Intro To Cardiovascular Physiology/pathophysiology

Front 1

Path of blood flow through heart and lungs with blood pressures listed:

Back 1

Front 2

Cardiac output is defined as:

Blood pressure is defined as:

Back 2

CO = Stroke Volume X Heart Rate (~6L/min!)

BP = Cardiac Output X Systemic Vascular Resistance
(think V=IR)

Front 3

3 components of diastole:

2 components of systole:

Back 3

Diastole: Isovolumic relaxation, Rapid Ventricular filling, Atrial contraction (“kick”)

Systole: Isovolumic contraction, L.V. Ejection

Front 4

Systole begins with what action?

Diastole begins with what action?

Back 4

S-- starts with closure of the mitral valve

D-- starts with closure of the aortic valve

Front 5

Discuss the volume change during LV filling:

Back 5

-Atrial kick accounts for only ~20% of ventricular filling. Most is passive filling.

Front 6

Pressure vs. time graph of the whole cardiac cycle:

Where's S1? S2?

Where's isovolumic contraction? relaxation?

Back 6

S1= closure of mitral and tricuspid valve.
[Systole between S1/S2]
S2= Closure of aortic valve and pulmonic valve
[Diastole between S2/S1]

Isovolumic contraction = between closure of MV and opening of AV.

Isovolumic relaxation = between closure of AV and opening of MV.

Front 7

pressure vs. volume curve of LV filling:

Back 7

*Relationship of pressure to volume defines L.V. “stiffness” or “non-compliance.”

*At low pressures, it's almost linear.

*More steep = less compliant.

Front 8

Compliance is proportional to:

Stiffness is proportional to:

Back 8

*“Compliance” is proportional to change in volume over change in pressure.

*“Stiffness” is the inverse. Stiffness is proportional to change in pressure over change in volume.

Front 9

Pressure vs. volume plot of a normal and a non-compliant LV:

Back 9

left = stiffer, less compliant

Front 10

What are 3 causes of Diastolic Dysfunction?

Back 10

*Left ventricular hypertrophy

*Myocardial ischemia or infarction

*Restrictive Cardiomyopathy

Front 11

What are 3 causes of LV hypertrophy?

Back 11

Chronic high blood pressure (“hypertension”)
Valvular heart disease
Cardiomyopathy

Front 12

What are the mediators of CO?

Back 12

Front 13

Definition of preload:

Definition of afterload:

Definition of wall tension:

Back 13

*Preload = the wall tension during diastole.

*Afterload = the wall tension during systole.

*Wall tension = (P x r) / 2h
h = wall thickness

Front 14

Effect of decreased LV compliance on preload:

What is the most important determinant of ventricular preload? 2nd most?

Back 14

Volume is the most important determinant of ventricular preload.

Compliance of the LV is also important (so be careful about giving too much fluids to an elderly patient).

Front 15

What is the major variable affecting LV pressure during systole?

Back 15

Aortic pressure. Therefore, aortic pressure is the most important determinant of ventricular afterload.

High BP = high afterload = reduced CO.

Front 16

How do we relate myocardial performance (cardiac output) to preload and afterload?

And how does “myocardial contractility” relate to cardiac output??

Back 16

*Frank-Starling Curves

Front 17

What are Frank-Starling Curves?

Back 17

*L.V. “performance” curves relating:
1) L.V.E.D.P. (i.e." preload”)
2) L.V.“performance” (i.e. cardiac output)

Front 18

Discuss the Frank-Starling curves in CHF:

Back 18

Curve gets flatter in failing hearts.

Only compensatory mechanism is a chronically high LVEDP.

Front 19

what's the one with the balloon? what does it measure?

Back 19

The Swan-Ganz Catheter--

measures Blood pressure, Cardiac output, Stroke volume, LVEDP, and Systemic vascular resistance

Front 20

What are the 2 methods of measuring CO? Briefly explain each.

Back 20

Fick Method: (O2 consumption) / (Arterial-Venous O2 difference)

Thermodilution method: “The Black Box”

Front 21

Discuss the Fick principle in more detail:

Back 21

*Looks at efficiency of O2 transfer to measure CO.
*Measure arterial O2 saturation and mixed venous O2 saturation in the pulmonary artery.
*Can do this with Swan-Ganz catheter.
*Uses standardized tables based on weight, gender.

Front 22

What is the Waters Hood?

Back 22

Measures O2 consumption directly.

Front 23

Discuss the Thermodilution Method in more detail:

Back 23

*Similar in principle to the Fick method

*Uses change in temperature per unit time, rather than change in O2 saturation

*Requires a thermal probe in the right side of the heart and an injection.

*A computer method.

Front 24

If the cardiac output is low, is the “mixed venous” O2 content:

A) Lower than normal
B) Higher than normal
C) The same as normal

Back 24

A) Lower than normal

Front 25

What happens to the Frank Starling curve with a surge of epinephrine?

A) Curve stays the same
B) Curve moves down and to the right
C) Curve moves up and to the left

Back 25

C) Curve moves up and to the left

Front 26

Discuss Pressure-Volume loops:
what do they relate?
what's their function?

Back 26

*Bottom curve = LV filling curve. Vertical lines are isovolumic contraction and relaxation.

*Relate L.V. pressure to L.V. volume in a single cardiac cycle

*Can be used to explore the effects of various therapies on stroke volume and L.V.E.D.P.

Front 27

More on pressure-volume loops:

What if you increase preload while holding contractility constant?

Back 27

*Holding afterload and contractility constant
*Varying “preload” measured as end-diastolic volume

*Increasing preload while holding contractility constant increases stroke volume.

Front 28

Exercise has what effects on CO?

Back 28

-Increases SV and HR.

-CO increases by 3 or 4 fold.

-Drop in systemic vascular resistance (vasodilation).

Front 29

What 3 things affect SV?

Back 29

SVCAP: Contractility, Afterload, Preload

Front 30

How is PCWP measured?

Why is PCWP important?

Back 30

Put a catheter with a balloon on it into the pulmonary artery. When it occludes, you can measure PCWP.

PCWP = Left atrial pressure = LVEDP