Important Physio Stuffs Flashcards
S1
- first heart sound, closure of mitral then tricuspid valves: two bursts, a mitral M1 and a tricuspid T1 component
- Occurs during R-S segment of EKG, and during the isovolumetric contraction
S2
- second heart sound (sounds like dub)
- An aortic A2 and a pulmonary P2 component: resulting from closure of aortic and pulmonary valves
OS
opening snap
- opening of a stenotic mitral valve
S3
- third heart sound: early diastole, soon after S2
- during rapid ventricular filling phase
- normal in younger people
- may indicate ventricular enlargement associated with heart failure; reduced distensibility/compliance
- diastolic filling gallop or ventricular or protodiastolic gallop
- “protodiastolic gallop” : S1-S2-S3 (“Ken-tuck-y”)
S4
- fourth heart sound: heard late diastole, just before S1
- Associated with unusually strong atrial contraction
- Indicative of pathology, ventricular wall stiffness and decreased compliance associated with hypertrophy
- atrial sound that creates an atrial or presytolic gallop
“Gallop” S1, S2 + S3 and/or S4
- Presystolic gallop: S4 - S1- S2
- (“Ten-nessee”)
splitting of S2
best heart during inspiration
On right side of heart:
- Relatively negative intrathoracic pressure –>greater VR to RA/RV –> increased EDV –> greater RV ejection volume
- Additional time for RV ejection delays pulmonary valve closure (P2) more
- Enhances physiological splitting of S2
Effect on left side of heart:
- Relatively negative intrathoracic pressure –>retention of blood in dilated pulmonary v.v. –>reduced VR to LA/LV –> decreased LV EDV & ejection
- Less time for LV ejection accelerates aortic valve closure (A2) more
- Enhances physiological splitting of S2
What are variations in S1, S2 splitting?
Louder S1 with Tachycardia
Valves are farther from being closed when contraction occurs (slam shut) vs. more time at slower HR to slowly begin closure
Pathologic S1 split
Additional increase in delay between Mitral and Tricuspid closure (M1 , T1)
Ex: Right Bundle Branch Block
Paradoxical S2 Splitting
A2 and P2 heard during expiration, not inspiration
Fixed S2 splitting
A2 and P2 heard throughout respiratory cycle
Mitral stenosis:
Valve stiffening may result in opening snap (OS) after S2, early diastole
Venous Pulse
Contributions to venous pulse:
(1) Retrograde action of the heartbeat during cardiac cycle
(2) Respiratory cycle
(3) Contraction of skeletal muscles
- same three waves as the atrial waves:
- a wave: RA contraction, closely related to venous return
- c wave: RV pressure in early systole (when all valves are closed and isovolumetric contraction occuring - bulging of tricuspid valve into RA)
- v wave: RA filling (tricuspid closed)
- increase pressure subsequent to y minimum –> occurs as VR continues with reduced ventricular filling
abnormal changes in a wave?
- RA contraction:
- no a waves: atrial fibrillation
- large a waves: tricuspid stenosis, right heart failure
- cannon (very large) a waves: third degree complete heart block (AV dissociation)
what causes an abnormal v wave?
RA filling (tricuspid bulging): large v wave (c-wave): tricuspid regurgitation
work performed by heart
W = P x V + 1/2mv2 + tension heat
- kinetic energy: factors work per beat including acceleration
- W = total external work
- P= pressure volume work
- 1/2mv is kinetic energy
Tension Heat: KT(change in heat)
- greatest energy cost
- splitting ATP during isovolumetric onctraction
- isometric: no “work” without movement
- T= ventricular wall tesnsion (afterload)
- change in time: time in systole
What are three main determinants of myocardial O2 demand?
- ventricular wall stress
- heart rate
- contractility (inotropic state)
Cardiac Output
CO = HR X SV
- normal = ~ 5 L/min at
Determinants: Preload, Afterload, Contractility/Inotropy
What is measured in right-sided heart catheterization? what about left-sided heart catheterization?
- RA, RV and pulmonary wedge pressure (left atrial pressure, wedged into a small pulmonary a.)
- LA, LV; insertion of catheter into artery and advanced into the left heart to measure pressure
what would you see with aortic stenosis?
- increased heart sound between S1–>S2 due to narrowing of the aortic valve
- Left ventricular pressure would be abnormally high, due to increased pressure needed to get blood through the narrow segment
What would you see with mitral stenosis?
- would hear sounds before from S2–>S1: diastole phase: sounds are due to the difficulty getting blood through the AV valves
- would see elevated pressure in the left atrium
What would you see with aortic regurgitation?
- would see abnormally elevated aortic pressure due to blood flowing back through aortic valve into the left ventricle
- hear abnormal sounds during diastolic phase; due to blood leaking back through into the ventricle
What would you hear with mitral insufficiency?
