Pericardial and Myocardial Cases-Henkin Flashcards

1
Q

Classification or Pericardial diseases

A

Pericarditis (Acute/recurrent/chronic), pericardial effusions, (without inflammation from other causes-traumatic, infiltrated) Pericardial compressive syndromes (cardiac tamponade, constrictive pericarditis), Other rare diseases (congenital absence, cysts, primary tumors-metastasis more common)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What determines whether or not fluid causes tamponade (contraction impedance)?

A
  1. Amount of fluid, 2. Rate of fluid production (gradual)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Most common causes of pericardial effusion/inflammation

A

Viral (assume unless proven otherwise) and idiopathic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Other causes of pericardial effusion/inflammation

A

Bacterial/fungal, Traumatic, mechanical after surgery (damage causing autoimmune reaction to pericardium), Kidney disease, dialysis patients will have fluid, Hypothyroidism, HIV more common, Metastasis, Pregnancy by itself (our patient!) can cause a small amount of PE dt fluid overload like peripheral edema (not autoimmune), Radiation therapy , Chemotherapy-some, Some medications that cause autoimmune reactions..

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the physical exam signs of pericarditis?

A

Normal BP, clear lungs, normal heart sounds, scratchy sound over precordium-pericardial frictino rub (like scratchy paper, louder when leans forward and heart is against chest wall. 3 components: diastole, presystole/atrial systole and systole), biphasic or monophasic systolic murmur.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does the EKG show in pericarditis?

A

ST elevation in almost all leads. PR depression. T wave doesn’t become inverted when ST still elevated. Can also be lower QRSs, some Pulsus alternans.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Lab tests in pericarditis

A

Inflammation, increased sedimentation rate (ESR), leukocytosis, increase in myocardial enzymes if myocarditis but often normal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the primary treatment for pericarditis?

A

Antiinflammatories

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the symptoms of pericarditis

A

Muscle and chest pain, fever. Retrosternal or epigastric can radiate to neck or trapezius area aggravated by cough and deep breath, recumbancy, eased by leaning forward.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Differential diagnoses with acute pericarditis

A

If not typical check enzymes for MI just in case. Pneumonia (fever and chest pain), dissecting aortic aneurysm.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the CXR like in constrictive pericarditis?

A

Large, waterbottle shape, equally large L and R sides.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How to measure pulsus paradoxis

A

inflate the BP sleeve to above systolic BP and slowly decrease pressure until start hearing a sound (systolic BP). At first will only hear it during expiry not inspiry. Only when decrease more will hear inspirum. Because during inspirum increases venous return. Sign of tamponade.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the 2 pericardial constrictive syndromes?

A

Cardiac tamponade (from fluid, acute), Constrictive pericarditis (chronic inflammation). Can also be in between.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens with increased diastolic pressure in one chamber?

A

Equilization across all 4 chambers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the effect of increased right sided pressure?

A

Impeded venous return: increased jugular venous pressure, increased CVP, hepatomegaly, edema, asciites.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the effect of increased left sided pressure:?

A

Decreased cardiac output, compensatory tachycardia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Pathophysiology in chambers of impared diastolic filling

A

Decreased ventricular volume, increased diastolic pressures, decreased diastolic compliance, preserved systolic function, ventricular coupling

18
Q

Mechanism of pulsus paradoxus

A

Usually during inspirum, get increase in venous return, with septum tending to bulge into LV because more blood in R side pushes septum towards left side but if pericardium is elastic, L side can also expand and doesn’t effect volume or pressure much. If fixed and doesn’t allow expansion, bulging of septum will reduce CO and reduce blood pressure.

19
Q

How are the signs of tamponade similar and different from pulmonary edema?

A

Both have low BP, extended JV, pulsus paradoxus. Clear lungs.

20
Q

What is the physical exam presentation in cardiomyopathy?:

A

Tachypnea, tachycardia, normal BP, extended jugular veins, mild rales, soft heart sounds, gallop rhythm with S4, enlarged liver, pitting edema in legs.

