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 STEMI⼀ACS_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(involving gingiva or oral mucosa)]
d. dental cleaning
e. [respiratory tract procedureinvolving incision or biopsy of mucosa]
f. surgical placement of prosthetic cardiac material
ptsHRC must receive [SAP] prior to any [SRS]
[⚠️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 nonbacterialmaranti(C)with its misc (C)] ..” causes [mitral>tricuspid*]IE … FROM JANE”.
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*
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]
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)]
What causes parasternal heave?
RVH
In peds, Digital clubbing is expected with ⬜ due to ⬜
Cyanotic heart disease ; R-to-L shunting
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
What is Monitored Carotid massage used for?
diagnoses [Syncope 2/2 carotid hypersensitivity (found in elderly with Carotid atherosclerosis)]
Name the major clinical signs of Dehydration (4)
- HR INC
- dry mucous membrane
- hemoconcentration
- BUN/Cr ratio INC
[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]}
Long term amiodarone is a/w what sx? (7)
- [Neuro (ataxia, peripheral neuropathy)]
- visual disturbance
- thyroid
- bradyarrhythmia
- [chronic interstitial pneumonitis]
- hepatotoxic
- blue gray skin
Cardiac Amyloidosis sx (3)
unexplained …
- [Echo: INC Vt wall thickness with nl LV cavity dimension]
- [HFpEF diastolic]
- EKG low voltage
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])
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
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]
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
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
From MOST effective to least effective, describe the 5 NonPharmacologic tx for decreasing high blood pressure
D>W>A>S>E
{[⬇︎Sat/Total Fats Dash diet ⇪Fruits/Vegetables]→ (⬇︎11mmHg) }
[Weight loss⬇︎10kg = ⬇︎6mmHg](if BMI ≥25)*
[Aerobic exercise30min/d x 5d/wk]
[Sodium(<1.5g PO/d)]
[ETOHM≤2 | W ≤1 (drink/day)]
_________________
*Use If BMI ≥25 | central obesity = greatest lifestyle RF for HTN
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
[Troponin-iii q6H x ≥3]⼀rises@4h, peaks 6-12h, falls@7-10d
[EKGq30m x ≥3]
[CKMB] ⼀rises@6h, peaks@24h, falls@2d
[NTGsublingual - prn active chest pain]C❌D{RV MI}
[ASA 325 mg](may trigger asthma)
“1st [TECNA] 2nd [“Really Always Needs OBAMA”]
initial Tx for [symptomatic varicose veins] is conservative and includes ⬜3
- compression stockings
- leg elevation
- wt loss
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)]
🔎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 👀∆ ,
HeartDAD arrhythmia
GINV/anorexia
“(VAQS) traps Digoxin” by preventing renal excretion → DigX Tox hurts [Brain, Eye, Heart, GI]
___________________________x____________________________________
🔎Verapamil|Amiodarone|Quinidine|Spironolactone
*🔎DigX = [Digoxin | Digitalis](Cardiac Glycoside)
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
_________________
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)
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)]
[mild/mod Aortic Stenosis] differs in clinical presentation than [SEVERE Aortic Stenosis]
________________
How does [SEVERE Aortic Stenosis] affect heart sounds? -2
- during inspiration[1 single soft second heart sound]
- [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)
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”
What is a normal Ejection Fraction?
> 50%
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
⬜ is the most common cause of [Dilated Cardiomyopathy HFrEF] and should be evaluated with what 2 test?
[Coronary Artery Diseasse] ;
stress test | coronary angiography
“the PIGS© PAID for Dilated Cardiomyopathy”
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/overStates HF status
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
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
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
List the common causes of Restrictive Cardiomyopathy - 8
RAMILIES
- Radiation Fibrosis (includes coronaries and valves)
- Amyloidosis (heterogenous misfolded proteins)
- Sarcoidosis= [Noncaseating granuloma formation] in multiple organs 2º to [CD4 Helper T] attack on unidentified antigen
- Metastatic Tumor
- Inborn metabolism errors
- Endomyocardial fibrosis= Common in [African/Tropic children]
- [Loeffler Endomyocardial fibrosis] = (Has [Peripheral blood eosinophilia and infiltrate])
- Idiopathic
Restrictive Cardiomyopathy =
-AKA infiltrative cardiomyopathy.
-Diastolic dysfunction
-low voltage EKG
Describe [3rd degree AV block]
[PR and QRS are completely independent]
[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]
peripheral edema is a side effect of which BP rx?
