P1 Spring Organs 2011-02-01 (Cardiac Output)

Front 1

What is the equation for stroke volume?

Back 1

Stroke vol = EDV - ESV
where
EDV is end diastolic vol (~120 ml)
ESV is end systolic vol (~50 ml)

Front 2

What is the equation for ejection fraction?

Back 2

EF = SV / EDV
where SV is stoke vol

eg EF = 70ml / 120 ml = 58%

Front 3

What is the equation for cardiac output?

Back 3

CO = HR * SV (per beat)
eg CO = 72beats/min * 70ml/beat = 5040ml/min = 5L/min

Front 4

List two ways to increase SV (stoke vol).

Back 4

1. Decrease the ESV
2. Increase EDV

Front 5

How can you decrease ESV?

Back 5

By increasing the contraction of the ventricles, the ESV is lower (and the SV is higher).

Front 6

How can you increase the EDV?

Back 6

By increasing the preload

Front 7

Whats preload, and how can you increase it?

Back 7

Preload is the volume of the ventricles at the end of diastole.
Increasing venous return increases the preload.

Front 8

What normally happens to your ejection fraction if you preload increases?

Back 8

It tends to stay the same.
eg 70/120 (58%) versus 87/150 (58%)

Front 9

When do you see a decrease in the ejection fraction when preload increases?

Back 9

During compensated heart failure.
eg 70/120 (58%) versus 70/150 (46%)

Front 10

What causes a decrease in SV?

Back 10

A higher afterload.

Front 11

What is afterload, and what causes it to increase?

Back 11

Afterload is the arterial/aortic pressure.
Ventricles must overcome the afterload to eject the blood out.
High blood pressure increases afterload.

Front 12

How does high blood pressure lead to heart failure (eventually)?

Back 12

High bp increases afterload so the heart has to work much harder to pump blood out, which cause hypertrophy and extra stress, both of which lead to failure.

Front 13

List things that change the ESV.

Back 13

1. Increased afterload increases ESV
2. Increased contractility decreases ESV
3. Increased preload increases ESV (eg 120-70 vs 150-87)

Front 14

What things increase, decrease, or do not change the ejection fraction?

Back 14

increase: inc contractility
decrease: compensated heart failure, inc afterload
remains the same: inc preload

Front 15

List causes of increased contractility of heart?

Back 15

1. athletes heart
2. Inc SNS

Front 16

Why do athletes have lower heartrates?

Back 16

Because they have higher stroke volume and normal cardiac output, so HR must decrease:
CO = SV * HR
CO tends to always be about 5L/min

Front 17

List the ways that cardiac output is regulated.

Back 17

1. Intrinsic regulation
2. SNS regulation
3. PSNS regulation

Front 18

Describe intrinsic regulation.

Back 18

Whatever blood is sent to the heart is pumped, according to the Frank Starling mechanism.
SV is proportional to EDV which is proportional to venous return.

Front 19

What is the positive chronotropic effect?

Back 19

The increase in heart rate by the SNS via the SA node.
Impulse received by B1 receptors.

Front 20

What is a negative chronotropic effect?

Back 20

The decrease in heart rate by the PSNS via SA node.
Impulse is sent via vagus nerve.

Front 21

Describe physiological hypertrophy.

Back 21

1. Enlarged heart
2. Seen in athletes
3. Higher contractile force results in higher ejection fraction due to more efficient heart.

Front 22

Describe pathological hypertrophy.

Back 22

1. Enlarged heart
2. Lower ejection fraction due to inefficient heart.
3. Causes: hypertension (chronically stresses heart), high afterload (same), poorly functioning valves

Front 23

Whats another name for a heart attack, and the cause?

Back 23

-Cardiac arrest.
-The heart has fibrilated (must be defibrilated).

Front 24

Whats another name for compensated cardiac failure, and the cause?

Back 24

-Congestive heart failure.
-Weak heart, CO decreases.

