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A Physiology > 2.4B. (Pump function of the heart.) Cardiac output and its control. > Flashcards

2.4B. (Pump function of the heart.) Cardiac output and its control. Flashcards

1
Q

I. Cardiac output
1. What is cardiac output?

A

Cardiac output (CO) is the volume of blood being pumped by the left ventricle into the aorta per minute
- CO = 5,6 L/min at rest
- CO = HR * SV = 70 beats/min * 80mL = 5600mL/min = 5,6 L/min

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2
Q

I. Cardiac output
2. How to calculate cardiac output (give the values as well)?

A
  • CO = 5,6 L/min at rest
  • CO = HR * SV = 70 beats/min * 80mL = 5600mL/min = 5,6 L/min
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3
Q

II. Total peripheral resistance (TPR)
1. Definition of Total peripheral resistance (TPR)

A

The ratio of arteriovenous pressure difference to the flow through the entire systemic vascular bed (essentially the CO)

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4
Q

II. Total peripheral resistance (TPR)
2. Formula of Total peripheral resistance (TPR)

A

The ratio of arteriovenous pressure difference to the flow through the entire systemic vascular bed
(essentially the CO)
=> MABP = CO * TPR

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5
Q

III. Stroke volume
1. What is Stroke volume?

A

SV = amount of blood transported to aorta during systole

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6
Q

III. Stroke volume
2. How to calculate the stroke volume?

A

The difference between the volume of blood in the ventricle before ejection (end diastolic volume) and the volume remaining in the ventricle after ejection (end systolic volume)
SV = EDV - ESV
- Less than half of the blood volume remains in the ventricles
- Stroke volume (SV) = EDV – ESV = 140mL – 60mL = 80mL

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7
Q

IV. Eject fraction (EF)
1. Definition of Eject fraction (EF)

A

A measure of how much blood the left ventricle pumps out with each contraction in percentage
- Refers to how well the left ventricle pumps blood with each beat

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8
Q

IV. Eject fraction (EF)
2. How to calculate Eject fraction (EF)

A
  • 0,5 < EF < 0,75 -> more than 1⁄2, but less than 3⁄4 of volume should be ejected
  • 0,50 < EF < 0,75 ↔ 1⁄2 < EV <3⁄4
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9
Q

V. 4 factors that determine the CO
1. What are the 4 factors that determine CO?

A
  1. Cardiac factors
    a) Heart rate
    b) Myocardial contractility
  2. Coupling factors (heart + circulation)
    a) Preload
    b) Afterload
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10
Q

V. 4 factors that determine the CO
2. Definition of cardiac factors

A

Cardiac factors: strictly cardiac factor, but influenced by hormonal + neural factors
a) Heart rate
b) Myocardial contractility

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11
Q

V. 4 factors that determine the CO
2B. What are characteristics of Myocardial contractility (a cardiac factor)

A

Myocardial contractility: ability of heart to increase contraction force
- Influenced by SYM activity
- Determines the SV + HR = CO

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12
Q

V. 4 factors that determine the CO
3A. Definition of the coupling factors?

A

Coupling factors (heart + circulation) – constitute a functional coupling of heart + vessels
a) Preload
b) After load

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13
Q

V. 4 factors that determine the CO - the coupling factors
3B. What is preload?

A

Preload: force that stretches the relaxed muscle fibers = (blood filling the wall during diastole)

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14
Q

V. 4 factors that determine the CO - the coupling factors
3C. What is afterload?

A

Afterload: force added to the muscle against which the contracting muscle must act = aortic pressure (left ventricle must generate a greater pressure than the aorta to open the valve)

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15
Q

VI. Regulation of cardiac output
1. What are the 2 types of regulations?

A
  1. Heterometric regulation
  2. Homometric regulation
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16
Q

VI. Regulation of cardiac output - heterometric regulation
2A. What is heterometric regulation?

A

Refers to how different initial fiber lengths impact the force of contraction

17
Q

VI. Regulation of cardiac output - heterometric regulation
2B. What are the 2 experiments contributing to the understanding of heterometric regulation?

