3⼀CARDIOLOGY Flashcards

(348 cards)

1
Q

5

What are the 2 most common cardiac tumors?
_________________

cp? (5)

A

[metastasis to heart] > [L atrial myxoma (most common 1º cardiac tumor)]

_________________

[“tumor plop”] [diastolic murmur] , HF, afib, [arterial embolization/occlusion]

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2
Q

{[NYHA⬜] with [EF⬜%]} indicates initiation of [6HOT]

In step wise order, state when each part of [6HOT] is clinically indicated -6

[6*part*-HFrEF Optimized Therapy]

A

[1-4 ; ≤40%]
_________________
{1a AB: [1-4 ≤40%]}
{1b D: [2-4 VO]}
{2 A: [2-4 ≤35%]}
{3 S: [2-4]}
{S i: Angiotensin🟥 intolerance}
{S d: REFRACTORY HF}

6HOT = NYHA HF tx

[(1aAB) - (1bD)]
[2A]
[3S]
{Si} and {Sd}

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3
Q

{[NYHA⬜] with [EF⬜%]} indicates initiation of [6HOT]

describe

[NYHA 1] (4)

[New York Heart Association (HF Class)1]

A

[1-4 ; ≤40%]
_________________
{[⊝Resting | ⊝Ordinary Activity]
= [No Activity Limitationmild HF]}

💔 = HF sx (fatigue, SOB, palpitation)
🔎6HOT = [6part-HFrEF Optimized Therapy]

{1a AB: [1-4 ≤40%]}
{1b D: [2-4 VO]}
{2 A: [2-4 ≤35%]}
{3 S: [2-4]}
{S i: Angiotensin🟥 intolerance}
{S d: REFRACTORY HF}

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4
Q

{[NYHA⬜] with [EF⬜%]} indicates initiation of [6HOT]

describe

[NYHA 2] (4)

[New York Heart Association (HF Class)2]

A

[1-4 ; ≤40%]
_________________
{[⊝Resting | 💔Ordinary Activity]
= [SLIGHT Activity Limitationmild HF]}

💔 = HF sx (fatigue, SOB, palpitation)
🔎6HOT = [6part-HFrEF Optimized Therapy]

{1a AB: [1-4 ≤40%]}
{1b D: [2-4 VO]}
{2 A: [2-4 ≤35%]}
{3 S: [2-4]}
{S i: Angiotensin🟥 intolerance}
{S d: REFRACTORY HF}

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5
Q

{[NYHA⬜] with [EF⬜%]} indicates initiation of [6HOT]

describe

[NYHA 3] (4)

[New York Heart Association (HF Class)3]

A

[1-4 ; ≤40%]
_________________
{[⊝Resting | (💔less thanOrdinary Activity)]
= [MARKED Activity LimitationMOD HF]}

💔 = HF sx (fatigue, SOB, palpitation)
🔎6HOT = [6part-HFrEF Optimized Therapy]

{1a AB: [1-4 ≤40%]}
{1b D: [2-4 VO]}
{2 A: [2-4 ≤35%]}
{3 S: [2-4]}
{S i: Angiotensin🟥 intolerance}
{S d: REFRACTORY HF}

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6
Q

{[NYHA⬜] with [EF⬜%]} indicates initiation of [6HOT]

describe

[NYHA 4] (4)

[New York Heart Association (HF Class)4]

A

[1-4 ; ≤40%]
_________________
{[💔RESTING | 💔ANY ACTIVITY ]
= [BEDBOUND⼀COMPLETE Activity LimitationSEVERE HF]}

💔 = HF sx (fatigue, SOB, palpitation)
🔎6HOT = [6part-HFrEF Optimized Therapy]

{1a AB: [1-4 ≤40%]}
{1b D: [2-4 VO]}
{2 A: [2-4 ≤35%]}
{3 S: [2-4]}
{S i: Angiotensin🟥 intolerance}
{S d: REFRACTORY HF}

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7
Q

{[NYHA⬜] with [EF⬜%]} indicates initiation of [6HOT]

In step wise order, name the parts of [6HOT] -6

[6*part*-HFrEF Optimized Therapy]

A

[1-4 ; ≤40%]
_________________
[(1aAB) - (1bD)]
[2A]
[3S]
{Si} and {Sd}

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8
Q

What therapies are used to treat [ACS NSTEMI]? -10

A

Pts with ACS {Really Always Need OBAMA}!

  1. Reperfusioncoronary angiography within 24H
  2. [AAA blood thinners (ASA/ADP P2Y12 R Blocker/Anticoag (Heparin)]
  3. NTG = VasoDilates Veins and Coronary Arteries (C❌D in R VT MI)
  4. Oxygen = Minimizes ischemia
  5. Beta Blockers = DEC HR –> DEC Arrhythmia risk and DEC O2 demand (C❌D in acute HF)
  6. [ACEk2 inhibitors within 24 hrs] = DEC [L Ventricle Dilation/Remodeling]
  7. Morphine = pain
  8. AtorvaSTATIN - comes later

ASA and Beta blockers can –> asthma exacerbation

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9
Q

Of the 10 therapies for ACS, which is contraindicated in RIGHT Ventricular MI?

A

Nitrates

(venoDilates → DEC preload(not good for preload dependent RV MI) & worsens hypOtension)
_________________
Pts with ACS { Really Always Need OBAMA }!

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10
Q

Of the 10 therapies for ACS, which [ACS therapy] is contraindicated when acute HF is superimposed?

A

BETA🟥

do NOT use β🟥 if [ACS c/b _acut_e HF]

Pts with ACS { Really Always Need OBAMA }!

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11
Q

What therapies are used to treat [ACSSTEMI] ?-10

A

Pts with ACS {Really Always Need OBAMA}!

  1. ReperfusionR4 criteria
  2. [AAA blood thinners (ASA/ADP P2Y12 R Blocker/Anticoag (Heparin)]
  3. NTG = VasoDilates Veins and Coronary Arteries (CTD in R VT MI)
  4. Oxygen = Minimizes ischemia
  5. Beta Blockers = DEC HR –> DEC Arrhythmia risk and DEC O2 demand (CTD in acute HF)
  6. [ACEk2 inhibitors within 24 hrs] = DEC [L Ventricle Dilation/Remodeling]
  7. Morphine = pain
  8. AtorvaSTATIN - comes later

ASA and Beta blockers can –> asthma exacerbation

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12
Q

What therapies are used to treat [ACSunstable angina]?-10

A

Pts with ACS{Really Always Need OBAMA}!

  1. Reperfusioncoronary angiography within 24H
  2. [AAA blood thinners (ASA/ADP P2Y12 R Blocker/Anticoag (Heparin)]
  3. NTG = VasoDilates Veins and Coronary Arteries (CTD in R VT MI)
  4. Oxygen = Minimizes ischemia
  5. Beta Blockers = DEC HR –> DEC Arrhythmia risk and DEC O2 demand (CTD in acute HF)
  6. [ACEk2 inhibitors within 24 hrs] = DEC [L Ventricle Dilation/Remodeling]
  7. Morphine = pain
  8. AtorvaSTATIN - comes later

ASA and Beta blockers can –> asthma exacerbation

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13
Q

When is Angina classified as Unstable -4

Aua

A

FREN [chest pain Occurrence] is UNSTABLE!

  1. [Freq ( cpO ⇪ in Frequency)]
  2. [Rest (cpO at rest)]
  3. [Exertion (cpO w low exertion)]
  4. [New (cpO is new)]

Aua: [ACS ⼀Unstable angina]

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14
Q

DDx for T-wave inversion - 6

A

“T wave Inverts my MUNDO, smh”

[Myocardial❌HYPERTROPHY|contusion|inflammation]

[Unstable Angina⼀ACS]

[NSTEMI⼀ACS]

[Digoxin OD]

[Old💔([Old Pericarditis]|[Old STEMI⼀ACS_especially if ⊕Q waves])}

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15
Q

What is Cardiac Syndrome X

________________

Lab findings?-3

A

[Exertional(stable angina-LIKE) cp] (usually Women) with accompanying [❌Abnl Exercise Stress EKG]

BUT…

[ ✅ NORMAL CORONARY ANGIOGRAM] and..
[ ✅Normal baseline EKG]

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16
Q

Based on the 3 characteristics of Angina [which are (⬜3)] , when is Angina:

TYPICAL?

________________

Atypical?

________________

NonAngina?

A

“Diagnose Angina cp using the [Angina PEN] “

[Pressure substernally >20m]

[Exertional]

[NTG or Rest relieves]

________________

[3/3 = TYPICAL] [2/3= Atypical | [0-1 = NonAngina]

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17
Q

Tx for Stable Angina -6

A

STABLE CAD management = stabLE

statin,

[tighten Lifestyle(BP/Glucose/🚭)],

aSA,

[(bBlocker**>ccb )+ (ACEK2 inhibitor)]

_________________
[Lab-for-coronary angio revascularization in high risk pts(STD at min exertion/VT arrhythmia/poor exercise capacity) or false neg stress test pts],

[Exercise stress = dx unless ⊕baseline EKG❌ → Pharmacologic stress imaging]

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18
Q

RanOlazine

MOA
_________________
Indication

A

inhibits late-phase Na+ influx –> ⬇︎myocardial Ca+ influx –> [⬇︎myocardial wall tension] → [ ⇪ Coronary a blood flow] = treats Stable Angina

Stable Angina 2/2 Atherosclerotic CAD

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19
Q

In patients c/f ACS, describe the minimal workup required if initial troponin/initial EKG are unremarkable ? (2)

A

[(troponin q6h) x 3] + [(EKG q30 min) x 3]

“1st TENA *2nd [“Really Always Needs OBAMA”]

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20
Q

What is the greatest risk factor for coronary stent thrombosis after cornary stent is placed?

_________________

describe this risk factor (2)

A

[noncompliance with postsurgical DAPT]
_________________

[low dose ASA]

+

[ADP P2Y platelet R blocker (Clopidogrel,Prasugrel,Ticagrelor)]
_________________

DAPT = DualAntiPlatelet Threapy

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21
Q

pts with underlying connective tissue disease are at ⇪ risk for what sudden heart complication?
________________

Describe the clinical presentation -5

A

[Chordae Tendineae rupture]

→ [acute MR( sx = Pulm edema, hypOtension, hyperdynamic❤️ +/- holosystolic murmur)]

🔎MR = Mitral Regurgitation

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22
Q

Brugada Syndrome

MOD

________________

tx -2

A

[AUTO DOM Na+ Channelopathy] ➜ [SUDDEN SLEEP DEATH OR SYNCOPE]

________________

ICD vs Quinidine

[Brugada-Pokkuri-SUNDS]AKA

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23
Q

Describe the approach to Cardiac arrest -10

A
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24
Q

what is the purpose of the [Upright Tilt Table Test]?

A

differentiates unclear Syncope into
{[VANS] vs. [Dysautonomia] vs. [Postural Orthostatic⼀Tachycardia Syncope]}

