3⼀CARDIOLOGY Flashcards
5
What are the 2 most common cardiac tumors?
_________________
cp? (5)
[metastasis to heart] > [L atrial myxoma (most common 1º cardiac tumor)]
_________________
[“tumor plop”] [diastolic murmur] , HF, afib, [arterial embolization/occlusion]
{[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]
[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}
[(1aAB) - (1bD)]
[2A]
[3S]
{Si} and {Sd}
{[NYHA⬜] with [EF⬜%]} indicates initiation of [6HOT]
describe
[NYHA 1] (4)
[New York Heart Association (HF Class)1]
[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}
{[NYHA⬜] with [EF⬜%]} indicates initiation of [6HOT]
describe
[NYHA 2] (4)
[New York Heart Association (HF Class)2]
[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}
{[NYHA⬜] with [EF⬜%]} indicates initiation of [6HOT]
describe
[NYHA 3] (4)
[New York Heart Association (HF Class)3]
[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}
{[NYHA⬜] with [EF⬜%]} indicates initiation of [6HOT]
describe
[NYHA 4] (4)
[New York Heart Association (HF Class)4]
[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}
{[NYHA⬜] with [EF⬜%]} indicates initiation of [6HOT]
In step wise order, name the parts of [6HOT] -6
[6*part*-HFrEF Optimized Therapy]
[1-4 ; ≤40%]
_________________
[(1aAB) - (1bD)]
[2A]
[3S]
{Si} and {Sd}
What therapies are used to treat [ACS ⼀NSTEMI]? -10
Pts with ACS {Really Always Need OBAMA}!
- Reperfusioncoronary angiography within 24H
- [AAA blood thinners (ASA/ADP P2Y12 R Blocker/Anticoag (Heparin)]
- NTG = VasoDilates Veins and Coronary Arteries (C❌D in R VT MI)
- Oxygen = Minimizes ischemia
- Beta Blockers = DEC HR –> DEC Arrhythmia risk and DEC O2 demand (C❌D in acute HF)
- [ACEk2 inhibitors within 24 hrs] = DEC [L Ventricle Dilation/Remodeling]
- Morphine = pain
- AtorvaSTATIN - comes later
ASA and Beta blockers can –> asthma exacerbation
Of the 10 therapies for ACS, which is contraindicated in RIGHT Ventricular MI?
Nitrates
(venoDilates → DEC preload(not good for preload dependent RV MI) & worsens hypOtension)
_________________
Pts with ACS { Really Always Need OBAMA }!
Of the 10 therapies for ACS, which [ACS therapy] is contraindicated when acute HF is superimposed?
BETA🟥
do NOT use β🟥 if [ACS c/b _acut_e HF]
Pts with ACS { Really Always Need OBAMA }!
What therapies are used to treat [ACS⼀STEMI] ?-10
Pts with ACS {Really Always Need OBAMA}!
- ReperfusionR4 criteria
- [AAA blood thinners (ASA/ADP P2Y12 R Blocker/Anticoag (Heparin)]
- NTG = VasoDilates Veins and Coronary Arteries (CTD in R VT MI)
- Oxygen = Minimizes ischemia
- Beta Blockers = DEC HR –> DEC Arrhythmia risk and DEC O2 demand (CTD in acute HF)
- [ACEk2 inhibitors within 24 hrs] = DEC [L Ventricle Dilation/Remodeling]
- Morphine = pain
- AtorvaSTATIN - comes later
ASA and Beta blockers can –> asthma exacerbation
What therapies are used to treat [ACS⼀unstable angina]?-10
Pts with ACS{Really Always Need OBAMA}!
- Reperfusioncoronary angiography within 24H
- [AAA blood thinners (ASA/ADP P2Y12 R Blocker/Anticoag (Heparin)]
- NTG = VasoDilates Veins and Coronary Arteries (CTD in R VT MI)
- Oxygen = Minimizes ischemia
- Beta Blockers = DEC HR –> DEC Arrhythmia risk and DEC O2 demand (CTD in acute HF)
- [ACEk2 inhibitors within 24 hrs] = DEC [L Ventricle Dilation/Remodeling]
- Morphine = pain
- AtorvaSTATIN - comes later
ASA and Beta blockers can –> asthma exacerbation
When is Angina classified as Unstable -4
Aua
FREN [chest pain Occurrence] is UNSTABLE!
- [Freq ( cpO ⇪ in Frequency)]
- [Rest (cpO at rest)]
- [Exertion (cpO w low exertion)]
- [New (cpO is new)]
Aua: [ACS ⼀Unstable angina]
DDx for T-wave inversion - 6
“T wave Inverts my MUNDO, smh”
[Myocardial❌HYPERTROPHY|contusion|inflammation]
[Unstable Angina⼀ACS]
[NSTEMI⼀ACS]
[Digoxin OD]
[Old💔(Old Pericarditis/[Old MI⼀especially if ⊕Q waves])]
What is Cardiac Syndrome X
________________
Lab findings?-3
[Exertional stable angina-like] cp usually in Women
- Normal coronary angiogram
- Normal EKG
- Abnormal Exercise Stress test
Based on the 3 characteristics of Angina [which are (⬜3)] , when is Angina:
TYPICAL?
________________
Atypical?
________________
NonAngina?
“Diagnose Angina cp using the [Angina PEN] “
[Pressure substernally >20m]
[Exertional]
[NTG or Rest relieves]
________________
[3/3 = TYPICAL] [2/3= Atypical | [0-1 = NonAngina]
Tx for Stable Angina -6
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]
RanOlazine
MOA
_________________
Indication
inhibits late-phase Na+ influx –> ⬇︎myocardial Ca+ influx –> [⬇︎myocardial wall tension] → [ ⇪ Coronary a blood flow] = treats Stable Angina
Stable Angina 2/2 Atherosclerotic CAD
In patients c/f ACS, describe the minimal workup required if initial troponin/initial EKG are unremarkable ? (2)
[(troponin q6h) x 3] + [(EKG q30 min) x 3]
“1st TENA *2nd [“Really Always Needs OBAMA”]
What is the greatest risk factor for coronary stent thrombosis after cornary stent is placed?
_________________
describe this risk factor (2)
[noncompliance with postsurgical DAPT]
_________________
[low dose ASA]
+
[ADP P2Y platelet R blocker (Clopidogrel,Prasugrel,Ticagrelor)]
_________________
DAPT = DualAntiPlatelet Threapy
pts with underlying connective tissue disease are at ⇪ risk for what sudden heart complication?
