Cardio: buzzwords/diseases Flashcards

1
Q

Dilated Cardiomyopathy

  • what type of HF
  • RF
  • Etiologies (6)and which is mc?
  • CM
  • PE
  • Diagnosis —TOC?
  • whats EF like?
A

reduced strength of contraction and systolic dysfunction–>leading to dilated weak heart–>right and/or left ventricular enlargement–incr risk for sudden cardiac death
SYSTOLIC HF*
RF: 20-60 YO and M>F

ETIOLOGIES:

  1. Idiopathic– MC–can be familial
  2. infections–viral MC (esp enteroviruses, coxsackievirus B, echovirus)
  3. postviral myocarditis, HIV, lyme dz, parovivrus B19 and Chagas dz
  4. Toxic: etoh, cocaine, anthracycline (Doxorubicin–chemo) and radiation
  5. Pregnany, autoimmune, HTN
  6. Metabolic: thryoid disorders, B1 (thiamine) deficiency

CM

  • systolic HF
  • ->LEFT SIDED: L for lungs….. dyspnea (exertional or at rest), fatigue, cough,
  • ->RIGHT SIDED: periph edema, JVD, hepatomegaly, GI s/s, loss of appetite,
  • embolic events, arrhythmias

PE

  • S3 gallop hallmark due to filling of a dilated ventricle
  • mitral or tricuspid regurg

Diagnosis:
TOC=echo–>left ventricular dilation— DECR EJEC FRAC
CXR: cardiomegaly
ECG: sinus tach or arrythmias

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2
Q

what is the MC type of cardiomyopathy

A

dilated (95%)

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3
Q

S3 gallop

  • physiologically whats happeneing
  • dz
A
  • filling of a dilated ventricle*

- dilated cardiomyopathy

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4
Q

dilated cardiomyopathy is assoc with what heart sound

A

s3

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5
Q

Hypertrophic Cardiomyopathy

  • what is it and how is it passed
  • type of HF (dia or systolic)
  • what makes it worse
  • what makes murmur decrease in intensity and increase? desribe murmur
  • common age group
  • MC s/s? other cM?
  • what is common cause of death
  • diagnosis
A

HOCM–hypertrophic obstructive cardiomyopathy

  • autosomal dom genetic disorder of inapp. LV and.or RV hypertrophy with DIASTOLIC dysfunction
  • subaortic outflow obstruction due to asymmetrical septal hypertrophy + systolic anterior motion (SAM) of the mitral valve

*WORSENS WITH
1. increased contractility–>exercise, Digoxin, Beta agonists
and/or
2. decreased LV volume–>dehydration, decr venous return, Valsava

MURMUR: harsh systolic murmur best heard at LSB

  • –>increased intensity with decreased venous return (Valsalva, standing)) or decrease after load (nitries)
  • ->decreased intensity with inreased venous return (squatting, supine, leg raise) or increased afterload (handgrip) ——>incr LV volume preserves outflow
***common presents at young age---->sudden cardiac death 
OTHER CM 
*Dyspnea MC s/s 
*fatigue 
*angina-CP 
*pre syncope 
*dizziness 
*arrhythmias
*sudden cardiac death--esp in young pt--esp during exercise/extreme exertion--MC from VFIB

DIAGNOSIS

  • ECHO: asymmetric ventrical wall thickness (esp septal)
  • ECG: LVH
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6
Q

murmur increased intensity with decreased venous return (Valsalva, standing)) or decrease after load (nitries)

A

HOCM

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7
Q

Murmur decreased intensity with incr venous return (squatting, supine, leg raise) or increased afterload (handgrip)

A

HOCM

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8
Q

Restrictive Cardiomyopathy

  • type of HF
  • etiologies–MC?
  • CM–most commmon?
  • PE
  • diagnosis–toc? def diagnosis?
A

Diastolic HF in a non-dilated ventricle— impedes ventricular filling (decr compliance)—stiff ventricle fill with great effort

ETIOLOGIES

  • infiltrative dz–>amyloidosis MC, sarcoidosis, hemochromatosis, scelroderma, CA METS,
  • chemo/radiation

CM

  • RIGHT HF»» LEFT HF s/s
  • RIGHT HF= periph edema, JVD, hepatomegaly, ascites, GI s/s

PE
*Kussmaul’s sign–>lack of an inspiratory decline or increase in JVP with inspiration

DIAGNOSIS

  • ECHO–>TOC: non-dilated ventricles with normal thickness, diastolic dysfunction, marked dilated of atria**
  • ->if amyloidosis is cause–>will see bright speckled myocardium
  • EKG: low voltage QRS, arrythmias
  • DEFINITIVE DIAGNOSIS: endomyocaridal biopsy–>if amyloidosis=apple-green birefringence with Congo-red staining
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9
Q