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25
On EKG, What constitutes as *[**PROLONG*** **QT** interval*]* in peds \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Male \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ FeMale
males \> 4**5**0 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Peds \> 4**6**0 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ FEMALES \> 4**7**0 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ | (ms) [peds = 1-15 yo]
26
pathologic Q waves on EKG are a sign of what?
prior MI
27
Mycotic Aneurysm is defined as ⬜ It can develop from ⬜ and lead to ⬜ as a complication
**[vessel wall aneurysm]** *specifically 2/2 [vessel wall infection *(i.e. from IE septic embolization)*] ➜ vessel wall destruction ➜ vessel wall aneurysm* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ {[vessel wall infection *(i.e. from IE septic embolization)*] ➜ vessel wall destruction ➜ vessel wall aneurysm*} \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [SubArachnoid Hemorrhage (from [vessel wall aneurysm] rupture) - *LOOK FOR NECK STIFFNESS*] ; | *🔎IE = Infective Endocarditis*
28
describe the algorithm used to determine if a [nonvalvular **afib**] patient needs [oral anticoagulation] for stroke px
## Footnote *💡oral anticoag = warfarin / dabigatrin / rivaroXaban / apiXaban*
29
Which parts of the heart does the [R Coronary artery] perfuse? -3
➜ SA node [➜ R marginal a ➜ RV] ➜ [**PDA** (in 70% popln)]
30
*[L Main Coronary] branches into [LAD] and [LCX]* What does the [LCX] perfuse? (2)
➜ **LATERAL** LV ➜ [**PDA** (in 10% of popln)]
31
*[L Main Coronary] branches into [LAD] and [LCX]* What does the [LAD] perfuse? (3)
➜ ***IVP***: I: ANT 2/3 V: ANT LV P: ANT LAT ## Footnote ✏️ IVP= Interventricular septum/ Vt Free Wall/ Papillary muscle
32
Name 3 major complications of acute **inferior wall** MI? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ management?- 3 | *AaS*
1. [RVMI](= Preload dependent = no Nitrate/no Diuretic/no Opioid):*Tx = {IVF-nitrates*} 2. [AV Block] 3. [Sinus Bradycardia]*Tx = {Atropine IV}* | *severe = unresponsive/hypOtension/dizziness/HF/syncope* ## Footnote \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 💊[P⼀harm[(IVF*-nitrates)*+AtropineIV]] 💊💊--(if severe)--\> [P⼀acetransQ|V] 💊💊💊→ [P⼀erfuse_PCI revascularization]
33
*In ["SBIE-Risk"-Settings], pts[with High Risk Cardiac_conditions] have ⇪ risk of developing [SBIE] = these ptsHRC require [SBIE abx px] prior to engaging [SBIE-Risk-Settings]}* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What are these [High Risk Cardiac Conditions] -4
## Footnote 1.Previous SBIE 2.Prosthetic heart valve 3 [Transplanted heart with valve structure❌] 4.[CHD-Congenital Heart Disease (with cyanosis or after repair)] *🔎SBIE = [[Subacute Bacterial Infective Endocarditis]*
34
Name the manifestations of [Infective Endocarditis ] -8 | *IE* ## Footnote (8)
"Bacteria **FROM JANE**" ## Footnote **F**ever [**R**etinal Roth Spots - *Immunologic phenomena*] [**O**sler "Ouch" Nodes- *Immunologic phenomena*] [**M**umur that's new] [**J**aneway's purplish nonpainful lesions of the palms&sole] **A**nemia [**N**ailbed Subungal _Splinter_ Hemorrhages] [**E**mboli from valvular (T\>A\>M) vegetations] ; \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_x\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *"Enterococcus⼀[STAph **A**], [STAph **E**]⼀[strEP **B**] [strEP **V**]* ⼀[*and nonbacterial**maranti(C)**with its misc (C)*] .." causes [mitral>tricuspid\*]IE ... *FROM JANE"*.
35
*In ["SBIE-Risk"-Settings], Pts [with ⬜] have ⇪ risk of developing [SBIE] = these Pts require [⬜] prior to engaging [SBIE-Risk-Settings]}* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Name the 6 *[SBIE-Risk-Settings]* (6) | *SBIE=Subacute Bacterial Infective Endocarditis*
[High Risk Cardiac Conditions] ; [SBIE abx px] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ A. [Surgery during (ACTIVE) GI infection] B. [Surgery during (ACTIVE) GU infection] c. [dental procedure*(involving gingiva or oral mucosa)*] d. dental cleaning e. [respiratory tract procedure*involving incision or biopsy of mucosa*] f. surgical placement of prosthetic cardiac material | *ptsHRC must receive [SAP] prior to any [SRS]* ## Footnote [⚠️SBIE = strEP Viridans = 💊CefTriaxone|aPG] *🔎HRC = High Risk Cardiac* *🔎SAP = [SBIE abx px]}* *🔎SRS = [SBIE-Risk-Setting]* *"Enterococcus⼀[STAph **A**], [STAph **E**]⼀[strEP **B**] [strEP **V**]* ⼀[*and nonbacterial**maranti(C)**with its misc (C)*] .." causes [mitral>tricuspid\*]IE ... *FROM JANE"*.
36
*Ventricular Tachycardia is one of the major causes of Cardiac Syncope* cp for [Cardiac Syncope from VTach]
patient with previous structural heart disease has random Vtach arrhythmia ➜ [**RANDOM SYNCOPE WITH NO PRECEDING SX**] ➜ rapid spontaneous patient recovery within min and no residual sx \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *this can ➜ SUDDEN CARDIAC DEATH eventually*
37
List ALL the causes of Cardiac Syncope? (6)
## Footnote 1. Sick Sinus Syndrome 2. AV Block 3. MMVT 4.{[PMVT_torsades des Pointes] *RF:(low K+, low Mg+, Long QT)*} 5. HOCM 6. Aortic Stenosis
38
causes of Multifocal Atrial Tachycardia -3 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ etx for MAT? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ how is this related to [Wandering atrial pacemaker]?
a. 1. pulmonary❌(disease|exacerbation) 2. electrolyte❌(K+|Mg+) 3. sepsis (catecholamine surge) | c. [(*wap*) < 100bpm ≤ (*MAT*)] ## Footnote b. MAT etx: *(PES) ➜ *:random firing of multiple ectopic foci in the atria ➜ [***3 DIFFERENT P-wave MORPHOLOGIES***with **irregularly irregular R-R** + **(rate ≥100bpm**)].
39
how do you diagnose MAT? -2 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ tx? -2
(dx = [EKG with P waves of 3 different morphologies] + [atrial rate \> 100]) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ tx =[treat *PES* cause*(Pulmonary/Electrolyte/Sepsis)❌*] --(if fail)--\> [VerapamilnCCB (AV node blockade)]
40
What is Acute Chest Syndrome? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ how do you diagnose it? -2
[infection (*peds*)] or [fat embolus (*ADULTS*)] ➜ life-threatening vasooclusioin of pulmonary vasculature in sickle cell patients \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [CXR New Pulmonary infiltrate] + ≥1 of : - WOB - Temp\>38.5C - Hypoxemia - chest pain
41
What are the 10 reversible causes of PEA (Pulseless Electrical Activity)?
## Footnote ***CVC*** = {[**C**.**O**.**D**.**E**.] ➜ [**VV.A.P.**]} ➜ [**C=A=R**]
42
Describe Approach to [Adult Cardiac Arrest] if pt has *Asystole*
[***CVC***⼀ACLS] *START CHEST COMPRESSIONS!* | *"C - V - C"* ## Footnote ***CVC*** = 1)[**C**.**O**.**D**.**E**.] ➜ 2)[V.(**A**).P.] 3)➜ [**C=A=R**]
43
Describe Approach to [Adult Cardiac Arrest] if pt has *PEA*
[***CVC***⼀ACLS] *START CHEST COMPRESSIONS!* | *"C - V - C"* ## Footnote ***CVC*** = 1){[**C**.**O**.**D**.**E**.] ➜ 2)[V.A.(**P**).] 3)➜ [**C=A=R**]
44
Describe Approach to [Adult Cardiac Arrest] if pt is in *VFib*
[***⚡CVC***⼀ACLS]\* *START CHEST COMPRESSIONS!* | *"{shock} C - V- C*" ## Footnote \* ***⚡CVC***④⼀*"{shock} C - V- C"* = 1) [**C**.O.D.E.] → 2) {[⊕(**V**) A.P.] = *--give-->**3) {⊕[(V)oltage\_SH⚡CK\_Debrillation]}* 4) → [**C**=A=R]
45
Describe Approach to [Adult Cardiac Arrest] if pt is in *pulseless VTach*
[***⚡CVC***⼀ACLS]\* *START CHEST COMPRESSIONS!* | *"{shock} C - V- C*" ## Footnote \* ***⚡CVC***④⼀*"{shock} C - V- C"* = 1) [**C**.O.D.E.] → 2) {[⊕(**V**) A.P.] = *--give-->**3) {⊕[(V)oltage\_SH⚡CK\_Debrillation]}* 4) → [**C**=A=R]
46
In a MVA, what is the most common cause of death associated with steering wheel injury?
AORTIC INJURY ## Footnote *secondary to rapid deceleration with shearing along the aortic arch*
47
What are the main features of [Takotsubo stress induced cardiomyopathy] -4
[**ABCQ** *"Takotsubo"*] 1. [stressor(s) ➜ catecholamine surge ➜ **A**NT MI presentation] *+* 2. [***B**alloon❤️*LV wall motion ∆] 2/2 3. [**C**oronary spasms transiently (withOUT coronary occlusion on Cath!)] and 4. [**Q**T prolongation] ## Footnote 🔎[*Balloon❤️* =Echo[(apical hypOkinesis) + (BASILAR HYPERkinesis)]
48
tx for [acute-chest-syndrome] -3
**a-c-s** [**a**zithromycin (*mycoplasma pna*)] [**c**eftriaxone (*strep pneumo*)] [**s**aline IVF w analgesia]
49
*Patient is diagnosed with HOCM* ⬜ (or ⬜ alternatively) both treat HOCM \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Describe how they treat HOCM?
beta blockers \> ([Verapamil*NCCB*] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ HOCM TX GOAL = **⇪ LV Volume to overcome outflow tract obstruction**. BB and nCCB achieve this 2 ways: Negative chronotropy ( ⬇︎HR) ➜ inc diastolic time to fill -> higher LV end-**diastolic** volume Negative inotropy ( ⬇︎contractility) ➜ decreases systolic ejection strength -> completes systole with higher LV end-**systolic** volume
50
What is [PEA-Pulseless Electrical Activity] ? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ how should it first be managed-2?
▶**PULSELESS (No palpable pulse)** *with* ▶electrical activity (organized rhythm ⼀that's not VF/VTp) on cardiac monitor \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ { [CPR x 2 min] + [Epi q 3-5 min]} until cause is determined! | *Note: [pulseless VT/VF] DO require defibrillation*
51
[Chronic primary mitral valve regurgitation] is defined as ⬜ . What is the normal ejection fraction for *these* patients?
mitral valve insufficiency 2/2 **intrinsic defect of mitral valve apparatus** (leaflets/chordae tendineae) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [normal EF for Chronic Primary MVR] \> 60% (*normally \> 50%*)
52
How are Major Depression and the Cardiovascular system related? (2)
1. [Major Depressive Disorder] = independent risk factor for [⇪ morbidity and mortality] from CV disease . 2. CVD = [independent risk factor for developing MDD] ## Footnote *Treat with SSRI*
53
In patients with DM and CAD occlusion, which is superior [*PCI* or *CABG*]? why? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ * PCI = [PerCutaneous Coronary Intervention (w drug eluting stents)]* * CABG = Coronary Artery Bypass Graft*
**CABG** \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ CABG has lower all-cause morTality, MI and repeat vascularization than PCI
54
Which Calcium Channel Blockers are a/w peripheral edema? Name them -2 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Tx for this?
dihydropyridine-CCB [Amlodipine | Nifedipine] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ACEK2 inhibitors
55
Prolonged Amiodarone tx can ➜ [FATAL ⬜ DISEASE] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ how do you manage this if it occurs? -2
**PULMONARY** **\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_** [DC amiodarone] ➜ [CTS if severe/life threatening]
56
*acute inferior MI is a/w ⬜ MI* What's the most important tx for this kind of MI ?-2 why?
RIGHT Ventricular MI ; {**[AGGRESSIVE IVF (BOLUS)] - [Nitrates]**} = ## Footnote ☞ RVMI tx = **PRELOAD DEPENDENT** = (need to INC preload with IVF and avoid Nitrates/diuretics/opioids that DEC preload) ☞ (add AtropineIV to treat associated AV Block and Sinus brady) 💊[P⼀harm[(IVF*-nitrates)*+AtropineIV]] → P⼀ace → P⼀erfuse_PCI]
57
When is Carotid Endarterectomy(CEA) indicated in Men-2 vs Women?
Men: [\> 60% occlusion and Symptomatic] or [\> 70% occlusion] Women: [\> 70% occlusion regardless of sx] ANY OF THESE --\> CAROTID ENDARTERECTOMY ​ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *ASA, antiHTN and Statin = medical mgmt*
58
When Carotid Endarterectomy(CEA) is not yet indicated for Carotid occlusion, medical management is used instead What is the *medical* management for Carotid occlusion? (3)
ASA*,* antiHTN *and* Statin
59
60
61
62
What is Cardiac Index?
[CARDIAC OUTPUT --corrected for *patient's size*(smaller people = smaller CO / Larger People = Larger CO) = **standardized measure of pump functioning** | [(⬇︎⬇︎ in cardiogenic shock) > (⬇︎ in hypOvolemic shock)]
63
What is Leriche triad? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ what does it indicate?​
[LE claudication (butt/thigh pain or weakness)] diminshed femoral pulses Erectile Dysfunction \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ BL AortoiLiac PAD​ *PATIENTS WITH ED SHOULD BE SCREENED FOR CVD/PAD BEFORE TX!*
64
Why should patients with Erectile Dysfunction be screened for ⬜ BEFORE receiving treatment?
PAD; PAD ➜ ED and ED is a strong predictor of CAD ED patients should receive diagnostic testing (ABI/Stress testing) BEFORE INITIATING TREATMENT FOR SEXUAL DYSFUNCTION
65
What side effect does Trastuzumab have on the heart?
**[REVERSIBLE** asx decline of LV EF (that may ➜ overt HF)] BUT AFTER DISCONTINUANCE ➜ COMPLETE REGAINMENT OF CARDIAC FUNCTION POSSIBLE ​ | *Trastuzumab is used in Breast CA*
66
What is the initial management for chest pain 2/2 acute Cocaine intoxication? (5) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What should you do if there is [persistent ST elevation (initial management fails)]?​
get a [**LOAN⼀aP**] to treat Coke! ## Footnote 1. [**L**orazepam\_ benzo (*HR/BP/psych control*)]IV 2. [**O**pioid🟢\_Morphine]IV 3. [**A**mlodipine\_dCCB] 4. [**N**TGIV] --(if persist)--→ 5. → [**a**lpha1🟥\_Phentolamine (if *P*ersistent)] 6. ➜ ➜ **P**CI (for coronary revascularization if sx still not alleviated)
67
Describe the complication IVC filters pose
ironically, although [IVC filters] [⬇︎PE risk x 2], it actually [⇪DVT RISK x 2]
68
List the 4 primary EKG changes for Hyperkalemia \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ how do you treat Hyperkalemia?​ (4)
1. tall (T) 2. Loss of (P) 3. [Wide/sinusoidal QRS] 4. (U) wave absent \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ {**1st** (*stabilizes cardiac membrane potential*): [IV Calcium Gluconate] or [IV Calcium Cl] } ➜ {-**2nd** *drive K+ into cells*: Beta agonist or [insulin-glucose]} \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *Hyperkalemia sx = weakness + cardiac*
69
[biventricular pacing device] is indicated for patients with what 3 clinical criteria ?
Patients with all 3: 1. **SINUS RHYTHM** + 2. [symptomatic HF EF<35%] 3. [LBBB with QRS\>150]
70
What is the 1st step to evaluate suspected Pulmonary hypertension? ​ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ why? (4)
TTE = Evaluates [RV function], [**Pulmonary Artery Pressure**], [L valve function] and [LV function]
71
Why are Benzodiazepines given early for Cocaine-chest pain ? -3
*{"with Cocaine [**L**orazepam_Benzo] targets [Psych / Pressure / Pain"]}* 1.[*Psych:*⬇︎Psychomotor agitation] 2.[*Pressure:*⬇︎sympathetic NS →⬇︎HTN] 3.[*Pain:*⬇︎myoscardial ischemia] | *Cocaine ODtx = [**LOAN-aP**]* ## Footnote ⚠*but do NOT give β🟥 (MAY ➜ UNOPPOSED ALPHA 1 ACTIVATION)*
72
Persistent chest pain and/or new neurologic symptoms in a Cocaine Chest Pain patient is s/f what complication? explain
acute *TAAAD* [Type A *ascending* Aorta Dissection] (severe HTN from cocaine can ➜ *TAAAD* = sharp ANT chest pain | and if *TAAAD* ascends into carotid artery ➜ [neuro weakness]) *dx = [Chest Spiral_CTA]*
73
Imaging modalities for Aortic Dissection-3