________________
Describe the clinical presentation -5
[Chordae Tendineae rupture]
→ [acute MR( sx = Pulm edema, hypOtension, hyperdynamic❤️ +/- holosystolic murmur)]
🔎MR = Mitral Regurgitation
Brugada Syndrome
MOD
________________
tx -2
[AUTO DOM Na+ Channelopathy] ➜ [SUDDEN SLEEP DEATH OR SYNCOPE]
________________
ICD vs Quinidine
[Brugada-Pokkuri-SUNDS]AKA
Describe the approach to Cardiac arrest -10
what is the purpose of the [Upright Tilt Table Test]?
differentiates unclear Syncope into
{[VANS] vs. [Dysautonomia] vs. [Postural Orthostatic⼀Tachycardia Syncope]}
On EKG, What constitutes as [PROLONG QT interval] in
peds
________________
Male
________________
FeMale
males > 450
________________
Peds > 460
________________
FEMALES > 470
________________
(ms)
[peds = 1-15 yo]
pathologic Q waves on EKG are a sign of what?
prior MI
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
describe the algorithm used to determine if a [nonvalvular afib] patient needs [oral anticoagulation] for stroke px
💡oral anticoag = warfarin / dabigatrin / rivaroXaban / apiXaban
Which parts of the heart does the [R Coronary artery] perfuse? -3
➜ SA node
[➜ R marginal a ➜ RV]
➜ [PDA (in 70% popln)]
[L Main Coronary] branches into [LAD] and [LCX]
What does the [LCX] perfuse? (2)
➜ LATERAL LV
➜ [PDA (in 10% of popln)]
[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
✏️ IVP=
Interventricular septum/
Vt Free Wall/
Papillary muscle
Name 3 major complications of acute inferior wall MI?
_________________
management?- 3
AaS
- [RVMI](= Preload dependent = no Nitrate/no Diuretic/no Opioid):Tx = {IVF-nitrates}
- [AV Block]
- [Sinus Bradycardia]Tx = {Atropine IV}
severe = unresponsive/hypOtension/dizziness/HF/syncope
_________________
💊[P⼀harm[(IVF-nitrates)+AtropineIV]]
💊💊–(if severe)–> [P⼀acetransQ|V]
💊💊💊→ [P⼀erfuse_PCI revascularization]
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
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]
Name the manifestations of [Infective Endocarditis ] -8
IE
(8)
“Bacteria FROM JANE”
Fever
[Retinal Roth Spots - Immunologic phenomena]
[Osler “Ouch” Nodes- Immunologic phenomena]
[Mumur that’s new]
[Janeway’s purplish nonpainful lesions of the palms&sole]
Anemia
[Nailbed Subungal Splinter Hemorrhages]
[Emboli from valvular (T>A>M) vegetations] ;
___________________________x____________________________________
“Enterococcus⼀[STAph A], [STAph E]⼀[strEP B] [strEP V] ⼀[and nonbacterialmaranti(C)with its misc (C)] ..” causes [mitral>tricuspid*]IE … FROM JANE”.
In [“SBIE-Risk”-Settings], Pts [with ⬜] have ⇪ risk of developing [SBIE] = these Pts require [⬜] prior to engaging [SBIE-Risk-Settings]}
________________</sup>
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<sup>*(involving gingiva or oral mucosa)*</sup>]
d. dental cleaning
e. [respiratory tract procedure<sup>*involving incision or biopsy of mucosa*</sup>]
f. surgical placement of prosthetic cardiac material
| < *<sub>pts</sub>HRC must receive [SAP] prior to any [SRS]* >
## Footnote
*🔎HRC = High Risk Cardiac*
*🔎SAP = [SBIE abx px]}
*🔎SRS = [SBIE-Risk-Setting]*
<sub>*"Enterococcus⼀[STAph **A**], [STAph **E**]⼀[strEP **B**] [strEP **V**]* ⼀[<sup>*and nonbacterial*</sup>*maranti(C)*<sup>*with its misc (C)*</sup>] ..<sup>" causes <sup>[mitral>tricuspid\*]</sup>IE ... *FROM JANE"*</sup>.</sub>
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
List ALL the causes of Cardiac Syncope? (6)
- Aortic Stenosis
- HOCM
- VTach
- [Torsades de pointes (look for ⬇︎K, ⬇︎Mg or ⇪ QT)]
- Sick Sinus Syndrome
- AV Block
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)]
b. MAT etx: (PES) ➜ </sup>:random firing of multiple ectopic foci in the atria ➜ [3 DIFFERENT P-wave MORPHOLOGIESwith irregularly irregular R-R + (rate ≥100bpm)].
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)]
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
What are the 10 reversible causes of PEA (Pulseless Electrical Activity)?
CVC = {[C.O.D.E.] ➜ [VV.A.P.]} ➜ [C=A=R]
Describe Approach to [Adult Cardiac Arrest] if pt has
Asystole
[CVC⼀ACLS]
START CHEST COMPRESSIONS!
“C - V - C”
CVC③ =
1)[C.O.D.E.] ➜
2)[V.(A).P.]
3)➜ [C=A=R]
Describe Approach to [Adult Cardiac Arrest] if pt has
PEA
[CVC⼀ACLS]
START CHEST COMPRESSIONS!
“C - V - C”
CVC③ =
1){[C.O.D.E.] ➜
2)[V.A.(P).]
3)➜ [C=A=R]
Describe Approach to [Adult Cardiac Arrest] if pt is in
VFib
[⚡CVC⼀ACLS]*
START CHEST COMPRESSIONS!
“{shock} C - V- C”
* ⚡CVC④⼀“{shock} C - V- C” =
1) [C.O.D.E.] →
2) {[⊕(V) A.P.] =
–give–>3) {⊕[(V)oltage_SH⚡CK_Debrillation]}
4) → [C=A=R]
Describe Approach to [Adult Cardiac Arrest] if pt is in
pulseless VTach
[⚡CVC⼀ACLS]*
START CHEST COMPRESSIONS!
“{shock} C - V- C”
* ⚡CVC④⼀“{shock} C - V- C” =
1) [C.O.D.E.] →
2) {[⊕(V) A.P.] =
–give–>3) {⊕[(V)oltage_SH⚡CK_Debrillation]}
4) → [C=A=R]
In a MVA, what is the most common cause of death associated with steering wheel injury?
