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*PANCE by subspecialty > Quick cards > Flashcards

Quick cards Flashcards

1
Q

Any change in carotid upstroke/pulse has to do with?

A

Aortic valve

Similarly anything that radiates to carotids = AORTIC VALVE

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2
Q

“Fixed splitting of S2”

A

= ASD

bc blood going thru defect & coming bacd around & causing valve to close slightly slower

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3
Q

S3 = ?

A

Volume overload -

Occurs during increased passive filling (increase preload)

CHF

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4
Q

S4 = ?

A

Occurs in stiff, noncompliant ventricle during atrial kick

= (atrial squeeze right at end of diastole to get rest of blood from atria –> ventricles)

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5
Q

S1 = ?

A

AV valve closure

Mitral
Tricuspid

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6
Q

S2 = ?

A

Semilunar valves closing

Aortic
Pulmonic

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7
Q

Physiologic splitting of S2 = ?

A

Delay in aortic valve closure in YOUNG active healthy person w/ large inspiration

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8
Q

Paradoxical splitting

A

ABNORMAL

Delay in aortic valve closure w/ large exhalation in young active = HOCM!!!

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9
Q

Fixed splitting

A

Delayed consistently w/ every beat in a L-R shunt (ASD)

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10
Q

MR. ASTR - PS - mnemonic that’s helpful for what?

A

These are the murmurs that are all systolic - if they give you a systolic murmur and a location, then you know what it’s from immediately

If they give you a diastolic murmur and a location, switch it from REGURG –> STENOSIS or vice versa but with same valve!!!

MR-TR - should be closed during systole b/c so backflow = REGURG

AS-PS - open during systolic so systolic murmurs a/w these valves = STENOSIS

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11
Q

Any valve disorder that causes or results in enlargement of either atria will lead to?

A

Afib

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12
Q

Any valve disorder that causes increased fluid in either ventricle will lead to?

A

Dilated CMP and HFrEF

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13
Q

Any valve disorder which causes increased pressure in either ventricle (stenotic aortic or pulmonic valve) will cause?

A

LVH and lead to HFpEF at first and then HFrEF later if not treated

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14
Q

Calcified (stenotic) aortic valve by age 40…(so young?)..you’re thinking?

A

Bicuspid aortic valve - taking bigger pressure hit over longer period of time = AS at much younger age than normal

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15
Q

Systolic murmur
HARSH, loud
Radiates to neck
Slow, rising, prolonged carotid pulse

+syncopal episode walking up stairs

A

AORTIC STENOSIS

Anything radiating to carotids/neck = aortic

Anything that affects carotid upstroke = aortic issue

Systolic w/ aortic features (MR. ASTR-PS) = aortic stenosis

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16
Q

Aortic murmurs in general are?

A

Harsh, loud

High-pitched

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17
Q

Mitral murmurs in general are?

A

Low-pitched

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18
Q

Aortic stenosis = which structural cardiac issues over time?

A

LVH, LAE, LAD on EKG

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19
Q

AS = CP - ?

A

AS = SAD

Syncope (on exertion)
Angina
Dyspnea (on exertion)

Fatigue
Weakness

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20
Q

Loud harsh systolic murmur w/ exertional angina

A

Aortic stenosis

not an MI

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21
Q

Regurgitation = ? volume or pressure overload in general

A

Volume overload = S3

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22
Q

Stenosis = ? in general

A

Pressure overload = ventricular remodeling = stiffening of tissue = S4

Pressure overload = concentric LVH

Similar pathology as seen in LVH due to increase pressure 2/2 hypertension - so can think of that as an example

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23
Q

Signs of aortic regurg

A

AR = Al roker = WIDE pulse pressure signs

DIASTOLIC, HIGH-pitched, at BASE, wide pulse pressure, S3 common

Regurg = volume overload = ventricular remodeling = LVH (cardiomegaly) - tolerated well for many years

MR. ASTR-PS = systolic so if at base and diastolic = opposite = AR

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24
Q

Which maneuvers increase venous return (therefore increasing all murmurs except MVP, HOCM)

A 
Squatting
Laying down (legs up)
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25
Q

Which maneuvers decease venous return? (therefore decreasing all murmurs except HOCM, MVP)

A

Valsalva

Standing

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26
Q

Inspiration does what?