Front 25

List symptoms of compensated cardiac failure.

Back 25

-Shortness of breath
-Chronic cough (due to fluid in the lungs)
-May not "feel" any symptoms until they do exercise.
-No cardiac reserve.
-Venous return > CO (right atrial pressure exceeds 0mmHg, goes up to 6mmHg)
-Normalized stroke volume
-High end diastolic volume (due to high blood volume and venous return)
-Decreased ejection fraction
-Pathological hypertrophy

Front 26

List the compensatory steps that occur in compensated heart failure.

Back 26

When CO↓ (BP↓) :
1. ↑SNS (↑HR, ↑contractility, ↑venous return) (Short term).
2. BP↑ via salt and water retention by kidneys, this ↑blood volume which ↑venous return (Long term).
End result: These all stress the heart leading to pathological hypertrophy.

Front 27

What is a positive inotropic effect?

Back 27

The increase in heart contraction by the SNS.
Impulse received by B1 receptors.

Front 28

Main difference between compensated and decompensated heart failure?

Back 28

In decomp. the frank starling mechanism has broken down, and the normalized stroke volume cant be maintained, so CO drops and tissues/brain dont receive enough oxygen/nutrients.

Front 29

List symptoms of decompensated heart failure.

Back 29

-Low stroke volume
-Kidneys stop working/filtering
-Very high fluid retention
-Very high right atrial pressure
-Very high EDV (up to 300ml)
-Very low ejection fraction
-More pulmonary edema (usually leading to death)

Front 30

Whats the treatment used for decompensated heart failure?

Back 30

-Diuretics to reduce excess fluid
-Digitalis to strengthen the heart

Front 31

List general differences between systolic and diastolic dysfunctions.

Back 31

Systolic (emptying problem):
-↓EF
-↓CO
Diastolic (filling problem) :
-EF unchanged
-↓EDV and ↓SV
-↓CO

Front 32

Is decompensated heart failure a diastolic or systolic dysfunction?

Back 32

Systolic dysfunction, the heart has trouble emptying.

Front 33

What is cardiac reserve?

Back 33

The ability to increase your CO, eg during exercise.

Front 34

List causes of heart valve lesions.

Back 34

1. Congenital/birth defect
2. Streptococcal infection (eg rheumatic fever)

Front 35

What is stenosis?

Back 35

Heart valve doesnt fully open, eg pin hole.

Front 36

Type of valve disorder with:
-Systolic dysfunction
-Aorta not opening properly
-Too much pressure in ventricle
-Systolic murmer
-Leads to LVH, ↓CO, pulmonary edema

Back 36

AVS (aortic valve stenosis).

Front 37

Type of valve disorder with:
-Systolic dysfunction
-Aorta not closing properly
-Too much volume in ventricle
-Diastolic murmer
-Leads to LVH, ↓CO, pulmonary edema

Back 37

Aortic regurgitation

Front 38

Type of valve disorder with:
-Systolic dysfunction
-Mitral valve not closing properly
-Too much volume in atrium and ventricle?
-Systolic murmer
-Leads to LVH, ↓CO, pulmonary edema, as well as RVH and atrial hypertrophy

Back 38

Mitral regurgitation

Front 39

Type of valve disorder with:
-Diastolic dysfunction
-Mitral valve not opening properly
-Underfilled left ventricle
-Diastolic murmer
-Leads to RVH, ↓CO, pulmonary edema, atrial hypertrophy, BUT NO LVH

Back 39

Mitral stenosis

Front 40

LVH, RVH, and atrial hypertrophy can lead to what?

Back 40

Fibrillation.
Atrial hypertrophy leads to atrial fibrillation, not vent fib.

Front 41

What is patent ductus arteriosis?

Back 41

-The duct between the aorta and pulmonary artery never closed.
-Causes decreased CO due to dumpage of blood back in PA
-Murmer heard during systole and first part of diastole.