- would hear relatively flat sound during systole due to the mitral valve leaking back through, would result in increased pressure in the left atrium during systole
Left Ventricular heart failure
increased LV pressure, increased LA pressure, increased pulmonary vv. pressure, pincreased pulmonary capillary hydrostatic pressure, results in increased filtration, increased pulmonary edema
What is the cause of pulmonary hypertension?
RV failure, results in RA failure, results in venous distension of the VC, results in hepatomegally, ascites and peripheral edema
what does increased afterload lead to?
increased afterload (aortic pressure) –> decreased outflow velocity, greater proportion of time in systole is spent in isovolumetric contraction
- decreased stroke volume
- increased end systolic volume: decreased ejection fraction
What does increased preload lead to?
- increased VR, increased EDV, increased contractility, increased SV, increased CO
- preload activates more Ca2+ release via stretch activated Ca2+ channels on sarcolemma
How does NE affect heart rate
- results in positive chronotropy: via binding Adrenergic B1 receptors; increases heart rate
- increases funny current (increased diastolic Na+): results in increased steepness of phase 4 depolarization
- increased Ca2+ current; increases steepness of phase 4 and makes threshold more negative (thus reached sooner)
- > these result in shorter diastolic duration and threshold reached more quickly thus increaseing heart rate
How does ACh affect heart rate?
- binds cholinergic M2 receptors and results in negativ chronotropy
- increases K+ conductance: more (-) max diastolic potential (RMP)
- decreases If: decreaed slow depolarization rate
- decreases ICa2+: decreases slow dep. rate; makes threshold more negative
What is SV? How is it realated to CO? when is it increased/decreased?
SV = volume of blood ejected in 1 heartbeat (ml/beat)
SV = EDV - ESV
CO = HR x SV
In general:
SV is increased when:
- End-diastolic volume is increased (EDV)
- Contractility of the heart is increased
SV is decreased when:
- Afterload is increased
What are six factors that promote increased EDV?
- increased central venous pressure
- decreased HR
- increased ventricular compliance
- increased atrial contraction (symp. NE/Epi)
- increased aortic pressure
- pathological conditions: systolic failure, aortic stenosis/regurgitation, pulmonary valve stenosis/regurgitation
Six factors resulting in decrease of EDV?
- decreased CVP
- increased HR
- decreased atrial contractility (atrial arrythmias/fibrillation)
- decreased afterloaddiastolic failure (ventricular hypertrophy/ lusitropy)
- mitral/tricuspid valve stenosis
Factors which may decrease ESV?
- increased preload/ increased EDV
- decreased afterload
- increased contractility
- increased HR (can decrease or increase…. see notes)
How is positive inotropy regulated by sympathetic control?
- increased contractility due to B1 adrenergic receptors
- increased Ca2+ availability results in increased contractile force and increased CO
- increased Ca2+ influx via L-type DHDP channels, increased Ca2+ inside of cell results in increased Ca2+ dep Ca2+ release from the SR
- increase sensitivity to RYR
- increased SERCA activity (phopholamban is phosphorylated and more calcium can be stored in SR)
- increased ECF Ca2+ influx, results in increased SR Ca2+ stores over time
What is ESPVR?
**End-Systolic Pressure-Volume Relationship **
Slope of relationship between volume remaining at end of systole and a given End-systolic LV pressure
Indicator of contractility:
Lowest ESV possible independent of preload/EDV
The lower the ESV at a given LV pressure, the greater the contractility
increased contractiliy results in steeper more positive slope and increased stroke volume! (independent of EDV)
Also, sidenote: increased contractiliy results in increased steepness of ventricular performance curve
What are 5 positive inotropic agents?
- results in increased contractility
- adrenergic agonists (B1): catecholamines (NE/Epi)
- cardiac glycosides
- increased ECF [Ca2+]: (hypercalcemia)…. or decreased… see notes
- decreased ECF [Na+] (hyponateremia)
- increased HR: “bowditch effect”
What are 5 negative inotropic agents?
decrease in contractility
- muscarinic agonists (M2)
- decreased ECF [Ca2+]
- Ca2+ channel blockers
- increased [Na+] ECF: hypernatremia
- decreased pH
what results in positive lusitropy?
increased rate of relaxation = increased time for diastolic filling, increased SV
- B1-adrenergic agonists
- phosphorylation of phospholamban
- phosphorylation of troponin I
What effects negative lustiropy?
- decreased rate of relaxation
- elevated Ca2+ levels
- impaired SERCA
- increase affinity of Troponin C
- pH changes
How is increased CO met during exercise with decreased filling time caused by increased HR?
Positive inotropy and lusitropy: increased diastolic function and SV at a give Hr by decreasing relaxation time and increased force of contraction
- due to B1 effects on heart
CO= ?
