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PANRE > Cumulative > Flashcards

Cumulative Flashcards

1
Q

Define Cardiomyopathy

What is the MC type?

A

Decreased myocardium function w/out ischemic or valvular etiology.

Dilated- systolic dysfunction of myocardium d/t idiopathic etiology.

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2
Q

What genetic defect can cause dilated cardiomyopathy?

What viral etiology can cause this?

What parasitic etiology can cause this?

A

TTN- controls protein connection w/in sarcomeres.

Coxsackie-B, HIV, Parvo B-19

T. Cruzi- Chaga’s Dz

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3
Q

What two medications can cause dilated cardiomyopathy?

Why/How does B1 (thiamine) deficiency cause dilated cardiomyopathy?

A

Doxorubicin, Trastuzumab

B1 stims pyruvate dehydrogenase conversion of pyruvate in AcoA. Inc’d pyruvate inc lactic acid - vasodilation - AV shunting

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4
Q

What is the Cardiac Output equation?

Define Pre/Afterload

What is Frank Sterling’s Law?

A

CO= SV * HR

Pre: blood in heart during diastole
After: resistance LV has to overcome to circulate blood

Inc sarcomere stretch = inc contractility

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5
Q

What 3 factors affect SV?

Define Eccentric/Concentric Hypertrophy

What is LaPlace’s Law?

A

Pre/Afterload, Contractility

Ecc: inc volume adds sarcomeres longitudinally; thin walls
Con: inc pressure adds sarcomeres parallel/vertically; thick walls

P=2T/R (pressure, tension, radius)
Inc wall pressure= inc tension

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6
Q

What is the Gold Standard for Dx dilated cardiomyopathy?

What hallmark sound is heard on exam?

What are the 6 Ds of etiology for this condition?

A

Echo- eccentric hypertrophy w/ HFrEF <50% (n= 55-70%)

S3

Drinking
Dunno
Deficient B1
Doxorubicin
Drugs
Dz

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7
Q

What are the Tx goals for dilated cardiomyopathy?

What meds are used for these goals?

A

Dec pre/afterload, remodel, arrhythmia
Inc contractility

Dec P: Nitro, ACEI, Diuretic, ARB
Dec A: Hydralazine, ACEI/ARB, ISDN
Dec R: Spironolactone, Eplerenone, ACEI/ARB
Dec Arr: BB (M/E-olol)
Inc Con: Digoxin

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8
Q

What is used for anti-coagulation in Pts w/ dilated cardiomyopathy?

When are these Pts candidates for ICDs?

What meds lower mortality vs are used for Sx control?

A

Native valve: DOAC/Dabigatran
Mechanical: warfarin

LVEF <35%

BB ACEI/ARB Spironolactone Hydralazine Nitrate (ISDN)
Sxs: Loops, Digoxin

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9
Q

Define Restrictive Cardiomyopathy

What are the two MCCs of this condition?

Pts are more likely to present w/ ? type of Sxs?

A

Fibrotic/infiltrative process causing diastolic dysfunction.

Idiopathic > Amyloidosis

R-sided HF Sxs

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10
Q

How does amyloidosis cause restrictive cardiomyopathy?

How does sarcoidosis cause restrictive cardiomyopathy?

How does hemochromatosis cause restrictive cardiomyopathy?

A

Mis-folded proteins deposited in endocardium.

Asteroid bodies causing non-caseating granuloma deposition.

Inc hepcidin protein (regulated feroprotein: transports Fe across GI lumen/release from spleen) causing inc Fe uptake/deposition.

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11
Q

Define Loeffler’s Endocarditis

How/why does cardiac ischemia place Pt at higher risk for VT/VF?

What are the 3 phases of diastolic filling?

A

Inc eosinophil production leading to fibrosis (parasite, drug, allergic, leukemia).

Dec perfusion = inc permeability for inc cation flow;
HCM>restrictive

Early: atrial blood falls down
Mid: blood from vasculature falls down
Late: atrial kick

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12
Q

What will be seen on EKG, Echo and biopsy in restrictive cardiomyopathy?

When are the ventricles most compliant w/ this condition?

What what is the MC presenting Sx and what will be found on PE?

A

Bi-phasic P-waves
Atrial enlargement
Apple green w/ Congo red stain

Early diastole

Dyspnea; Early: S3 Late: S4
Kussmaul sign: inspiration increases JVD

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13
Q

What finding during cardiac cath suggests restrictive cardiomyopathy?