1. [**TEE**- *unstable or renal CXD*] 2. [Chest Spiral CT Angio]- *Stable vitals*] 3. [MRI-*NonEmergency*] ## Footnote *TEE is great because it's used in renal pts*
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What are the sx of Aortic Dissection (5)
1. [SEVERE SHARP TEARING (CHEST⼀*TAAAD*) OR (BACK⼀*tBDAD*) PAIN] 2. [BUE SBP discrepancy \> 20 mmHg] 3. [Aortic Regurgitation ➜ [pericardial effusion/tamponade/Hemothorax] 4. [LE paraplegia (*⼀spinal a*​)] 5. [Horner's *MAP* (⼀*carotid sympathetic plexus*)] | * biggest RF = HTN* ## Footnote * TAAAD = [Type A Ascending Aorta Dissection] || tBDAD = [Type B Descending Aorta Dissection]*
75
The most common cause of mitral stenosis is ⬜. When does this typically present? ​ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ clinical presentation (6)
[Rheumatic Mitral Stenosis]; [10-20 years after Rheumatic Fever] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ​ ## Footnote 1. **LOUD** S1 2. [mid-diastolic rumble @ apex] 3. DYSPENA 4. orthopnea 5. paroxysmal nocturnal dyspnea 6. hemoptysis
76
Describe the 2 methods for determining Heart Rate on EKG
77
What does a negative Exercise stress test mean for the patient?
\<1% risk of CV events within the next year \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *NEGATIVE stress test = ≥85% of Max HR with no major EKG* ∆ ​
78
diagnosis?
Acute pericarditis ## Footnote *diffuse ST elevations with PR depression*
79
What's the leading cause of death in [Systemic Lupus Erythematosus] patients? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ why is this?
Cardiovascular events \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ SLE is major risk factor for [**premature coronary atherosclerosis**] which ➜ fatal CV events
80
EKG findings for [ACS*⼀*NSTEMI] (2)
1. [ST8️⃣-9️⃣ **Depressions**] 2. [T🔟 inversions] | *🔎{#️⃣} = MEGAN (McCalister ECG Graph Association Number]* ## Footnote 💡[ST{8️⃣-9️⃣}*segment* **Depressions**] 💡[T🔟*wave* inversions
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EKG findings for ***Aua*** (2) | *🔤 **Aua** = [**A**CS⼀**u**nstable **a**ngina]*
1. ST **Depressions** 2. T Wave inversions ## Footnote *same EKG as **AanS** = [**A**CS⼀**a**cute **n****S**TEMMI]*
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*Pts with [ACS⼀acute STEMI] {**R**eally **A**lways **N**eed **OBAMA**}!* How do you determine [**R**eperfusion coronary revascularization]? (4) | *AaS*
[ACS acute STEMI] R4 criteria * * * * **R0**: Revascularize only if **[SX ≤ 12h]** * **R**1: [iHP = PCI ≤90 min eDB] * **R**2: [OHP ≤120m eDB TFR] = [PCI ≤120 min eDB] * **R**3: [OHP \>120m eDB TFR] = [*ART*-tPA fibrinolysiswithin 30m] ## Footnote * * * * iH/OHP: in/OUT HousePCI Institute* * TFR: Transfer* * eDB: estimated Door→Balloon*
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What is the diagnostic EKG criteria for [ACS⼀acute STEMI]-2 | AaS
New [**\> 1 mm** ST-Elevation (J point to baseline)] in [≥2 contiguous leads (*except V2,V3\**)] ​ \**V2,V3= [women ≥1.5mm]| [( ≥2.5)\<--m40--\> (≥2mm)]* \_\_\_\_\_\_OR\_\_\_\_\_\_\_ [New LBBB with ACS sx]
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Diagnostic EKG criteria for RBBB (2)
< **V1** [R1º (second R wave)] \>​ \_\_\_\_\_\_\_\_\_with\_\_\_\_\_\_\_\_ < **V6** [Fat *(widened)* S wave] \>
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Name the anticoagulation used for mechanical prosthetic valves (3) * * * how long do they require this? ​
- [(AVRRF*) = warfarin2.**5**-3.**5** ] - [(MVR) = warfarin2.**5**-3.**5** ] ​ - [(AVR) = warfarin2-3 ] ​ [+ ASAL (if severe CAD\*)] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ LIFELONG​ *RF = old-gen replacement valve, afib, LVHF, hypercoagulable, prior Thromboembolism // ASAL = Low dose ASA*
86
Which 3 drug groups are a/w Orthostatic hypOtension?
**DAN** is always droppin' orthostatic ## Footnote • **D**iuretics **• A**lpha R blocker • **N**itrates
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⬜ is the most common congenital heart disease in patients with Down syndrome
[**S**eptal endocardial cushion defect] ## Footnote {[**SHEEPPS**]*traits* & [**SHALA** **H**as **D**own **S**yndrome]*conditions*}
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Athletes in intense training can develop **non**pathologic CV changes such as what? (2)
- [Sinus Bradycardia (+/- 1º AV Block)] -*2/2 heightened vagal tone* - [EKG LVH]*-* *responsive LV thickness will meet EKG LVH voltage criteria*
89
What is Sudden Cardiac Death? (2)
1. [fatal Vt Arrhythmia triggered by intense exertion io\ [structural heart❌(*HOCM, coronary a anomalous origin*)] \> [conduction❌(*long QT, Brugada-Pokkuri*)] 2. leading COD age < 35
90
Describe **Pulsus Paradoxus**
[Systolic BP] ⬇︎more than 10 **during inspiration** ## Footnote "Pulsus for **CAPOT**"
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In Hypertensive Crisis (Urgency & Malignant Emergency), what's the rate for lowering MAP?-2
**[10-20% in 1st hour] --\> [5-15% over next 23 hours]** * * * | Normal MAP: 65-110 ## Footnote Malignant HTN Emergency = [Hypertensive Urgency (BP\>180/120)] PLUS Papilledema/Retinal Hemorrhages
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What is the normal range for Mean Arterial Pressure (MAP)? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Formula?
65-110 \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
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Tx for symptomatic Sinus Bradycardia -6
*(while investigating/treating underlying cause)* 1st : [**Atropine IV + IVF**] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 2nd : [**Glucagon IV**(⇪intracell cAMP)**] *⼀BB toxicity* 3rd: [Epigtt |DOPAminegtt] 4th: [transQ/V pacing]
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In Afib pt, when can you **NO LONGER** cardiovert?
\> 2 Days after onset
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List the 4 treatment options for [*HDS* aFib]
*MA * VZ * A * D* ## Footnote 1st: {BB: [**M**etoprolol10 mg start] | | [**A**tenolol] - *rCTD IN HF or hypOtension*} 2nd: {NCCB: [**V**erapamil] | [diltia**Z**em([0.25 mg/kg bolus] → [0.35 mg/kg DRIP])]) -*rCTD IN HF or hypOtension*] 3rd: [**A**miodarone+ Cardio consult] 4th: [**D**igoxin+ Cardio consult]
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List the treatment options for *UnStable* Afib -5
**100J CARDIOVERSION** **\_\_\_\_\_\_\_\_(unless duration ≥48h) ________ ➜** [Clots on Echo?] ➜ No = [Heparin ➜ 100J Cardioversion STAT] YES = [Warfarin x 3 wks ➜ Cardioversion when Warfarin therapeutic]
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# Aortic Dissection treatment? (4)
1. Surgery for *TAAAD* 2. [Esmolol β🟥]IV 3. Nitroprusside IV(if SBP >120) 4. Pain
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Why shouldn't Hydralazine ( ⬜*MOA*) be used to ⬇︎[acute Aortic Dissection HTN] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How is this related to Sodium Nitroprusside in AD?
(primary arterial vasoDilator) ; arterial vasoDilation ➜ [reflex tachycardia ➜ ⇪ LV contractility] ➜ [⇪ aortic wall shear stress] ➜ [worsens aortic dissection] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [Sodium Nitroprusside*(mixed vasoDilator/venoDilator)*] should **only** be used to ⬇︎ [AD **SBP \> 120**] | *never use Hydralazine ⼀ only use Nitrop if SBP > 120*
99
Why are Beta Blockers 1st line tx for HOCM?
BB allow for more time for LV to fill with blood ➜ more LV blood DEC outflow tract obstruction (and ⬇︎murmur) ➜ improves HOCM cardiac output
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Name 3 Lifestyle regimens to ⬇︎CVD in Obese patients
Exercise | Mediterranean diet | DASH diet
101
Which drugs are a/w [drug-induced acquired Long QT Syndrome]? (5) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Which factor INC risk of [drug-induced acquired Long QT Syndrome] deteriorating into torsades de pointes?
antiPsychotics / antiDepressants / antiFungals /[antiBioticMacrolides] / [antiBioticFluoroquinolones] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ **B**radyarrhythmia (*sinus brady, AV block*) | "[HIS **B**EDS] gave me arrhythmia"
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what is the diagnosis? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ tx for this condition?(2) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ px for this condition?
[PMVT Torsade de Pointes] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1.{[**MgSO4IV**]pharm cardioversion} 2.{--(if persist)--\>[Temporary transVenous pacing]} \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [MgSO4IV] | *give regardless of preexisting baseline Mg*
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*A patient with aFib has failed rate control* What are the 2 anti-arrhythmic options for afib patients with... CAD (no HF)?
1. Sotalol[3] 2. Dronedarone[3]
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*A patient with aFib has failed rate control* What are the 2 anti-arrhythmic options for afib patients with... LVH?
1. Dronedarone[3] 2. Amiodarone[3]
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*A patient with aFib has failed rate control* What are the 2 anti-arrhythmic options for afib patients with... [no CAD and no structural heart disease]?
1. Flecainide[1C] 2. Propafenone[1C]
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*A patient with aFib has failed rate control* What are the 2 anti-arrhythmic options for afib patients with... HF?
1. **A**miodarone[3] 2. do**F**etilide[3]
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*pt presents 3 days s/p acute MI with this EKG* Tx? (2)
self limited --(if persist)--\> [ASA650 TID] | [acute pericarditis] ## Footnote *(NO NSAIDs or CTS as these impair myocardial healing and ➜ vt rupture)* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
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Dx?
Acute Pericarditis \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ | *can → calcified+fibrous → cardiac decline = Constrictive pericardiits* ## Footnote *diffuse PR depression + diffuse ST elevation*
109
What are the 3 indications for Statin therapy?
"give that **LAD** a *StatinM/H*!" 1. [**L**DL ≥190] 2. [**A**SCVD10y \> 7.5-10%] 3. [**D**M ≥40 year old] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *ASCVD10y = AtheroSclerotic CVD 10 year estimated risk | StatinM/H = Moderate/HIGH Intensity*
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Why are HOCM pts at greater risk for developing ⬜ or ⬜ tachyarrhythmia ? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ how are each caused? how are each managed?
1. afib (L Vt hypertrophy ➜ LAE ➜ afib) = [EKGamb ➜ [antiCoag + rate/rhythm control] 2. **VT (L Vt ischemia and fibrosis ➜ Vtach --****(if sustained)****--\>SCD (most common COD for HOCM) = [EKGamb ➜ ICD]** * * * *[AMBULATORY EKG (24H Holter)] to diagnose both*
111
What 3 *Coronary Heart Disease* risk factors are the most significant predictors of poor CV outcomes?
1. [noncoronary Atherosclerosis (PAD, Carotid, AAA)] 2. CKD 3. [DM (*note: strict glycemic control only ⬇︎ **micro**vascular complication*)] ***these factors are AKA "CHD equivalents"*** = carries same risk to of damaging CV health ... as having CHD itself
112
*After MI, pts are classified as [low risk] or [HIGH risk] for resuming SEXUAL ACTIVITY* what factors makes a patient HIGH risk? (4) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ how does this translate for patients?
* NYHF**4** * refractory angina * arrhythmias * valvular disease \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [low = sex ≥1 wk post ✔︎CRV] || [HIGH = requires assessment before sex]
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What are the major effects of radiation to the heart? (5)
1. Restrictive cardiomyopathy with diastolic dysfxn 2. constrictive pericarditis 3. valve damage 4. conduction damage 5. MI
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# *fill-in-blank*
115
diagnosis? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ tx? (4)
mmVT \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [***SLAP***pharm cardioversion] ## Footnote -mmVT = monomorphic VT -***SLAP*** = Sotalol3 |Lidocaine1B |Amiodarone3|Procainamide1A
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diagnosis? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ tx?-2
[PMVT Torsades de Pointes] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1.{[**MgSO4IV**]pharm cardioversion} 2.{--(if persist)--\>[Temporary transVenous pacing]} ## Footnote PMVT = POLYMORPHIC VT
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diagnosis? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ tx? (4)
mmVT \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [***SLAP***pharm cardioversion] ## Footnote -mmVT = monomorphic VT -***SLAP*** = Sotalol3 |Lidocaine1B |Amiodarone3|Procainamide1A
118
diagnosis? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ tx? (2)
[atrial Tachycardia *(looks like aflutter THAT'S MISSING SAWTOOTH PATTERN)* ] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ***BB***|***nCCB*** rate control ## Footnote -[BB=Beta Blocker] / [NCCB=nonDihydropyridine Calcium Channel Blocker (Verapamil|Diltiazem)]
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diagnosis? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ tx? (3)
[AV**N**RT]*PSVT* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ stable: -vagal maneuevers stable: -adenosine ⚠️unstable: DC Cardioverson ## Footnote [AVnRT = AtrioVentricular (nodal) Reentrant Tachycardia]
120
diagnosis? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ tx? (2)
[atrial flutter *(look for sawtooth pattern)* ] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ***BB***|***nCCB*** rate control ## Footnote -[BB=Beta Blocker] / [nCCB=NonDihydropyridine Calcium Channel Blocker (Verapamil|Diltiazem)]
121
diagnosis?
[AVRT orthodromic*retrograde P wave* SVT] | *Look for **[retrograde P waves]**!*
122
diagnosis? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ tx? (4)
[atrial fibrillation] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [*MA* * *VZ* * *A* * *D*]rate control | [irregular R⼀R] / [no P wave] / [narrow QRS] ## Footnote [*MA* * *VZ* * *A* * *D*]rate control **(M|A)*** **(V|Z)** * **A** * **D**
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diagnosis? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ tx?
[⚡mmVT**pulseless**] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [***⚡CVC***⼀ACLS]*START CHEST COMPRESSIONS!* ## Footnote -mmVT = monomorphic VT -***⚡CVC*** = **C**ODE| **V**AP| **C**=A=R (⚡= *give* [Voltage Defibrillation SHOCK])
124
diagnosis? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ tx?
[⚡VF] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [***⚡CVC***⼀ACLS]*START CHEST COMPRESSIONS!* ## Footnote -VF: Ventricular Fibrillation \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ **⚡CVC** : **C**ODE| **V**AP| (**C**=A=R)] -{VF = [***⚡CVC***⼀ACLS] tx--regardless of pulse}
125
diagnosis? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ tx?
[⚡VF] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [***⚡CVC***⼀ACLS]*START CHEST COMPRESSIONS!* ## Footnote -VF: Ventricular Fibrillation \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ -[***⚡CVC** : **C**ODE| **V**AP| (**C**=A=R)] -{VF = [***⚡CVC***⼀ACLS] tx--regardless of pulse}
