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Nayla Foundations > Myocarditis > Flashcards

Myocarditis Flashcards

1
Q

What are the 3 structural types of cardiomyopathies

A 
Dilated (most common- systolic dysfunction)
hypertrophic
restrictive (diastolic dysfunction)
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2
Q

What is the leading cause of congestive HF

A

idiopathic dilated CM

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3
Q

What is dilated CM

A

LV enlarges (w/o hypertrophy) and can’t expel blood (reduced EF)

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4
Q

What happens to compensate for systolic dysfunction

A

HR and/or SV increase

CO=HRxSV, and CO is reduced in dilated CM

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5
Q

What causes dilated CM

A

**Idiopathic

also tons of others; genetics, myocarditis, etc.

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6
Q

What are the ABCD PIG for Dilated Cardiomyopathy

A 
Alcohol
Beriberi
Coxsackie/Chagas
Drugs (cocaine, chemo)
Pregnancy 
Idiopathic/infection
Genetic
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7
Q

What is Ischemic CM the most common cause of

A

HF due to systolic dysfunction

also causes Dilated CM

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8
Q

What happens in ischemic CM

A

LVEF <35-40% from CAD, often after MI

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9
Q

How do you treat Ischemic CM

A

ASA, high intensity statin, BB, Ace

Loop if fluid overloaded

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10
Q

What is Hypertensive CM

A

Concentric LVH that progresses to LV dilation

Usually causes systolic HF (but can rarely cause diastolic)

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11
Q

What is alcoholic cardiomyopathy

A

excess alcohol causes myocardial dysfunction

>90g (7-8 drinks) per day for 5 years (less for women)

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12
Q

What’s a characteristic ECG finding for alcoholic CM

A 
Prolonged QTc (cause ventricular arrhythmia)
Hypo-Mg and K prolong QT even more
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13
Q

What is peripartum CM

A

Development of HF late in pregnancy (36 wks) or 5 mo. postpartum
Wean therapy only after LVEF >50% for 6 mo.
Requires heart transplant
10% mortality in 2 years

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14
Q

What are RF for peripartum CM

A 
age
african descent
cocaine
pre-eclampsia
multiple fetuses
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15
Q

What is Takotsubo CM

A

Stress CM, broken heart syndrome
Transient ballooning of LV during systole
Associated with physical and emotional stress
WITHOUT CAD present (If present, probably not takotsubo)

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16
Q

How do Takotsubo patients present

A

Like MI (substernal CP)
7x elevated Troponin
ST elevation
decreased LVEF (ballooning)

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17
Q

How do you treat Takotsubo

A

recovery in 1-4 weeks!

BB if at risk for recurrence

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18
Q

What are dilated CM patients usually misdiagnosed as

A

Viral URI in young adults (viral myocarditis)

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19
Q

What are key points that indicate Dilate CM in History

A 
insomnia (sleeping sitting up) 
SOB,Cough, PND, orthopnea
Hx Breast cancer
alcohol or drug use
Fix sudden cardiac death
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20
Q

What would you see on dilated CM PE

A 
cariogenic shock, tachypnea
L/RHF symptoms
Hypoxia (clubbing, cyanosis)
Heaves, shifted PMI
(Kerley B lines on CXR)
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21
Q

What CMP finding in dilated CM indicates poor prognosis

A

Hyponatremia

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22
Q

How do you treat dilated CM

A 
Same as HF; 
ACE (great if EF <35%)
ARB
BB (great if HFrEF and LVEF <40%)
aldosterone antagonist (reduce M&amp;M in Class III-IV HF)
23
Q

What is sacubitril-Valsartan

A

Drug that reduces M&M in HFrEF patients

24
Q

What are the positive functions of the drugs used to treat Dilated CM

A

ACE: decrease preload and after load
BB: reduce HR and decreased afterload

25
Q

What are surgical options for dilated CM

A

LVAD
CRT (LVEF <35%)
AICD (LVEF <30-35%)
Heart transplant

26
Q

What is hypertrophic CM

A

Unexplained LV hypertrophy >15 mm (w/o dilation) with high incidence of sudden cardiac death
AKA: IHSS and ASH

27
Q

What causes hypertrophic CM

A

Familial HCM
structural abn
subendocardial ischemia

28
Q

What is the pathophysiology of HCM

A

higher systolic outflow= more severe disease
Increased ventricular filling pressure
Mitral Regurgitation

29
Q

What are the two types of HCM

A

Obstructive (due to systolic anterior motion of mitral valve obstructing flow)
Non-obstructive

30
Q

What happens when you increase LVOTO (L ventricular outflow tract obstruction)