AORTIC INJURY
secondary to rapid deceleration with shearing along the aortic arch
What are the main features of [Takotsubo stress induced cardiomyopathy] -4
[ABCQ “Takotsubo”]
1. [stressor(s) ➜ catecholamine surge ➜
ANT MI presentation]
+
2. [Balloon❤️LV wall motion ∆]
2/2
3. [Coronary spasms transiently (withOUT coronary occlusion on Cath!)]
and
4. [QT prolongation]
🔎[Balloon❤️ =Echo[(apical hypOkinesis) + (BASILAR HYPERkinesis)]
tx for [acute-chest-syndrome] -3
a-c-s
[azithromycin (mycoplasma pna)]
[ceftriaxone (strep pneumo)]
[saline IVF w analgesia]
Patient is diagnosed with HOCM
⬜ (or ⬜ alternatively) both treat HOCM
________________
Describe how they treat HOCM?
beta blockers > ([VerapamilNCCB]
________________
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
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
[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%)
How are Major Depression and the Cardiovascular system related? (2)
- [Major Depressive Disorder] = independent risk factor for [⇪ morbidity and mortality] from CV disease .
- CVD = [independent risk factor for developing MDD]
Treat with SSRI
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
Which Calcium Channel Blockers are a/w peripheral edema?
Name them -2
________________
Tx for this?
dihydropyridine-CCB
[Amlodipine | Nifedipine]
________________
ACEK2 inhibitors
Prolonged Amiodarone tx can ➜ [FATAL ⬜ DISEASE]
________________
how do you manage this if it occurs? -2
PULMONARY
________________
[DC amiodarone] ➜ [CTS if severe/life threatening]
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]} =
☞ 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]
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
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
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)]
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!
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
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
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!
- [Lorazepam_ benzo (HR/BP/psych control)]IV
- [Opioid🟢_Morphine]IV
- [Amlodipine_dCCB]
- [NTGIV]
–(if persist)–→
- → [alpha1🟥_Phentolamine (if Persistent)]
- ➜ ➜ PCI (for coronary revascularization if sx still not alleviated)
Describe the complication IVC filters pose
ironically, although [IVC filters] [⬇︎PE risk x 2], it actually [⇪DVT RISK x 2]
List the 4 primary EKG changes for Hyperkalemia
_________________
how do you treat Hyperkalemia? (4)
- tall (T)
- Loss of (P)
- [Wide/sinusoidal QRS]
- (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
[biventricular pacing device] is indicated for patients with what 3 clinical criteria ?
Patients with all 3:
- SINUS RHYTHM
+
- [symptomatic HF EF<35%]
- [LBBB with QRS>150]
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]
Why are Benzodiazepines given early for Cocaine-chest pain ? -3
{“with Cocaine [Lorazepam_Benzo] targets [Psych / Pressure / Pain”]}
1.[Psych:⬇︎Psychomotor agitation]
2.[Pressure:⬇︎sympathetic NS →⬇︎HTN]
3.[Pain:⬇︎myoscardial ischemia]
Cocaine ODtx = [LOAN-aP]
⚠but do NOT give β🟥 (MAY ➜ UNOPPOSED ALPHA 1 ACTIVATION)
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]
Imaging modalities for Aortic Dissection-3
- [TEE- unstable or renal CXD]
- [Chest Spiral CT Angio]- Stable vitals]
- [MRI-NonEmergency]
TEE is great because it’s used in renal pts
What are the sx of Aortic Dissection (5)
- [SEVERE SHARP TEARING (CHEST⼀TAAAD) OR (BACK⼀tBDAD) PAIN]
- [BUE SBP discrepancy > 20 mmHg]
- [Aortic Regurgitation ➜ [pericardial effusion/tamponade/Hemothorax]
- [LE paraplegia (⼀spinal a)]
- [Horner’s MAP (⼀carotid sympathetic plexus)]
* biggest RF = HTN*
- TAAAD = [Type A Ascending Aorta Dissection] || tBDAD = [Type B Descending Aorta Dissection]*
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]
_________________
- LOUD S1
- [mid-diastolic rumble @ apex]
- DYSPENA
- orthopnea
- paroxysmal nocturnal dyspnea
- hemoptysis
Describe the 2 methods for determining Heart Rate on EKG
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 ∆
diagnosis?
Acute pericarditis
diffuse ST elevations with PR depression
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
EKG findings for [ACS⼀NSTEMI] (2)
- ST Depressions
- T Wave inversions
EKG findings for Aua (2)
🔤 Aua = [ACS⼀unstable angina]
- ST Depressions
- T Wave inversions
same EKG as AanS = [ACS⼀acute nSTEMMI]
Pts with [ACS⼀acute STEMI] {Really Always Need OBAMA}!
How do you determine [Reperfusion coronary revascularization]? (4)
AaS
[ACS acute STEMI] R4 criteria
- R0: Revascularize only if [SX ≤ 12h]
- R1: [iHP = PCI ≤90 min eDB]
- R2: [OHP ≤120m eDB TFR] = [PCI ≤120 min eDB]
- R3: [OHP >120m eDB TFR] = [ART-tPA fibrinolysiswithin 30m]
- iH/OHP: in/OUT HousePCI Institute*
- TFR: Transfer*
- eDB: estimated Door→Balloon*
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]
Diagnostic EKG criteria for
RBBB (2)
< V1 [R1º (second R wave)] >
_________with________
< V6 [Fat (widened) S wave] >
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
Which 3 drug groups are a/w Orthostatic hypOtension?
DAN is always droppin’ orthostatic
• Diuretics
• Alpha R blocker
• Nitrates
⬜ is the most common congenital heart disease in patients with Down syndrome
[Septal endocardial cushion defect]
{[SHEEPPS]traits & [SHALA Has Down Syndrome]conditions}
Athletes in intense training can develop nonpathologic 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
What is Sudden Cardiac Death? (2)
- [fatal Vt Arrhythmia triggered by intense exertion io\ [structural heart❌(HOCM, coronary a anomalous origin)] > [conduction❌(long QT, Brugada-Pokkuri)]
- leading COD age < 35
Describe Pulsus Paradoxus
[Systolic BP] ⬇︎more than 10 during inspiration
“Pulsus for CAPOT”
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
Malignant HTN Emergency = [Hypertensive Urgency (BP>180/120)] PLUS Papilledema/Retinal Hemorrhages
What is the normal range for Mean Arterial Pressure (MAP)?
________________
Formula?
65-110
________________
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]
In Afib pt, when can you NO LONGER cardiovert?
