8VQ
Mitral Regurgitation Murmur Sounds like Best heard at Enhanced with Due to
Holosystolic, high-pitched “blowing murmur”
Mitral - loudest at apex and radiates toward axilla
Enhanced by maneuvers that increase TPR (squatting, hand grip) or LA return (expire)
MR due to ischemic heart disease, MVP, LV dilation; rheumatic fever and infective endocarditis
To hear: https://www.youtube.com/watch?v=MMJBSd5Z_Uc
Tricuspid Regurgitation Murmur Sounds like Best heard at Enhanced with Due to
Holosystolic, high-pitched “blowing murmur”
Tricuspid - loudest at tricuspid area and radiates to right sternal border
Enhanced by maneuvers that increase RA return (inspire)
TR due to RV dilation; rheumatic fever and infective endocarditis
To hear: https://www.youtube.com/watch?v=Jk50shI9vV8
Aortic Stenosis Sounds like Also heard at Other signs Due to Can cause
Crescendo-decrescendo systolic ejection murmur following ejection click (due to abrupt halting of valve leaflets)
Radiates to carotids/heart base
Pulsus parvus et tardus - pulses are weak with a delayed peak
LV»_space; aortic pressure during systole; age-related calcific aortic stenosis or bicuspid aortic valve
Can lead to syncope, angina, dyspnea on exertion (SAD)
To hear: https://www.youtube.com/watch?v=Gbk2465HO98&list=UUkiESbCo0zbmPwovRiXC8VQ
VSD
Sounds like
Best heard at
Enhanced by
Holosystolic, hard sounding murmur
Loudest at tricuspid area
Enhanced by hand grip bc increased afterload
To hear: https://www.youtube.com/watch?v=7oKz6J0Ay_I
MVP Sounds like Best heard at Enhanced by Due to
Late systolic crescendo murmur with midsystolic click (due to sudden tensing of chordae tendineae)
Best heard over apex, loudest at S2
Enhanced by maneuvers that decrease venous return (standing/Valsalva)
Due to valvular lesion but benign usually or myxomatous degeneration, rheumatic fever, chordae rupture; predispose to infective endocarditis
Mid-systolic click: https://www.youtube.com/watch?v=PsmGx2XMxF8&list=UUkiESbCo0zbmPwovRiXC8VQ
Aortic regurgitation Sounds like Enhanced/depressed by Other sx Due to
Immediate high-pitched “blowing” diastolic decrescendo murmur
Enhanced by hand grip, vasodilators decrease intensity
Wide pulse pressure when chronic - present with bounding pulses and head bobbing
Due to aortic root dilation, bicuspid aortic valve, endocarditis, rheumatic fever
To hear: https://www.youtube.com/watch?v=42IahK-zxj0&list=UUkiESbCo0zbmPwovRiXC8VQ
Mitral stenosis
Sounds like
Enhanced by
Due to
Follows opening snap (due to abrupt halt in leaflet motion in diastole after rapid opening due to fusion at leaflet tips); delayed rumbling late diastolic murmur
Enhanced by maneuvers that increase LA return (expire)
LA»_space; LV pressure during diastole
Occurs 2ndary to rheuamtic fever, chronic MS can result in LA dilation
To hear: https://www.youtube.com/watch?v=L5DEqvgS_xs
Opening snap: https://www.youtube.com/watch?v=E0fDFsmVQfY&list=UUkiESbCo0zbmPwovRiXC8VQ
PDA
Sounds like
Best heard at
Due to
Continuous machine-like murmur, loudest at S2
Best heard at left infraclavicular area
Congenital rubella or prematurity
To hear: https://www.youtube.com/watch?v=UOOylGXPsyQ
Ventricular action potential (and at bundle of His and Purkinje fibers) - Phase 0
Phase 0 = rapid upstroke, voltage gated Na+ channels open
Ventricular action potential (and at bundle of His and Purkinje fibers) - Phase 1
Phase 1 = initial repolarization - inactivation of voltage-gated Na+ channels. Voltage-gated K+ channels begin to open
Ventricular action potential (and at bundle of His and Purkinje fibers) - Phase 2
Phase 2 = plateau - Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflus. Ca2+ influx triggers Ca2+ relase from sarcoplasmic reticulum and myocyte contraction
Ventricular action potential (and at bundle of His and Purkinje fibers) - Phase 3
Phase 3 = rapid repolarization - massive K+ efflus due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca2+ channels
Ventricular action potential (and at bundle of His and Purkinje fibers) - Phase 4
Phase 4 = resting potential - high K+ permeability through K+ channel
Hows is ventricular different than skeletal muscle?
