Heart Failure Part 2

Front 1

What is the clinical scenario for heart failure with "preserved ejection fraction?"

Back 1

Elderly patient
Long-standing hypertension (with obesity) and concentric left ventricular hypertrophy now with impaired compliance

Bulking up for years and years against excess afterload until compliance finally gives way.

Front 2

What is the pathway to systolic dysfunction heart failure with decreased ejection?

Back 2

Draw it!

Front 3

What is the spectrum of patients with heart failure?

Back 3

Draw it.

Front 4

True or false. Patients with large myocardial infarctions go straight to heart failure with systolic dysfunction and decreases ejection fraction.

Back 4

True! (they do not go through a phase of diastolic dysfunction, heart failure with preserved ejection fraction)

Front 5

What are the four classifications for acute heart failure hemodynamics?
What percentage of each die?

Back 5

Warm and dry (10%)
Warm and wet
Cold and dry
Cold and wet (40%)

Warm = perfusion, cold = low perfusion
Dry = no pulmonary edema, wet = pulmonary edema

Front 6

What are the three general principles of heart failure?

Back 6

From the slide.

Front 7

What can septic, cardiogenic, and hypovolemic shock be classified as?

Common effects of each?

Back 7

Distributive shock

Vasodilation (capacitance too big for amount of blood available)

Front 8

What is a cause of cardiogenic shock?

What is a cause of obstructive shock?

Back 8

1. Large pulmonary thromboembolus blocking pulmonary circulation
2. Hemopericardium causing cardiac tamponade

Front 9

Label each.

Back 9

Distributive shock --> Hypovolemic shock --> Cardiogenic shock --> Obstructive shock

Front 10

What is the most common type of shock? Least common?

Back 10

Common = distributive
Least = Obstructive

Front 11

What three things is the diagnosis of shock based on?

Back 11

Clinical, hemodynamic, and biochemical signs.

Front 12

What is the biochemical sign of shock?

Back 12

Elevated serum lactate from anaerobic metabolism required because the body is inadequately perfused

Front 13

What are the hemodynamic signs of shock?

Back 13

Hypotension (different for each patient)

Front 14

The clinical signs of shock are observed through which three windows of the body?

Back 14

Behavior, skin, urine

Front 15

What are behaviors that can be observed (clinical windown #1) in shock?

Back 15

Disorientation, confusion, obtundation (decreased level of alertness)

Front 16

What are the skin changes that can be observed in shock (clinical window #2)

Back 16

Mottled, cold, clammy, pale, or cyanotic

Front 17

What are unine changes that can be observed in shock (clinical window #3)?

Back 17

Decreased output

Front 18

We should probably know this slide.

Back 18

Draw it!

Front 19

Aortic regurgitation due to severe dilatation of aortic root.
Name and describe the microscopic pathology indicated by arrow.

Can you name the disease that would cause this?

Back 19

Front 20

Why does she have mitral regurgitation? What is the reason?

Back 20

Ruptured papillary muscle

Front 21

Why does she have a ruptured papillary muscle? Here is the reason. Can you find it, describe and diagnose it?

Back 21

1. Posterior left ventricle
2. Area of mottled tan, red, light, and dark brown myocardium
3. Acute MI

Front 22

A 90-year-old white male has a history of an old myocardial infarction. He presents with increasingly disabling dyspnea on exertion, waking up short of breath and needing three pillows to prop him up for sleep.

His temperature is 37, heart rate 110, blood pressure 110/70, respirations 20 and saturation 95%. He has a third heart sound, but no murmurs. He has pulmonary crackles one-third of the way up his back bilaterally. His abdomen is distended, but not tender. He has leg edema up to the knees.
Why does he have leg edema?

Back 22

This is why?

Front 23

Why does he have tachycardia?

Back 23

Sympathetic nervous stimulation
Epinephrine & norepinephrine from adrenals

Front 24

Why does he have pulmonary crackles?

Back 24

Pulmonary alveolar edema

Front 25

Why does he have pulmonary alveolar edema?

Back 25

Hydrostatic pressure buildup from the excess blood the left heart is failing to pump, being transmitted back to the pulmonary capillaries, which are leaking fluid transudate into alveoli.

Front 26

What is the answer?

Back 26

B-type natriuretic peptide

Front 27

Which hormone opposed what the other hormones are doing in heart failure?

What is an excellent blood test for heart failure?

Back 27

ANP

B-type natriuretic peptide (BNP) levels

Front 28

What do you think the patient has?

Back 28

Ankle swelling + pulmonary crackles = heart failure

Diastolic murmur = valve disease (NO INNOCENT DIASTOLIC MURMURS)

AORTIC REGURGITATION!

Front 29

Let’s assume that her baseline left ventricular
end-diastolic pressure (LVEDP) was 10 mm Hg.
Assume her baseline left ventricular
end-diastolic volume (LVEDV) was 150 ml.
Assume her stroke volume (SV) was 100 ml.
That would make her ejection fraction (EF) 67%

It would make her left ventricular end-systolic
volume (LVESV) 50 ml.

Make sure the numbers reflect heart failure also!

Back 29

Only been three days, so regurge is not compensated.
E

Front 30

Marfan Syndrome:
What is defective?

Back 30

Defective synthesis of fibrillin --> abnormal sequestration of TGF-B in aortic wall --> dilation due to dysregulated signaling and progressive loss of elastic tissues

Front 31

What does Marfan's syndrome lead to?

Back 31

Inadequate extracellular matrix synthesis and accumulation of increasing amounts of amorphous proteoglycans --> cystic medial degeneration

Can also occur in scurvy.

Front 32

A 60-year-old obese white female smoker with diabetes (for 30 years), hypertension and hypercholesterolemia presents with rapidly progressive dyspnea over 3 hours associated with abdominal distension and ankle swelling.
Her temperature is 37.6, pulse 100 and blood pressure 90/30. She is diaphoretic. She has a grade III/VI blowing holosytolic heart murmur, bibasilar pulmonary crackles, mild abdominal distension
and mild pedal edema.

Back 32

Mitral regurgication

Not aortic stenosis (female and wrong type of murmur quality)

Front 33

She had an MI that led to papillary rupture and mitral regurgitation. Why didn't she have chest pain?

Back 33

Silent myocardial infarctions

More common in diabetics, usually involves about 10% of LV

Front 34

Let’s assume that her baseline left atrial pressure (LAP) was 10 mm Hg. Assume her baseline left ventricular end-diastolic volume (LVEDV) was 150 ml. Assume her stroke volume (SV) was 100 ml. That would make her ejection fraction (EF) 67% It would make her left ventricular end-systolic volume (LVESV) 50 ml. Now, with her mitral regurgitation and heart
failure, her stroke volume is partly going in reverse back into the left atrium (RSV) and partly going forward (FSV). Since there are 2 papillary muscles and she has lost one, let’s assume half of her SV is RSV…

Back 34

E
Acute myocardial regurgitation =
Elevated atrial pressure, decreased LVESV with part of stroke volume going backward

Chronic = less elevated left atrial pressure, more increased LVEDV to compensate for stroke volume reverse --> higher than normal LVESV at the end of systole

Front 35

What happens when chronic mitral regurgitation passes limit of compensation and becomes decompensated?

Back 35

Hemodynamics take on bad features of acute and chronic mitral regurgitation:

LAP increases
LVEDV really high
LVESV increase way up (because decompensated heart can't pump out so much) --> FORWARD STROKE VOLUME FALLS