A

decrease preload
decrease after load
increased inotropy (contraction)
–Achieved by standing quickly or valsalva

31
Q

How do you decrease LVOTO

A

supine with legs up

this increases chamber size and decreases inotropy

32
Q

What makes HCM related to sudden cardiac death

A

increased risk for ventricular and supra ventricular arrhythmias

33
Q

What are risk factors for sudden cardiac death in HCM

A 
Hx syncope 
FHx
LV wall >30 mm
abn BP with exercise 
<30 y/o
34
Q

How do HCM patients usually present

A

asymptomatic (until VTach)

-Fatigue, dyspnea, angina, palpitations, syncope, PMN/orthopnea, dizziness

35
Q

What will you see on PE for HCM

A

Double apical impulse (S3 gallop)
S4
Systolic ejection crescendo/decrescendo murmur at apex/LSB (increased with low preload/afterload aka valsalva)

36
Q

How do you diagnose and treat HCM

A

TEE to diagnose

Risk stratify, restrict physical activity, avoid volume depletion

37
Q

What is pharmacologic treatment for HCM

A

Arrhythmias: BB (- inotropy but not vasodilator)
HCM and AFib: Anticoagulation!
Sx despite BB: replace BB with Non-DHP CCB (Verapamil)
Disopyramide: anti arrhythmic, STRONG - inotrope (more than BB and CCB), prolongs QT, accelerates AV (use WITH BB)

38
Q

What is surgical treatment for HCM

A

surgical septal myectomy

alcohol septal ablation

39
Q

What is restrictive CM

A

Ventricles impaired filling WITHOUT hypertrophy or dilation (diastolic dysfunction)
Severe cases have bi-atrial enlargement

40
Q

What are the causes of restrictive CM

A 
Idiopathic 
Loeffler eosinophilic endomyocardial disease (#1 world wide)
Amyloidosis (#1 in US)
High incidence in tropics
Resembles constrictive pericarditis
41
Q

How dos RCM present clinically

A

Late stage with pronounced Sx

Exercise intolerance, SOB, fatigue, orthopnea, palpitations, syncope

42
Q

What will you see on RCM PE

A

RHF Sx
Cardiac cachexia
amyloidosis signs (easy bruising, periorbital purpura, macroglossia)
JVD (Kussmaul’s sign)

43
Q

How do you diagnose RCM

A 
*Echo!
Cardiac MRI 
ECG: ST depression, AFib, low voltage QRS
Cardiac cath 
Ventricular biopsy (last resort)
44
Q

What will lab findings for RCM show

A

eosinophilia
LFT
high NT-pro-BNP

45
Q

How can you tell the difference between RCM and constrictive pericarditis

A

Cardiac cath

NT-pro-BNP elevated in RCM but NOT in constrictive pericarditis

46
Q

How do you manage RCM

A

want to reduce filling pressure w/o reducing CO- BB, CCB
Diuretics (but use caution)
ACE and ARB not for amyloidosis
Anticoagulate if in AFib
-Treat underlying disease (chemo for amyloidosis) (phlebotomy for hemochromatosis)
-Pacemaker, LVAD

47
Q

What is cardiac amyloidosis

A

deposition of amyloid fibrils systemically, infiltrating the heart
4 types with varying prognosis

48
Q

What is Myocarditis

A

inflammation of myocardium associated with CAD
can be rapidly progressive and manifest in otherwise healthy patient
-Usually cause systolic dysfunction

49
Q

What are the types of myocarditis

A

Fulminant myocarditis (after viral prodrome)
acute myocarditis
chronic active myocarditis (fibrosis on biopsy)
chronic persistent myocarditis (no systolic dysfunction)

50
Q

What causes myocarditis

A

Idiopathic
**Viral in developed countries (enterovirus, coxsackie B, adenovirus, CMV, EBV)
developing countries (rheumatic carditis, chagas, HIV

51
Q

What is the prognosis of Myocarditis

A

Fulminant myocarditis survivors: good prognosis
1/3 develop DCM
Mild Sx recover completely
Postpartum CM have 50% mortality at 1 yr

52
Q

How does Myocarditis present clinically

A

Acute decompensating HF (**edema, S3 gallop, tachycardia)
Recent URI, flu Sx (1-2 wk)
CP (pericardial friction rub)

53
Q

How do you diagnose myocarditis

A

Endomyocardial biopsy***

indicate in fulminant HF w/in 2 wks/new onset HF w/o treatment response

54
Q

How do you treat Myocarditis

A

avoid strenuous activity
supportive care
If fulminate myocarditis, manage as if HF

Nayla Foundations (18 decks)

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