> 2 Days after onset
List the 4 treatment options for [HDS aFib]
MA * VZ * A * D
1st: {BB: [Metoprolol10 mg start] | | [Atenolol] - rCTD IN HF or hypOtension}
2nd: {NCCB: [Verapamil] | [diltiaZem([0.25 mg/kg bolus] → [0.35 mg/kg DRIP])]) -rCTD IN HF or hypOtension]
3rd: [Amiodarone+ Cardio consult]
4th: [Digoxin+ Cardio consult]
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]
Aortic Dissection
treatment? (4)
- Surgery for TAAAD
- [Esmolol β🟥]IV
- Nitroprusside IV(if SBP >120)
- Pain
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
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
Name 3 Lifestyle regimens to ⬇︎CVD in Obese patients
Exercise | Mediterranean diet | DASH diet
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]
_________________
Bradyarrhythmia (sinus brady, AV block)
“[HIS BEDS] gave me arrhythmia”
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
A patient with aFib has failed rate control
What are the 2 anti-arrhythmic options for afib patients with…
CAD (no HF)?
- Sotalol[3]
- Dronedarone[3]
A patient with aFib has failed rate control
What are the 2 anti-arrhythmic options for afib patients with…
LVH?
- Dronedarone[3]
- Amiodarone[3]
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]?
- Flecainide[1C]
- Propafenone[1C]
A patient with aFib has failed rate control
What are the 2 anti-arrhythmic options for afib patients with…
HF?
- Amiodarone[3]
- doFetilide[3]
pt presents 3 days s/p acute MI with this EKG
Tx? (2)
self limited –(if persist)–> [ASA650 TID]
[acute pericarditis]
(NO NSAIDs or CTS as these impair myocardial healing and ➜ vt rupture)
_________________
Dx?
Acute Pericarditis
_________________
can → calcified+fibrous → cardiac decline = Constrictive pericardiits
diffuse PR depression + diffuse ST elevation
What are the 3 indications for Statin therapy?
“give that LAD a StatinM/H!”
- [LDL ≥190]
- [ASCVD10y > 7.5-10%]
- [DM ≥40 year old]
___________________
ASCVD10y = AtheroSclerotic CVD 10 year estimated risk | StatinM/H = Moderate/HIGH Intensity
Why are HOCM pts at greater risk for developing ⬜ or ⬜ tachyarrhythmia ?
_________________
how are each caused?
how are each managed?
- afib (L Vt hypertrophy ➜ LAE ➜ afib) = [EKGamb ➜ [antiCoag + rate/rhythm control]
-
VT (L Vt ischemia and fibrosis ➜ Vtach –(if sustained)–>SCD (most common COD for HOCM) = [EKGamb ➜ ICD]
* * *
[AMBULATORY EKG (24H Holter)] to diagnose both
What 3 Coronary Heart Disease risk factors are the most significant predictors of poor CV outcomes?
- [noncoronary Atherosclerosis (PAD, Carotid, AAA)]
- CKD
- [DM (note: strict glycemic control only ⬇︎ microvascular complication)]
these factors are AKA “CHD equivalents” = carries same risk to of damaging CV health … as having CHD itself
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?
- NYHF4
- refractory angina
- arrhythmias
- valvular disease
_________________
[low = sex ≥1 wk post ✔︎CRV] || [HIGH = requires assessment before sex]
What are the major effects of radiation to the heart? (5)
- Restrictive cardiomyopathy with diastolic dysfxn
- constrictive pericarditis
- valve damage
- conduction damage
- MI
fill-in-blank
diagnosis?
_________________
tx? (4)
mmVT
_________________
[SLAPpharm cardioversion]
-mmVT = monomorphic VT
-SLAP = Sotalol3 |Lidocaine1B |Amiodarone3|Procainamide1A
diagnosis?
_________________
tx?-2
[PMVT Torsades de Pointes]
_________________
1.{[MgSO4IV]pharm cardioversion}
2.{–(if persist)–>[Temporary transVenous pacing]}
PMVT = POLYMORPHIC VT
diagnosis?
_________________
tx? (4)
mmVT
_________________
[SLAPpharm cardioversion]
-mmVT = monomorphic VT
-SLAP = Sotalol3 |Lidocaine1B |Amiodarone3|Procainamide1A
diagnosis?
_________________
tx? (2)
[atrial Tachycardia (looks like aflutter THAT’S MISSING SAWTOOTH PATTERN) ]
_________________
BB|nCCB rate control
-[BB=Beta Blocker] / [NCCB=nonDihydropyridine Calcium Channel Blocker (Verapamil|Diltiazem)]
diagnosis?
_________________
tx? (3)
[AVNRT]PSVT
_________________
stable: -vagal maneuevers
stable: -adenosine
⚠️unstable: DC Cardioverson
[AVnRT = AtrioVentricular (nodal) Reentrant Tachycardia]
diagnosis?
_________________
tx? (2)
[atrial flutter (look for sawtooth pattern) ]
_________________
BB|nCCB rate control
-[BB=Beta Blocker] / [nCCB=NonDihydropyridine Calcium Channel Blocker (Verapamil|Diltiazem)]
diagnosis?
[AVRT orthodromicretrograde P wave SVT]
Look for [retrograde P waves]!
diagnosis?
_________________
tx? (4)
[atrial fibrillation]
_________________
[MA * VZ * A * D]rate control
[irregular R⼀R] / [no P wave] / [narrow QRS]
[MA * VZ * A * D]rate control
(M|A)*
(V|Z) *
A *
D
diagnosis?
_________________
tx?
[⚡mmVTpulseless]
_________________
[⚡CVC⼀ACLS]START CHEST COMPRESSIONS!
-mmVT = monomorphic VT
-⚡CVC = CODE| V⚡AP| C=A=R
(⚡= give [Voltage Defibrillation SHOCK])
diagnosis?
_________________
tx?
[⚡VF]
_________________
[⚡CVC⼀ACLS]START CHEST COMPRESSIONS!
-VF: Ventricular Fibrillation
_________________
⚡CVC : CODE| VAP| (C=A=R)]
-{VF = [⚡CVC⼀ACLS] tx–regardless of pulse}
diagnosis?
_________________
tx?
[⚡VF]
_________________
[⚡CVC⼀ACLS]START CHEST COMPRESSIONS!
-VF: Ventricular Fibrillation
_________________
-[*⚡CVC : CODE| VAP| (C=A=R)]
-{VF = [⚡CVC⼀ACLS] tx–regardless of pulse}
diagnosis?
[ACS ⼀STEMI](anterolateral)
Erectile Dysfunction in the setting of still having [nonsexual nocturnal erections] suggest what etiology?
psychogenic etx
(Do Detailed Psychological assessment/counseling)
Physical Exam findings for Aortic Stenosis-3
- {[Crescendo Decrescendo Systolic murmur w/delayed carotid pulse @ R 2nd ICS]}
- [Pulsus Parvus et Tardus(delayed carotid pulse)]
- [S4(from LV hypertrophy)]
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 Ass, that’ll turn it up!”