126
diagnosis?
[ACS ⼀STEMI](*anterolateral*)
127
Erectile Dysfunction in the setting of still having [nonsexual nocturnal erections] suggest what etiology?
psychogenic etx (*Do Detailed Psychological assessment/counseling*)
128
Physical Exam findings for Aortic Stenosis-3
1. {[Crescendo Decrescendo Systolic murmur w/*delayed* carotid pulse @ R 2nd ICS]} 2. [Pulsus Parvus et Tardus(*delayed* carotid pulse)] 3. [S4(from LV hypertrophy)]
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A. Diagnose and Describe murmur (*Auscultation Site is attached*) B: Maneuvers that INC (2) C: Maneuvers that DEC
**Aortic Stenosis** *[Crescendo-Descrescendo Systolic Ejection Murmur]* "**Lean forward**...& then **Squat** with that *As*s, that'll turn it up!" B: INC with... 1. Leaning Forward 2) Squatting C: DEC with...handgrip (*INC afterload*)
130
Which Murmur? ## Footnote (*Auscultation Site is attached*)
**M**itral **V**alve **P**rolapse *[**MidSystolic NON-Ejection Click** + Late Systolic Crescendo Murmur]*
131
Which Murmur? B: Name the Auscultation Site -2 C: Maneuvers that INC sound
**Mitral Stenosis** *[Diastolic delayed **Opening Snap** followed by Rumbling]* B: [Apex + **LLDP** (L Lateral Decubitus Position)] C: Maneuvers that [INC Afterload] (i.e. handgrip)
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Which Murmur? (*Auscultation Site is attached*)
**Hypertrophic Cardiomyopathy** *[Holosystolic **Harsh** Blowing Murmur + palpable thrill] @ [L Sternal 2/3 ICS]*
133
Which Murmur? ## Footnote (*Auscultation Site is attached*)
**V**entricular **S**eptal **D**efect *[Holosystolic **Harsh** Blowing Murmur + palpable thrill] @ [tricuspid area]*
134
# pt with CHF exacerbation also has hypOnatremia How is [CHF exacerbation *hypOnatremia*] treated? (3)
N=none**[*****(Sx *(😵‍|🫨)* or Na < 120)*****?]**Y=Water restriction (c/s Tolvaptan if Na<120 + chronic HF) ## Footnote *hypOnatremia sx (confusion😵‍, seizure🫨) ||* [**Tolvaptan** *(Vasopressin-2 ADH R blocker)*]
135
Oral Salt tablets are used to treat hypOnatremia in [**⬜** CHF exacerbation | SIADH]
SIADH ## Footnote \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *NEVER give Oral salt tablets to edematous/volume overload CHFE*
136
MOA for how Beta Blockers work on the heart? (2)
inhibition of B1 R ➜ [⬇︎intracellular cAMP] in… ## Footnote ▶[cardiac **contractile** myocytes] ➜ DEC heart contractility ➜ DEC BP *(poor perfusion/confusion if OD)* ▶[cardiac **pacemaker** myocytes] ➜ DEC [phase 4 depolarization slope] ➜ DEC HR* (arrest/AV block if OD) * *_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_* *BBtox tx = IVF, atropine, glucagon*
137
# Pt p/w bradycardia to 40 bpm, likely 2/2 beta blocker toxicity Treatment? (3) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Which of these is specific to beta blocker toxicity and how does it work?
1. IVF (if hypOtension) 2. atropine (symptomatic bradycardia) 3. **GLUCAGON** **= BB toxicity tx ⼀*****activates glucagon R ➜ directly INC intracellular cAMP = bypasses adrenergic blockade from BB and restores HR and contractility in setting of BB toxicity***
138
1st line treatment for Calcium channel blocker toxicity
Calcium **gluconate** \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *INC intracellular Ca+ ➜ restores arterial smooth m tone and cardiac contractility*
139
# [Bicuspid aortic valve] mode of inheritance is either ⬜ or ⬜ When diagnosed, the first step in management is ⬜
- [AUTO DOM *with incomplete penetrance*] or - sporadic \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [screen 1st degree relatives for [bicuspid aortic valve] with echo]
140
# On an EKG 1 LARGE box **=** ⬜**mm **(*← ⇪*) = **⬜ms** (*← →*) = ⬜**mV **(⇪ ⬇︎)
5; 200; 0.5
141
# On an EKG 1 small box **=** = ⬜**mm **(*← ⇪*) **⬜ms** (*← →*) = ⬜**mV **(⇪ ⬇︎)
1; 40; 0.1
142
# On EKG, How does Potassium affect the P-wave? (2)
“*K* [(*lifts up the* 🆃), (*sits on the* 🄿),*(widens 1st interval* **Q**) & *(suppresses the 🅄]*” ## Footnote = [⇪ K] ➜ [widening & flattening of *P*] ➜ [No *P*]
143
# On EKG, How does Potassium affect the T-wave? (2)
“*K* [(*lifts up the* 🆃), (*sits on the* 🄿),*(widens 1st interval* **Q**) & *(suppresses the 🅄]*” ## Footnote = ([⇪ K] ➜ [peaked *T*]) or ([⬇︎ K] ➜ [flat *T*])
144
# On EKG, How does Potassium affect the [QRS interval]? (4)
“*K* [(*lifts up the* 🆃), (*sits on the* 🄿),*(widens 1st interval* **Q**) & *(suppresses the 🅄]*” ## Footnote = ([⇪ K] ➜ [wide *QRS*]) ([⇪⇪ K] ➜ [very wide *QRS*]) ([⇪⇪⇪ K] ➜ [sinusoidal vs Torsades *QRS*])
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# On EKG, How does Potassium affect the [U wave]? (2)
“*K* [(*lifts up the* 🆃), (*sits on the* 🄿),*(widens 1st interval* **Q**) & *(suppresses the 🅄]*” ## Footnote = ([⬇︎ K] ➜ [visible *U*]) ([⬇︎⬇︎ K] ➜ [prominent *U*])
146
# MOD of Wolff Parkinson White syndrome (5)
## Footnote *🔎A**A**S = [AVRT **A**ntiDROMIC(delta wave) **S**VT]* *🔎BKAP ⼀Bundle of Kent accessory pathway* 💡delta wave = 2/2 fusion of both conduction ☞ [*early but slow* myocardial depolarization via *BKAP*] ..with the [normal AV node depolarization]
147
Diagnosis?
[Wolff Parkinson White] ## Footnote *🔎BKAP ⼀Bundle of Kent accessory pathway*
148
# Patients with WPW are at risk of sudden cardiac death ▨ Explain Why \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ◮ How do you *ultimately* treat WPW?
◮[*BKAP* **ABLATION***via Catheter*] Obliterates accessory pathway ## Footnote *🔎A**A**S = [AVRT **A**ntiDROMIC(delta wave) **S**VT]* *🔎BKAP ⼀Bundle of Kent accessory pathway*
149
# As their GP, your patient presents requesting pre-operative assessment and approval for an upcoming surgery How do you evaluate [pre-operative cardiovascular risk] for a noncardiac surgery using solely the RCRI index? (2)
✔︎ {DO✅SURGERY \<-- **[****(****0-1****pt (LR≤1%)**|***Revised Cardiac Risk Index***|**(****≥2****pt (HR\>1%)**|**]** --\> [DELAY❌SURGERY*(unless can concomitantly perform ≥4METS)*]} ✔︎ Pts {[≥2pt (HR\>1%)] *but* can perform ≥4 METs} = DO✅SURGERY also ## Footnote * [Revised Cardiac Risk Index] has 6 scoring variables, each 1 pt* * \*Delay❌Surgery= to assess cardiac functional capacity* * METs = Metabolic Equivalent*
150
Radionuclide ventriculography is typically used to measure ⬜ due to ⬜. How is this applied in the clinical setting?
LV Ejection Fraction ; [High accuracy & reproducibility] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [Radionuclide ventriculography (AKA Multigated Acquisition Scan)] is used clinically for [initial, ongoing and follow up monitoring of [LV EF] in patients receiving cardiotoxic chemo (like doxo/daunarubicin) = [a *DEC in EF by ≥10% during chemo➜ Discontinue chemo]*
151
What's the most specific diagnostic finding for cardiac tamponade? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ What are the other diagnostic findings? (5)
**ECHO: early diastolic [R heart (atria & ventricle) collapse]** **\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_** 2. Echo: IVC plethora 3. EKG: electrical alternans 4. EKG: low voltage QRS 5. CXR: enlarged cardiac silhouette 6. CXR: clear lungs with HF-like sx
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# Cardiac Tamponade Treatment (2)
1. IVF( ⇪ R Heart preload) 2. Drainage(via pericardiocentesis or pericardial window)
153
# Cardiac Tamponade Clinical Signs (2)
1. [Beck's triad (hypOtension, JVD, muffled heart sounds)] 2. [Pulsus Paradoxus(SBP ⬇︎\> 10 during inspiration)]
154
Identify each number in this ⬜ tracing
Jugular Venous Tracing ## Footnote 1. [**a**trial on RIGHT contracts⼀*RA contracts*] 2. [**c**ontraction of RV ➜ tricuspid bulge ⼀ *RV contracts*] 3. [rela**x**ation of RA ⼀*RA relaxes*] 4. [ **v**enous blood fills RA ⼀*RA fills*] 5. [ empt**y**ing of RA passively after tricuspid valve opens ⼀*RA emptys*]
155
In a Jugular venous tracing, a large ***v*** wave is seen in patients with ⬜
severe Tricuspid Regurgitation ## Footnote 1. [**a**trial on RIGHT contracts⼀*RA contracts*] 2. [{**c**losure *(& bulge)* of tricuspid}⼀ *2/2 RV contracts -> tricuspid closure/bulge] 3. [rela**x**ation of RA ⼀*RA relaxes* and subsequently fills with {venous IVC blood}] 4. [{ **v**enous IVC blood cont to fill RA}] 5. [ empt**y**ing *(passively)* of RA into RV)]
156
Aortic Coarctation is a congenital narrowing located ⬜, associated with ⬜ syndrome, but mostly affects which patients?
[(Distal to L subclavian artery) & (Proximal to Ductus Arteriosus)]; Turner ; MALES
157
Aortic Coarctation Sx (6)
1. UE HTN 2. LE hypOtension 3. LE weak and delayed distal pulses 4. LE claudication 5. [CXR: “3” sign from aortic narrowing + rib notching from collateral vessels] -**dx** ***confirmed by echo*** 6. [+/- murmur (if [PDA-continuous] or [L sternal -turbulent flow] present)]
158
What causes parasternal heave?
RVH
159
In peds, Digital clubbing is expected with ⬜ due to ⬜
Cyanotic heart disease ; R-to-L shunting
160
Which HOCM patients require [ICD⼀***PRIMARY*** SCD px] ? (5) | *Sudden Cardiac Death*
1. SCD fam hx 2. Syncope 3. [holter nonSustained VT] 4. exertional hypOtension 5. [LVH \> 3 cm]
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Which HOCM patients require [ICD⼀***secondary*** SCD px] ? (2) | *Sudden Cardiac Death*
1. survivor of cardiac arrest 2. [holter Sustained ventricular arrhythmias]
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*Pt p/w sx suspicious for Stable coronary artery disease* How do you work them up?
## Footnote *Stable* CAD management = **stabLE** = **s**tatin, [**t**ighten Lifestyle(BP/Glucose/no smoking]), **a**SA, [**b**Blocker\>ccb + ACEK2i],[**L**ab_for_coronary angio revascularization in high risk/false neg], [**E**xercise stress = dx *unless ⊕baseline EKG❌ → Pharmacologic stress imaging*] *HIGH RISK= ST depression at min exertion, Vt arrhythmia, poor exericse capacity*
163
What is Monitored Carotid massage used for?
diagnoses [Syncope 2/2 carotid hypersensitivity (*found in elderly with Carotid atherosclerosis*)]
164
Name the major clinical signs of Dehydration (4)
1. HR INC 2. dry mucous membrane 3. hemoconcentration 4. BUN/Cr ratio INC
165
[***C***onstrictivePericarditis] Causes (6)
1. Surgerycardiac 2. idiopathic 3. TB 4. viral*Coxsackie* 5. radiation 6. other[Uremia/CA/MI_Dressler] "*Surgeons* are *viral* *idiots* to **constrict** my *TV*, *radio* and *More*"
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[***C***onstrictivePericarditis] clinical features (8)
1. Fatigue / DOE 2. R HF [Peripheral edema/ascites/INC JVP] 3. **Early diastole Pericardial knock** 4. **[JVD with ⊕Kussmaul** *(paradoxic INC JVP with inspiration)***]** 5. **Prominent** ***y*** **descent** 6. **CXR pericardial calcifications** 7. **TTE: biatrial enlargement with nml Vt wall** 8. EKG: low voltage QRS 9. {[acute pericarditis] {*C*an → [*C*alcified fibrous thickening of Pericardium] → [*C*ardiac compromise with decline] = ***C***onstrictivePericarditis]} ***T***x = {[anti-inflammatory Rx]--(*refractory)*--\>[pericardiectomy]}
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Long term amiodarone is a/w what sx? (7)
1. [Neuro (ataxia, peripheral neuropathy)] 2. visual disturbance 3. thyroid 4. bradyarrhythmia 5. [chronic interstitial pneumonitis] 6. hepatotoxic 7. **blue gray skin**
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Cardiac Amyloidosis sx (3)
*unexplained …* 1. [Echo: INC Vt wall thickness with nl LV cavity dimension] 2. [HFpEF diastolic] 3. EKG low voltage
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Why should you 1st give atropine to an [inferior MI] with bradycardia, profound hypOtension and pulmonary edema?
Inferior MI often causes [R Vt wall and SA node ischemia] which → **INC Vagal Tone** → sinus bradycardia (+ R HF and L HF sx) = atropine tx (*blocks INC Vagal tone*)
170
Name the 8 types of SVT
1. [AV**N**RT]*PSVT* 2. [A**O**S]\* 3. Sinus Tachycardia SVT 4. [atrial tachycardia SVT] 5. [atrial Flutter SVT] 6. [aFib SVT]*⚠️irregular* 7. [A**A**S] \* 8. [aberrant SVT]*⚠️WIDE* | *SVT are typically Regular and Narrow unless ⚠️* ## Footnote \* **AOS**: [**A**VRT **O**RTHOdromic*retrOgrade P wave* **S**VT] **AAS**: [**A**VRT **A**ntidromic*deltA wave* **S**VT]
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# During initial tx and dx: For [*✅HDS*SVT⼀unidentified] pts [⬜ or vagal maneuvers] are given 1st vs. For [*❌HD**U**S*SVT⼀unidentified] pts ⬜ is given 1st \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ | *HDUS = hypOtension, AMS*
(AdenosineIV) * * * \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [synchronized DC cardioversion]
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Why do we 1st give [⬜ and/or vagal maneuvers] to *HDS*SVT pts? (2) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *HDUS = hypOtension, AMS*
[AdenosineIV and/or vagal maneuvers]: 1. *Dx*: temporarily slows AV node conduction and unmask “hidden” P waves on EKG for dx. 2. *Tx*: also causes transient AV nodal block → terminates AV node-dependent arrhythmias (i.e. [AV**N**RT]*PSVT* and [AOS-*AVRT orthodromic SVT*])
173
Head bobbing with each heart beat or Head pounding is c/w ⬜
Aortic Regurgitation \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *Head bobbing with each heart beat = de Musset sign and is sign of widened pulse pressure*
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Which conditions causes a [**FIXED** Widened S2 Splitting]?
Atrial Septic Defect
175
What makes up the Femoral Triangle (3)
1. [Inguinal Ligament *Superiorly*] 2. Sartorius M. *Laterally* 3. [ADDuctor Longus M. *Medially*]
176
Describe [**SHAC** Syndrome - Supine hypOtensive Aortocaval Compression]
Pregnant Women *\> 20 weeks gestation* can experience hypOtension when [gravid uterus] (while **supine**) compresses IVC --\> [DEC Venous Return] --\> DEC CO
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Name the location in the heart where ectopic foci that causes aFib are found
Pulmonary Veins *Myocardial sleeves extends around PVs and are supposed to be a sphincter to prevent reflux during atrial systole*
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# *Pt just had a stroke recently and now needs clot px* From the [**B.A.L.T.I.C.***post stroke px*], list the *blood thinning* regimens used for prevention of stroke? - 3
1. Give [**A**SA + ADP P2Y12 R Blocker]*alt: ( vs ASA vs Warfarin)* *(unless)* 2.*#2nd stroke → Warfarin⚠️* 3.*⊕aFib present → Warfarin⚠️|NOAC* | B**A**LTIC ## Footnote *⚠️Cont ASA/ADP🟥 if Warfarin CXD* *Also make sure pt is on a Statin* ✏️START WARFARIN FOR SURE **after second stroke** (if warfarin contraindicated, use only ASA) ✏️Give WARFARIN vs NOAC if pt has **aFib** after ANY stroke
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Why should you use ____ to treat *aFib*[Wolff Parkinson White syndrome] instead of [adenosineIV] beta blockers, calcium blockers or digoxin?
**Procainamide** ; the others are AV nodal blockers and may ⬆︎condution through the [BKAP] | *🔎BKAP = Bundle of Kent accessory pathway* ## Footnote *🔎A**A**S = [AVRT **A**ntiDROMIC(delta wave) **S**VT]*
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What is the life expectancy for patients with HOCM? (2)
