Cardiac

Question 0

Cardiac Output

Answer 0

= 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)

Question 1

Fick Principle

Answer 1

CO= Rate of O2 consumption / (Arterial O2 content - Venous O2 content)

Question 2

Mean Arterial Pressure

Answer 2

2/3 Diastolic + 1/3 Systolic
Diastolic + 1/3 Pulse Pressure (systolic - diastolic)

MAP = Afterload

**Pulse Pressure => Stroke Volume

Question 3

Stroke Volume

Answer 3

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

Question 4

Contractility

Answer 4

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)

Question 5

Increased Myocardial O2 Demand By:

Answer 5

Increasing one or more of the following:
Afterload
Contractility
Heart Rate
Heart Size (increased wall tension)

Question 6

Factors that influence turbulence

Answer 6

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.

Question 7

Vascular Resistance

Answer 7

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)

Question 8

Resistance

Answer 8

Directly proportional to viscosity and vessel length and inversely proportional to the radius to the 4th power.

Question 9

Pan Systolic Murmur

Answer 9

Mitral or Tricuspid Regurgitation

Question 10

Crescendo-decrescendo systolic murmur

Answer 10

Aortic Stenosis

LV»> aortic pressures, pulses are weak with a delayed peak.
Can lead to syncope, angina, dyspnea

Question 11

Late crescendo murmur

Answer 11

Mitral valve prolapse

follows a midsystolic click due to the sudden tensing of the chordae tendineae (best heard over the apex)

Question 12

Diastolic Decrescendo murmur

Answer 12

Aortic Regurgitation

Question 13

Delayed diastolic rumbling murmur

Answer 13

Mitral stenosis

Question 14

Continuous murmur, loudest at S2

Answer 14

PDA

Question 15

Phase 0 of Vent. action potential

Answer 15

Rapid upstroke (depolarization), Voltage gated Na+ channels open

Question 16

Phase 1 Vent. Action Potential

Answer 16

Initial Repolarization- Inactivation of Na+ channels, Voltage gated K+ channels begin to open.

Question 17

Phase 2 Vent Action Potenntial

Answer 17

Plateau- Ca++ influx (voltage gated) balances K+ efflux.

Ca++ influx triggers Ca++ release from SR and myocyte contraction.

Question 18

Phase 3 Vent. Action Potential

Answer 18

Rapid repolarization - opening of slow K+ rectifier channels, closure of Ca++ channels

Question 19

Phase 4 Vent. Action Potential

Answer 19

Resting Potential - High K+ permeability (Na/K pump, and Na/Ca exchanger active at this stage as well)

Question 20

Respiratory Pump

Answer 20

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.