Other Flashcards
1
Q
Control of myocardial O2 supply
A
coronary arterioles
o Normal heart: 60-80% of capillaries are open
o Arterial hypoxia: recruitment of capillaries
2
Q
Major determinants of myocardial O2 demand
A
- HR => acutely regulate contractile state (w Starling law and autonomic control
o incr O2 demand by incr external work + enhancing force of ventricular contraction
Bowditch staircase effect: force frequency relationship
Rapid stimulation => incr intra¢ Na+ and Ca2+ => overload Na+/K+ pump => Na+ overload incr Na+/Ca2+ exchanger fct => incr Ca2+ => incr inotropy - Myocardial wall stress => afterload
- Velocity of contraction => contractility
o incr contractility => incr velocity of contraction
Adrenergic stimulation
Digitalis
Inotropic agents
3
Q
Indices of myocardial O2 uptake
A
- HR
- Double product
o Systolic pressure x HR - Triple product
o Systolic pressure x HR x systolic ejection time - Time-tension index (or time-pressure)
- Pressure-volume area
- Pressure-work index: integral of pressure and flow during ejection period
4
Q
Myocardial metabolism
A
- Fatty acids: major source of E
o Anaerobic glycolysis: max 5-7% of normal E requirements - Limited energy reserve => require high rate of ATP production + continuous O2 supply
5
Q
phases of the Valsalva maneuver
A
- Forceful expiration against closed glottis => incr intrathoracic pressure (contracting rib cage)
o decr venous return + compression of cardiac chambers => decr cardiac filling/preload => decrCO
o Compression of thoracic Ao => incr Ao pressure for few seconds (phase I)
decr Ao pressure after 2nd to decr CO (phase II)
o BaroR reflex: reciprocal changes in HR
Phase I: decr HR because of incr BP
Phase II: incr HR because of decr BP - When normal breathing is restored => removal of external compression
o Brief decr Ao pressure + HR (phase III)
o incr cardiac filling pressures => incr CO => incr Ao pressure + decr HR as CO decr
o BaroR + adrenergic incr in PVR also incr Ao pressure
6
Q
Anrep effect
A
- Acute incr afterload (BP) => incr contractility
o Intrinsic change in inotropy
o incr afterload => incr LV end diastolic volume (decr CO) => incr inotropy through Frank Starling mechanism
If maintained => contraction force incr further (10-15min) => decr end diastolic volume
o Partially compensate incr end systolic volume and decr SV 2nd to incr afterload - Initial response: Frank Starling => incr TnC sensitivity to Ca2+
- Delayed response: promote incr Ca2+ release by SR
o Mediators: ET1, Ang II released by cardiac cell in response to stretch
o incr LV wall tension => myocardial mechanoR => incr cytosolic Ca2+
7
Q
Austin Flint murmur
A
DYING WHALE
* Severe AI => mid-diastolic to presystolic murmur
o Premature MV closure => disturbed diastolic flow through MV orifice/ bulging
o Best heard at L apex
o S1 soft, S2 obscured by soft regurgitant murmur and louder, low pitched late diastolic murmur
8
Q
Bainbridge reflex
A
- incr atrial pressure => stretch R at jct of PVs => incr HR
o ↑ blood volume → incr venous return => ↑ β fiber firing → signals to brain → modulation of ∑ and p∑ influence on SA node → ↑ HR → incr CO
Small effect on contractility and SV: incr SV through Frank Starling
incr HR through ∑ stimulation
o Blocked by atropine or cutting vagus nerve - Involved in sinus arrhythmia: inspiration → ↓ intrathoracic P → ↑ venous return → ↑ stretch R stimulation → Bainbridge reflex → ↑ HR
9
Q
Bezold-Jarisch reflex
A
- Powerful vagal reflex
o Reflex bradycardia: slow SA node PM + 2AVB Mobitz I
o Vasodilation and hypotension
Renin release
Vasopressin secretion
o ↑ coronary flow - Cardiac sensory R in LV, inferoposterior wall
o Stimulated by stretch, chemical substances, drugs
symp overactivity: ↓ preload, myocardial infarction → contraction of under filled LV
o Sense underfilled LV → activate high pressure C fiber afferent nerve → non myelinated vagal afferent signals: incr psmp, decr symp → paradoxical bradycardia + ↓ contractility → hypotension - Treated w volume repletion and atropine
10
Q
Branham reflex
A
- Sudden occlusion of AV fistula/shunt → sudden ↑ in BP → bradycardia
o Exaggerated Bezold-Jarish reflex
o Shunt closure → excess CO forced into systemic circulation → sudden ↑ in diastolic BP → baroR stimulation → bradycardia
11
Q
Brockenbrough-Braunwald-Morrow sign
A
- Hemodynamic technique to diagnose DLVOTO
o ↓ in BP after VPC + ↑ in peak LVP - Normally: VPC will cause post extrasystolic potentiation
o Compensatory pause → longer filling period → ↑ LV end diastolic volume → ↑ SV and BP
12
Q
Rivero-Carvallo sign
A
- TV: indicate TR or TS
- Louder murmur during inspiration
o Inspiration → ↓ intrathoracic P → ↑ venous return → ↑ R heart filling → ↑ regurgitant volume
o TR: ↑ fillinf → ↑ regurgitatnt volume
o TS: ↓ P in RV > vs RA → ↑ PG and filling force → louder murmur - Helps distinguish MR from TR
13
Q
Bowditch staircase effect or Treppe effect
A
- incrHR => incr contractility
o Positive inotropic effect of activation or force-frequency relationship
o incr Na+ and Ca2+ entry => overload Na+/K+ pump => incr [Na2+] => Ca2+ entry by Na+/Ca2+ exch
14
Q
Corrigan’s pulse
A
- Bounding or water-hammer pulse: large and strong pulse w normal contour
o PDA, AI, peripheral AV fistula : ↑ pulse pressure 2nd to diastolic runoff
15
Q
Frank-Starling law
A
- Frank : incr diastolic heart volume => ventricular stretch → incr contraction velocity + force = + inotropic effect
- Starling: energy of contraction is a fct of the initial length of the muscle fiber
o incr venous pressure => incr stretch fiber at end of diastole => incr contraction force - Frank-Starling: ability of heart to change its force of contraction and SV in response to venous return
o incr venous return => incr ventricular filling/end diastolic volume => incr initial stretching of myo¢ => incr sarcomere length => incr inotropy + SV
o incr preload => incr active tension on muscle fibers => incr velocity of fiber shortening
o incr sarcomere length => incr TnC Ca+ sensitivity => incr cross bridge attachment/detachment - Normal curve: red dashed
o Afterload and inotropy define slope of curve
↑ afterload or ↓ contractility → shift down and R → ↓ SV
↓ afterload or ↑ contractility → shift up and L → ↑ SV
o Preload/volume define position on normal curve