[dihydropyridineCCB] (ex: amlodipine, nifedipine)
a. Describe the 3 vascular complications of cardiac catheterization
b. dx?
a. “
b. ultrasound
What is PostOperative Atrial Fibrillation (POAF)? -4
- COMMON occurring afib after cardiac surgery
- caused by INC sympathethetic tone (from surgery itself)
- spontaneously converts to sinus rhythm within few days
- likely indicates underlying substrate ➜ recurrent afib ➜ subsequent complications (stroke, HF)
[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
GFR threshold for hemodialysis
7.5 - 15
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)]
Tx for [Peripheral Arterial Disease] -5
FIRST
1A. AntiPlatelet
1B. [STATIN high intensity]
1C. [Lifestyle ∆ (EXERCISE PROGRAM, no smoking)]
_______(THEN ⬇️)___________
- [Cilostazol PDE inhibitor] for sx
______(THEN ⬇️⬇️)_________
- [Surgical Revascularization]
causes of Dilated Cardiomyopathy (9)
“the PIGS© PAID for Dilated Cardiomyopathy”
- Post Viral Myocarditis (Coxsackie B)
- Iron Overload: [Hereditary Hemochromatosis] or [Multiple Blood Transfusion Hemosiderosis] = Iron accumulates and interferes with myocytes
- Genetic (affects cytoskeleton)
- {[Sad Broken Heart ABCQ Takatsubo] (apical ballooning octopus on echo)}
- ⭐©AD = MOST COMMON CAUSE OF DILATED CARDIOMYOPATHY ⭐
- PeriPostpartum (late in pregnancy : 5 mo. post partum)
- Alcohol related (direct toxicity vs. nutritional deficiency)
- Idiopathic
- [Doxorubicin, Daunarubicin and Traztuzumab Chemo] (dose-dependent)
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
What are the 5 Causes ofX [High Cardiac Output failure] -5
- Wet Beri Beri
- chronic Anemia
- Arteriovenous fistula
- Paget’s bone disease
- HYPERthyroid
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.i.
_________________
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]
In [ACS⼀acute STEMI], Revascularization of coronary blood flow with [PCI (PerCutaneous Intervention)] should be administered per what 4 criteria ?
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
“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]
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+ 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] ➜[INITIALssDD] ➜
▶🔋causes … [Ca+ TVGC] open ➜minor[Ca+ iNflux] ➜ [ENDssDD] 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
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: 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
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]
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
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
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
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]
Propafenone
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.
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]
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
Amiodarone
A: MOA (4)
B: Effect (3)
C: Antiarrhthymia Class
A: “Amy BLOCKED the NBC-K channel”
[Blocks Na+ / Beta receptors / Ca+ / 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]
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
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
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?
” Nervous Barry Killed Carrie “
Class 1: Na+ channel Blockers (A vs. B vs. C)
Class 2: Beta Blockers
Class 3: [K+ channel blocker(* = prolongs action potential duration*)]
Class 4: [Ca+ L-type channel blockers - Non-Dihydropyridine]
[Vascular smooth m. / cardiac myocytes / SA node / AV Node]
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.
Sotalol
A: MOA (2)
B: Indications (2)
C: Antiarrhthymic Class
A:
- [General β-blocker] (L-isomer only)
- 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
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:
- [1st choice- Supraventricular arrhythmias]
- Re-entry arrhythmias/tachycardias involving AV node.
- Slows ventricular rate in atrial flutter/fib
🔎NCCB = Nondihydropyridine Calcium Channel Blocker
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
Verapamil side effects = “even CHAPELS hurt from CCB!”
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
MAGNESIUM
A: MOA (2)
B: Antiarrhythmic Class
A: Inhibits [Na+,K+-ATPase] and [Na+/ K+/ Ca+ channels]—> alters membrane surface charge
B: NO CLASS
POTASSIUM
A: MOA (HYPER vs. hypOkalemia)
B: Antiarrhythmic Class
A:
- Hyperkalemia; depolarizes resting membrane potential
- Hypokalemia; decreases K+ permeability
B: NO CLASS
[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”
ShOUT PIN ⼀COUT SIN
▶ [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
ADENOSINE
Side Effect (5)
❌flushing
❌hypOtension
❌chest pain
❌impending doom
❌bronchospasm = CXD IN PTS WITH BRONCOSPASTIC DISEASE
✏️similar to ACh.
✏️acts on Atrial and AV node primarily
MAGNESIUM
Effect (2)
- Anti-arrhythmic effects[PMVT Torsades de Pointes] in some patients with normal Mg+ levels.
- May inhibit afterdepolarizations.
🧠MOA = Inhibits [Na+,K+-ATPase] and [Na+/ K+/ Ca+ channels]—> alters membrane surface charge
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).