B: INC with…
- Leaning Forward
2) Squatting
C: DEC with…handgrip (INC afterload)
Which Murmur?
(Auscultation Site is attached)
Mitral Valve Prolapse
[MidSystolic NON-Ejection Click + Late Systolic Crescendo Murmur]
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)
Which Murmur?
(Auscultation Site is attached)
Hypertrophic Cardiomyopathy
[Holosystolic Harsh Blowing Murmur + palpable thrill] @ [L Sternal 2/3 ICS]
Which Murmur?
(Auscultation Site is attached)
Ventricular Septal Defect
[Holosystolic Harsh Blowing Murmur + palpable thrill] @ [tricuspid area]
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)
hypOnatremia sx (confusion, seizure) | [Tolvaptan (Vasopressin-2 ADH R blocker)]
Oral Salt tablets are used to treat hypOnatremia in [⬜ CHF exacerbation | SIADH]
SIADH
_________________
NEVER give Oral salt tablets to edematous/volume overload CHFE
MOA for how Beta Blockers work on the heart? (2)
inhibition of B1 R ➜ [⬇︎intracellular cAMP] in…
▶[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
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?
- IVF (if hypOtension)
- atropine (symptomatic bradycardia)
- 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
1st line treatment for Calcium channel blocker toxicity
Calcium gluconate
_________________
INC intracellular Ca+ ➜ restores arterial smooth m tone and cardiac contractility
[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]
On an EKG
1 LARGE box =
⬜mm (← ⇪)
= ⬜ms (← →)
= ⬜mV (⇪ ⬇︎)
5;
200;
0.5
On an EKG
1 small box =
= ⬜mm (← ⇪)
⬜ms (← →)
= ⬜mV (⇪ ⬇︎)
1;
40;
0.1
On EKG,
How does Potassium affect the P-wave? (2)
“K [(lifts up the 🆃), (sits on the 🄿),(widens 1st interval Q) & (suppresses the 🅄]”
= [⇪ K] ➜ [widening & flattening of P] ➜ [No P]
On EKG,
How does Potassium affect the T-wave? (2)
“K [(lifts up the 🆃), (sits on the 🄿),(widens 1st interval Q) & (suppresses the 🅄]”
=
([⇪ K] ➜ [peaked T]) or
([⬇︎ K] ➜ [flat T])
On EKG,
How does Potassium affect the [QRS interval]? (4)
“K [(lifts up the 🆃), (sits on the 🄿),(widens 1st interval Q) & (suppresses the 🅄]”
=
([⇪ K] ➜ [wide QRS])
([⇪⇪ K] ➜ [very wide QRS])
([⇪⇪⇪ K] ➜ [sinusoidal vs Torsades QRS])
On EKG,
How does Potassium affect the [U wave]? (2)
“K [(lifts up the 🆃), (sits on the 🄿),(widens 1st interval Q) & (suppresses the 🅄]”
=
([⬇︎ K] ➜ [visible U])
([⬇︎⬇︎ K] ➜ [prominent U])
MOD of
Wolff Parkinson White syndrome (5)
🔎AAS = [AVRT AntiDROMIC(delta wave) SVT]
🔎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]
Diagnosis?
[Wolff Parkinson White]
🔎BKAP ⼀Bundle of Kent accessory pathway
Patients with WPW are at risk of sudden cardiac death
▨ Explain Why
_________________
◮ How do you ultimately treat WPW?
◮[BKAP ABLATIONvia Catheter] Obliterates accessory pathway
🔎AAS = [AVRT AntiDROMIC(delta wave) SVT]
🔎BKAP ⼀Bundle of Kent accessory pathway
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 <– [(0-1pt (LR≤1%)|Revised Cardiac Risk Index|(≥2pt (HR>1%)|] –> [DELAY❌SURGERY(unless can concomitantly perform ≥4METS)]}
✔︎ Pts {[≥2pt (HR>1%)] but can perform ≥4 METs} = DO✅SURGERY also
- [Revised Cardiac Risk Index] has 6 scoring variables, each 1 pt*
- *Delay❌Surgery= to assess cardiac functional capacity*
- METs = Metabolic Equivalent*
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]
_________________
- Echo: IVC plethora
- EKG: electrical alternans
- EKG: low voltage QRS
- CXR: enlarged cardiac silhouette
- CXR: clear lungs with HF-like sx
Cardiac Tamponade
Treatment (2)
- IVF( ⇪ R Heart preload)
- Drainage(via pericardiocentesis or pericardial window)
Cardiac Tamponade
Clinical Signs (2)
- [Beck’s triad (hypOtension, JVD, muffled heart sounds)]
- [Pulsus Paradoxus(SBP ⬇︎> 10 during inspiration)]
Identify each number in this ⬜ tracing
Jugular Venous Tracing
- [atrial on RIGHT contracts⼀RA contracts]
- [contraction of RV ➜ tricuspid bulge ⼀ RV contracts]
- [relaxation of RA ⼀RA relaxes]
- [ venous blood fills RA ⼀RA fills]
- [ emptying of RA passively after tricuspid valve opens ⼀RA emptys]
In a Jugular venous tracing, a large v wave is seen in patients with ⬜
severe Tricuspid Regurgitation
- [atrial on RIGHT contracts⼀RA contracts]
- [{closure (& bulge) of tricuspid}⼀ *2/2 RV contracts -> tricuspid closure/bulge]
- [relaxation of RA ⼀RA relaxes and subsequently fills with {venous IVC blood}]
- [{ venous IVC blood cont to fill RA}]
- [ emptying (passively) of RA into RV)]
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
Aortic Coarctation Sx (6)
- UE HTN
- LE hypOtension
- LE weak and delayed distal pulses
- LE claudication
- [CXR: “3” sign from aortic narrowing + rib notching from collateral vessels] -dx confirmed by echo
- [+/- murmur (if [PDA-continuous] or [L sternal -turbulent flow] present)]
Which HOCM patients require [ICD⼀PRIMARY SCD px] ? (5)
Sudden Cardiac Death
- SCD fam hx
- Syncope
- [holter nonSustained VT]
- exertional hypOtension
- [LVH > 3 cm]
Which HOCM patients require [ICD⼀secondary SCD px] ? (2)
Sudden Cardiac Death
- survivor of cardiac arrest
- [holter Sustained ventricular arrhythmias]
Pt p/w sx suspicious for Stable coronary artery disease
How do you work them up?