How to Tx/manage this condition?

A

Square root/Dip and plateau sign- end diastolic pressure rapidly increases.

Dec Pre: Na/Water restriction, diuretics
Dec Aft: ACEI/ARB, Hydralazine, ISDN
Arr: BB/CCBs
Coag: DOAC/Warfarin

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14
Q

What genetic mutation causes HOCM?

What triad d/o can occur w/ this condition?

Why is there an increase in septal wall growth?

A

Autosomal dominant mutation of heavy chain of myosin causing decreased sarcomere function.

Trinucleotide repeat of GAA= Frederick Ataxia: DM, HCM, Ataxia: loss of body function.

Dec sarcomere function stims release of GF causing concentric myocyte growth.

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15
Q

Why is the anterior leaflet of the MV pulled anteriorly during systole in HOCM?

What will be seen/heard on PE?

A

Venturri effect: volume under pressure passing through small area pulls on leaflet.

MR
JVP A-wave: RA contracting against resistance
Apical lift
Biphasic radial pulse
S4

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16
Q

What causes murmur of HOCM to increase?

What causes murmur of HOCM to decrease?

A

Inc preload: squat/leg raise
Inc afterload: hand grips

Dec preload: stand/valsalva
Dec afterload: vasodilators (amylnitrate, hydralazine)

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17
Q

How to manage HOCM?

What needs to be avoided?

A

Increase preload: hydrate
Maintain HR/contractility: BB, Non-DHP CCB

Dec afterload: dilation decreases blood return to heart= inc SV/dec ESV increasing obstruction
Inc contractility: worsens obstruction while increasing O2 demand

18
Q

What are the two definitive Txs for HOCM?

What are the Echo Dx criteria?

A

Myomectomy
Alcohol septal ablation

15mm septal thickness
13mm w/ +FamHx

19
Q

What are the cardiac causes of Afib?

What are the non-cardiac causes?

A

HTN/Hypertrophy
Ischemia/inflammation
MR/S
Stretch (CHF/DCM)

Post-surgical catecholamine response
E+ abnormality (hypoK/Mg)
Hypoxia
Thyrotoxicosis: inc T3/4 inc B-adrenergic receptors=inc SNS
Sepsis- fight/flight response to HOTN
Pheo ETOH Drugs: meth/coke

20
Q

What is the MC location for the ectopic foci causing Afib?

What is the equation for MAP

A

Pulmonary veins

2(DBP)+SDP/3
Goal: 70-100 to perfuse kidney/brain

21
Q

What are the four classifications of Afib?

What determines if they’re hemodynamically unstable?

A

Mitral valve
Onset/Duration
Hemodynamics
Ventricular rate: >100bpm= Afib w/ RVR; <60bpm= Afib w/ SVR

Chest pain HOTN AMS Pulm edema

22
Q

What are the four groups of timing classifications?

How is unstable Afib Tx?

A

New: <72hrs
Paroxysmal: <7days
Persistent: >7days
Long standing: >12mon
Permanent: >7days w/out attempt to convert to NSR

+CHAP= cardio convert

23
Q

How is stable Afib Tx?

When is conversion considered in stable Afib?

What is procedure/confirmation imaging is preferred before converting?

A

Rate control (Amiodarone, BB, CCB, Digoxin)
Anti-coagulate (DOAC/LMWH)

Afib <48hrs w/ low CHADSVASC score w/ anti-coag x 4wks

TEE

24
Q

What is the risk of using Amiodarone for rate control in Afib?

BBs are c/i for use if ? exists?

CCBs are c/i for use if ? exists?

When is Digoxin preferred?

A

Pulmonary fibrosis

Asthma/COPD

Decompensated HF

HOTN/HF due to vagus nerve stimulation to inc acetylcholine

25
Q

What are the four methods of rhythm control for Afib?

What is the scoring system for anticoagulating these Pts?

A

Maze procedure, Ablation Chemical (Ia, Ic, 3) Electrical

CHA2DS2VASC:
CHF HTN Age>75 DM Stoke/TIA Vascular dz Age 65-74y/o Sex M=0, F=1)

0= low risk, no anti-coag
1= possible
2 or more= anti-coag

26
Q

Criteria for unstable Aflutter

How are these Pts Tx?

