Other Flashcards
Control of myocardial O2 supply
coronary arterioles
o Normal heart: 60-80% of capillaries are open
o Arterial hypoxia: recruitment of capillaries
Major determinants of myocardial O2 demand
- 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
Indices of myocardial O2 uptake
- 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
Myocardial metabolism
- 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
phases of the Valsalva maneuver
- 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
Anrep effect
- 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+
Austin Flint murmur
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
Bainbridge reflex
- 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
Bezold-Jarisch reflex
- 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
Branham reflex
- 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
Brockenbrough-Braunwald-Morrow sign
- 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
Rivero-Carvallo sign
- 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
Bowditch staircase effect or Treppe effect
- 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
Corrigan’s pulse
- Bounding or water-hammer pulse: large and strong pulse w normal contour
o PDA, AI, peripheral AV fistula : ↑ pulse pressure 2nd to diastolic runoff
Frank-Starling law
- 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
Kussmaul’s sign
- incr jugular venous pressure w inspiration
o Indicative of limited RV filling due to R heart dysfct => incr blood flow backup into venous system => jugular venous distension
o DDX: constrictive pericarditis, RCM, RV infarctus, cardiac tumor, TV stenosis, PTE - Normally = inspiration => decr intrathoracic pressures => incr venous return in highly compliant RA
- Kussmaul breathing: deep and labored breathing 2nd to severe metabolic acidosis (DKA, Kid failure)
o Hyperventilation: ↓ CO due to ↑ rate and depth of respiration
Graham Steele murmur
- PV: associated w/ PI
o Louder, higher pitched, decrescendo
o Earlier in diastole
o Best heard at L apex after S2 - icnr intensity w inspiration unlike AI murmur
o decr w vagal stimulation - Associated w/ PH >55mmHg → dilation of PV annulus → PI
Cushing reflex
- Cranial perfusion pressure = mean BP – intracranial BP
o Cranial blood flow = cranial perfusion pressure/cranial vascular resistance - incr ICP => compression of brain/arteries => CNS ischemic response => incr BP → ↑ cerebral blood flow
o ∑ system response:
Activation of A1R => peripheral vasoconstriction => incr BP
incr HR + contractility => incr CO
o p∑ response: BaroR in Ao arch detect icnr BP => reflex bradycardia via vagal stimulation
o Distortion of brainstem 2nd to icnr ICP => loss control of involuntary breathing => irregular respiratory pattern/apnea - Leads to triad
o Irregular, decr/slow repiration
o Bradycardia
o Widening pulse pressure, systolic hypertension
Seldinger technique
- Vascular access technique: vessel is puncture w needle/KT => guidewire advanced through lumen => sheath/cannula passed over guidewire
Guyton curves
- Guyton: important research on cardiovascular physiology and author of textbook (AKA part of general boards trauma) → discovered need for tissue O2 determines CO and BP regulation by kids
- Guyton curves: describe relation ship btwn RAP and CO
o Venous return: ↓ as RAP ↑
Curve slope = resistance to venous return
o Cardiac function curve:
o Mean circulatory filling P: BP at which venous return is 0
o Intersection of venous return curve and CO → functioning preload of RV
Lewis-Wigger diagram
Cardiac cycle diagram: LV contraction, relaxation, filling
Harvey
1st physician to describe systemic circulation and blood pumped from the heart
Sones
1st to develop cardiac angiography + 1st coronary bypass sx