Cardiology Review

Tailored for USMLE*

Mazen Al Hammoud
Cardiologist Med Student Cardiologist
Outline
1. Syncope 8. Cardiomyopathies
2. Primary Prevention of ASCVD 9. Rapid Fire Cardiomyopathies
3. Chest Pain ECGs
4. Acute Coronary Syndrome 10. Heart Failure
5. Complications of MI 11. Valular Heart Diseases
6. Stable Angina 12. Imaging for VHD
7. Rapid Fire Ischemia ECGs
Syncope
Section 1
Definition
• Syncope is a sudden transient loss of consciousness associated with
absence of postural tone followed by complete and usually rapid
recovery.
• Think of syncope in 4 big buckets:
1. Orthostatic
2. Reflex-Mediated
3. Cardiac – Obstructive
4. Cardiac – Electrical
• If patient has lateral tongue biting => this is a seizure and not a
syncope!
Four Buckets of Syncope
Reflex-mediated Orthostatic Cardiac-obstructive Cardiac-electrical

• Typically has a • Occurs when rising • Structural • Tachyarrhythmias

prodrome (nausea, from recumbency. obstruction (i.e., (usually either
diaphoresis, • Associated with aortic stenosis, young people with
warmth) orthostatic SBP HCM, mitral SVT or VT or older
drop by >20 mmHg stenosis, pulmonary people with
• Encompasses or DBP >10 mmHg embolism) => With ischemic disease)
vasovagal syncope, with a reflex exertion • Bradyarrhythmias
situational syncope, tachycardia. • Lesions which limit (older people with
and carotid • Think of the stroke volume syncope),
hypersensitivity. dehydration or (i.e., pericardial • Often without a
hypovolemia tamponade, prodrome.
causing orthostasis! pulmonary
hypertension.
HY Sycope
• Vasovagal syncope occurs for a very brief period of time after a prodrome
indicating a hightened parasympathetic discharge.
• Etiology: Young women
• Dx: Clinically if history and ECG normal. Tilt-test table if uncertain.
• Tx: Reassurance (1 episode); Avoid triggers and counterpressure maneuvers (if
multiple recurrent episodes)
• Carotid sinus hypersensitivity
• Think of someone adjusting their tight neck collars or shaving.
• Dx: carotid sinus massage
• Tx: permanent pacemaker
• Orthostatic Hypotension due to decreased baroreceptor sensitivity,
hypovolemia, meds, or neuropathy. May have lightheadedness prior.
Primary Prevention of ASCVD
Section 2
Atherosclerosis
• Atherosclerosis is an inflammatory disease of the tunica intima that
begins with endothelial dysfunction as a response to shear stress.
• Most common location at bifurcation of abdominal aorta (L4).
• You would see fatty streaks on a biopsy of a young male. Females tend to
have slower onset because of the protective role of estrogen.
• Macrophages => oxidize lipids => foamy cells => release PDGF => recruit
smooth muscle cells => differentiation into myofibroblasts => release
collagen in ECM.
Atherosclerosis (Con’t)
• Intimal plaque = necrotic lipid core + fibromuscular cap
• Plaque rupture depends on increased metalloproteases.
• Risk factors for progression: Diabetes > Smoking > Hypertension
• Most protective step to decrease risk of MACE => smoking cessation
• #1 risk factor for MI, a previous MI J
• Neuro tip but relevant: asking about stroke risk factors (AF > HTN >
smoking)
Hyperlipidemia
• Statins => Inhibits HMG-CoA reductase => upregulation of LDL-
receptors on hepatocytes.
• Statins in:
• LDL > 190
• Diabetics
• Young with FHx + elevated LDL
• 100 < LDL < 190 but with ASCVD risk factors
• Statins => myopathy + mild elevated liver enzymes. Cannot combine
with fibrates because high risk of rhabdo due to CYP450 interaction.
Hyperlipidemia (Con’t)
• Ezetimibe blocks cholesterol absorption in the small bowel.
• Bile acid sequestrants (cholestyramine) results in liver pulling more
cholesterol out of the blood.
• Pay attention, Ezetimibe and Cholestryamines INCREASE
CHOLESTEROL SYNTHESIS TO DEPLET BLOOD CHOLESTEROL)
• Fibrates (BEST FOR HIGH TG not LDL!) it upregulates PPAR-alpha ad
lipoprotein lipases.
• PCSK9 inhibitors.
• Niacin increases HDL. Causes flushing tx with NSAIDs. Increases FBS.
Chest Pain
Section 3
The 4 + 2 + 1 Rule to Not Kill Anyone
• Four cardiac
• ACS
• Aortic Dissection