[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)
MAGNESIUM
Indication (2)
_________________
Route of Admin
-[(CardiacGlycoside-induced arrhythmia) in the setting of hypOmagnesemia]
-[PMVT Torsades de Pointes]
_________________
IV
PMVT = POLYMORPHIC Ventricular Tachycardia
POTASSIUM
- A: Indication*
- B: Route of Admin (2)*
- Maintain normal plasma K+
B: IV or PO
[CARDIAC GLYCOSIDES]
Indication (3)
(Digoxin | Digitalis)
- HF
- [aFib(slows RVR)]
- [aFlutter(slows RVR)]
💡In (atrial flutter/afib) CG parasympathomimetic effects slow AV nodal conduction,—->slows [afib/aflutter associated_Rapid Ventricular Rates]
[DIGITALISCARDIAC GLYCOSIDES]
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.
What is the primary determinant of the ventricular muscle refractory period?
Action Potential Duration (Phase 2) (QT)
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
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. 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 cardiacdFUSt = [depolarizing & (FREQUENTLY-USED-STATE) tissue ] - 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!
- “Antiarrhythmics are better acting when the M-Lid is up frequently”*
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: 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
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]
Non-Pharmacologic Anti-Arrhythmic Therapies:
Synchronized Electrocardioversion/Defibrillation
Indications (3)
- [HDUS atrial fibrillation]
- [Ventricular Fibrillation]
- [Ventricular Tachycardiapulseless]
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)
Antiarrhythmics used for conversion to sinus Rhythm? (3)
“Adele and Ami converted me to Flex”
Adenosine / Amiodarone/ Flecainide
Antiarrhythmics used for Maintenance of sinus rhythm (5)
“Maintain ur F-PPAD man”
Flecainide
Propafenone
Propranolol
Amiodarone
Dronedarone
Antiarrhythmics used for Ventricular Rate Control (4)
” V EDP”
Diltiazem/Verapamil / Propranolol/Esmolol
Which Drugs for:
Ventricular tachycardia in patients without heart disease (2)
“Ur having VTach without Heart Dz..? Go to LA”
Lidocaine
Amiodarone
Which tx for:
AV Block (2)
Atropine
Pacemaker
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
[Propranolol (as an antiarrhythmic)]
Indications) (6)
” Propranolol uses VARAMA cream “
- Vt Rate Control
- Atrial arr
- Reinfarct POST MI tx
- AfterDepolarization (EAD/DAD) tx
- Maintains Sinus Rhythm
- AV Nodal Re-entry tx
Why are [Ca+ Channel Blockers] and [Beta Blockers] Contraindicated in Acute CHF?
[Ca+ Channel & BB Blockers] have NEGATIVE INOTROPIC EFFECTS!
[DigitalisCardiac Glycoside]
Indication (2)
- CHF
- [RVR(in aFib RVR/aFlutter RVR )]
(since DigX slows ventricular rate)
Major unique Adverse Effect of [Nifedipine Dihydropyrdine Ca+ channel Blocker]
Reflex Tachycardia
_____\
(in addition to CHAPELS)
Nesiritide
A: Indication (2)
B: MOA (4)
A:
- [CHF exacerbation] in hospitalized patients
- HTN
B:
- [Human BNP recombinant] that…
- [renal BNP🟢] → DCT Natriuresis
- [vascular smooth muscle NPR1/2🟢] → [renal Afferent arteriole]vasoDilation–> INC GFR
- INC cGMP in [vascular smooth muscle] –> [peripheral arteriole] vasoDilation
🧠[Nesiritide = artificial BNP] = [Nesiritide BNP]
prolonged QT predisposes to [Torsades de Pointes Polymorphic VT]
What are the major causes of acquired prolonged QT? (7)
antiABCDEKG
-[antiArrhythmics (class 1A, 3)]
-[antiBiotics (macrolide)]
-[anti”C“ychotics (haloperidol)]
-[antiDepressants (TCA)]
-[antiEmetics (ondansetron)]
-[anti-K = ⬇︎K+]
-[anti-Mg = ⬇︎Mg]
both low K+ and low Mg+ can prolong QT
Baroreceptors and Chemoreceptors of the Aortic Arch send its afferent information to ⬜ via ⬜
[solitary nucleus of medulla] ← [Vagus CN10]
Baroreceptors and Chemoreceptors of the Carotid Sinus send its afferent information to the ⬜ via ⬜
[solitary nucleus of medulla] ← [Glossopharyngeal CN9]
ANP
clinical features (4)
- released from atrial myocytes when [blood volume ⇪] or [atrial pressure ⇪]
- [⇪GFR (promotes diuresis)] - via dilates Afferent arteriole /constricting efferent arteriole
- vasoDilation
- ⬇︎Na+ ReAbsorption at CD
BNP
clinical features (4)
- from Vt myocytes in response to ⇪ pressure
- similar to ANP but longer 1/2 life
- good NPV for HF dx
- available to treat HF as Nesiritide
NPV = Negative Predictive Value
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
What are the primary diagnostics for MI (3)
a. [EKG (STEMI/ST Depression/hyperacute T/TWI/new LBBB/Q/poor R progression)] = gold standard Hours 1-6 post MI
b. [Troponin-iii] rises@4h, peaks@6-12h, falls@7-10d
c. [CKMB (also released from sk muscle)] rises@6h, peaks@24h, falls@2d (returns to baseline 48h post MI = useful for diagnosing reinfarction)
“1st [TECNA] 2nd [“Really Always Needs OBAMA”]
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
CALCIUMN CHANNEL BLOCKERS
a. MOA
b. [Nondihydropyridine CCB] act on [____ (vasc smooth m) | (heart)]
c. Name the 2 NCCB.
