Cardiac Flashcards
Cardiac Output
= Stroke Volume x Heart Rate
= O2 Consumption / Arterial - Venous O2 content (Fick Principle)
= MAP / TPR (total peripheral resistance)
Early Exercise CO is maintained by Increased HR and SV. Late exercise CO is maintained by increased HR only
If HR is too high Diastolic filling is incomplete and CO decreases (eg. VT)
Fick Principle
CO= Rate of O2 consumption / (Arterial O2 content - Venous O2 content)
Mean Arterial Pressure
2/3 Diastolic + 1/3 Systolic
Diastolic + 1/3 Pulse Pressure (systolic - diastolic)
MAP = Afterload
**Pulse Pressure => Stroke Volume
Stroke Volume
The amount of blood ejected from the heart per beat.
Affected by Contractility, Afterload, Preload
Increased SV w/ Increased Preload, Decreased Afterload, or Increased Contractility
Contractility
Force of contraction at a given muscle length.
Increase (and SV) with:
Catecholamines (activity of Ca++ pump in SR)
Intracellular Ca++
Decreased extracellular Na+ (decreased Na/Ca exchanger)
Digitalis (blocks Na/K pump –> intracellular Na and decreased Na/Ca exchanger)
Increased Myocardial O2 Demand By:
Increasing one or more of the following: Afterload Contractility Heart Rate Heart Size (increased wall tension)
Factors that influence turbulence
Increase in Turbulence:
High velocity flow
Large vessel diameter
Blood density
Decrease in turbulence:
Increased Viscosity
All together make up Reynolds Number. when >2000 laminar flow becomes turbulent.
Vascular Resistance
Increases with increased blood volume venomotor tone (will result in increased right atrial pressure)
Decreases with hemorrhage and venodilation.
***(Vasoconstriction decreases blood flow, BUT Veinoconstriction increases blood flow)
Resistance
Directly proportional to viscosity and vessel length and inversely proportional to the radius to the 4th power.
Pan Systolic Murmur
Mitral or Tricuspid Regurgitation
Crescendo-decrescendo systolic murmur
Aortic Stenosis
LV»> aortic pressures, pulses are weak with a delayed peak.
Can lead to syncope, angina, dyspnea
Late crescendo murmur
Mitral valve prolapse
follows a midsystolic click due to the sudden tensing of the chordae tendineae (best heard over the apex)
Diastolic Decrescendo murmur
Aortic Regurgitation
Delayed diastolic rumbling murmur
Mitral stenosis
Continuous murmur, loudest at S2
PDA
Phase 0 of Vent. action potential
Rapid upstroke (depolarization), Voltage gated Na+ channels open
Phase 1 Vent. Action Potential
Initial Repolarization- Inactivation of Na+ channels, Voltage gated K+ channels begin to open.
Phase 2 Vent Action Potenntial
Plateau- Ca++ influx (voltage gated) balances K+ efflux.
Ca++ influx triggers Ca++ release from SR and myocyte contraction.
Phase 3 Vent. Action Potential
Rapid repolarization - opening of slow K+ rectifier channels, closure of Ca++ channels
Phase 4 Vent. Action Potential
Resting Potential - High K+ permeability (Na/K pump, and Na/Ca exchanger active at this stage as well)
Respiratory Pump
Increased venous return to right atrium on inspiration.
Decreased intrathoracic pressure –> expanded thoracic veins –> blood from head fills vena cave –> increased flow in vena cava –> increased venous return to RA
ALSO contraction of the diaphragm during inspiration increases abdominal pressure resulting in increased venous return.