A

Increases preload = all right sided murmurs = louder, L-sided murmurs quieter

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27
Q

Exhalation does what?

A

Increases venous return to left side = all L-sided murmurs louder& right sided murmurs quieter

**Why L-sided murmurs are best heard after maximal expiration

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28
Q

MS ==>

A

MS = diastolic opening snap / diastolic rumble - heard best at APEX, radiates to axilla - low-pitched = use bell

MS. DOSSA - laying on left side - slut - got strep - rheumatic fever

Rheumatic fever = MCC

Pulm edema, hoarseness, cough, LAE, afib:

So much pressure backed up into LA b/c can’t get thru stenotic valve - so it backs up into pulm - so get pulmonary symptoms & get hoarseness b/c l recurrent pharyngeal nerve gets stretched out

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29
Q

MR etiologies - acute vs chronic

A

Acute:
Infective endocarditis
Chordae tendinae rupture
Papillary mu ischemia/infarction

Chronic:
MC form - can be asx for years or forever
Marfan’s syndrome
Rheumatic, congenital, MVP

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30
Q

Acute MR

A

NO LA enlargement - blood just backs up due to huge sudden volume overload

Remember blood coming from lungs into LA -> LV

So if Mitral valve not working, blood backs up into..? LUNGS = ACUTE PULMONARY EDEMA

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31
Q

Chronic MR

A

Blood flows back from LV to LA during systole = volume overload = prominent S3

LA will become enlarged
LV will dilate to accomodate

Results in dilated heart failure (EF < 40%) =

Afib
DOE
Fatigue

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32
Q

Chronic MR management

A

Yearly Echo

Cards referral if > mild

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33
Q

MVP = ? murmur? CP?

A

MVP = MSC (mid-systolic click)

Up to 10% of females 2/2 floppy valve

ASX in most - found incidentally

CP = palpitations, CP, dyspnea, fatigue

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34
Q

MVP management

A

If murmur, send to cards

Bb for palps

SSRI’s for anxiety

MV repair

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35
Q

Tricuspid stenosis = ?

A

RAE, RVH –> right HF = dependent edema, hepatometaly, ascites (fluid backs up to body if RHF)

Holosystolic murmur along LLSB, increases w/ inspiration

(inspiration = increased preload = all R-sided murmurs get louder)

Valve replacement

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36
Q

Left heart failure, fluid backs up to?

A

BODY - systemic
LIVER -portosystemic

LEFT side = blood coming from LUNGS

RIGHT side = blood coming from BODY

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37
Q

Stenotic mitral valve, fluid backs up to?

A

Left atria

Then lungs

LEFT side = blood coming from LUNGS

RIGHT side = blood coming from BODY

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38
Q

Who gets abx ppx with dental procedures?

A

Prosthetic cardiac valves

Previous infective endocarditis

Congenital anomalies - shunts, unrepaired cyanotic heart disease

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39
Q

Controlling sx in HFrEF

A

Reduce cardiac workload:
Dec afterload! (control HTN)

Reduce preload: (control excessive fluid!!)
- Diet, diuretics, vasodilators

Increase contractility (+inotropes)

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40
Q

Which med is given to improve QOL in the later stages of CHF?

A

Digoxin = positive cardiac inotrope

Does NOT PROLONG life, makes QOL better - makes heart pump harder so decreases sx but heart might poop out sooner

Also + inotrope = milrinone

In cardiogenic shock - can use pressors = IV + inotropes = Epi, NE, dobutamine, and dopamine

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41
Q

Vasodilator drugs

A

CCB
Alpha-1 blockers

Hydralazine
Minoxodil
Nitropress

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42
Q

What is BiDil? Who should get it?

A

BiDil = medication for AA w/ HF

BiDil = isosorbid dinitrate + hydralazine = dec BP & dec vascular resistance

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43
Q

Nitrates are used for?