*** with EARLY DX & APPROPRIATE TX …*** **[NORMAL]****MAJORITY **\> \> [poor pgn 2/2 LV systolic dysfunction]minority
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Explain why Standing [**⬜** INC | DEC] HOCM murmur
INC
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Explain why Squatting [**⬜** INC | DEC] HOCM murmur
DEC
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From MOST effective to least effective, describe the 5 *Non*Pharmacologic tx for decreasing high blood pressure
**D**\>**W**\>**A\>S\>****E** * * * {[**⬇︎**Sat/Total Fats **D**ash diet ⇪Fruits/Vegetables]*→ (⬇︎11mmHg) *} [**W**eight loss⬇︎10kg = ⬇︎6mmHg]*(if BMI ≥25)** [**A**erobic exercise30min/d x 5d/wk] [**S**odium(<1.5g PO/d)] [**E**TOHM≤2 | W ≤1 (drink/day)] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *\*Use If BMI ≥25 | central obesity = greatest lifestyle RF for HTN*
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*pts with _any_ c/f ACS must receive the bare minimum [ACSprimary] management. Suspicion greater than mild → graduate to [ACSSECONDARY (includes “Really Always Needs OBAMA” tx)] management.* *\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_* What all makes up [ACSprimary] management? (5)
*“call **TECNA*** *for [ACSprimary] = ALWAYS DO THIS FOR ANY ACS* [**T**roponin-iii q6H x ≥3]⼀rises@4h, peaks 6-12h, falls@7-10d [**E**KGq30m x ≥3] [**C**KMB] ⼀rises@6h, peaks@24h, falls@2d [**N**TGsublingual - prn active chest pain]*C❌D{RV MI}* [**A**SA 325 mg](may trigger asthma) ## Footnote *“1st [**TECNA**] 2nd ["**R**eally **A**lways **N**eeds **OBAMA**"]*
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initial Tx for [symptomatic varicose veins] is conservative and includes ⬜3
- compression stockings - leg elevation - wt loss
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diagnosis?
**Prior** MI \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *II/III/avF: contiguous TWI and Q waves are representative of previous MI* | "T wave *Inverts* my **MUNDO**, smh"
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Patients with CAD and/or prior MI should be started on ⬜ secondary prevention of cardiovascular events. What 4 components does this entail?
**ABCD** | *[**ABCD** 2º prevention of CV events]* ## Footnote **A**CE inhibitor/ARB **B**eta blocker [**C**holesterol lowering HIGH INTENSITY STATIN] [**D**ual anti-Platelet(ASA + ADP P2Y12 R Blocker)]
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# 🔎DigX = [Digoxin | Digitalis]*(Cardiac Glycoside)* sx of DigX Toxicity (6) * * * Which 4 drugs are HIGH RISK for causing digoxin toxicity? why?
"DigX Tox hurts *Brainconfusion* , *Eyeyellow-green 👀∆ * , *Heart*DAD arrhythmia *GI*NV/anorexia ## Footnote “(**VAQS**) traps Digoxin” by preventing renal excretion → DigX Tox hurts *[Brain, Eye, Heart, GI]* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_x\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 🔎***V**erapamil|**A**miodarone|**Q**uinidine|**S**pironolactone* *🔎DigX = [Digoxin | Digitalis]*(Cardiac Glycoside)*
189
Describe the preop cardiac evaluation for noncardiac nonemergency surgery
✔︎ {DO✅SURGERY \<-- **[****(****0-1****pt (LR≤1%)**|***Revised Cardiac Risk Index***|**(****≥2****pt (HR\>1%)**|**]** --\> DELAY❌SURGERY} ✔︎ Pts {[≥2pt (HR\>1%)] *but* can perform ≥4 METs} = DO✅SURGERY also \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_
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Because chronic HF → INC risk for frequent hospitalization, this risk should be mitigated using [multidisciplinary strategy that target ⬜ and ⬜] Give an example of this type of strategy
home environment; health literacy * * * [In-person (*at pt's home*) medication reconciliation/management/education] by RN case manager (in patient home \> clinical setting)
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a. diagnostic criteria for [Severe Aortic Stenosis] (3) * * * b. Indications for Aortic Valve Replacement (4)
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In the setting of *Severe Aortic Stenosis*, [_Onset of symptoms_*(angina/syncope/exertional dyspnea)*] vs ⬜ vs ⬜] are the 3 independent factors associated with ⇪ *Severe AS* mortality*📖→ ( ... and therefore also 3 independent indicators for aortic valve replacement⼀which ⬇︎Severe AS mortality)*
1.[Onset of Sx*(angina/syncope/DOE)*] *or* 2.**LVEF < 50%** *or* 3.**Undergoing other Cardiac Surgery** | *AV replacement* = [(Severe AS) + (1|2|3)]
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*[mild/mod Aortic Stenosis] differs in clinical presentation than [SEVERE Aortic Stenosis]* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How does [SEVERE Aortic Stenosis] affect heart sounds? -2
1. during inspiration[1 single soft second heart sound] 2. [**LATE** peaking systolic murmur] (early = mid/mod Aortic Stenosis) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *(normally, inspiration ⇪ blood into right heart ➜ pulmonic valve closes after aortic valve -- but in SEVERE Aortic Stenosis, the stenotic Aortic valve will have delayed closure also ➜ single second heart sound)*
194
Describe the Pre-operation management for aFib
195
What's important to remember regarding BNP in Obese patients?
Obesity causes **FALSELY LOW** **BNP** levels --> **underestimates their HF** \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *"Bigger people have Bigger BNP than you think"*
196
What is a normal Ejection Fraction?
\> 50%
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*Patient is diagnosed with HOCM* what would an [Implantable Cardioverter-defibrillator] be used to prevent in HOCM pts? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ diagnostic criteria? -2
Sudden Cardiac Death \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [**Sx**HOCM] + [≥1 SCD (1º vs 2º px) risk factor]\* ## Footnote SCD (1º vs 2º px) risk factors: 1º : SCD fhx/ syncope/ holter VT/ exertional hypOtension/LVH 2º: cardiac arrest survivor, sustained VT
198
Patients with bicuspid aortic valve are also at risk for developing what 3 aortic abnormalities?
aortic DISSECTION aortic ANEURYSM aortic DILATION \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *screen aortic root and proximal aorta*
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⬜ is the most common cause of [Dilated Cardiomyopathy HFrEF] and should be evaluated with what 2 test?
[Coronary Artery Diseasse] ; stress test | coronary angiography ## Footnote *"the **PIGS© PAID** for Dilated Cardiomyopathy"*
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Why is BNP an unreliable marker of volume status in patients taking [(ARNI) Angiotensin Receptor/Neprilysin Inhibitor] ? \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *ARNI = [sacubitril-valsartan]*
Neprilysin normally degrades BNP ➜ ARNI ➜ falsely higher BNP/**over**States HF status
201
# Infective Endocarditis *Name the 6 causes of IE*
*"Enterococcus⼀[STAph **A**], [STAph **E**]⼀[strEP **B**] [strEP **V**]* ⼀[*and nonbacterial**maranti(C)**with its misc (C)*] .." causes [mitral>tricuspid\*]IE ... *FROM JANE"*. \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. [Enterococcus= 💊*amp-gent*] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 2. [STAph **A**ureus#ACUTE⼀HIGH virulence➜RAPID+LARGE on NML Valves = 💊*Vanc*] 3. [STAph **E**pidermidis#prosthetic valves= 💊*Vanc*] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 4. [strEP **B**ovis #present in colon CA] 5. [strEP **V**iridans #subACUTE⼀low virulence➜ gradual+small on dz valves #dental = 💊*[cefTriaxone|aPG]*] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 6. [*maranti(C)*(misC (C)auses:*(C)A|(C)lotting/SLE) ***non***bacterial vegetations*] | *(aPG = aqueous Pencillin G IV)* ## Footnote *✏️tricuspidSBIE is a/w IVDU*
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# Infective Endocarditis [*(If present)*List💊 tx for each cause of IE
*"Enterococcus⼀[STAph **A**], [STAph **E**]⼀[strEP **B**] [strEP **V**]* ⼀[*and nonbacterial**maranti(C)**with its misc (C)*] .." causes [mitral>tricuspid\*]IE ... *FROM JANE"*. \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. [Enterococcus= 💊*amp-gent*] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 2. [STAph **A**ureus#ACUTE⼀HIGH virulence➜RAPID+LARGE on NML Valves = 💊*Vanc*] 3. [STAph **E**pidermidis#prosthetic valves= 💊*Vanc*] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 4. [strEP **B**ovis #present in colon CA] 5. [strEP **V**iridans #subACUTE⼀low virulence➜ gradual+small on dz valves #dental = 💊*[cefTriaxone|aPG]*] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 6. [*maranti(C)*(misC (C)auses:*(C)A|(C)lotting/SLE) ***non***bacterial vegetations*] | *(aPG = aqueous Pencillin G IV)* ## Footnote *✏️tricuspidIE is a/w IVDU*
203
S3 on auscultation typically indicates ⬜, but why is S3 less useful in younger patients \< 40 yo?
Ventricular Enlargement (HF) ; **S3 = NORMAL FINDING IN YOUNG PTS\<40 y/o**
204
Why are pts with Ehlers Danlos Syndrome at ⇪ risk for acute mitral regurgitation?
EDS = in addition to [Skin/Msk/GU] sx... EDS also cuases myxomatous degeneration (and ultimately RUPTURE) of the **chordae tendineae**
205
* [SEVERE HYPERTRIGLYCERIDEMIA] occurs when serum level TAG is ⬜ mg/dL. SEVERE HYPERTRICLYCERIDEMIA is a risk factor for developing ⬜* * \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_* Name tx for SEVERE HYPERTRICLYCERIDEMIA -3
\>1000 ; [HTAP - HyperTriglyceridemia Associated **PANCREATITIS**] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [Insulin or Apheresis (to lower serum TAG acutely)] + [FIBRATES (for HTAP tx and px)] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *Pts with HTAP hx require long term Fibrates for acute tx and prevention*
206
List the common causes of **Restrictive** Cardiomyopathy - 8
**RAMILIES** 1. **R**adiation Fibrosis (includes coronaries and valves) 2. **A**myloidosis (heterogenous misfolded proteins) 3. **S**arcoidosis= [Noncaseating granuloma formation] in multiple organs 2º to [CD4 Helper T] attack on unidentified antigen 4. **M**etastatic Tumor 5. **I**nborn metabolism errors 6. **E**ndomyocardial fibrosis= Common in [African/Tropic children] 7. [**L**oeffler Endomyocardial fibrosis] = (Has [Peripheral blood eosinophilia and infiltrate]) 8. **I**diopathic ## Footnote Restrictive Cardiomyopathy = -AKA *infiltrative* cardiomyopathy. -Diastolic dysfunction -low voltage EKG
207
Describe [3rd degree AV block]
[*PR* and *QRS* are completely independent]
208
[1st degree AV block] Tx
observation
209
describe [1st degree AV block] EKG
[*PR* prolonged \> [1 LOX (200 ms)] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *LOX = LARGE bOX*
210
2nd degree AV Block: Mobitz Type 1 Describe **where** block is, **EKG** findings and describe **QRS**
[2nd degree AV Block: Mobitz Type 1 Wekenbach] where = AV Node EKG = [(*Narrow*QRS Clusters) with ("*Wenke*" PR intervals)] until ➜ **Random Beat Drop** QRS is Narrow "*Wenke = gets longer and longer*
211
# [2nd degree AV Block: Mobitz Type 2] Describe **where** block is, **EKG**-3 findings and describe **QRS**-2
Bundle of His \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ [(*wide vs narrow*QRS clusters) +(constant PR)] ➜ [**RANDOM QRS Drop**] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ (*wide vs narrow*QRS groups | *[2nd degree AV Block: Mobitz Type 2] ("2 and 2")*
212
# [2nd degree AV Block: Mobitz Type 2] tx
Pacemaker
213
[NONtraumatic lens dislocation] indicates further evaluation for _____? Why?
Marfan Syndrome (AUTO DOM) [Aortic Dissection] r/o
214
how do you differentiate Marfan Syndrome from Homocystinuria ? - 2
1.Homocystinuria = auto recessive / Marfan = AUTO DOM 2.Homocystinuria = [*TALL* Marfan Sx] [+ DVT] [- intelligence]
215
Describe capillary refill for the 3 phases of [Acute Limb Ischemia]: *(Viable • Threatened • NonViable)*
Intact ➜ delayed ➜ ABSENT
216
name the 5 clinical values that determine Limb viability (*Viable vs Threatened vs Nonviable*) after severe [Acute Limb ischemia]
**SAVED** ## Footnote **S**ensory/Motor deficit **A**rterial doppler **V**enous doppler [**E**mpty-to-full (capillary refill)] [**D**olor (PAIN)]
217
Management for each phase of [Acute Limb Ischemia] - 3 *(Viable-2 • Threatened • NonViable)*
* Viable[Catheter or Surgical Revascularization] * Threatened[Surgical Revascularization STAT] * NonViable[Amputation]
218
peripheral edema is a side effect of which BP rx?
[dihydropyridineCCB] *(ex: amlodipine, nifedipine)*
219
a. Describe the 3 vascular complications of cardiac catheterization b. dx?
a. " b. ultrasound
220
What is PostOperative Atrial Fibrillation (POAF)? -4
1. COMMON occurring afib after cardiac surgery 2. caused by INC sympathethetic tone (from surgery itself) 3. spontaneously converts to sinus rhythm within few days 4. likely indicates underlying substrate ➜ recurrent afib ➜ subsequent complications (stroke, HF)
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# [Atrial Fibrillation SVT] is the most common tachyarrhythmia. It is often precipitated by what 9 things?
**LHEMM CHOP** makes *afib*! 1. [**L** atrial enlargement*(2/2 HF/HTN/Mitral dz)*] 2. ⭐[**H**TN = MOST COMMON CAUSE]⭐ 3. **E**tOH 4. **M**itral/Rheumatic❤️ dz 5. **M**I/CAD 6. [**C**atecholamines*i.e. sympathetics*] 7. **H**YPERthyroid 8. **O**bstructing PE 9. **P**ericarditis
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Mngmt for [Post-CABG related Afib] -3
▶*resolves spontaneously if rate is controlled with:* ▶HDS: (Beta Blockers vs Diltiazem vs Amiodarone3) ▶HDUS: DC Conversion | *This type of Afib is common*
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Marfan Syndrome s/s -4
**TALL** 1. {[**T**all/slender/flat feet] with [bone❌*breastbone∆ + (scoliosis vs kyposis)* 2. {[**A**ortic root disease\**(Aortic Dissection | Aortic Aneurysm)* + MVP ➜ SCD 3. {**L**ens dislocation*(ectopia lentis)* ➜ myopia} 4. {**L**ong [fingers*( = arachnodactyly ⼀Steinberg thumb/wrist), *], [arms] and [LEGS] with [hypermobile joints]} ## Footnote 🧠 Aortic Root Disease 2/2 idiopathic cystic medial degeneration which → Aortic Dissection|Aortic Aneurysm
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GFR threshold for hemodialysis
7.5 - **15** | *"GFR under fif-teen? then dia-lyze mee"*
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Describe [Malignant HTN Emergency] - 2
[Hypertensive Urgency (BP\>180/110)] + Papilledema/Retinal Hemorrhages
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list the causes of **secondary** hypertension -8
## Footnote 1. [Coarctation of Aorta] 2. [THYROID❌*(HYPERthyroid)*] 3. [THYROID❌*(hypOthyroid)*] 4. HYPERParathyroid 5. Pheochromocytoma 6. Cushing Syndrome 7. [RENAL❌*(-vascular)*] 8. [RENAL❌*(-parenchymal)*]
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Tx for [Peripheral Arterial Disease] -5
FIRST 1A. AntiPlatelet 1B. [STATIN high intensity] 1C. [Lifestyle ∆ (EXERCISE PROGRAM, no smoking)] \_\_\_\_\_\_\_(THEN ⬇️)\_\_\_\_\_\_\_\_\_\_\_ 2. [Cilostazol PDE inhibitor] for sx \_\_\_\_\_\_(THEN ⬇️⬇️)\_\_\_\_\_\_\_\_\_ 3. [Surgical Revascularization]
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causes of Dilated Cardiomyopathy (9)