21
Q

What is the appearance of the CXR in cardiomyopathy?

A

Enlarged left heart.

22
Q

Definition of cardiomyopathy

A

A disease involving the heart muscle of unknown etiology. Primary so must exclude: MI, HTN, congenital HF, valvular, pericardial.

23
Q

Primary classification of cardiomyopathies

A

Dilated (DCM), hypertrophic (HCM), Restrictive.

24
Q

Secondary classification of CMP

A

Infective (usually viral), Familial storage diseases (accumulation of glycogen or polysaccharides in myocardium), electrolyte/vimatim deficiencies, infiltrations of other cells or substances (hemochromatosis/iron accumulation), Toxic causes, Peripartum (two months before or after birth), drugs

25
Q

Drugs causing CMP

A

Chemo (Doxorubicin, cyclophsphamide, 5FU, herceptin), cocaine (blood vessels, small MIs)

26
Q

Exclusionary differential diagnoses with secondary CMP:

A

Alcohol (abstinence), hypo and hyperthyroid, hemochromatosis (can remove iron), hypocalcemia/phosphatemia, HIV, chronic tachycardia (from arrhythmias like afib that can weaken the heart over time, treatment restores contraction to normal), Tako-Tsubo, peripartum (last few weeks of pregnancy, can be reversible but can’t get pregnant again), noncompaction (embryogenesis)

27
Q

What is Tako Tsubo

A

Stress cardiomyopathy more common in women often, can see ST elevation like an MI, base of ventricle looks normal then see ballooning. Catheterize and all vessels are open with no obstruction. Not a true MI because after a few days disappears, outsurge of catecholamines, after a few days pt rests and goes away.

28
Q

Treatment of CMP

A

Like any other heart failure (beta blockers, etc)

29
Q

Physical exam in Hypertrophic cardiomyopathy

A

Brisk pulse, jugular veins not extended, clear lungs, S4 heart sound, mid/late systolic murmur (at left sternal border/apex).

30
Q

How is the EKG in hypertrophic cardiomyopathy?

A

LV hypertrophy, sinus rhythm, ST depression and T inversion .

31
Q

What appears in the echo of hypertrophic cardiomyopathy:?

A

Bulging of septum, mitral valve blocks aortic outflow, systolic anterior motion (SAM) of mitral valve.

32
Q

What needs to be excluded to diagnose cardiac myopathy?

A

HTN, aortic stenosis, LV dilation.

33
Q

Hypertrophic cardiomyopathy classification

A

Non-obstructive and obstructive, Assymetric (more in obstructive) and Symmetric.

34
Q

What causes diastolic dysfunction in Hypertrophic CMP?

A

Thick myocardium that can’t contract properly. Stiff and impedence to filling, high resistance/LVEDP.

35
Q

Mechanical difference between aortic stenosis and hypertrophic CMP?

A

Aorta is constantly constricted in aortic stenosis whereas starts normal in HC and pressure drops and valve flops in the way.

36
Q

Factors that increase and lengthen murmur or make it stronger in hypertrophic cardiomyopathy

A

Hypertrophy increases by decreasing afterload (LV size decreases and obstruction increases), increased contractility (LV contracts). Ex: Valsalva (increases venous return), standing up, exercise (increases contractility), hypovolemia, tachycardia and medications.

37
Q

Factors that decrease obstruction in hypertrophic cardiomyopathy

A

Increase venous return with increased afterload.

38
Q

Complications of hypertrophic CMP

A

AFib, dilated CMP, ischemia (thick with no new vessels, high pressure), arrhythmias and sudden cardiac death, dilated cardiomyopathy with systolic dysfunction.

39
Q

What treatment should be avoided in HCMP?

A

Digitalis or anything that increases contractility or decreases volume of the ventricle.

40
Q

Treatment for hypertrophic CMP

A

Beta blockers and calcium channel blockers to reduce contractility. A pacemaker will decrease contractility-dyssynchrony of contraction. ICD to prevent arrhythmia and sudden death. Surgery: septal myectomy to decrease symptoms if no other treatment worked.