- Cardiac muscle AP has a plateau - due to Ca2+ influx and K+ efflux
- Myocyte contraction occurs due to Ca2+ induced Ca2+ release from SR
- Cardiac nodal cells spontaneously depolarize during diastole resulting in automaticity due to I-f channels (slow mixed Na+/K+ inward current)
- Cardiac myocytes are electrically coupled to each other by gap junctions
Pacemaker action potential - Phase 0 (SA and AV nodes)
Phase 0 = upstroke - opening of voltage gated Ca2+ channels. Fast voltage gated Na+ channels are permanently inactivated bc 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
Pacemaker action potential - Phase 2 (SA and AV nodes)
Phase 2 = plateau is absent
Pacemaker action potential - Phase 3 (SA and AV nodes)
Phase 3 = inactivation of Ca2+ channels and increase activation of K+ channels leading to K+ efflux
Pacemaker action potential - Phase 4 (SA and AV nodes)
Phase 4 = slow diastolic depolarization - membrane potential spontaneously depolarizes as Na+ conductance increases. Accounts for automaticity of SA and AV nodes. Slope of phase 4 in SA = HR.
ACh/adenosine decrease rate of diastolic depol and decrease HR
Catechols increase depol and HR
SNS stim increase the chance that I-f channels are open and thus increase HR
Pulmonary stenosis
to hear: https://www.youtube.com/watch?v=SWW1PTL9Jbw&list=UUkiESbCo0zbmPwovRiXC8VQ
Aortic arch receptor
transmits via what?
to what?
responding to what?
transmits via vagus nerve to solitary nucleus of medulla
responds only to increased BP
Carotid sinus receptor
transmits via what?
to what?
responding to what?
transmits via glossopharyngeal nerve to solitary nucleus of medulla
responds to increase and decrease in BP
Baroreceptor response to hypotension
decrease arterial pressure –> decrease stretch –> decrease afferent baroreceptor firing –> increase efferent sympathetic firing and decrease efferent parasympathetic stimulation –> vasoconstriction, increase HR/contractility/BP.
Important in severe hemorrhage
Carotid massage
increase pressure on carotid artery –> increase stretch –> increase afferent baroreceptor firing –> decrease HR
How do baroreceptors contribute to Cushing reaction?
Cushing reaction: HTN, bradycardia, and respiratory depression
Increase intracranial pressure constricts arterioles –> cerebral ischemia and reflex sympathetic increase in perfusion pressure (HTN) –> increase stretch –> reflex baroreceptor induced-bradycardia
Peripheral chemoreceptors where?
Stimulated by?
Peripheral - carotid and aortic bodies
Stimulated by decrease in PO2 (<60 mmHg), increase PCO2, and decrease pH of blood (acid)
Central chemoreceptors
Stimulated by?
stimulated by changes in pH and PCO2 of brain interstitial fluid which in turn are influenced by arterial CO2. Do no directly respond to PO2
Organ with the largest blood flow
Lung = 100% of cardiac output
Organ with largest share of SYSTEMIC cardiac output
Liver
Organ with highest blood flow per gram of tissue
Kidney
Organ with largest arteriovenous O2 difference because O2 extraction is 80%.
Heart - therefore increase O2 demand is met by increase coronary blood flow, not by increase extraction of O2
PCWP approximates what
How does mitral stenosis effect it?
How is it measured?
Pulmonary capillary wedge pressure is a good approximation of left atrial pressure. In mitral stenosis the PCWP > LV diastolic pressure
Measured with pulmonary artery catheter (Swan-Ganz)
Autoregulation
How blood flow to an organ remains constant over a wide range of perfusion pressures
Factors determining autoregulation of the heart
Local metabolites (vasodilatory) - CO2, adenosine, NO
Factors determining autoregulation of the brain
Local metabolites (vasodilatory) - CO2 (pH)
Factors determining autoregulation of the kidneys
Myogenic and tubuloglomerular feedback
Factors determining autoregulation of the lungs
Hypoxia causes vasoconstriction
Factors determining autoregulation of the skeletal muscles
Local metabolites - lactate, adenosine, K+
Factors determining autoregulation of the skin
Sympathetic stimulation most important mechanism - temperature control
How does hypoxia effect the pulmonary vasculature?
Hypoxia causes vasoconstriction so that only well-ventilated areas are perfused. In other organs, hypoxia causes vasodilation.
What determines the fluid movement through capillary membranes? Name all four.
Starling forces
Pc = capillary pressure - pushes fluid out of capillary
Pi = interstitial fluid pressure - pushes fluid into capillary
(Pi)c = plasma colloid osmotic pressure - pulls fluid into capillary
(Pi)i = interstitial fluid colloid osmotic pressure - pulls fluid out of capillary
Net filtration pressure of capillaries?
P net = [(Pc - Pi) - ((Pi)c - (Pi)i)]
What is the filtration constant and what does it represent?
Kf = filtration constant = capillary permeability
Net fluid flow?
Jv = net fluid flow = (Kf)(P net)
Causes of edema
Excess fluid outflow into interstitium caused by:
Increase capillary pressure (Pc; heart failure)
Decrease plasma proteins ((Pi)c; nephrotic syndrome, liver failure)
Increase capillary permeability (Kf; toxins, infections, burns)
Increase interstitial fluid colloid osmotic pressure ((Pi)i; lymphatic blockage)
