Cardiac Cycle & Control of Cardiac Output - Quiz 3 Flashcards Preview

Spring 2020 - Physiology 1 > Cardiac Cycle & Control of Cardiac Output - Quiz 3 > Flashcards

Flashcards in Cardiac Cycle & Control of Cardiac Output - Quiz 3 Deck (40)
Loading flashcards...
1
Q

Ventricular Systole

A

Phase 2: Isovolumic Contraction

Phase 3: Rapid Ejection

Phase 4: Reduced Ejection

2
Q

Ventricular Diastole

A

Phase 5: Isovolumic Relaxation

Phase 6: Rapid Filling

Phase 7: Diastasis

Phase 1: Atrial Systole

3
Q

Atrial contraction is ____ essentatial for ventricular filling.

A

NOT Essential

More important for faster heart rates

Accounts for 10% of LV filling

4
Q

When does most of ventricular filling occur?

A

Phase 6: Rapid Ventricular Filling

  • AV valves open, Aortic and Pulmonic Vavles Close
  • Passive filling
5
Q

Opening of AV Valve produces what sound?

A
  • No heart sounds opening of any normal valves
  • S3 may be present and normal in children during rapid filling d/t tensing of chordae tendinae and AV ring.
  • Not normal in adults = Ventricular Dilation
6
Q

Closure of Aortic and Pulmonic Valve produces what sound?

A

Produce S2

7
Q

Closure of AV Valves produce what sound?

A

Produce S1

8
Q

What does the incisura or dicrotic notch of aortic pressure tracings mark the beginning of ?

A

Diastole

Aortic and Pulmonic Valve Closure

9
Q

During what cardiac phase does the Mitral and Aortic valve both close?

A

Phase 5: Isovolumic Relaxation

  • All valves closed
  • Ventricular volumes constant
10
Q

Various Waves of CVP

A

a: atrial contraction
c: ventricle contraction
v: slow atrial filling, AV valves close

11
Q

What signifies the first heart sound?

A

Closure of the AV Valves

(Triscuspid and Mitral)

12
Q

What signifies the second heart sounds?

A

Closure of Aortic and Pulmonic Valves

13
Q

When does the majority of blood ejection from the LV happen?

A

Phase 3: Rapid Ejection

  • Aortic and Pulmonic valves open, AV valves stay closed
  • About 70% ejected
14
Q

How much does Atrial Kick contribute to Ventricular Filling?

A

About 10%

  • At Higher HR, atrial kick up to 40%
  • In A-Fib, atrial kick is 0%
15
Q

4 Major Determinants of Cardiac Output

A

Heart Rate, Contractility, Preload, and Afterload

CO = HR x SV

SV = EDV - ESV

EF = SV
EDV

16
Q

How can Stroke Volume normally be increased?

A

Increase End Diastolic Volume (EDV)

OR

Decrease End Systolic Volume (ESV)

17
Q

What is the Bowditch Effect?

A

Autoregulation - Increase in heart rate will cause Positive Intropy

AKA: Treppe Effect/Staircase Phenomenon

Due to Na/K ATP pump unable to keep up with influx of NA at higher rates –> more intracellular calcium.

18
Q

Why do extremely high heart rates result in decreased Cardiac Output?

A

Decreased Stroke Volume due to decrease filling time –> decreases End Diastolic Volume

19
Q

The name of the phenomenon where Preload increases and Cardiac Output increases

A

Frank-Starling Mechanism - Upward curve shift

20
Q

As PRELOAD decreases, CARDIAC OUTPUT decreases. This is called?

A

Frank-Starling Mechanism - Downward curve shift

21
Q

What keeps the CARDIAC OUTPUT of the ventricle matched with venous return?

A

Frank-Starling Relationship - Stretching of the ventricle results in increased force of contraction

22
Q

What keeps the CARDIAC OUTPUT of the right and left ventricles matched?

A

Frank-Starling Mechanism

23
Q

Factors that Affect Ventricular Preload

A
  • Venous BP
  • Venous Volume
  • Filling Time (HR)
  • Ventricular Compliance
  • Atrial Contraction
  • Inflow/Outlfow Resistance
  • Ventricular Systolic Failure
24
Q

What is Part of the Venous Volume

A

Venous Return

Total Blood Volume

Respiration

Exercise/Muscle Contraction

Gravity

25
Q

What is the Frank-Starling Relationship?

A

Increases venous return, ventricular filling, and preload leads to increased stroke volume

26
Q

What is the Y-Axis of the Starling Curve?

A

Stroke Volume

27
Q

What is the X-Axis on the Starling Curve

A

Left Ventricule End Diastolic Pressure (LVEDP)

28
Q

Factors that Cause Increased Afterload

A

Aortic Pressure

Increased SVR

Aortic Stenosis

Ventricular Dilation

29
Q

How does After Load effect Cardiac Output

A

Increase in Afterload decreases Cardiac Output

30
Q

Wall stress can be used to help understand what determinant of Cardiac Output

A

Afterload?

31
Q

What is Contractility?

A

Capacity of myocardium to contract independently of changes in afterload or preload

32
Q

What is another name for Contractility?

A

Inotropy

33
Q

What is the Anrep Effect?

A

Modest increase in inotropy after an abrupt increase in afterload

34
Q

When are S4 heart sounds produced?

A

Sometimes heard during atrial contraction - vibration of ventricular wall with reduced compliance

35
Q

Phase 2: Isovolumic Contraction

A

All Valves Closed

QRS - Ventricular Depolarization

Rise in Ventricular pressure, but volumes stays the same

36
Q

Phase 4: Reduced Ejection

A

T Wave - Ventricular Repolarization

37
Q

When would an S3 sound be produced?

A

Not normal. May happen during Rapid refilling - tensing of chordae, tendinae and AV ring.

38
Q

Phase 7: Diastasis

A

Reducing Ventricular Filling

39
Q

What is the most important mechanism regulating inotropy?

A

Autonomic Nerves

  • Sympathetic nerves have big role in intropic regulation.
  • Parasympathetic have big negative inotropic effects in atria, but little in ventricles.
40
Q

What valve closes at the dicrotic notch?

A

Aortic Valve