Cardiomyopathy and Pericardial Disease Large Group-Silverstien Flashcards

1
Q

What is responsible for Chagas Disease? Where is this most common?

A

Parasite Trypanosoma cruzi

transmission by leaving feces on skin and biting–> get into circulation

common in Central and South America

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2
Q

When will the titer be high in Chagas Disease? What are the symptoms at this stage and can it be cured?

A

Acute phase

usually asymptomatic but can cause myocarditis.

can cure

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3
Q

What does chronic Chagas Disease often cause?

A

inflammation leading to chronic multifocal fibrosing myocarditis –> conduction problems

hard to treat

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4
Q

What EKG changes are classic for Chagas? Presentation?

A

Classic : RBBB +/- LAFB , Multiform PVCs, Ventricular tachycardia

often presents as a young person who travelled to central/south america

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5
Q

What findings are associated with chronic Chagas?

A

apical aneurysm

progressive biventricular systolic dysfunction

thromboembolism

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6
Q

Who should you treat for Chagas? What is the treatment? (3)

A

those under 50 yo with chronic infection without end-stage cardiac disease

acute infection

congenital infeciton

chronic in children

immunosuppressed

Treatment:
Benznidazole, nifurtimox and amiodarone (anti-trypanosomal activity, NOT anti-arrhythmic)

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7
Q

What are the potential causes for dilated cardiomyopathy?

A
  • idiopathic
  • familial
  • inflammatory (inc. CT diseases and sarcoidosis)
  • toxic (chronic EtOH and chemo drugs)
  • metabolic: hypothyroid and chronic hypocalcemia
  • neuromuscular: muscular or myotonic dystrophy
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8
Q

What is the hallmark finding in hypertrophic cardiomyopathy?

A

asymmetric septal hypertrophy in the absence of chronic pressure overload (HTN or aortic stenosis)

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9
Q

What is the most common cause of sudden cardiac death in young athletes in the US?

A

hypertrophic cardiomyopathy

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10
Q

What is the genetic mutation in hypertrophic cardiomyopathy?

A

genes for sarcomere proteins (beta myosin heavy chain, myosin binding protein C are the most common)

autosomal dominant but not 100% penetrance

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11
Q

What causes sudden death in pts with hypertrophic cardiomyopathy?

A

monomorphic V tach due to fibrosis and myofibrillar disarray

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12
Q

What PE findings will there be in association with hypertrophic cardiomyopathy?

A

Crescendo-decrescendo murmur at LLSB that increases with Valsalva (enlargement of the septum can cause sub aortic stenosis that will worsen with decreased preload)

May have accompanying MR murmur

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13
Q

What ECG findings are seen in hypertrophic cardiomyopathy?

A

Giant, “dagger like” Q waves in the lateral leads

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14
Q

What is the pharmacological treatment of hypertrophic cardiomyopathy? What should be avoided?

A

Treatment:

  • beta blockers
  • Ca2+ channel blockers
  • DIsopyramide (dec contractility)

AVOID nitrates–> cause decrease preload=BAD

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15
Q

What is the only thing that reduces the mortality risk in hypertrophic cardiomyopathy? Who should receive this treatment?

A

AICD (defibrillator)

indications:

  • family hx of sudden death
  • wall thickness >30 mm
  • unexplained syncope
  • hx of ventricular arrhythmias
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16
Q

What is Kussmaul’s sign? What can cause it?

A

JVP rises with inspiration

Restrictive and Constrictive Pericarditis

17
Q

What is the most likely diagnosis in a pt with SEVERE bi-atrial enlargement?

A

restrictive pericarditis/cardiomyopathy

this is a diastolic heart failure–> ventricles are non-compliant and require high P in the atria to fill –> cause the atria to enlarge

18
Q

What is the disease associated with ventricular thickening without systolic dysfunction but low voltage on an EKG?

A

amyloidosis

19
Q

What is the number one cause of Restrictive Cardiomyopathy? How is this diagnosed?

A

amyloidosis –> misfolded fibrils deposit in the tissue

can be caused by a plasma cell tumor –> multiple myeloma

  • consider with renal, neuropathy, macroglossia and easy bruising in weird places (nasal folds)
  • diagnose with congo red stain-green birefringence
20
Q

What heart sound is associated with pericarditis?

A

Friction rub with 3 phases (heard best with the pt leaning forward and exhaling)

21
Q

What is the treatment for pericarditis? What should be avoided?

A

NSAIDS and high dose Aspirin –> normally self-limited 1-3 weeks

AVOID steroids (inc likelihood of recurrent pain)

22
Q

What is the number one cause of constrictive pericarditis? What are some other causes?

A

Tuberculosis–> pericardial thickening and blood fluid

malignant (lung, breast, lymphoma), bacterial, post-MI, Uremic, radiation, rheumatologic, drug induced (procainamide)

23
Q

If tamponade is suspected, what test should be done immediately?

A

Echo

should see early diastolic RV collapse and late diastolic RA collapse

-respiratory variation in output >25%

24
Q

What is Beck’s Triad for Cardiac Tamponade?

A
  1. tachycardia and hypotension
  2. muffled heart sounds
  3. Jugular venous distension
25
Q

What is pulses paradoxus?

What is associated with a wide pulsus?

A

pulsus=fall in systemic Pressure >10 mmHg during inspiration

Take BP. at first, hear sounds in expiration only and then measure until you hear constant sounds and measure the difference. >10-12 is significant

*cardiac tamponade

26
Q

What can cause a rapid pericardial effusion? A slow?

Which type will be able to hold more volume before the pt experiences tamponade?

A

Rapid: punctures of the wall, aortic dissection –> bleeding into the pericardial space

slow: heart failure, lupus, renal failure

slow can accommodate more volume

27
Q

What ECG finding is associated with cardiac tamponade?

A

changes in the appearance (height) of the QRS from the heart swinging.

Low voltage
limb leads <10

28
Q

What chest x-ray finding is associated with cardiac tamponade?

A

Enlarged cardiac silhouette
Globular
“Water bottle”

29
Q

What is the gold standard for cardiac tamponade?

A

Right heart cath

BLUNTED Y descent in RA

(Y descent is ventricular filling)

30
Q

What is the treatment of cardiac tamponade?

A

pericardiocentesis (removal of the fluid)

31
Q

Will pulsus or Kussmaul be seen in constrictive pericarditis?

A

Kussmaul will (blood will pool in the veins and distend them in inspiration)

not pulsus because the stiff pericardium does not respond to the change in intrathoracic pressure well

32
Q

What disease has a RA STEEP Y descent? Why?

A

constrictive pericarditis because the ventricles will be allowed to fill rapidly and then shut off quickly by the rigid pericardium