A

They are anti-anginal agents- for PPX and treatemnt

NTG - SL tab, patch, ointment - used to treat acute CHF/angina, MI –> paste you can rub off! - Caution can cause hypotension

Isosorbid dinitrate - for AA w/ CHF or PO tab for angina

Nitrates MOA - get converted to nitrous oxide = smooth muscle relaxation & vasodilation =

Dec preload
Dec afterload

Nitrates C/I in inferior MI (preload dependent) and hypotension

Note: PDE-5 inhibitors (sildenafil, tadalafil) work on same pathway to cause vasodilation! Used in P. aa. HTN. Not used w/ nitrates = severe hypotension

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44
Q

Initial management stable afib

A

RATE CONTROL

BB (metoprolol)
CCB (Diltiazem)
Dig in CHF/Hypotension

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45
Q

Preferred agent for rate control in Afib if elderly with significant comorbid conditions of CHF or severe hypotension?

A

Digoxin

= + cardiac inotrope

Improves LVEF, reduces hospitalizations for CHF but NO IMPROVEMENT IN MORTALITY

For standard CHF tx - still use ACEI + BB + DIURETIC

46
Q

Which drug reduces # hospitalizations in CHF?

A

Digoxin

47
Q

Standard maintenance management of CHF

A

ACEI

BB

Diuretic

48
Q

Stable afib: After rate control what are other considerations?

A

Rhythm control - use direct synchronized cardioversion most commonly - can do if:

Afib < 48 hrs, anticoagulated 3-4 weeks & TEE shows no clots in LA

IF UNSTABLE CARDIOVERT RIGHT AWAY

Or can use anti-arrhythmic agent (amiodarone, ibutilide, flecainide etc)

49
Q

CHA2DS2-VASc components?

A 
CHF 
HTN
Age > or equal to 75 - 2pt
DM
Stroke, TIA, thrombus - 2pt

Vascular dz (MI, PAD)
Age > or equal to 65-74
Sex (female 1 pt)

Total of 9 points max

> or equal to 2 = moderate to high risk of clot - chronic oral anti-coag recommended

1 = low risk = based on clinical judgement - benefit vs risk

0 = low risk - no anticoagulation

50
Q

Drugs that prolong QT…why prolonged QT is dangerous? How prolonged QT can present clinically?

A 
Drugs: 
Macrolides
Fluoroquinolones
TCAs 
First gen antipsychotics
Anti-arrhythmics (amio) --> GET EKG BEFORE STARTING

ELECTROLYTE ABNL can also prolong QT!!! AKA Hypocalcemia, hypo-Mg2+, hypo-K+

Presents clinically as recurrent syncope - get electrolytes & EKG…or can present as SCD in otherwise young healthy b/c can be congenital

Can lead to torsades - polymorphic ventricular tachycardia that leads to vfib –> death

51
Q

Two types of SVT

A

AV nodal reentry tachycardia (AVNRT) –> two pathways WITHIN node = MC type

Extra pathways = extra impulses sent to ventricles

AV reciprocating tachycardia (AVRT) = less common, MORE dangerous - accessory pathway OUTSIDE AV node = WPW

**Often preceded by a PAC that kicks it on –> SVT is frequently fast on, fast off

52
Q

Orthodromic AVNRT, AVRT = ? wide or narrow? Stable or unstable? Tx?

A

Can to orthodromic (normal direction thru AV Node) ==> leads to STABLE, NARROW complex SVT

Tx: Vagal maneuvers, Adenosine

53
Q

Antidromic AVNRT, AVRT = wide or narrow QRS? Stable or unstable?

A

WIDE QRS (going wrong direction thru AV node)

Usually less stable but if pt is doing okay (HD stable), can try meds first –> NO ADENOSINE, need an anti-arrhythmic (Look at ALCS algorithm)

Tx: Amiodarone

**If suspect WPW, then PROCAINAMIDE = tx

54
Q

WPW = what on EKG?

A

Delta wave = wide QRS

Upward slope of QRS

Short PR interval

55
Q

MAT a/w what dz? definitoin = what?

A

Multifocal atrial tachycardia = rate > 100, > 3 p wave morphologies

A/w SEVERE COPD

56
Q

Unstable SVT or unstable WPW

A

Direct synchronized cardioversion

If stable and WPW - use procainamide

57
Q

Which drugs must you avoid in WPW?

A

AV nodal blockers - ABCD

Adenosine
Beta blockers
CCB
Digoxin

These are avoided b/c they can cause preferential conduction through the fast (pre-excitation) pathway = worsening of the tachy-arrhythmia

58
Q

Causes of increased JVP

A

JVP & crackles = CHF

JVP & normal pulm exam = tamponade or constrictive pericarditis

JVP & decrease breath sounds = tension PTX

59
Q

Young asian male w/ sudden cardiac syncope = ?