*"the **PIGS© PAID** for Dilated Cardiomyopathy"* ## Footnote 1. **P**ost Viral Myocarditis (Coxsackie B) 2. **I**ron Overload: [Hereditary Hemochromatosis] or [Multiple Blood Transfusion Hemosiderosis] = Iron accumulates and interferes with myocytes 3. **G**enetic (affects cytoskeleton) 4. {[**S**ad Broken Heart *ABCQ Takatsubo*] (apical ballooning octopus on echo)} 5. ⭐**©**AD = MOST COMMON CAUSE OF DILATED CARDIOMYOPATHY ⭐ 5. **P**eriPostpartum (late in pregnancy : 5 mo. post partum) 6. **A**lcohol related (direct toxicity vs. nutritional deficiency) 7. **I**diopathic 8. [**D**oxorubicin, Daunarubicin and Traztuzumab Chemo] (dose-dependent)
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# The 5 causes of [High Cardiac Output failure] include*WET beri beri What is MOD for **WET Beri Beri**[High Cardiac Output failure]
low ATP ➜ DEC ability to vasoconstrict peripheral arterioles ➜ VERY DILATED peripheral arterioles ➜ DEC afterload resistance ➜ HIGH CARDIAC OUTPUT ➜ chronic INC venous return ➜ Dilated Cardiomyopathy
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What are the 5 Causes of**X** [High Cardiac Output failure] -5
1. Wet Beri Beri 2. chronic Anemia 3. Arteriovenous fistula 4. Paget's bone disease 5. HYPERthyroid
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When is rhythm control indicated for [aFib SVT]? how is rhythm control achieved? -4
rate control failed\* | *(io\ [MA-VZ-A-D rate control rx] pt still unable to tolerate aFib sx)* ## Footnote *❤️ → Rhythm Rx* ▶Normal → F.P. ▶⊕CAD → S.D. ▶⊕LVH → A.D. ▶⊕HF → A.i. \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Use Rhythm Chart (*see image*)
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in [aFib SVT], when is Ablation indicated ?
**RHYTHM** control(after Rate control failure 1st ) failed also\* | *symptomatic afib patients who can NOT tolerate antiarrhythmic agents*
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Name the 4 Classes of Anti-Arrhythmic agents
Class… [1*(a/b/c)*: **Na+**Channel blocker] [2: **Beta** blocker] [3: **K+**Channel blocker] [4: **Ca+**Channel blocker]
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indications for [ (*\_\_\_\_\_\_ J*) defibrillation] -3
*360 J* 1.VF 2.mmVT*p* 3.[PMVT⼀TDP)]*p* ## Footnote 1. VF = VFib 2. [mmVT]p = [monomorphic VT *pulseless*] 3. [PMVT⼀TDP]p = [POLYMORPHIC VT⼀TORSADES DE POINTES *pulseless*]
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In [ACS⼀acute STEMI], **R**evascularization of coronary blood flow with [PCI (*PerCutaneous Intervention*)] should be administered per what 4 criteria ?
STEMI R4 criteria * * * * **R0**: Revascularize only if **[SX ≤ 12h]** * **R**1: [iHP = PCI ≤90 min eDB] * **R**2: [OHP ≤120m eDB TFR] = [PCI ≤120 min eDB] * **R**3: [OHP \>120m eDB TFR] = [*ART*-tPA fibrinolysiswithin 30m] ## Footnote * * * ▶* iH/OHP: in/OUT HousePCI Institute* ▶ TFR: Transfer ▶ eDB: estimated Door→Balloon
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*"Surgical Emergency patient develops new onset **HDS** afib"* management?
(if HDS) [BB/NCCB Rate Control] to [100-110 bpm] *[beta blocker/nondihydropyridine Calcium Channel Blocker]*
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This rhythm is ⬜ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Identify the 4 differentiating qualities about this rhythm
"[AV🅽🆁🆃 (subtype of)🅿︎SVT]" \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 1. **🅽arrow QRS** 2. **🆁egular rhythm** 3. PSV**🆃achycardia>100 bpm** 4. **🅿︎ wave❌**: ⭐4A) ["hidden" burried within QRS = MOST COMMON] and/or 4b) *V1* lead[pseudo R'(tiny blip 2/2 retrograde P wave) ] ✏️ and/or 4c) *"Southern"* lead[pseudo S'2/2 retrograde P wave] ✏️ | "AV... **NRT** -(suptype of ) **P** SVT" ## Footnote ✏️ [*AV****NRT******P****SVT*] *Retrograde P waves possibly appear as spikes at beginning/end of QRS or as inverted P waves* *Southern lead = inferior leads (II, III, avF)*
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Name the 7 causes of arrhythmia
**HIS BEDS** *gave me arrhythmia* 1. [**H**ypoxia & ishchemia] 2. **I**nflammation 3. **S**ympathetic stimulation 4. **B**radycardia 5. [**E**lectrolyte❌ (K/Ca+/Mg)] 6. **D**rugs 7. [**S**tretched chambers (enlarged/hypertrophied atria/Vt ➜ arrhythmia)]
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**Procainamide** A: Mechanism (2) B: Effect (4) C: Antiarrhythmia Class
A: Blocks [Na+ Phase 0] and K+ channels B: - [Slow upstroke of AP and AP conduction → ⇪ AP duration] - [Prolongs QRS complex → ⇪ *Effective Refractory Period*] - Direct depressant actions on [SA/AV nodes] - use/state-dependent C: [Class 1A]
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# *Myocardial* action potential is used by the Myocardium, ⬜ and ⬜ Describe the phases of *Myocardial* action potential ⼀7
bundle of his; purkinje fibers ## Footnote Phase 0: [Na+VGC] open ➜[Na+ influx] =**rapid upstroke and depolarization** \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Phase 1: eventually, [K+ VGC] *begin* to open ➜ [K+ efflux] = **initial repolarization** \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Phase 2: -but soon thereafter, [Ca+ VGC] also open ➜ allows [Ca+ influx] to balance [K+ Efflux] and this causes PLATEAU. -,[Ca+ influx] also triggers Ca+ release from Sarcoplamic reticulum which ultimately ➜ **MYOCYTE CONTRACTION** \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Phase 3: -[Ca+VGC] close -[*slow* K +VGC] open ➜ MASSIVE [K+ EFFLUX] = **RAPID REPOLARIZATION** \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Phase 4: high K+ permeability ➜ **resting potential** until Phase 0 again
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# *Pacemaker* action potential is used in the ⬜ and ⬜ Describe the phases of *Pacemaker* action potential ⼀8
[SA node] and [AV node] ## Footnote Phase **0**: ⚡ ▶at -40 mV📈: [Ca+ LVGC] Open*(while [Ca+ T-VGC] close)*MAJOR[Ca+ iNflux] ➜ [*SUAD*] {🚧} \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Phase **3**: 🪫 ▶at 0 mV: [Ca+ LVGC] closE ▶[K+ VGC] Open ➜ [K+ Efflux] ➜ *repolarization* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Phase **4**: 🔌 ▶at -60 mV: 🔌[Na+ iNflux] via [Na+ i(funny) channels] ➜[INITIAL*ssDD*] ➜ ▶🔋causes ... [Ca+ **T**VGC] open ➜minor[Ca+ iNflux] ➜ [END*ssDD*] until -40mV ✏️Phase 4 *slope* determines [SA node HR] =*responsible for SA/AV node automaticity* ✏️ -( *ACh/adenosine ⬇︎ rate/speed of *ssDD* which ➜ ⬇︎[node HR]) -(catecholamines ⇪ diastolic depolarization) -(sympathetic stimulation ⇪ chance that i(funny) channels are open →⇪rate/speed of *ssDD* thus ➜ ⇪ HR) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *🔎ssDD = *slow spontaneous Diastolic Depolarization* *🔎SUAD = [*slow upstroke _AP_ depolarization*]* \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ {🚧}:✏️[*fast* Na+ VGC] are permanently inactivated 2/2 negative resting voltage (-60mV) of SA/AV nodes = slows conduction velocity in both SA and AV node... BUT! AV node uses this to prolong transmission from atria to ventricles
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**Procainamide** A: Clinical Application (2) B: Route of Admin (3) C: Metabolized into ______ and is eliminated by \_\_\_\_\_\_
A: \*[Atrial Arrhythmias] \*[2nd choice for Ventricle Arrhythmias after acute MI] B: PO / IV / IM C: Metabolized into **NAPA** and eliminated via **RENAL**
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**Procainamide** *Side Effects* (4) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ How is **Quinidine** related to **Procainamide**?
- Torsades des pointes, - hypOtension - Anticholinergic effects - SLE-like syndrome B: Similar to Procainamide AND SAME CLASS but with stronger anticholinergic effects. _Rarely used due to cardiac and other (HA/tinnitus) adverse effects._
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A: How is **DISOPYRAMIDE** related to Procainamide? B: Effects (2); What does this require to work? C: Adverse Effects (3) D: Indication
A: Similar to Procainamide but anticholinergic effects \>\> Procainamide and Quinidine, B: Its Anti-cholinergic effects INC [sinus rate and AV conduction] but requires co-administration of drugs that slow AV conduction. C: \*Negative inotropic effects, \*may induce heart failure. \*extra-cardiac side effects from atropine-like actions. D: Approved only for *ventricular arrhythmias*, Not drug of 1st or 2nd choice
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A: Class 1 Antiarrhythmic Drugs are ⬜ that have a ⬜ action ## Footnote B: - Name the 3 *kinetic* Subtypes - .. and their Effect on action potential
A: Class 1 Antiarrhythmic Drugs are [*dFUSt(AKA "state") dependent* Phase 0 Na+ Channel Blockers] that have a [local anesthetic] action ## Footnote B: 3 Subtypes 1A: **Intermediate** kinetics and [prolongs action potential *duration*] 1B: **FAST** kinetics and [DEC action potential *duration*] 1C: **Slow** kinetics and [NO EFFECT ON ACTION POTENTIAL* duration *] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ {*🔎**dFUSt**-dependent = ⛔[**d**epolarizing (**F**REQUENT **U**SE-**S**TATE) **t**issue]** ( = ⛔tachycardic and ischemic tissue)}
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**Lidocaine** A: Mechanism B: Effect (2) C: Antiarrhthymia Class
A: [***dFUSt** dependent* Phase 0 Na+ Channel Blocker] B: - Generally no effect on _overall conduction_ *(since recovery from block occurs between action potential*). - Selective depression of conduction in [**depolarized** ischemic purkinje and ventricular cells] *(binds and blocks phase 0 Na+ channels that are active/in depolarized state)* C: [Class 1B] ## Footnote *🔎**dFUSt** = [**d**epolarized (**F**REQUENT **U**SE-**S**TATE) **t**issue]*
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**Lidocaine** A: Indication (2) B: route of admin for Arrhythmias C: Metabolization D: Side Effects (3)
A: - [ventricular arrhythmias after MI]. - [_1st choice - [Vtach and fib]_ after cardioversion in the setting of ischemia/infarction] B: **IV ONLY** in Arrhythmias C: First Pass-**Hepatic** metabolism D: (x) Least cardiotoxic in Class 1 (x) Neurological SE from local anesthetic properties (x) hypOtension with large doses
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**Mexiletine** A: _____ Active _____ analog! B: Adverse Effects C: Indications (3)
A: Orally Active Lidocaine analog! *(is also Class 1B)* B: SE similar to Lidocaine C: - Chronic Pain - Diabetic Neuropathy - Nerve Injury
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**Flecainide** A: MOA (2) B: Effect on Action Potential (3) C: Indication (2)
A: [Na+ and K+ channel] blockade B: -[prolongs ERP in AV node and accessory bypass tracts (but no ERP ∆ to Purkinje and Vt tissue)] -K+ blocker but has NO EFFECT ON ACTION POTENTIAL DURATION -No Anticholinergic Effects C: 1. [SVT (***especially aFib***) in pt with normal hearts] 2. Maintains NSR
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**Flecainide** * A: Elimination (2)* * B: Contraindications (3)* * C: Antiarrhythmia class*
A: Liver and Kidney B: patients with.. * ventricular tachyarrhythmias, * ventricular ectopy * previous MI C: [Class 1C]
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**Propafenone** ## Footnote A: MOA (2) B: Structural similarity to _____ but with weak\_\_\_\_\_\_ activity. C: Indication D: Adverse effects (4)
A: [Class 1C] Potent blocker of Na+ channels, / may also block K+ channels. B: Structural similarity to propanolol with weak β-blocking activity. C: Used for [supraventricular arrhythmias] in patients with otherwise normal hearts. D: Adverse effects/toxicity: - sinus bradycardia (from β-blockade). - bronchospasm (from β-blockade). - Metallic taste - constipation.
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**Propranolol** A: MOA B: Effect (4)
A: [**Class 2** General β-blocker] B: - inhibits sympathetic influences on cardiac electrical activity. - DEC heart rate by DEC pacemaker currents (SA node automaticity) - reduces conduction - decreases [catecholamine induced DAD] and [EAD mediated arrhythmias]
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**Propranolol** B: Adverse Effects (5) C: Contraindications D: How is it related to DM pts?
B: (x) Bradycardia (x) DEC excercise capacity (x) Heart Failure (x) hypOtension (x) AV Block C: pts with: \*Pulmonary Dz \*bradycardia \*AV Block D: May mask tachycardia associated with hypOglycemia in diabetic patients
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**Amiodarone** A: MOA (4) B: Effect (3) C: Antiarrhthymia Class
A: "Amy BLOCKED the **NBC-K** channel" [Blocks **N**a+ / **B**eta *receptors* / **C**a+ / **K**+ channels] B: * Prolongation of action potential duration (QT interval) by prolonging refractoriness * slows conduction (prolongs QRS)--\> suppresses abnormal automaticity * can slow normal sinus automaticity. C: [Class 3]
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**Amiodarone** Indication (Oral-3 vs. IV-3)
A: Oral: - [Recurrent VTach resistant to other drugs] - [Recurrent VF resistant to other drugs] - aFib *IV*: ▶ [1st choice-out of hospital Cardiac Arrest] ▶VT termination ▶VF termination
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**Amiodarone** B: Adverse Effects (7) C: Explain how it is related to Thyroid problems (2)
B: * Highly lipophilic--\> accumulation in several organs (heart, lung, liver, cornea). * Bradycardia in SA/AV node disease * heart block in patients with SA/AV node disease. * Pulmonary toxicity * hepatic toxicity, * photodermatitis, * cornea microdeposits. C: -Structural analogue of thyroid hormone--\>blocks conversion of T4 to T3, -source of inorganic iodine: Hypo- and hyperthyroidisms
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Describe What the Antiarrhythmia Classes below are A: Class 1 (A vs. B vs. C) B: Class 2 C: Class 3 D: Class 4 D2: What 4 sites does Class 4 act on?
" **N**ervous **B**arry **K**illed **C**arrie " Class 1: **N**a+ channel Blockers (A vs. B vs. C) Class 2: **B**eta Blockers Class 3: [**K**+ channel blocker(* = prolongs action potential duration*)] Class 4: [**C**a+ L-type channel blockers - *Non-Dihydropyridine*] [Vascular smooth m. / cardiac myocytes / SA node / AV Node]
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**Dronedarone** is a _____ analogue of **Amiodarone** A: What is the differences and what was it desinged for? B: Indications (2) C: Contraindications
A: Structural analogue of amiodarone but **without iodine atoms**,. Designed to eliminate effects on thyroxine metabolism. B: Indications: atrial fibrillation/flutter. Contraindicated in severe or recently decompensated symptomatic heart failure.
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**Sotalol** A: MOA (2) B: Indications (2) C: Antiarrhthymic Class
A: 1. [General β-blocker] *(L-isomer only)* 2. inhibits delayed rectifyer and possibly other K+ currents B: Indications: - [Ventricular and supraventricular arrhythmias]. - [Maintenance of sinus rhythm in patients with afib] C: Class 3
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**Verapamil** A: MOA B: Effect (3) B2: Which tissue does it affect most? C: Clinical Application (3)
