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Pathophysiology - Cardiovascular > Cardiac Cycle & LV Mechanics / Circulatory Hemodynamics > Flashcards

Cardiac Cycle & LV Mechanics / Circulatory Hemodynamics Flashcards

1
Q

When does systole begin and end, and how much of the cardiac cycle does this comprise?

A

1/3, begins when ventricles start to contract (isovolumetric contraction) and ends when the ejection stops (just BEFORE isovolumetric relaxation)

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2
Q

Is atrial systole a part of systole or diastole?

A

Diastole - occurs just before ventricular systole and is considered the last part of diastole.

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3
Q

When does isovolumetric relaxation begin and end? What does it correspond to on ECG? What is this volume?

A

Since it is the first part of diastole, it must begin with the end of ejection

Begins: Semilunar valves close
Ends: When ventricular pressure falls below atrial pressure, allowing AV valves to open

Corresponds to end of T wave on ECG -> ventricular repolarization

Volume = End systolic volume (ESV)

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4
Q

At normal heart rates, how much of ventricular filling is passive / active? When does this become more important?

A

75% is passive, 25% is active

In high exercise states, diastole shortens so there is less passive filling time -> atrial contraction becomes more important

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5
Q

What does atrial contraction coincide with on ECG?

A

Just after the P wave

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6
Q

What does isovolumetric contraction coincide with on ECG? What is this volume?

A

Peak of the R wave (in QRS complex)

Volume = End diastolic volume

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7
Q

When do the atria fill with blood?

A

All the time, even during ventricular systole, EXCEPT for atrial systole (part of diastole).

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8
Q

What are normal RA, RV, and PA pressures?

A 
RA = 0-5mmHg
RV = 25/5 mmHg (diastole corresponds to RAP)
PA = 25/10 mmHg (diastole corresponds to LAP)
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9
Q

What are normal LA, LV, and Aortic pressures?

A 
LA = 8-10 mmHg
LV = 120/10 mmHg (Diastole corresponds to LAP)
Aortic = 120/80 mmHg
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10
Q

Why is preload a thing in cardiac muscle but not skeletal muscle?

A

Cardiac muscle has more connective tissue which makes it more resistant to stretch -> stretching it like a rubber band will store up some potential energy.

-> contraction will begin when the sarcomere is near its full length

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11
Q

What is a good measurement approximator for preload? What two systemic factors will increase it?

A

ventricular EDV -> lets us know the end-diastolic length of the sarcomeres

Increased by: 1. Increased venous tone (more blood back to heart) 2. Increased blood volume

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12
Q

How is afterload defined, and what happens if afterload > contraction force?

A

Force that the muscle cell must overcome to begin to shorten

-> if afterload > contraction force, isometric contraction will occur (no shortening possible)

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13
Q

What changes the inotropy of cardiac muscle?

A

This is contractility - independent of preload and afterload

-> tends to be changed by biochemical environment of muscle bundle

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14
Q

Your graph is stroke volume vs LV EDP. What will happen to the curve if something increases inotropy?

A

Slope will increase / shift to the left -> greater stroke volume at any given LV EDP.

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15
Q

How is ejection fraction calculated?

A

SV / EDV

Where stroke volume = EDV - ESV

So

(EDV - ESV) / EDV

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16
Q

What accounts for the majority of the increased cardiac output during exercise?

A

The heart rate

-> stroke volume plateaus very early

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17
Q

Other than blood volume and venous tone, give a few other factors which can influence venous return to the heart and hence preload?

A
  1. Posture -> i.e. lying down with legs up
  2. Pericardial constraint -> i.e. pericardial thickening or effusion will limit distensibility of heart
  3. Atrial contraction presence / efficiency
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18
Q

Other than venous return, what other factor influences preload?

A

Ventricular compliance

-> hypertrophy will lower it

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19
Q

How does ventricular compliance change with ventricular volume?

A

At higher volumes, a higher pressure will be needed to get an increase in volume.

  • > due to its compliance characteristics
  • > becomes more stiff / less compliant

Stiffness = pressure / volume, compliance = volume / pressure

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20
Q

How can relaxation help myocardial compliance?

A

Reuptake of calcium into the SR rapidly will break actin-myosin crossbridges via an ATP-dependent process

  • > explains why phospholamban phosphorylation of Ca+2-ATPase on SR, and phosphorylation of TnI increasing relaxation is a good thing
  • > improvement of compliance will improve preload
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21
Q

What happens when atrial filling pressures increase greater than physiologically needed for optimal preload?

A

There comes a point when increased venous return is not needed

  • > volume overload
  • > will lead to pulmonary congestion and ultimately left-sided heart failure due to so much preload with every pump
22
Q

What is the formula for wall stress? What increases / decreases it?

A

Wall stress = (Pressure x Radius) / 2(wall thickness)
-> force with cardiomyocytes must push against

Increased by greater radius from center to wall of ventricle, and systolic pressure (afterload)

Stress is normalized via increasing wall thickness

23
Q

Why is afterload approximated by mean arterial pressure?

A

Afterload is actually wall stress -> Force per unit area the heart must push against

However, we assume that ventricular radius and wall thickness are pretty much constant, so pressure (in the numerator of wall stress equation) is a pretty good proxy.

Pressure = Force per area
Radius = length (i.e. cm)
Wall thickness = length (i.e. cm)

(F/A * cm) / cm = F/A, Laplace’s law

24
Q

How does wall stress change during ejection?

A

It decreases because

  1. The size of the LV cavity decreases -> Radius decreases
  2. LV wall thickness increases -> more sarcomeres pushed together
25
Q

What does dilated cardiomyopathy do to wall stress?