A

Brugada syndrome

EKG: RBBB & ST elevations (downsloping) in V1-V2

60
Q

Why is digoxin good for rate control in people with hypotension or CHF?

A

Because it is a positive inotrope (inc contractility) but a negative chronotrope (dec rate)

61
Q

First line chronic management angina

A

Beta blocker

Reduces mortality
Decreases sx
Prevents ischemic occurrences

62
Q

Tx Prinzmental angina

A

CCB

Prevents/terminates ischemia induced by coronary vasospasm

63
Q

Why do we use nitoglycerin in angina?

A

Nitro - SL

Reduces coronary vasospasm
Decreases demand/cardiac workload by dec preload

Increases myocardial blood supply - increased collateral blood flow to iischemic myocardium, coronary artery vasodilation

64
Q

Both DHPs and Non-DHPs cause peripheral dilation - which group have direct effects on the heart as well?

A

Non-DHPs - Diltiazem, verapamil

Think Non-DHPs = Non-selective - affect heart (negative chorno/dromo/inotrope) and peripheral blood vessels

Therefore caution in CHF, in combination w/ BB (do same thing, different mech), pre-existing AV block= WORSE

65
Q

Medication regimen chronic stable angina

A

Nitro SL PRN
Beta-blocker (FIRST LINE)
ASA

66
Q

Tx NTEMI/STEMI caused by cocaine (coronary artery vasospasm)

A

BETA BLOCKERS CONTRAINDICATED (usually part of first line management in acute and

67
Q

When are BB contraindicated in acute management of NSTEMI/STEMI?

A

Severe bradycardia (<50) - inferior / RV might present w/ this

Hypotension (SBP <90) 
Decompensated CHF
Heart block (2nd-3rd deg) 
Cardiogenic shock 
Cocain-induced MI
Severe asthma/COPD
68
Q

Medications unstable angina/ NSTEMI

A

MONA +

Clopidogrel
(caution if CABG planned)

UFH
(dec mortality - add in pt w/ EKG change or + cardiac biomarkers)

Beta-blocker
(CCB in pt who cannot have Bb)
Nitrate (no dec in mortality, dec anginal sx)

69
Q

R ventricular (inferior wall) MI - DO NOT give??

A

Nitrates
Caution w/ morphine too

Causes unsafe drop in preload
Give IV fluids to keep preload up

70
Q

Management STEMI

A

MONA + EKG (w/in 10 imn) + troponin

Heparin
Consider clopidogrel
Beta blocker
ACEI

PCI = most important (w/in 90 min)

71
Q

Complications of MI

A 
Arrhythmias (Vfib)
Ventricular aneurysm/rupture
Cardiogenic shock
Papillary muscle dysfunction
Heart failure
LV wall rupture

Post-MI pericarditis (dressler syndrome)

72
Q

Signs left-sided HF

A

Pulmonary edema = chronic nonproductive cough (or pink frothy), dyspnea (MC symptom)

PE: S3, rales, rhonchi

73
Q

Signs right-sided HF

A

Fluid backs up into systemic sx = JVD, LE pitting edema, hepatic congestion (hepatomegaly) + hepatogugular reflex

74
Q

Management acute decompenstated HF

A

LMNOP

Lasix
Morphine +/-
Nitrates 
Oxygen 
Position

+ Inotropic support if severe!
Digoxin - (HF + AFIB, dec hospitalizations but NO MORTALITY BENEFIT), dobutamine, dopamine etc

75
Q

Long term management of CHF

A
  1. ACEI
    (FIRST LINE TX OF CHF) - dec mortality , prevents rehospitalization, reverses pathology by decreasing renin/SNS activation = dec ventricular remodeling

PLUS

  1. Diuretic
    (Most effective tx for SYMPTOMS caused by CHF - spironolactone also a/w dec mortality

Then add if needed:

+/- 3. Beta blocker
(dec mortality, added AFTER ACEI)

+ 4. Implantable cardioverter defibrillator in pt w/ EF < 35% (b/c they tolerate arrhythmias poorly)

