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
define pathological Q wave
Q wave > 1 box in depth or width
26
Giant Cell Arteritis - what is it - RF - cm - tx - mc complication
* *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
HA worsens with masticationr
Giant cell arteritis
28
rule of 50 for GCA
Age greater than 50 Sed rate greater than 50 Steroids greater than 50 (will start patient typically on 60 mg of prednisone)