A

1) Otto Franck’s experiment
2) Starling’s experiment

18
Q

VI. Regulation of cardiac output - heterometric regulation
2B. What are the 2 experiments contributing to the understanding of heterometric regulation?

A

1) Otto Franck’s experiment
2) Starling’s experiment

19
Q

VI. Regulation of cardiac output - heterometric regulation
2C. Explain Otto Franck’s experiment

A
  • Within physiological limits, the contraction force is directly proportional to the initial fiber length
  • Higher diastolic filling (preload) -> stronger contraction (systolic pressure)
  • Higher fiber length -> more forceful contraction
  • An increase in the initial fiber length of the muscle fiber beyond a certain point will no longer increase the pressure
20
Q

VI. Regulation of cardiac output - heterometric regulation
2C. Explain Starling’s experiment

A

Concluded that increased venous return (diastolic filling) to the heart, which increased the filling pressure (EDV) of the left ventricle -> led to a greater SV
- Frank-Starling Law: SV of the heart increases in response to an increase in the blood volume in the ventricles (EDV) when all other factors remain constant
- Heterometric regulation: EDV↑ -> SV↑

21
Q

VI. Regulation of cardiac output - heterometric regulation
2D. What is Frank-Starling mechanism?

A
  • It states that SV of heart increases in response to an increase in the volume of blood in the ventricles before contraction. The larger vol of blood flows into ventricle, as a consequence, stretches the cardiac muscle fibres, leading to an increase in the force of contraction
  • As a muscle fiber is stretched (change in the initial fiber length). Active tension is created by alternating the overlap of thick and thin filaments
    -> At this point, interaction between the active binding site on the actin fiber and some myosin heads are inhibited, as there is an overlap of actin fibers
  • The greatest isometric active tension is developed when a muscle is at its optimal length
    -> All of the myosin heads are intact with the binding sites on the actin fiber, and there is no excess in both ways
22
Q

VI. Regulation of cardiac output - heterometric regulation
2E. Describe Inotropic mechanism

A
  • As a muscle fiber is stretched, sarcomeres must increase in length simultaneously
  • The increased sarcomere length increases the sensitivity of troponin C (TnC) to Ca2+
  • Increased TnC-sensitivity increases both the rate of cross-bridge attach/detachment and the strength of tension developed by muscle fiber, resulting in a greater SV
23
Q

VI. Regulation of cardiac output - heterometric regulation
2F. What are the 2 factors that affect the force of contraction?

A

Increased preload
Increased afterload

24
Q

VI. Regulation of cardiac output - heterometric regulation
2G1. How can increased preload affect force of contraction?

A

↑venous return -> ↑ventricular filling (EDV) -> ↑SV

25
Q

VI. Regulation of cardiac output - heterometric regulation
2G2. How can Increased afterload affect force of contraction?

A

↑systemic vascular resistance ->↑aortic pressure -> ↓SV

  • Increase in afterload leads to arterial pressure rapidly increasing
    +) Both systolic and diastolic pressures increase, but the difference between them stays the same, because venous inflow is the same
  • When afterload is increased, the first heartbeat is unable to pump out the usual amount of blood (due to a greater-than-normal pressure). So, once again, EDV increases
    -> More forceful contraction
    -> Occurs at a constant venous flow (constant preload)
26
Q

VI. Regulation of cardiac output - heterometric regulation
2H. What are the Determinants of ventricular filling?

A
  1. Venous return: venous pressure, central venous pressure (CVP), right atrial pressure
  2. Heart rate (duration of diastole): if HR↑ = diastole↓ -> limited time for ventr. filling
    - Atrial systole (20%) -> increases ventricular filling
    - The border between the atria and ventricles move toward the apex of the heart during (ventricular) systole -> suction of blood from the veins
27
Q

VI. Regulation of cardiac output - Homometric regulation
3A. What are the characteristics of homometric regulation?

A
  • The force of contraction is changed independently of the fiber length
  • The extrinsic regulatory mechanisms (ex: nervous, chemical) may override the intrinsic mechanism to regulate CO
28
Q

VI. Regulation of cardiac output - Homometric regulation
3A. What are the characteristics of homometric regulation?

A
  • The force of contraction is changed independently of the fiber length
  • The extrinsic regulatory mechanisms (ex: nervous, chemical) may override the intrinsic mechanism to regulate CO
29
Q

VI. Regulation of cardiac output - Homometric regulation
3B. What are the 2 types of nervous control of Homometric regulation?