76
Q

Meds that decrease mortality in CHF

A

ACEI
Beta-blockers
Nitrates + Hydralazine (BIDIL)
Spironolactone

77
Q

EKG changes pericarditis

MCC pericarditis

A

MCC - idiopathic, after viral infection (ENTEROVIRUSES - coxackie, echo)

CP: PPPP - pleuritic, persistent, postural (worse supine, relieved leaning forward), Pericardial friction rub

EKG: DIFFUSE ST elevations in PRECORDIAL (V1-V6) leads & assocated PR DEPRESSIONS

78
Q

EKG findings pericardial effusion

A

Low voltage QRS

Electrical alternans

79
Q

PE findings pericardial tamponade

A

Pulsus paradoxus

(exaggerated > 10mmHg dec in systolic blood pressure w/ inspiration - increased filling of R side of heart during inspiraiton dec left sided ventricular filling, leading to pulsus paradoxus)

+ Beck’s triad

80
Q

Beck’s triad

A

Hypotension
JVD
Muffled heart sounds

Triad of pericardial tamponade!!!

81
Q

Kussmaul’s sign

A

Increased JVD during inspiration

Inspiration = increased filling of the R heart --> 
r-I-ght = INc during INspiration

Rn disease where R heart cannot fill (constrictive pericarditis, restrictive CMP, R heart failure) = fluid backs up into jugulars b/c R heart cannot keep up

82
Q

CP/PE constrictive pericarditis

A 
Right sided heart failure signs: 
Dyspnea
Kussmaul's sign 
Inc JVD
Peripheral edema
Hepatojugular reflux

PERICARDIAL KNOCK
High-pitched 3rd heart sound due to sudden cessation of ventricular filling in early diastole from thickened inelastic pericardium - sounds like an S3

83
Q

Myocarditis - MCC, CP/PE, Tx

A

MCC Infections - enteroviruses - COXSACKIE- Also Lyme, SLE, rheumatic fever - similar to pericarditis

Myocarditis = muscle is inflamed = HEART failure!!!! –> impaired systolic function (heart muscle is sick) =…..

CP/PE: DOE, S3, tachycardia, hepatomegaly

Dx:
CXR = CARDIOMEGALY 2/2 dilated CMP
+ TROPONIN - helps distinguish myocarditis from chronic dilated CMP
Echo - ventricular dysfunction

Endomyocardial bx = GOLD standard

Tx: supportive + standard HF tx (diuretic, ACEI, inotrope if severe)

84
Q

Someone w/ viral prodrome (fever, myalgias, malaise) for several days who now comes in hypotensive, SOB, tachycardic, found to have hepatomegaly on exam

A

MYOCARDITIS - had coxackie B –> which infiltrated heart muscle & now has HEART FAILURE

May also have si/sx pericarditis concurrently

85
Q

HOCM Murmur

A

Harsh systolic crescendo-decrescendo murmur best heard at LLSB (sounds similar to AS but in different location & patient population)

Tx: Beta blockers = first line medical therapy, surgical = definitive (reserved for severe)

86
Q

Dx criteria rheumatic fever

A

Two Major OR one major + two minor

JONES = MAJOR
Joint (migratory arthralgias (LE-UE, LG)
Oh my heart! Active carditis - myo, valves (mit)
Nodules (subcutaneous) - over joints
Erythema marginatum - annular rash on trunk
Sydenham’s chorea - jerky nonrhythmic mvmt

MINOR: 
Fever
Arthralgia 
Inc ESR/CRP
EKG prolonged PR interval

PLUS evidence of strep infection - rapid, cultures, ASO titer

Tx: Aspirin 2-6 weeks w/ taper + PCN G

87
Q

HTN urgency

A

Lower BP by ~25% max over 24-48 hours using ORAL agents

Clonidine
Catopril
Furosemide
Labetalol
Nicardipine

Goal is to get < 160/100

88
Q

HTN + OP

A

Thiazide diruetic

89
Q

AA first line HTN

A

Thiazide

not 2/2 RAAS, ACEI less effective

90
Q

Aortic stenosis complications

A

= ASC

Angina
Syncope
CHF

91
Q

HTN + Systolic HF

A

ACEI !!!