Stable CAD management = stabLE = statin, [tighten Lifestyle(BP/Glucose/no smoking]), aSA, [bBlocker>ccb + ACEK2i],[Lab_for_coronary angio revascularization in high risk/false neg], [Exercise stress = dx unless ⊕baseline EKG❌ → Pharmacologic stress imaging]
HIGH RISK= ST depression at min exertion, Vt arrhythmia, poor exericse capacity
[ConstrictivePericarditis]
Causes (6)
- Surgerycardiac
- idiopathic
- TB
- viralCoxsackie
- radiation
- other[Uremia/CA/MI_Dressler]
“Surgeons are viral idiots to constrict my TV, radio and More”
[ConstrictivePericarditis]
clinical features (8)
- Fatigue / DOE
- R HF [Peripheral edema/ascites/INC JVP]
- Early diastole Pericardial knock
- [JVD with ⊕Kussmaul (paradoxic INC JVP with inspiration)]
- Prominent y descent
- CXR pericardial calcifications
- TTE: biatrial enlargement with nml Vt wall
- EKG: low voltage QRS
- {[acute pericarditis] {Can → [Calcified fibrous thickening of Pericardium] → [Cardiac compromise with decline] = ConstrictivePericarditis]}
Tx = {[anti-inflammatory Rx]–(refractory)–>[pericardiectomy]}
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)
Name the 8 types of SVT
- [AVNRT]PSVT
- [AOS]*
- Sinus Tachycardia SVT
- [atrial tachycardia SVT]
- [atrial Flutter SVT]
- [aFib SVT]⚠️irregular
- [AAS] * <sup⚠️WIDE</sup>
- [aberrant SVT]⚠️WIDE
SVT are typically Regular and Narrow unless ⚠️
*
AOS: [AVRT ORTHOdromicretrOgrade P wave SVT]
AAS: [AVRT AntidromicdeltA wave SVT]
During initial tx and dx:
For
[✅HDSSVT⼀unidentified] pts [⬜ or vagal maneuvers] are given 1st
vs.
For
[❌HDUSSVT⼀unidentified] pts ⬜ is given 1st
_________________
HDUS = hypOtension, AMS
(AdenosineIV)
_________________
[synchronized DC cardioversion]
Why do we 1st give [⬜ and/or vagal maneuvers] to HDSSVT pts? (2)
_________________
HDUS = hypOtension, AMS
[AdenosineIV and/or vagal maneuvers]:
- Dx: temporarily slows AV node conduction and unmask “hidden” P waves on EKG for dx.
- Tx: also causes transient AV nodal block → terminates AV node-dependent arrhythmias (i.e. [AVNRT]PSVT and [AOS-AVRT orthodromic SVT])
Which conditions causes a [FIXED Widened S2 Splitting]?
Atrial Septic Defect
What makes up the Femoral Triangle (3)
- [Inguinal Ligament Superiorly]
- Sartorius M. Laterally
- [ADDuctor Longus M. Medially]
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
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
- Give [ASA + ADP P2Y12 R Blocker]alt: ( vs ASA vs Warfarin)
(unless)
2.#2nd stroke → Warfarin⚠️
3.⊕aFib present → Warfarin⚠️|NOAC
BALTIC
⚠️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
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
🔎AAS = [AVRT AntiDROMIC(delta wave) SVT]
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
Explain why Standing [⬜ INC | DEC] HOCM murmur
INC
Explain why Squatting [⬜ INC | DEC] HOCM murmur
DEC
diagnosis?
Prior MI
_________________
II/III/avF: contiguous TWI and Q waves are representative of previous MI
“T wave Inverts my MUNDO, smh”
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]
ACE inhibitor/ARB
Beta blocker
[Cholesterol lowering HIGH INTENSITY STATIN]
[Dual anti-Platelet(ASA + ADP P2Y12 R Blocker)]
Describe the preop cardiac evaluation for noncardiac nonemergency surgery
✔︎ {DO✅SURGERY <– [(0-1pt (LR≤1%)|Revised Cardiac Risk Index|(≥2pt (HR>1%)|] –> DELAY❌SURGERY}
✔︎ Pts {[≥2pt (HR>1%)] but can perform ≥4 METs} = DO✅SURGERY also
_________________
a. diagnostic criteria for [Severe Aortic Stenosis] (3)
* * *
b. Indications for Aortic Valve Replacement (4)
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)]
Describe the Pre-operation management for aFib
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”
Patient is diagnosed with HOCM
what would an [Implantable Cardioverter-defibrillator] be used to prevent in HOCM pts?
________________
diagnostic criteria? -2
Sudden Cardiac Death
________________
[SxHOCM]
+
[≥1 SCD (1º vs 2º px) risk factor]*
SCD (1º vs 2º px) risk factors:
1º : SCD fhx/ syncope/ holter VT/ exertional hypOtension/LVH
2º: cardiac arrest survivor, sustained VT
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
Infective Endocarditis
Name the 6 causes of IE
“Enterococcus⼀[STAph A], [STAph E]⼀[strEP B] [strEP V] ⼀[and nonbacterialmaranti(C)with its misc (C)] ..” causes [mitral>tricuspid*]IE … FROM JANE”.
_______________________________________________________
- [Enterococcus= 💊amp-gent]
_________________ - [STAph Aureus#ACUTE⼀HIGH virulence➜RAPID+LARGE on NML Valves = 💊Vanc]
- [STAph Epidermidis#prosthetic valves= 💊Vanc]
_________________ - [strEP Bovis #present in colon CA]
- [strEP Viridans #subACUTE⼀low virulence➜ gradual+small on dz valves #dental = 💊[cefTriaxone|aPG]]
_________________ - [maranti(C)(misC (C)auses:(C)A|(C)lotting/SLE) *nonbacterial vegetations*]
(aPG = aqueous Pencillin G IV)
✏️tricuspidSBIE is a/w IVDU
Infective Endocarditis
[(If present)List💊 tx for each cause of IE
“Enterococcus⼀[STAph A], [STAph E]⼀[strEP B] [strEP V] ⼀[and nonbacterialmaranti(C)with its misc (C)] ..” causes [mitral>tricuspid*]IE … FROM JANE”.