A
  • Sympathetic: acts through β1-AR (Gs)
  • Parasympathetic: acts through M2-R (Gi)
30
Q

VI. Regulation of cardiac output - Homometric regulation
3C1. What is the molecular mechanism of sympathetic nervous control of homometric regulation?

A

NE -> β1-AR (Gs) -> AC activity↑ -> [cAMP]↑ -> PKA-activity↑ -> phosphorylation of following proteins:
- L-type VDCC: (same as RyR) becomes activated, allows larger influx of Ca2+
- Ryanodine receptors: responsible for much of the calcium from the lumen of SR
- Troponin I (TnI): inhibits binding of Ca2+ by troponin C (TnC)
-> Tropomyosin returns to its original position (blocking interaction), and facilitates cardiac relaxation
- Phospholamban activated, which regulates the Ca2+-ATPase pump that brings Ca2+ into the SR (SERCA pump)
-> This decreases [Ca2+]IC, but allows for faster relaxation

31
Q

VI. Regulation of cardiac output - Homometric regulation
3C2. What are the effects of sympathetic nervous control of homometric regulation?

A

Sympathetic: acts through β1-AR (Gs)
1. Positive chronotropic (HR) effect: ↑If
2. Positive dromotropic (conduction velocity) effect: ↑ICa
3. Positive inotropic (contractility) effect: ↑ICa
4. Positive lusitropic (relaxation) effect: ↑SERCA, ↓troponin Ca2+-affinity

=> Same effects can be achieved by isoproterenol (β-AR agonist)

32
Q

VI. Regulation of cardiac output - Homometric regulation
3D1. What is the molecular mechanism of parasympathetic nervous control of homometric regulation?

A
  • Parasympathetic: acts through M2-R (Gi)
  • ACh -> M2-R (Gi) -> ↓AC activity -> ↓[cAMP] -> ↓PKA
    -> Phosphorylation of various structures noted above (ex: Ca2+-ch, TnI) does NOT occur
    -> GIRKs are activated through M2-R -> Gβγ-dimer interacts with GIRKs to open them
    -> IK-ACh in atria and conduction system are affected
33
Q

VI. Regulation of cardiac output - Homometric regulation
3D2. What are the effects of Parasympathetic nervous control of homometric regulation?

A
  1. Parasympathetic: acts through M2-R (Gi)
  2. 4 effects
    - Negative chronotropic (HR) effect: ↓If, ↑IK-ACh
    - Negative dromotropic (conduction velocity) effect: ↓ICa,
    - Negative inotropic (contractility) effect: ↓ICa, ↑IK-ACh (ONLY IN ATRIA)
    - Positive lusitropic (relaxation) effect: ↓SERCA, ↑troponin Ca2+-affinity
34
Q

VII. Further factors that influence contractility
1. What are other factors that influence contractility?

A
  1. Temperature
  2. Ionic concentration
  3. Hypoxia, ischemia:
35
Q

VII. Further factors that influence contractility
2. How can Temperature influence contractility

A
  • Low temperature exerts negative inotropic (contractility) and chronotropic (HR)
    effects on the isolated heart
36
Q

VII. Further factors that influence contractility
3. How can Ionic concentration influence contractility

A
  • [Ca2+]EC ↑: positive inotropic effect (=↑ICa)
  • [K+]EC ↑: negative inotropic effect
37
Q

VII. Further factors that influence contractility
4. How can Hypoxia, ischemia: influence contractility

A
  • Not enough O2
  • Shortening of the ventricular AP, IK,ATP ↑
  • Loss of normal ion gradients (especially K+) across the membrane
  • Pacemaker channels remain inactivated in depolarized cells

A Physiology (88 decks)

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