A

HOTN Angina AMS

Stable: vagal, BB/CCB and anti-coagulate
unstable: synch’d conversion
Definitive: ablation

27
Q

Acronym for normal conduction pathway in the heart?

For AV blocks, what EKG measurement is used to determine presence?

A

Send A Big Bounding Pulse
SA AV BOH Bundles Purkinje

PR: time from atrial depolarization to ventricular depolarization
Norm: .12-.20ms (.20=one large box)

28
Q

Define 1* AV Block

What are the etiologies for this condition by age?

A

Abnormally slow conduction through AV node >.2ms

Young: athlete/inc vagal tone
Old: fibrosis

29
Q

What are the four AV blocking meds?

How are unstable 1* blocks Tx?

Define 2-1* AV Block

A

ABCDs: Adenosine BBs CCBs Digoxin

Atropine (first) then Epi

Impaired AV conduction leading to conduction delays until non-conducted impulse is sent

30
Q

Mnemonics for AV block etiologies

How are unstable 2-1* AB Blocks Tx

A

BLOCKS:
BBs
Lyme dz
Ordinary variant
CCBs
K, hyper
Stemi

HOTN AMS Angina= Atropine to Pacing to Pacemaker

31
Q

Define 2*-2 AV Block

Difference in location of block between 2-1 and 2-2

A

Dz of conduction system leading to dropped beat w/ fixed/normal PR interval

2-1: at AV node
2-2: below AV node/at BOH

32
Q

How are 2*-2 Tx?

Why is the use of atropine use avoided in the Tx of 2*-2?

A

Stable: transcutaneous pacing
Unstable: B-agonist (dopamine, epi) to pacemaker

Atropine decreases refractory time/inc speed through AV node

33
Q

Define 3* AV block

How are unstable 3* AV blocks Tx

A

Defected conduction system where all atrial impulses fail to reach ventricles= complete dissociation between atria/ventricles

Atropine
B-agonists: Dopamine/Epi
Pacing to pacemaker

34
Q

Define PSVT

What are the two types

A

Tachyarrhythmia originating above ventricles w/ HR of 150-250bpm

AVNRT (MC)- accessory pathway in AV node
AVRT- accessory pathway outside of AV node

35
Q

How will the two types of PSVT appear on EKG

How are they Tx

A

Orthodromic (MC)- narrow and tachy
Antidromic- wide and tachy

Stable, narrow: vagal, adenosine, BB, CCB, Digoxin
Stable, wide: amiodarone/procainamide
Unstable: synch’d conversion
Definitive: ablation

36
Q

MOA and dosage of Adenosine

MOA of Amiodarone

A

Slows AV conduction
6mg w/ 10ml flush then
12mg w/ 10ml flush

Class 3 K blocker to prolong action potential for atrial and ventricular arrhythmias; s/e: pulmonary fibrosis

37
Q

Define Sick Sinus Syndrome

What is the MCC

How are unstable Pts Tx?

A

Dysfunctional node causing periods of arrest followed by brady/tachy arrhythmias

Fibrosis

Atropine (FL) then Epi/Dopamine then Pacing
Pacemaker/IDC

38
Q

Define VFib

How are these Pts Tx

A

Ineffective ventricular contractions MC d/t ischemia

Unsynch’d defib w/ CPR

39
Q

What is the MC type of cardiomyopathy?

What are the etiologies of this MC?

A

Dilated- systolic dysfunction of myocardium w/out valvular or ischemic pathology.

A Bunch Can Cause Cardiac Dilation:
Acohol Beriberi Coxsackie Coke Chagas Doxorubicin
6 Ds:
Dunno Drugs Drinking Deficiency B1 Doxorubicin Dz, viral

40
Q

Define Preload

Define Afterload

A

Blood in heart during diastole

Pressure LV must overcome to circulate blood.

41
Q

What are the two types of remodeling that can occur within the heart?

What is the GS for Dx dilated cardiomyopathy?

A

Volume= eccentric, thin wall
Pressure= concentric, thick wall

Echo: ventricular enlargement w/ eccentric remodeling and HFrEF <50%

42
Q

How is dilated cardiomyopathy Tx to reduce mortality?

How is it symptomatically Tx?

A

BB
ACEI/ARB
Spironolactone/Eplenerone
Hydralazine/ISBDN

Diuretic, Digoxin

PANRE (2 decks)

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