_______________________________________________________
- [Enterococcus= 💊amp-gent]
_________________ - [STAph Aureus#ACUTE⼀HIGH virulence➜RAPID+LARGE on NML Valves = 💊Vanc]
- [STAph Epidermidis#prosthetic valves= 💊Vanc]
_________________ - [strEP Bovis #present in colon CA]
- [strEP Viridans #subACUTE⼀low virulence➜ gradual+small on dz valves #dental = 💊[cefTriaxone|aPG]]
_________________ - [maranti(C)(misC (C)auses:(C)A|(C)lotting/SLE) *nonbacterial vegetations*]
(aPG = aqueous Pencillin G IV)
✏️tricuspidIE is a/w IVDU
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
- [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
[1st degree AV block] Tx
observation
describe [1st degree AV block] EKG
[PR prolonged > [1 LOX (200 ms)]
________________
LOX = LARGE bOX
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 = [(NarrowQRS Clusters) with (“Wenke” PR intervals)] until ➜ Random Beat Drop
QRS is Narrow
“Wenke = gets longer and longer
[2nd degree AV Block: Mobitz Type 2]
Describe where block is, EKG-3 findings and describe QRS-2
Bundle of His
_________________
[(wide vs narrowQRS clusters)
+(constant PR)]
➜ [RANDOM QRS Drop]
_________________
(wide vs narrowQRS groups
[2nd degree AV Block: Mobitz Type 2] (“2 and 2”)
[2nd degree AV Block: Mobitz Type 2]
tx
Pacemaker
[NONtraumatic lens dislocation] indicates further evaluation for _____?
Why?
Marfan Syndrome (AUTO DOM)
[Aortic Dissection] r/o
how do you differentiate Marfan Syndrome from Homocystinuria ? - 2
1.Homocystinuria = auto recessive / Marfan = AUTO DOM
2.Homocystinuria = [TALL Marfan Sx] [+ DVT] [- intelligence]
Describe capillary refill for the 3 phases of [Acute Limb Ischemia]:
(Viable • Threatened • NonViable)
Intact ➜ delayed ➜ ABSENT
name the 5 clinical values that determine Limb viability (Viable vs Threatened vs Nonviable) after severe [Acute Limb ischemia]
SAVED
Sensory/Motor deficit
Arterial doppler
Venous doppler
[Empty-to-full (capillary refill)]
[Dolor (PAIN)]
Management for each phase of [Acute Limb Ischemia] - 3
(Viable-2 • Threatened • NonViable)
- Viable[Catheter or Surgical Revascularization]
- Threatened[Surgical Revascularization STAT]
- NonViable[Amputation]
a. Describe the 3 vascular complications of cardiac catheterization
b. dx?
a. “
b. ultrasound
[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. ⭐[HTN = MOST COMMON CAUSE]⭐
3. EtOH
4. Mitral/Rheumatic❤️ dz
5. MI/CAD
- [Catecholaminesi.e. sympathetics]
- Hyperthyroid
- Obstructing PE
- Pericarditis
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
Marfan Syndrome s/s -4
TALL
- {[Tall/slender/flat feet] with [bone❌breastbone∆ + (scoliosis vs kyposis)
- {[Aortic root disease*(Aortic Dissection | Aortic Aneurysm) + MVP ➜ SCD
- {Lens dislocation(ectopia lentis) ➜ myopia}
- {Long [fingers( = arachnodactyly ⼀Steinberg thumb/wrist), ], [arms] and [LEGS] with [hypermobile joints]}
🧠 Aortic Root Disease 2/2 idiopathic cystic medial degeneration which → Aortic Dissection|Aortic Aneurysm
Describe [Malignant HTN Emergency] - 2
[Hypertensive Urgency (BP>180/110)]
+
Papilledema/Retinal Hemorrhages
list the causes of secondary hypertension -8
- [Coarctation of Aorta]
- [THYROID❌(HYPERthyroid)]
- [THYROID❌(hypOthyroid)]
- HYPERParathyroid
- Pheochromocytoma
- Cushing Syndrome
- [RENAL❌(-vascular)]
- [RENAL❌(-parenchymal)]
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)
❤️ → Rhythm Rx
▶Normal → F.P.
▶⊕CAD → S.D.
▶⊕LVH → A.D.
▶⊕HF → A.F.
_________________
Use Rhythm Chart (see image)
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
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]
indications for [ (______ J) defibrillation] -3
360 J
1.VF
2.mmVTp
3.[PMVT⼀TDP)]p
- VF = VFib
- [mmVT]p = [monomorphic VT pulseless]
- [PMVT⼀TDP]p = [POLYMORPHIC VT⼀TORSADES DE POINTES pulseless]
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
-
🅿︎ 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”
✏️ [AVNRTPSVT]
Retrograde P waves possibly appear as spikes at beginning/end of QRS or as inverted P waves
Southern lead = inferior leads (II, III, avF)
Name the 7 causes of arrhythmia
HIS BEDS gave me arrhythmia
1. [Hypoxia & ishchemia]
2. Inflammation
3. Sympathetic stimulation
4. Bradycardia
5. [Electrolyte❌ (K/Ca+/Mg)]
6. Drugs
7. [Stretched chambers (enlarged/hypertrophied atria/Vt ➜ arrhythmia)]
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]
Myocardial action potential is used by the Myocardium, ⬜ and ⬜
Describe the phases of Myocardial action potential ⼀7
bundle of his; purkinje fibers
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
Pacemaker action potential is used in the ⬜ and ⬜
Describe the phases of Pacemaker action potential ⼀8
[SA node] and [AV node]
Phase 0:
▶at -40 mV: [Ca+ L-VGC] Open ➜ slow upstroke
✏️[fast Na+ VGC] are permanently inactivated 2/2 negative resting voltage 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
_________________
Phase 3:
▶[Ca+ L-VGC] closE
▶[K+ VGC] Open ➜ [K+ efflux]
_________________
Phase 4:
▶at -60 mV: slow spontaneous diastolic depolarization via [Na+ influx viai(funny) channels
✏️Phase 4 slope determines [SA node HR] =responsible for SA/AV node automaticity
✏️( *ACh/adenosine ⬇︎ rate of diastolic depolarization which ➜ ⬇︎[node HR])
(catecholamines ⇪ diastolic depolarization)
(sympathetic stimulation ⇪ chance that i(funny) channels are open, thus ➜ ⇪ HR)
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
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.
A: Class 1 Antiarrhythmic Drugs are ⬜ that have a ⬜ action
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
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 = ⛔[depolarizing (FREQUENT USE-STATE) tissue]** ( = ⛔tachycardic and ischemic tissue)}
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]
🔎dFUSt = [depolarized (FREQUENT USE-STATE) tissue]
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:
- [SVT (especially aFib) in pt with normal hearts]
- Maintains NSR
What is the primary determinant of the ventricular muscle refractory period?