Kussmaul’s sign

A

seen in restrictive cardiomyopathy

lack of an inspiratory decline or increase in JVP with inspiration

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10
Q

MCC of myocarditis

A

viral–enteroviruses–Coxsackievirus B

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11
Q

Viral Myocarditis

  • MC age
  • mc etiology
  • cm
  • diagnosis– gold standard?
A

-inflamm of heart muscle
-MC in young adults
MCC=enteroviruses–Coxsackievirus B

CM

  • Viral prodrome–>s/s of SYSTOLIC dysfunction aka dilated cardiomyopathy
  • HF s/s= S3 gallop, dyspnea, fatigue, exercise intolerance
  • OTHER: megacolon, pericarditis

DIAGNOSIS

  • CXR: cardiomegaly=classic
  • EKG: nonspecific ST MC
  • LABS: +/- cardiac enzymes, incr ESR
  • ECHO: ventric systolic dysf
  • GOLD STANDARD= endomyocardial biopsy–infiltration of lymphocytes w/ myocardial tissue necrosis—this is done for refractory or severe cases
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12
Q

this rhythm increases with inspiration and decrs with expiration

A

sinus arrhythmia

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13
Q

sinus arrest with alternating paroxysms of atrial tachycardia and bradycardia

A

sick sinus syndrome

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14
Q

define paroxysmal AFIB

A

self terminating within 7 days (usuaully <24hrs)

+/- recurrent

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15
Q

define persistent AFIB

A

fails to self terminate
lasts >7 days
-requires medical or electrical termination

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16
Q

define permanent afib

A

> 1 year

-refractory to cardioversion or cardioversion never tried

17
Q

define lone AFIB

A

paroxysmal, persistent or permanent without evidence of heart disease

18
Q

pSVT

-where originate

A

*above ventricles

19
Q

MAT

-assoc with what dz

A

COPD
-same as wondering atrial pacemaker except the HR is >100
EKG shows over 3 p-wave morphologies

20
Q

WPW

  • where is accessory pathway
  • EKG findings
  • CM
  • TX—stable, unstable and definitive
A
  • bundle of kent–outside AV node—it preexcites tbe venrticles
  • type of AV reciprocating tachycardia *AVRT)

WPW—“WPW”

  • W=wave–>delta wave
  • P=PR–>short PR interval
  • W=wide QRS (>0.12)

CM

  • most are asympto
  • prone to develop tachyarrythmia
  • can become unstable

TX **** (what i missed on packrat)

  1. STABLE: wide complex tachycardia:
    * antiarrhythmics–> Procainamide 1st choice— can use amino too
    * AVOID AV NODE BLOCKING AGENTS (ABCD–> Adenosine, BB, CCBs, Digoxin)
  2. UNSTABLE
    - cardiovert
  3. DEFINITIVE
    * radiofrequency catheter ablation
21
Q

delta wave

A

WPW

-slurred upstroke in QRS with a short PR interval

22
Q

ABDC pneumonic stands for

A

AV NODE BLOCKING AGENTS

A= adenosine
B=BBs
C= CCBs
D=digoxin

23
Q

Left BBB EKG findings

A
  • wide QRS >0.12
  • broad, slurred R wave in V5, 6
  • Deep S wave V1
  • ST elevations V1-3
24
Q

Right BBB ekg findings

A

wide QRS >0.12 sec
RsR’ in V1, 2
Wide S wave V6

25
Q

define pathological Q wave

A

Q wave > 1 box in depth or width

26
Q

Giant Cell Arteritis

  • what is it
  • RF
  • cm
  • tx
  • mc complication
A
  • *large and medium vessel granulomatous vasculitis of the extracranial branches of carotid artery (temporal artery, occipital artery, etc)
  • same clinical spectrum as POLYMYALGIA RHEUMATICA

RF

  • women >50
  • northeastern europeans

CM
-CLASSIC S/S–>HA, jaw claudication with mastication, visual changes
HA=new in onset, unilateral and lancinating in temporal area
+/- scalp tenderness
+/- constitutional s/s

DX

  • clinical
  • labs: incr ESR and CRP, normocytic normochromic anemia
  • temporal bipsy=definitve
  • temporal artery US–> thickening halo sign

TX (what i missed on packrat)

  1. high dose corticosteroids once suspected to prevent blindness******* DO NOT DELAY TX
  2. Methotrexate, Azathioprine
  3. low dose ASA
MC complication=blindness
Amaurosis fugax (temporary monocular blindness)
27
Q

HA worsens with masticationr

A

Giant cell arteritis

28
Q

rule of 50 for GCA

A

Age greater than 50
Sed rate greater than 50
Steroids greater than 50 (will start patient typically on 60 mg of prednisone)