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
CALCIUMN CHANNEL BLOCKERS
side effects (7)
“even CHAPELS hurt from CCB!”
❌Constipation
❌[Hyperprolactinemia(Verapamil)]
❌[AV Block= nCCB = (in pts: high dose | nodal dz | on β🟥) - treat with atropine]]
❌[Peripheral Edema(DCCB)]
❌[Everything’s Spinning ⼀Dizziness/hypOtension]
❌[Large gums⼀gingival hyperplasia]
❌[Skin Flushing(and skin Rxn = Verapamil IV)]
[blocks Calcium L-VGC] ➜ *DCCB*[⬇︎muscle contractility] /*nCCB*[⬇︎AV node conduction]
LARGE vessel vasculitis includes [Giant Cell Temporal Arteritis] and ⬜
[Giant Cell Temporal arteritis]
clinical features (7)
[Giant Cell Temporal Arteritis] and [Takayasu Pulseless arteritis]
- elderly female
- uL temporal artery (from Carotid a) HA
- jaw claudication
- ophthalmic artery (from Carotid a) occlusion may ➜ irreversible blind
- a/w PolyMyalgia Rheumatica
- ⇪ ESR with Focal granulomatous inflammation
- tx (prevent blindness) = [(CTS⼀HD) f/b Temporal artery bx]
LARGE vessel vasculitis includes ⬜ and [Takayasu Pulseless arteritis]
[Takayasu Pulseless arteritis]
clinical features (4)
[Giant Cell Temporal Arteritis] and [Takayasu Pulseless arteritis]
- asian young <40 yof
- “pulseless” = [granulomatous thickening (⇪ ESR) ➜ narrowing of aortic arch & proximal great vessels] ➜ weak UE pulses
- fv, night sweats, skin ∆, ocular ∆
- tx = CTS
Medium vessel vasculitis are Polyarteritis Nodosa, ⬜ and ⬜
Polyarteritis Nodosa
clinical features (5)
Medium vessel vasculitis are [Polyarteritis Nodosa], [Kawasaki disease], [Buerger Thromboangiitis Obliterans]
_________________
- Young adults
- HBV in 30% of patients
- -Const: Fever, wt loss, malaise
-Cardiac: HTN
-GI: abd pain, melena - [Immune complex mediated ⼀renal and visceral vessels (renal microaneurysms) ⼀arterial wall transmural inflammation with fibrinoid necrosis]
- tx = cyclophosphamide and CTS
Medium vessel vasculitis are ⬜ , ⬜, [Buerger Thromboangiitis Obliterans]
[Buerger Thromboangiitis Obliterans]
clinical features (4)
Medium vessel vasculitis are [Polyarteritis Nodosa], [Kawasaki disease], [Buerger Thromboangiitis Obliterans]
- <40 yom Smokers
- etx = [Segmental thrombosing vasculitis] ➜ Intermittent Claudication ➜ gangrene/digital autoamputation
- ⊕Raynaud phenomenon
- tx = smoking cessation
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)
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
[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]}
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
[ 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)]]
[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
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
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
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
What is [persistent truncus arteriosus]?
Truncus arteriosus fails to divide into pulmonary trunk and aorta 2/2 aorticopulmonary septum formation (usually accompanied with VSD)
name the local metabolites responsible for Skeletal Muscle autoregulation during exercise (6)
- lactate
- adenosine
- K+
- H+
- CO2
- sympathetic tone (at rest)
[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
What effect does carotid massage have on atrial flutter?
INC aFlutter AV Block
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
fill-in-Blank (15)
🔤< RCA/SA node/coronary perfusion/heart >
Briefly describe ion movement during all 4 phases of SA/AV node action potential