Action Potential Duration (Phase 2) (QT)
4 Main Ways Antiarrhythmic Drugs can treat Arrhythmia in the [SA/AV node]
- Reduction of phase 4 slope
- Increase [max. Resting Potential]
- Increase of threshold potential
- Increase of action potential duration
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]
B: Procainamide1A / Quinidine1A / Disopyramide1A
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)
ADIDaS rx: Amiodarone⼀Dronedarone / ibutilide / Dofetilide / and Sotalol
Non-Pharmacologic Anti-Arrhythmic Therapies:
Radiofrequency ablation & Cryoablation
B: MOA
C: Indication
B: interruptsreentrant | accessory pathway
C:[Nonpharm rhythm control] s/p {[rate control failure] and [pharmacologicrhythm control failure]}
frequently replaces [pharmrhythm control]
Antiarrhythmics used for Ventricular Rate Control (4)
” V EDP”
Diltiazem/Verapamil / Propranolol/Esmolol
Which Drugs for:
VENTRICULAR FIBRILLATION (3)!
1st:⭐-{Debrillation (plus Epinephrine*])}
_________________
2nd/Alt:
-{Debrillation (+/- [Amiodarone3])}
OR
-{Debrillation (+/- [Lidocaine1B])}
Amiodarone 3 or Lidocaine 1B in place of epinephrine
PDA is necessary during fetal development but should close by birth
Which substance maintains an open ductus arteriosus?
“[PGE Prostaglandin] – keEps a PDA”
*🔎PDA = patent ductus arteriosus *
[Indomethacin/NSAIDs inhibit [PGE Prostaglandin] synthesis! ➜ Closes ductus arteriosus
5 antiHLD categories = (FBENS).
[🍔Fibrates]
a. Target
b. MOA (2)
c. Rx (4)
d. side effects (2)
a. ⬇︎TAG
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)]
5 antiHLD categories = (FBENS).
[🍔Statins]
a. Target
b. MOA (2)
c. Rx (5)
d. side effects (2)
a. ⬇︎⬇︎⬇︎LDL Cholesterol
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.)
5 antiHLD categories = (FBENS).
[🍔Niacin 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]
b.
-[VLDL synthesis requires DGA2]. Niacin blocks DGA2 ➜ [⬇︎VLDL]
c.
📝Niacin B3
d.
❌Flushing (px = NSAIDs)
❌HYPERUricemia
❌HYPERGlycemia
5 antiHLD categories = (FBENS).
[🍔Ezetimibe]
a. Target
b. MOA (2)
c. Rx
d. side effects (2)
a. ⬇︎LDL Cholesterol
b.
-Prevent [Cholesterol] absorption at small intestine brush border ➜ body uses internal [LDL Cholesterol] ➜ [⬇︎ LDL Cholesterol]
c.
📝Ezetimibe
d.
❌Diarrhea
❌rare ⇪ LFTs
5 antiHLD categories = (FBENS).
[🍔Bile acid resins]
a. Target
b. MOA
c. Rx (3)
d. side effects
a. ⬇︎LDL Cholesterol
b.
[prevents intestinal Bile ReAbsorption ➜ forces liver to replace Bile using LDL Cholesterol = ⬇︎LDL Cholesterol
c.
📝Cholestyramine
📝 Colestipol
📝 Colesevelam
d.
❌Fat Malabsorption
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
✏️Increases K+ conductance (hyperpolarization) and inhibits [camp-Ca+ currents] both via purinergic receptors
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)]
WGP
1. {[c-ANCA] binds to [PR3 antigen] = antiproteinase 3} ➜ [WGP Triad]
- [⛔ASTHMA⼀✅Granulomas ]
a/w - [WGP Triad]:
WGP-1.[Focal necrotizing vasculitis]
WGP-2.[Necrotizing granulomas in ELK],
WGP-3.[Necrotizing Glomerulonephritis] - 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]
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”
“pPAGING churg-strauss”
- {[p-ANCA](binds to [MPO neutrophil antigen] = antiMyeloPerOxidase} ➜
- Polyps in Nose with rhinitis, sinusitis and skin nodules
- ⊕[Asthma ( ⇪ IgE)]
- ⊕[Granulomas on necrotizing vasculitis with eosinophilia]
- immune-pauci glomerulonephritis
- [Neuropathy (wrist/foot drop) +/- GI or heart involvement]
- ⊕[Granulomas on necrotizing vasculitis with eosinophilia]
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)]
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]
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)]
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
Patient in ER p/w new EKG…..
Fill-in-blank(s)
(USR⼀Upright, Smooth, Rounded)
Patient in ER p/w new EKG…..
Fill-in-blank(s)
(USR⼀Upright, Smooth, Rounded)
Patient in ER p/w new EKG…..
Fill-in-blank(s)
(USR⼀Upright, Smooth, Rounded)
Patient in ER p/w new EKG…..
Fill-in-blank(s)
(USR⼀Upright, Smooth, Rounded)
Patient in ER p/w new EKG…..
Fill-in-blank(s)
(USR⼀Upright, Smooth, Rounded)
[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 = Acute Pericarditis usually self limited –(if persist)–> ASA 650 TID]
——–
CP6. {Chronic Pericarditis → [Calcified fibrous thickening of Pericardium] → [Cardiac compromise and decline] = ConstrictivePericarditis]}
{⭐differentiate from [ConstrictivePericarditis] which has [EKG: low QRS voltage]}
[ST Elevations or Q waves] in leads V1-V2 indicate MI of the ⬜ heart ⼀which is perfused by the ⬜ artery
SeptalAnterior ; pLAD
[ST Elevations or Q waves] in leads [1 \ aVL] indicate MI of the ⬜ heart ⼀which is perfused by the ⬜ artery
LATERAL high ; LCX
[ST Elevations or Q waves] in leads [2\ 3\ aVF] indicate MI of the ⬜ heart ⼀which is perfused by the ⬜ artery
inferior ; RCA
[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
[ST Elevations or Q waves] in leads V3-V4 indicate MI of the ⬜ heart ⼀which is perfused by the ⬜ artery
ANTERIOR ; LAD
[RRAIB-MC] = systematic approach to EKG
describe
Rate
[RRAIB-MC] = systematic approach to EKG
describe
Rhythm
[RRAIB-MC] = systematic approach to EKG
describe
Axis
[RRAIB-MC] = systematic approach to EKG
describe
Interval
[RRAIB-MC] = systematic approach to EKG
describe
B⼀R⼀Q⼀T
|Bundle Branch Block | R | Q | T |
|Bundle Branch Block | R | Q | T |“Be Our CuTie”
[RRAIB-MC] = systematic approach to EKG
describe
Morphology
[RRAIB-MC] = systematic approach to EKG
describe
Chamber Enlargement
For all 12 leads, delineate:
A. Anatomic correlation
B. arterial perfusion
For all 12 leads, delineate (if present):
Any Exceptions to the rule
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
fill-in-Blank (15)
🔤< RCA/SA node/coronary perfusion/heart >
Briefly describe ion movement during all 4 phases of SA/AV node action potential