A: {**NCCB** blocks activated and inactivated [L-Type Ca+ channels] in the heart} B: * [Directly slows AV node conduction] and [increases AV node refractoriness]*( →⇪ PR interval)* , * slows SA node automaticity.--\> Lowers heart rate * Use/state-dependent action. B2: Major effects in slow- response tissues- (i.e. SA/AV node). C: 1. [**1st choice**- Supraventricular arrhythmias] 2. Re-entry arrhythmias/tachycardias involving AV node. 3. Slows ventricular rate in atrial flutter/fib ## Footnote *🔎NCCB = Nondihydropyridine Calcium Channel Blocker*
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**Verapamil** A: Antiarrhythmic Class B: Metabolism
A: Class 4*(NCCB: Blocks [Calcium L-VGC] in Heart)* B: Extensive Hepatic --\> can cause Liver Dysfunction | *🔎L-VGC = L-type Voltage Gated Channels* ## Footnote Verapamil side effects = "even **CHAPELS** hurt from CCB!"
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A: How is **Diltiazem** compared to **Verapamil** B: Additional uses of **Diltiazem** (3) C: Antiarrhythmic class of **Diltiazem**
Similar to Verapamil but with _lower cardioselectivity_, B: used also for - HTN - Angina - Exercise Tolerability **INCREASE** by [decreasing angina freq. and myocardial demand] C: Class 4
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**MAGNESIUM** A: MOA (2) B: Antiarrhythmic Class
A: Inhibits [Na+,K+-ATPase] and [Na+/ K+/ Ca+ channels]---\> alters membrane surface charge B: **NO CLASS**
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**POTASSIUM** A: MOA (HYPER vs. hypOkalemia) B: Antiarrhythmic Class
A: * Hyperkalemia; depolarizes resting membrane potential * Hypokalemia; decreases K+ permeability B: **NO CLASS**
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**[CARDIAC GLYCOSIDE]** A: MOA B: Antiarrhythmic Class C: examples (2)
A. DGC\* inhibits [(ShOUT PIN) Na+/K+ ATPase] which ➜ [⇪ intracell Na+] ➜ prevents [(COUnT SIN) Na+/Ca+ exchanger] (since there will be already too much [intracell Na+] for "SIN") and this leaves more intracell Ca+ = [⇪ cardiac contractility] B: **NO CLASS** C. {[DiGoxin | DiGitalis]Cardiac Glycoside}= DGC | "*ShOUT PIN ⼀COUnT SIN*" ## Footnote **S**hOUT **P**IN ⼀**C**OUT **S**IN ▶ [Na+/K+ ATPase pump] = 3 Na+ OUT, 2 K+ in ▶[Na+/Ca+ exchange] = 2 Ca+ OUT, 3 Na+in \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ShOUT = Sodium Out PIN = Potassium IN - - - - COUnT = Calcium Out SIN = Sodium IN
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**ADENOSINE** *Side Effect (5)*
❌flushing ❌hypOtension ❌chest pain ❌impending doom ❌**bronchospasm** = **CXD IN PTS WITH BRONCOSPASTIC DISEASE** ## Footnote ✏️similar to ACh. ✏️acts on Atrial and AV node primarily
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**MAGNESIUM** *Effect (2)*
* Anti-arrhythmic effects*[PMVT Torsades de Pointes]* in some patients with normal Mg+ levels. * May inhibit afterdepolarizations. ## Footnote *🧠MOA = Inhibits [Na+,K+-ATPase] and [Na+/ K+/ Ca+ channels]---\> alters membrane surface charge*
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**POTASSIUM** *Effect (HYPER vs. hypOkalemia)*
* Hyperkalemia--\> slows conduction (may lead to re-entrant arrhythmias and AV nodal block). * hypOkalemia---\>enhances ectopic automaticity, lengthens action potential duration which can lead to EADs (torsades de pointes).
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**[CARDIAC GLYCOSIDES]** *Effect (2)* | (Digoxin | Digitalis)
* Positive inotropic actions (used widely in heart failure) * Parasympathomimetic effects: increase AV nodal refractoriness and slow AV node conduction.(treats RVR from afib/aflutter)
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**MAGNESIUM** Indication (2) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ Route of Admin
-[(CardiacGlycoside-induced arrhythmia) in the setting of hypOmagnesemia] -[PMVT Torsades de Pointes] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ IV ## Footnote PMVT = POLYMORPHIC Ventricular Tachycardia
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**POTASSIUM** * A: Indication* * B: Route of Admin (2)*
* Maintain normal plasma K+ B: IV or PO
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**[CARDIAC GLYCOSIDES]** *Indication (3)* | (Digoxin | Digitalis)
* HF * [aFib*(slows RVR)*] * [aFlutter*(slows RVR)*] ## Footnote 💡In (atrial flutter/afib) CG parasympathomimetic effects slow AV nodal conduction,----\>slows [afib/aflutter associated_Rapid Ventricular Rates]
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**[DIGITALIS*CARDIAC GLYCOSIDES*]** ## Footnote A: Elimination by the ⬜ with a ⬜ therapeutic window. B: drug interactions (3) B2: Which conditions enhance toxic effects? (2) . C:Adverse Effects (4) D: How do you *Reverse* Severe digitalis toxicity
A: kidney ; **Narrow**. B: Many drug interactions (amiodarone, verapamil, flecainide)!!! B2: Hypokalemia/magnesemia enhance toxic effects. C: "DigX Tox hurts *[Brain, Eye, Heart, GI]*" D: Severe digitalis toxicity can be reversed by digoxin antibodies.
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What is the **primary** determinant of the ventricular muscle refractory period?
Action Potential Duration (Phase 2) (QT)
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A: hypOkalemia and Acidosis can each cause what change to the SA Node? B: EAD usually occurs at ____ HR from the \_\_\_\_\_\_\_ C: DAD usually occurs at ____ HR from the \_\_\_\_\_
A: **Disturb Impulse Formation** and cause premature stimulation --\> INC HR B: EAD (*early afterdepolarization)* usually occurs at SLOW HR from the [Phase 2 Plateau] C: DAD (Delayed afterdepolarization) usually occurs at FAST HR from the Resting Potential
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4 Main Ways Antiarrhythmic Drugs can treat Arrhythmia *in the **[SA/AV node]***
1. Reduction of phase 4 slope 2. Increase [max. Resting Potential] 3. Increase of threshold potential 4. Increase of action potential duration
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A. Explain what [Use-dependent or state-dependent] drug action actually means B: Example (2) C: Why is tx of _asymptomatic_ or _minimally symptomatic_ arrhythmias **DISCOURAGED AGAINST**?
A. antiarrhythmic rx selectively depresses cardiac**dFUSt** = [**d**epolarizing & (**F**REQUENTLY-**U**SED-**S**TATE) **t**issue ] - *tissue frequently* used *[ AKA in a depolarized state with M-Lid up(tachycardia/ischemic)]! * \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ B: e.g. - during fast tachycardia (many channel *depolarizations frequently*) - [ischemic/infarcted tissue have more positive resting potential = will reach action potential threshold sooner = will reach (be in) [depolarized used/inactive state] = more likely to interact with [use/state**"dFUSt"** dependent antiarrhythmic]] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ C: Antiarrhythmics CAN STILL ACT ON NORMAL Cells with "RESTING" Na+ channel M-Lids! ---\> Drug induced Arrhythmia! ## Footnote * "Antiarrhythmics are better acting when the **M-Lid** is up frequently"*
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A: How do Antiarrhythmic Class 1 work? (3) B: Name the 3 [Class 1 Antiarrhythmics] that actually INC Action Potential Duration
*Class 1* * Reduce Conduction Velocity*(in especially [**DAUST** {= tachycardic & ischemic tissue}])* * ...by blocking [Phase 0 Fast AP Na+ VGC] → DEC rate and magnitude of [Phase 0 Fast Action Potential Upstroke] → alters ERP \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ * Some Class 1 affect K+ channels ---\> Prolonged Repolarization ---\> Prolonged Action Potential Duration | *🔎DAUST = [Depolarized⼀ACTIVELY USED-STATE TISSUE]* ## Footnote B: Procainamide1A / Quinidine1A / Disopyramide1A
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A: What is **NAPA**? B: Antiarrhythmic Class C: Elimination (2) D: Adverse Effects (3)
A: Metabolite from [Procainamide1A] B: Is actually Class 3! and C: eliminated via Liver and Kidney(requires dose reduction in renal failure ) D: - hypOtension - Torsade De pointes - Lupus Erythematosus with long term usage! | *Procainamide1A --(breaks down into)--> NAPA3*
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A: Which class antiarrhythmic is most associated with ⇪ QT prolongation? B: Why? C: This Antiarrhthymic class works better with which Heart Rate (fast vs slow)?
A./B.: **CLASS 3** - Antiarrhythmics --\> Prolongs Action Potential Duration as a K+ channel Blocker C: _WORKS BETTER WITH SLOW HR_ (even tho this may cause Torsades De Pointes) ## Footnote ADIDaS rx: Amiodarone⼀Dronedarone / ibutilide / Dofetilide / and Sotalol
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# _Non-Pharmacologic_ Anti-Arrhythmic Therapies: **Radiofrequency ablation & Cryoablation** B: MOA C: Indication
B: interrupts*reentrant | accessory* pathway C:[**Nonpharm** rhythm control] s/p {[rate control *failure*] and [*pharmacologic*rhythm control *failure*]} | frequently **replaces** [*pharm*rhythm control]
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# _Non-Pharmacologic_ Anti-Arrhythmic Therapies: **Synchronized Electrocardioversion/Defibrillation​** Indications (3)
- [*HD**U**S* atrial fibrillation] - [Ventricular Fibrillation] - [Ventricular Tachycardia*pulseless*]
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_Non-Pharmacologic_ Anti-Arrhythmic Therapies **Vagal Maneuver** A: Examples (3) B: MOA C: Indication
Vagal maneuvers A: carotid sinus message, [diving reflex (cold water on face)], [Valsalva maneuver]. B: slows conduction through AV node. C: Acute treatment for paroxysmal supraventricular tachycardia (PSVT)
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Antiarrhythmics used for conversion to sinus Rhythm? (3)
"_Adele_ and _Ami_ *converted* me to _Flex_" Adenosine / Amiodarone/ Flecainide
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Antiarrhythmics used for **_Maintenance_** of sinus rhythm (5)
"Maintain ur **F**-**PPAD** man" Flecainide Propafenone Propranolol Amiodarone Dronedarone
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Antiarrhythmics used for Ventricular Rate Control (4)
" **V EDP**" Diltiazem/**V**erapamil / Propranolol/Esmolol
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Which Drugs for: Ventricular tachycardia in patients without heart disease (2)
"Ur having VTach *without* Heart Dz..? Go to **LA**" **L**idocaine **A**miodarone
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Which tx for: AV Block (2)
Atropine Pacemaker
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Which Drugs for: VENTRICULAR FIBRILLATION (3)!
1st:⭐-{Debrillation (plus **Epinephrine***])} \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ 2nd/Alt: -{Debrillation (+/- [Amiodarone*3*])} OR -{Debrillation (+/- [Lidocaine*1B*])} | Amiodarone 3 or Lidocaine 1B in place of epinephrine
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[**Propranolol** (as an antiarrhythmic)] Indications) (6)
" Propranolol uses **VARAMA** cream " 1. **V**t Rate Control 2. **A**trial arr 3. **R**einfarct POST MI tx 4. **A**fterDepolarization (*EAD/DAD)* tx 5. **M**aintains Sinus Rhythm 6. **A**V Nodal Re-entry tx
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Why are [Ca+ Channel Blockers] and [Beta Blockers] **Contraindicated** in Acute CHF?
[Ca+ Channel & BB Blockers] have **NEGATIVE INOTROPIC EFFECTS!**
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[**Digitalis**Cardiac Glycoside] Indication (2)
1. CHF 2. [RVR*(in aFib RVR/aFlutter RVR )*] | *(since DigX slows ventricular rate)*
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Major **unique** *Adverse Effect* of [**Nifedipine** Dihydropyrdine Ca+ channel Blocker]
Reflex Tachycardia _\_\_\_\_\ *(in addition to **CHAPELS**)*
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**Nesiritide** *A: Indication (2)* *B: MOA (4)*
A: 1. [CHF exacerbation] in hospitalized patients 2. HTN B: 1. **[Human BNP recombinant]** that... 2. [**renal BNP🟢]** → DCT _Natriuresis_ 3. [**vascular smooth muscle NPR1/2🟢]** → [renal Afferent arteriole]*vasoDilation*--\> INC GFR 4. INC cGMP in [**vascular smooth muscle**] --\> [peripheral arteriole] *vasoDilation* | 🧠[Nesiritide = *artificial* BNP] = [Nesiritide BNP]
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# prolonged QT predisposes to [Torsades de Pointes Polymorphic VT] What are the major causes of acquired prolonged QT? (7)
anti**ABCDEKG** -[anti**A**rrhythmics (class 1A, 3)] -[anti**B**iotics (macrolide)] -[anti"**C**"ychotics (haloperidol)] -[anti**D**epressants (TCA)] -[anti**E**metics (ondansetron)] -[anti-**K** = ⬇︎K+] -[anti-M**g** = ⬇︎M**g**] | *both low K+ and low Mg+ can prolong QT*
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*Baroreceptors and Chemoreceptors of the **Aortic Arch** send its afferent information to ⬜ via ⬜*
[solitary nucleus of medulla] ← [Vagus CN10]
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*Baroreceptors and Chemoreceptors of the **Carotid Sinus** send its afferent information to the ⬜ via ⬜*
[solitary nucleus of medulla] ← [Glossopharyngeal CN9]
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ANP clinical features (4)
1. released from atrial myocytes when [blood volume ⇪] or [atrial pressure ⇪] 2. [⇪GFR (promotes diuresis)] - via dilates Afferent arteriole /constricting efferent arteriole 3. vasoDilation 4. ⬇︎Na+ ReAbsorption at CD
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BNP clinical features (4)
1. from Vt myocytes in response to ⇪ pressure 2. similar to ANP but longer 1/2 life 3. good NPV for HF dx 4. available to treat HF as *Nesiritide* ## Footnote NPV = Negative Predictive Value
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# *PDA is necessary during fetal development but should close by birth* Which substance maintains an open ductus arteriosus?
"[PG**E** Prostaglandin] -- *ke**E**ps a PDA*" | *🔎PDA = patent ductus arteriosus * ## Footnote [Indomethacin/NSAIDs inhibit [PGE Prostaglandin] synthesis! ➜ Closes ductus arteriosus
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What are the primary diagnostics for MI (3)
a. [**E**KG (STEMI/ST Depression/hyperacute T/TWI/new LBBB/Q/poor R progression)] = gold standard Hours 1-6 post MI b. [**T**roponin-iii] rises@4h, peaks@6-12h, falls@7-10d c. [**C**KMB (also released from sk muscle)] rises@6h, peaks@24h, falls@2d (returns to baseline 48h post MI = useful for diagnosing reinfarction) ## Footnote *“1st [**TECNA**] 2nd ["**R**eally **A**lways **N**eeds **OBAMA**"]*
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# 5 antiHLD categories = (**FBENS**). [🍔***F**ibrates*] a. Target b. MOA (2) c. Rx (4) d. side effects (2)
a. ⬇︎TAG ## Footnote b. -[upregulates (LPL)] ➜ [ ⇪VLDL to IDL]➜ [ ⇪ TAG clearance via HDL] -[activates PPARα ➜ ⇪ HDL ➜ [ ⇪ TAG clearance via ⇪ HDL] c. 📝gemFIBrozil 📝cloFIBrate 📝bezaFIBrate 📝FenoFIBrate d. ❌Cholesterol Gallstones ❌[Myopathy *(⇪ with Statins)*]
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# 5 antiHLD categories = (**FBENS**). [🍔***S**tatins*] a. Target b. MOA (2) c. Rx (5) d. side effects (2)
a. ⬇︎⬇︎⬇︎LDL Cholesterol ## Footnote b. *[HMG-CoA reductase inhibitor]* -Inhibits conversion of [HMG-CoA ➜ mevalonate (*necessary for (LDL Cholesterol) synthesis*)] ❗️⬇︎Mortality in CAD patients c. 📝Atorvastatin 📝Simvastatin 📝Pravastatin 📝Rosuvastatin 📝Lovastatin d. ❌HEPATOTOX (*⇪ with F.N.*) ❌MYOPATHY ( *⇪ with F.N.*)