CO= MAP/TPR
CO = HR x SV
Q =
CO= VO2 / A - VO2 difference
MAP =
MAP = DBP + 1/2 (SBP - DBP)
PP = ?
PP = SBP - DBP
SV =
SV = EDV - ESV
EF = ?
EF = SV/EDV
NET FILTRATION PRESSURE =
(Pc + osmotic IF) - (Osmotic capillary + Pif)
(out) - (in)
What are 6 major effects of angiotensin II?
- vasoconstriction
- stimulates aldosterone production
- stimulates ADH/AVP
- stimulates thirst
- stimulates Na+ reabsorption
- stimulates SNS activity
What does Aldosterone do?
- ANG II triggers secretion of Aldosterone from the adrenal medulla
- Aldosterone promotes renal Na+ reabsorption
- H2O follows by osmosis to increase effective circulating volume and increase MAP
What are the humoral regulations of blood pressure?
- RAAS: increased MAP
- ADH/AVP: increased MAP
- ANH/ANP: decreased MAP
What is the timing of neural and hormonal responses in the regulation of BP?
Fast acting:
- baroreceptors
- CNS ischemic
- chemoreceptors
Intermediate:
- capillary fluid shift
- renin-angiotensin vasoconstriction
Long-Term:
- aldosterone
- renal-blood volume pressure control
What are six regulations of MAP?
ANS
- Specific CV control reflexes (ex: baroreceptor reflex)
- Generalized ANS activation (ex: fight-or-flight response)
Respiratory
- Ventilation: modification of intrinsic chemoreceptor response
- Respiration: negative intra-thoracic pressure –>increased VR
- Respiration: water evaporation can impact blood volume over time, without compensation
Hematopoietic organs and liver
- Control of blood composition
- Hematocrit & large proteins: blood viscosity and flow
- Plasma protein: colloid osmotic pressure and Starling forces –> distribution ECF between interstitium and blood plasma
GI/Urinary:
- Long-term BP regulation: control of electrolyte & H2O input/output –> impacts ECF volume and composition
Endocrine System:
- Influence vascular tone, fluid volume & electrolyte composition (renal and G.I. actions), epinephrine
Temperature Regulation system:
- CV system is important in thermoregulation
- Blood distribution: core –> skin promotes heat loss
- Sweating –> loss of ECF, decreased ECV
What is the integrated CV response during exercise?
- Exercise pressor reflex
- Sensitivity of baroreflexes
- Skeletal m. vasodilation
- Circulating epinephrine
- Venous return
- Temperature regulation
what are main trends of exercising to cardiovascular control?
increased HR and VR: increased CO
decreased TPR
general increase in MAP and PP
vasoconstriction in inactive beds
vasodilation in active beds: allows for perfusion of active tissues
What are effects of training and exercise in cardiovascular demands?
Training:
- improves O2 extraction
- increased capiillary density
- oxidative enzymes
- mitochondrial density
- myoglobin
CV adaptations:
- Lower resting HR: increased vagal tone and decreased Symp at rest
- Greater SV
- Lower TPR (especially in muscle)
—> Endurance training: increased LV volume (with minimal change in wall thickness), increased filling
–> Resistance training: increased LV wall thickness (concentric hypertorphy); little effect on ventricular volume
What does medulla oblongata do?
“cardiovascular center” or “vasomotor area”
- regulates MAP; mediates S/PS response
- receives input from baroreceptors, chemoreceptors, hypothalamus, cerebral cortex and local concentrations of O2 and CO2
What do high pressure baroreceptors register? what happens? where are they located? when is their response most dominant?
- located at carotid sinus and aortic arch
- decreased firing with decreased MAP (and decreased PP), due to decreased stretch, results in greater PS and less S –> results in vasoconstriction and tachycardia
- dominant responders to volume depletion
Where are low pressure baroreceptors located: when are they most active???
- cardiac chambers and large pulmonary vessels
- increased firing rate with increased stretch of vena cava b/c of increased VR (opposite for decreased stretch)
- regulate volume rather than MAP
- affarent fibers go to medulla and decerase renal vasoconstriction in order to increase urine output and decrease effective circulating volume
What does Bainbridge reflex do?
couterbalances high pressure baroreceptor reflex
with increased VR/RAP results in increased HR
- most dominant during volume loading
where are peripheral chemoreceptors located?
- bifurcation of carotid body and aortic arch/aortic bodies
- detect changes in O2 and CO2
- primarily function in regulating respiration, which in turn regulates heart rate/CO
Where is central chemoreceptor located?
medulla oblangata
detects high levels of CO2 and stimulates vasoconstriction
integrated physiological response to increased CO2?
stimulates increased ventilation
stretches pulmonary stretch receptors
negativiely inhibits cardioinhibitory center
increases HR
results in increased TPR and MAP