A

Increases it by increasing the radius in Laplace’s law

26
Q

How does heart rate increase contractility?

A

Decreases the ability of Ca+2 to leave the cytoplasm -> more calcium for next contraction.

27
Q

How does the B1 adrenoceptor increase contractility?

A

Phosphorylates the Ca+2 channels, increasing Ca+2 entry and thus Ca+2-induced Ca+2 release.

Also, phosphorylates phospholamban to reuptake Ca+2 into SR faster for quicker relaxation, and phosphorylates TnI for faster recovery.

28
Q

What effect will increased preload have on the LV pressure volume loops (LV pressure vs LV volume)?

A

Increases the EDV and thus stroke volume since you will still return to the same ESV.

29
Q

What effect will increased afterload have on the LV pressure volume loops (LV pressure vs LV volume)?

A

Increases the ESV and thus decreases stroke volume since you will have the same EDV.

ESV will move up the same slope of the ESPVR curve (same contractility).

30
Q

What effect will increased contractility have on the LV pressure volume loops (LV pressure vs LV volume)?

A

Shifts the ESPVR curve to the left, increasing its slope. This will decrease the ESV while keeping EDV the same.
-> increased stroke volume.

31
Q

What is normal ejection fraction?

A

55-60%

32
Q

What will increasing preload, afterload, and contractility do to ejection fraction?

A

Preload - increase EF (to a point, until fibers are overstretched and excess blood will be held in ventricle)
Afterload - decrease EF
Contractility - increase EF (lower ESV / greater SV)

33
Q

What does concentric hypertrophy happen in response to, and what is its pathogenesis?

A

In response to increased afterload
-> Lay down more sarcomeres in parallel, decreasing LV cavity size and increasing wall thickness, which decreases wall stress.

34
Q

Give a few conditions causing concentric hypertrophy?

A

Uncontrolled HTN
Aortic valve stenosis
Pulmonic valve stenosis (thickening of RV)

35
Q

What does eccentric hypertrophy happen in response to, and what is its pathogenesis?

A

In response to chronically increased preload

  • > Lay down more sarcomeres in series to accommodate increased volume
  • > Increased volume increases wall stress (radius is larger)
  • > Lay down sarcomeres in parallel to increase wall thickness and decrease cavity size
36
Q

Give a few conditions causing eccentric hypertrophy?

A

Aortic, mitral, pulmonic, and tricuspid regurgitation states.
-> will dilate one chamber of the heart each time.

37
Q

Why is LV hypertrophy bad?

A
  1. Volume of myocytes increases disproportionately to capillary growth -> decreased coronary reserve in situations of high demand (i.e. tachycardia)
  2. Sarcomeres increase more than mitochondria -> inefficient energy use
  3. Decreased contraction efficiency in myosin ATPase
  4. Increased collagen deposition -> increased LV stiffness
38
Q

What is concentric remodeling?

A

Reversible and physiologic hypertrophy which happens in athletes

39
Q

What is “remodeling”?

A

LV dilatation related to primary myocyte structural or functional loss, as in MI or non-ischemic cardiomyopathy

40
Q

How does the thermodilution method of testing cardiac output work?

A

Put a pulmonary artery catheter in via the femoral vein. Cold saline is injected via proximal right atrial catheter and temperature is measured via distal thermometer in pulmonary artery

Drop in temperature correlates with velocity of blood / stroke volume

41
Q

What is the Fick equation and how is it used to measure cardiac output?

A

Cardiac output = VO2 (measured via inspiration / expiration, in mL/min) / AV oxygen difference (mL O2 / liter of blood)

Measure the patients arterial and venous O2 concentrations for the AV oxygen difference.

42
Q

How is vascular resistance (afterload) measured? Units?

A

Mean pressure difference across a vascular bed / mean blood flow

Mean blood flow is measured in volume / time (cm^3/sec)

Thus, units are (Dynes/cm^2) / (cm^3 / sec) = dynesseccm^-5

43
Q

What is the conversion between dynesseccm^-5 and Woods Units?

A

1 Wood Unit = 80 dynesseccm^-5

So 10 Woods Units = 800 dynesseccm^-5

44
Q

What does pulmonary capillary wedge pressure (PCWP) approximate?

A

Left atrial pressure (diastolic pressure from a balloon catheter inserted into the pulmonary artery) -> LVEDP -> preload

45
Q

How is the systemic vascular resistance calculated and what is the normal range?

A

SVR = (MAP - Mean RAP) / CO

RAP = right atrial pressure

Normal = 900-1300 dynesseccm^-5

46
Q

How is the pulmonary vascular resistance calculated and what is the normal range?

A

PVR = (Mean PAP - Mean LAP) / CO

LAP = Left atrial pressure = PCWP

Normal = 40 to 90 dynesseccm^-5

47
Q

What things increase SVR or PVR?

A

SVR -> systemic vasoconstriction

PVR -> pulmonary vasoconstriction from hypoxia or by clotting or scarring

48
Q

What things decrease SVR or PVR?

A

SVR -> systemic vasodilation, i.e. sepsis, anemia

PVR -> pulmonary vasodilation

49
Q

How do you calculate Mean Arterial Pressure with Cardiac output and total peripheral resistance?

A

MAP = CO * TPR

V = I*R

50
Q

How do you calculate MAP and pulse pressure with systolic / diastolic pressure?

A

MAP = 2/3 diastolic + 1/3 systolic, or diastolic + 1/3 pulse pressure

Pulse pressure = Systolic - diastolic

Pathophysiology - Cardiovascular (24 decks)

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