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# 5 antiHLD categories = (**FBENS**). [🍔***N**iacin B3*] a. Target (2) b. MOA c. Rx d. side effects (3)
a1. [⬇︎VLDL*(by blocking [DGA2] which is needed in VLDL synthesis)*] a2. [ ⇪ HDL] ## Footnote b. -[VLDL synthesis requires DGA2]. Niacin blocks DGA2 ➜ [⬇︎VLDL] c. 📝Niacin B3 d. ❌Flushing (px = NSAIDs) ❌HYPERUricemia ❌HYPERGlycemia
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# 5 antiHLD categories = (**FBENS**). [🍔***E**zetimibe*] a. Target b. MOA (2) c. Rx d. side effects (2)
a. ⬇︎LDL Cholesterol ## Footnote b. -Prevent [Cholesterol] absorption at small intestine brush border ➜ body uses internal [LDL Cholesterol] ➜ [⬇︎ LDL Cholesterol] c. 📝Ezetimibe d. ❌Diarrhea ❌rare ⇪ LFTs
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# 5 antiHLD categories = (**FBENS**). [🍔***B**ile acid resins*] a. Target b. MOA c. Rx (3) d. side effects
a. ⬇︎LDL Cholesterol ## Footnote b. [prevents intestinal Bile ReAbsorption ➜ forces liver to replace Bile using LDL Cholesterol = ⬇︎LDL Cholesterol c. 📝Cholestyramine 📝 Colestipol 📝 Colesevelam d. ❌Fat Malabsorption
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**Adenosine** a. MOA (5) b. Indication (2)
A. 1.given as [6 mg rapid IV bolus](similar to ACh. Atrial tissue affected more) 2.[**slows AV node conduction***(causes 15 second AV node depolarization delay by ⬇︎Ca+ influx)*]produces transient cardiac arrest 3.[**prolongs AV node refractory***(by causing AV node hyperpolarization via activating K+ efflux]produces transient cardiac arrest 4.blunted by theophylline (Adenosine R Blocker) 5.blunted by caffeinee (Adenosine R Blocker) \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ b. ✅SVT diagnostics ✅SVT abolishment ## Footnote ✏️Increases K+ conductance (hyperpolarization) and inhibits [camp-Ca+ currents] both via purinergic receptors
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**CALCIUMN CHANNEL BLOCKERS** a. MOA b. [Nondihydropyridine CCB] act on [____ (vasc smooth m) | (heart)] c. Name the 2 NCCB. ## Footnote NCCB = [Nondihydropyridine CCB]
a. [blocks Calcium L-VGC] ➜ *dCCB*[⬇︎muscle contractility] /*NCCB*[⬇︎AV node conduction] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ b. heart c. Verapamil>Diltiazem | "even **CHAPELS** hurt from CCB!"*= side effect*
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**CALCIUMN CHANNEL BLOCKERS** side effects (7)
"even **CHAPELS** hurt from CCB!" ❌**C**onstipation ❌[**H**yperprolactinemia*(Verapamil)*] ❌[**A**V Block*= nCCB = (in pts: high dose | nodal dz | on β🟥) - treat with atropine]*] ❌[**P**eripheral Edema*(DCCB)*] ❌[**E**verything's Spinning ⼀Dizziness/hypOtension] ❌[**L**arge gums⼀gingival hyperplasia] ❌[**S**kin Flushing*(and skin Rxn = Verapamil IV)*] ## Footnote *[blocks Calcium L-VGC] ➜ *DCCB*[⬇︎muscle contractility] /*nCCB*[⬇︎AV node conduction]*
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# LARGE vessel vasculitis includes [Giant Cell Temporal Arteritis] and ⬜ **[Giant Cell Temporal arteritis]** clinical features (7)
[Giant Cell Temporal Arteritis] and [Takayasu Pulseless arteritis] ## Footnote 1. elderly female 2. uL temporal artery *(from Carotid a)* HA 3. jaw claudication 4. ophthalmic artery *(from Carotid a)* occlusion may ➜ irreversible blind 5. a/w PolyMyalgia Rheumatica 6. ⇪ ESR with Focal granulomatous inflammation 7. tx (prevent blindness) = [(CTS⼀HD) f/b Temporal artery bx]
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# LARGE vessel vasculitis includes ⬜ and [Takayasu Pulseless arteritis] **[Takayasu Pulseless arteritis]** clinical features (4)
[Giant Cell Temporal Arteritis] and [Takayasu Pulseless arteritis] ## Footnote 1. asian young <40 yof 2. "pulseless" = [granulomatous thickening (⇪ ESR) ➜ narrowing of aortic arch & proximal great vessels] ➜ weak UE pulses 3. fv, night sweats, skin ∆, ocular ∆ 4. tx = CTS
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# Medium vessel vasculitis are Polyarteritis Nodosa, ⬜ and ⬜ **Polyarteritis Nodosa** clinical features (5)
Medium vessel vasculitis are [Polyarteritis Nodosa], [Kawasaki disease], [Buerger Thromboangiitis Obliterans] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ ## Footnote 1. Young adults 2. HBV in 30% of patients 3. -Const: Fever, wt loss, malaise -Cardiac: HTN -GI: abd pain, melena 4. [Immune complex mediated ⼀renal and visceral vessels (renal microaneurysms) ⼀arterial wall transmural inflammation with fibrinoid necrosis] 5. tx = cyclophosphamide and CTS
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# Medium vessel vasculitis are ⬜ , ⬜, [Buerger Thromboangiitis Obliterans] **[Buerger Thromboangiitis Obliterans]** clinical features (4)
Medium vessel vasculitis are [Polyarteritis Nodosa], [Kawasaki disease], [Buerger Thromboangiitis Obliterans] ## Footnote 1. <40 yom Smokers 2. etx = [Segmental thrombosing vasculitis] ➜ Intermittent Claudication ➜ gangrene/digital autoamputation 3. ⊕Raynaud phenomenon 4. tx = smoking cessation
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# Name the 4 small vessel vasculitis **-[WGP ⼀Wegener Granulomatosis with polyangiitis]** clinical features (4)
-[MP ⼀microscopic polyangiitis] -[WGP ⼀Wegener Granulomatosis with polyangiitis] -[CEGP ⼀Churg strauss Eosinophilic Granulamtosis with Polyangiitis] -[BrIAN-hSP ⼀Berger IgA Nephropathy (*Henoch Schonlein purpura*)] ## Footnote **WGP** 1. {[**c**-ANCA] binds to [PR3 antigen] = antiproteinase 3} ➜ [WGP Triad] 2. [⛔ASTHMA⼀✅Granulomas ] *a/w* 3. [WGP Triad]: WGP-1.[Focal necrotizing vasculitis] WGP-2.[Necrotizing granulomas in ELK], WGP-3.[Necrotizing Glomerulonephritis] 4. tx = [cyclophosphamide and CTS] \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_x\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ *🔎ELK = ENT/Liver/Kidney* ENT\LK: -E:Otitis media -N:nasal septum perforation, chronic sinusitis -T: hemoptysis, dyspnea -L: CXR large nodular densities -K: hematuria, RBC cast, [Necrotizing Glomerulonephritis]
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# Name the 4 small vessel vasculitis **[CEGP ⼀Churg strauss Eosinophilic Granulamtosis with Polyangiitis]** clinical features (7)
-[MP ⼀microscopic polyangiitis] -[WGP ⼀Wegener Granulomatosis with polyangiitis] -[CEGP ⼀Churg strauss Eosinophilic Granulamtosis with Polyangiitis] -[BrIAN-hSP ⼀Berger IgA Nephropathy (*Henoch Schonlein purpura*)] | **CEGP** = *"**pPAGING** churg-strauss"* ## Footnote *"**pPAGING** churg-strauss"* 1. {[**p**-ANCA](binds to [MPO neutrophil antigen] = antiMyeloPerOxidase} ➜ 2. **P**olyps in Nose with rhinitis, sinusitis and skin nodules 3. ⊕[**A**sthma ( ⇪ IgE)] 4. ⊕[**G**ranulomas on necrotizing vasculitis with eosinophilia] 5. **i**mmune-pauci glomerulonephritis 6. [**N**europathy (wrist/foot drop) +/- GI or heart involvement] 7. ⊕[**G**ranulomas on necrotizing vasculitis with eosinophilia]
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# Name the 4 small vessel vasculitis **[MP ⼀microscopic polyangiitis]** clinical features (4)
-[MP ⼀microscopic polyangiitis] -[WGP ⼀Wegener Granulomatosis with polyangiitis] -[CEGP ⼀Churg strauss Eosinophilic Granulamtosis with Polyangiitis] -[BrIAN-hSP ⼀Berger IgA Nephropathy (*Henoch Schonlein purpura*)] ## Footnote **MP** 1.{[**p**-ANCA](binds to [MPO neutrophil antigen] = antiMyeloPerOxidase} ➜ 2.[⛔ASTHMA ⼀ ⛔GRANULOMAS] *but will →* 3.*necrotizing vasculitis of* LKS -Lung: Hemoptysis -Kidney: [pauci-immune glomerulonephritis] -Skin: palpable purpura 4.[tx= cyclophosphamide and CTS]
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# Name the 4 small vessel vasculitis **[BrIAN-hSP ⼀Berger IgA Nephropathy (*Henoch Schonlein purpura*)]** clinical features (4)
-[MP ⼀microscopic polyangiitis] -[WGP ⼀Wegener Granulomatosis with polyangiitis] -[CEGP ⼀Churg strauss Eosinophilic Granulamtosis with Polyangiitis] -[BrIAN-hSP ⼀Berger IgA Nephropathy (*Henoch Schonlein purpura*)] ## Footnote **BrIAN-hSP** 1. TRIAD: [GI Pain / Palpable Purpura on Butt-Legs/ Arthralgias] 2. Vasculitis 2/2 IgA immune complex deposition 3. occurs Post-URI 4. most common childhood systemic vasculitis
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# *Patient in ER p/w new EKG.....* | Fill-in-blank(s)
## Footnote *(USR⼀Upright, Smooth, Rounded)*
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# *Patient in ER p/w new EKG.....* | Fill-in-blank(s)
## Footnote *(USR⼀Upright, Smooth, Rounded)*
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# *Patient in ER p/w new EKG.....* | Fill-in-blank(s)
## Footnote *(USR⼀Upright, Smooth, Rounded)*
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# *Patient in ER p/w new EKG.....* | Fill-in-blank(s)
## Footnote *(USR⼀Upright, Smooth, Rounded)*
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# *Patient in ER p/w new EKG.....* | Fill-in-blank(s)
## Footnote *(USR⼀Upright, Smooth, Rounded)*
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a. What is Kussmaul sign? b. in which conditions do you see it? (4)
a. inspiration ➜ [ ⇪ JVP ( *instead of normal ⬇︎JVP)*] due to impaired RV filling b. -constrictive pericarditis -restrictive cardiomyopathy -RA tumor -RV tumor
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[Pericarditis *(Acute & Chronic)*] clinical features (6)
Ap1. **⭐[EKG: diffuse ST elevation with PR depression]** Ap2. [sharp pain exacerbated by inspiration, alleviated by sitting up/leaning forward] Ap3. friction rub Ap4. {etx: [idiopathic (viral)] > Coxsackie > CA > autoimmune > uremia > [CV (STEMI/Dressler)] > radiation} Ap5. [tx = *A*cute Pericarditis usually self limited --(if persist)--> ASA 650 TID] -------- CP6. {*C*hronic Pericarditis → [*C*alcified fibrous thickening of Pericardium] → [*C*ardiac compromise and decline] = ***C***onstrictivePericarditis]} ## Footnote {⭐differentiate from [***C***onstrictivePericarditis] which has [EKG: low QRS voltage]}
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clinical features of Rheumatic Fever (6)
1.consequence of GASP pharyngeal infection 2.{Rheumatic heart disease affects heart valves (mitral [MVR ➜ MS]) > aortic >\> tricuspid} 3.[Aschoff bodies (granuloma with giant cells)] 4.[⇪ ASO titers] 5.tx and px = PCN 6.[J.❤️.N.E.S] = major criteria ## Footnote [ J.❤️.N.E.S] Joint migratory polyarthritis ❤️ Carditis Nodules subcutaneously in Skin Erythema Marginatum Sydenham chorea 🧠[⇪ ASO titers [Type 2 hypersensitivity {Ab to GASP M -protein cross react with self antigen (molecular mimicry)]]
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[ST Elevations or Q waves] in leads **V1-V2** indicate MI of the ⬜ heart ⼀which is perfused by the ⬜ artery
SeptalAnterior ; pLAD
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[ST Elevations or Q waves] in leads [**1 \ aVL**] indicate MI of the ⬜ heart ⼀which is perfused by the ⬜ artery
LATERAL high ; LCX
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[ST Elevations or Q waves] in leads **[2\ 3\ aVF]** indicate MI of the ⬜ heart ⼀which is perfused by the ⬜ artery
inferior ; RCA
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[ST Elevations or Q waves] in leads **V5-V6** indicate MI of the ⬜ heart ⼀which is perfused by the ⬜ and ⬜ arteries
LATERAL low ; LCX or dLAD
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[ST Elevations or Q waves] in leads **V3-V4** indicate MI of the ⬜ heart ⼀which is perfused by the ⬜ artery
ANTERIOR ; LAD
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# List the congenital cardic defect a/w with ______ a. Fetal Alcohol Syndrome (4) b. Congenital rubella (3) c. Down Syndrome (2) d. Prenatal lithium
A. *FAS* = VSD| ASD| PDA| Tetralogy of Fallot B. *congenital Rubella* = PDA | Septal defects | pulmonary artery stenosis c. *Down Syndrome*= [VSD | ASD ⼀(endocardial cusion defect)] d.*Prenatal lithium* = Ebstein anomaly
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# List the congenital cardic defect a/w with ______ a. a. Turner syndrome (2) b. Williams syndrome c. 22q11 syndromes (2)
a. Bicuspid aortic valve | coarctation of aorta b. Supravalvular Aortic Stenosis c. Truncus arteriosus | Tetralogy of Fallot
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What is Eisenmenger syndrome? (4)
**uncorrected [L to R shunt** (VSD/ASD/PDA)] ➜ [pulmonary HTN 2/2 remodeling] ➜ RVH ➜ reverses {from [L to R] **into** **[R to L] shunt**} = -late cyanosis -clubbing -polycythemia
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What is [persistent truncus arteriosus]?
Truncus arteriosus fails to divide into pulmonary trunk and aorta *2/2 aorticopulmonary septum formation* (usually accompanied with VSD)
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name the local metabolites responsible for *Skeletal Muscle* autoregulation *during exercise* (6)
1. lactate 2. adenosine 3. K+ 4. H+ 5. CO2 6. sympathetic tone (at rest)
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# [**R**RAIB-MC] = systematic approach to EKG *describe* **R**ate
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# [R**R**AIB-MC] = systematic approach to EKG *describe* **R**hythm
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# [RR**A**IB-MC] = systematic approach to EKG *describe* **A**xis
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# [RRA**I**B-MC] = systematic approach to EKG *describe* **I**nterval
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# [RRAI**B**-MC] = systematic approach to EKG *describe* **B**⼀R⼀Q⼀T | |Bundle Branch Block | R | Q | T |
## Footnote |Bundle Branch Block | R | Q | T |*"Be Our CuTie"*
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# [RRAIB-**M**C] = systematic approach to EKG *describe* **M**orphology
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# [RRAIB-M**C**] = systematic approach to EKG *describe* **C**hamber Enlargement
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*For all 12 leads, delineate:* A. Anatomic correlation B. arterial perfusion
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*For all 12 leads, delineate (if present):* Any Exceptions to the rule
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Explain the difference in pathophysiology between aFib and aFlutter
aFlutter = **single** constant reentrant circuit (above AV node ⼀ usually around tricuspid annulus), atrial rate ~ 250-350 bpm ➜ *regular* saw tooth EKG pattern vs \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ aFib = **MULTIPLE** UNPREDICTABLE reentrant circuitS ... inundate AV node which randomly allows impulses to pass ➜ irregularly irregular R-R interval, no P waves, narrow QRS, atrial rate~120-180 bpm
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What effect does carotid massage have on atrial flutter?
INC aFlutter AV Block ## Footnote atrial flutter typically has 2:1 block (2 flutter and 1 QRS), but increasing vagal tone slows AV conduction which ➜ worsens time for flutters to occur before QRS is delivered ➜ 5:1 block
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# *fill-in-Blank (15)*
## Footnote *🔤< RCA/SA node/coronary perfusion/heart >*
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Briefly describe *ion movement* during all 4 phases of SA/AV node action potential