Diuretic

92
Q

DM + HTN

A

ACEI

93
Q

Aortic dissection - medical management

A

For DESCENDING

Esmolol

94
Q

Best drug to increase HDL

A

Niacin

95
Q

Best drug to decrease LDL

A

HmgCOa reductase inhibitors

Statins

96
Q

Best drug to decrease triglycerides

A

Fibrates

97
Q

Duke criteria endocarditis

A

MAJOR:
Sustained bacteremia (2+ Bl Cx w/ organism known to cause endocarditis)
AND
Endocardial involvement (Echo = vegetations, NEW valvular regurgitation)

MINOR:
Predisposing condition (IVDA, abnl valve, indwelling catheter)
Fever (100.4)
Vascular & embolic phenomena
+ Bl cx not meeting major criteria
+ echo findings not meeting major (worsening of existing murmur)

TWO MAJOR or ONE major & THREE minor

Odd but can have + ESR/RF too…?

98
Q

MCC subacute endocarditis

A

Indolent infection of ABnormal valve w/ less virulent organism

S. viridans

99
Q

MC organism endocarditis prosthetic valve (PVE)

A

Staph epidermis if w/in 60 d of implant

If late, same as acute endo (staph aureus)

100
Q

Mainstay of PAD treatment

A

Cilostazol

Control other RF (DM, HTN, HLD)

101
Q

When to repair AAA (prerupture)

A

> 5.5 cm - immediate repair even if asx

102
Q

Unique PE finding Aortic dissection

A

> 20 mmHg between left and right arm
Decreased peripheral pulses

Dx: CT scan w/ contrast = initial test of choice - MRI angiogram = gold standard

Tx: Esmolol if descending (type III/B) w/ target SBP 100-120 & pulse < 60 +/- sodium nitroprusside

If Type A, Type I/II - aka acute proximal = SURGERY

103
Q

Signs coarctation of aorta

A

High UE BP
Low LE BP

A/w Bicuspid aortic valve

A/w TURNER syndrome - bicuspid valve looks like a T

104
Q

Superficial thrombophlebitis

A

Thrombophlebitis = swelling/inflammation of a vein caused by a blood clot - superficial = superficial thrombophlebitis - deep = DVT

RF: Virchow’s triad, IV cath, trauma, pregnancy, varicose veins

Tx: supportive management = MAINSTAY - extremity elevation, warm compresses, NSAIDs, elastic compression stockings

105
Q

Etiologies cardiogenic shock

A

Massive PE
Pericardial tamponade
Tension PTX
Aortic dissection

Tx underlying cause!!!

106
Q

SIRS criteria

A

HR > 90
RR > 20
Temp > 100.4
WBC > 12,000

Sepsis = SIRS + focus of infection (a/w inc lactate)))

Septic shock = Sepsis + refractory hypotension despite resuscitation

107
Q

Neurogenic shock

A

Form of distributive shock (along w/ septic, anaphylactic, endocrine)

Hypotension WITHOUT reflex tachycardia –> AKA HYPOTENSION w/ BRADYCARDIA = weird!!!

108
Q

4 findings TOF

A

1 of 5 cyanotic heart diseases

Pulmonary aa. stenosis =RVOF obs
Overriding aorta
RVH
VSD

= DOE, cyanosis worsens w/ age
“Tet-spells”= cyanotic spells relieved by inc venous return

109
Q

Murmur of VSD

A

Non-cyanotic - L–>R shunt

= HHHH

Harsh, High-pitched, Holosystolic best heard at LLSB (think of where ventricles are & which way it’s blowing L–>R)

110
Q

PE of ASD

A

Left to right = NON-cyanotic (Lefties = good)

Systolic ejection crescendo-decrescendo murmur

ASD, AS, HOCM are all described as crescendo decrescendo - but all in DIFFERENT areas - ASD = pulmonic area, AS = aortic area (RUSB), HOCM = LLSB/Erb’s point

111
Q

PDA murmur/ CP

A

Loud harsh continuous machinery murmur heard at pulmonic area

Bounding pulses - like a hammer - everything aggressive in PDA

IV indomethacin = tx, surgical correction if fails before 1-3 years of age

112
Q

Cyanotic congenital heart lesions

A

The 5 T’s
Pulmonary atresia
Tricuspid atresia

KEEP PFO/PDA OPEN w/ prostaglandin until surgical correction

*PANCE by subspecialty (22 decks)

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