• Pericarditis or Myocarditis First initial step for chest pain is always an ECG
• Cardiac tamponade within 10 minutes of FMC and measure hs-
Troponin regardless of the etiology.
• Two pulmonary
• Pulmonary Embolism
• Pneumothorax
• One gastrointestinal
• Esophageal Perforation
DDx of Chest Pain
Description Diagnosis
• Stabbing and sharp pain Pericarditis
• Increases with deep inhalation
• Worse with lying down and improves while leaning forward
• Recent Hx of infection
• ECG: diffuse ST elevations ± PR depressions
• PE: Dyspnea, cough, fever, pericardial friction rub
• Stabbing and sharp pain Pneumothorax or Pulmonary
• Increases with deep inhalation Embolism
• Respiratory distress
• Hypoxia
• Sudden severe tearing pain Aortic dissection
• Radiates to back
• Associated in elderly with HTN and ASCVD
• Associated in younger with Connective Tissue Disorders
DDx of Chest Pain (Con’t)
Description Diagnosis
• Substernal pain ± radiation Coronary Artery Disease
• Pressure, tightness quality
• Worsens with exertion
• Improves with rest or NG
• Non-exertional at night, relieved by PPIs => GERD Gastrointestinal Etiologies
• May be brought by stressors => DES
• Associated with regurgitation, nausea, dsyphagia
• Remember that achalasia + cardiomyopathy + megacolon => Chagas
Disease (T. cruzii)!
• Persistent pain Musculoskeletal Etiologies
• Worse with activity
• Tenderness => costochondritis esp. in young females
Summary of Chest Pain Management in ED
1. Vital signs and obtain venous access
2. Stabilize patient if hemodynamically unstable
3. Obtain ECG and CXR
4. Administer aspirin if low risk of aortic dissection
5. Supplement with O2 if SpO2 < 90%
Acute Coronary Syndromes
Section 4
STEMI Protocol
HY Notes on RV/Inferior MI
• Avoid drugs that decrease preload in RV MI (diuretics, nitrates, opiates)
• Most sernsitive and specific for RV infarct is lead V4r.
• To optimize preload in RV MI => IV fluids if hypotensive with no pulmonary
edema. If hypotensive despite IV fluids => inotropes!
• Inferior MI (RCA > LCx) mostly associated with bradycardia due to increased vagal
tone in first 24 hrs and decreased blood supply to SA node (can help
differentiating PE from MI)
• If patient severe bradycardia + pulmonary edema => choose atropine > IV fluids as best
next step.
• Mobitz II common in RCA blockage due to AV supply.
• S4 is common in MI
NSTE-ACS
Long Term Management
• Thrombotic Management
• First 12 months DAPT followed by ASA (1) monotherapy indefinitely
• Anticoagulation (UFH) should be discontinued after intervention
• Lipid Lowering Medications
• Beta Blockers (2)*
• ACEi or ARNI
• MRA (eplerenone) if EF < 40% or diabetic (UWorld Step 2) (3)
• Influenza vaccine!
• No survival benefit of nitrates.
Variant Angina
• Most common cause => smoking
• Cocaine, stress, cold etc.
• Most commonly occurs at site of atherosclerosis
• Associated with younger patients ± migraines and Raynauld’s
• Transient ST elevations that resolve without other ischemic ECG changes
• Can cause arrhythmias due to sudden reperfusion
• First Line Tx: CCBs (Usually diltiazem)
• Gold standard: Provocative angio with ergonovine or Ach
• Avoid Aspirin AND non-selective BB
Cocaine-Induced STEMI
Complications of MI
Section 5
HY Complications
• Arrhythmias (most common)
• Papillary muscle rupture more common with PDA occlusion
(posteromedial papillary muscle) => 2nd mitral regurgitation =>
holosystolic murmur at apex* => flash pulmonary edema.
• Ventricular septal rupture => due to macrophage destruction of
septum => harsh holosystolic murmur at LLSB => acute onset RHF.
• LV free wall rupture => mostly during removal of necrotic tissue (5-14
days s/p MI) => hypotension, muffled heart sounds, JVD => cardiac
tamponade.
• LV pseudoaneurysm => can lead to CHF or thrombosis (stroke!)
HY Complications (Con’t)
• Dressler Pericarditis (> 2 weeks) => Type IV hypersensitivity => Treat
with NSAIDs (aspirin) and sometimes colchicine.
• Peri-infarction Pericarditis (1-3 days) => caused by neutrophils leaking
out into pericardium so cannot happen except in transmural
infarcts=> AVOID NSAIDs
• ICD in patients post-MI with LV EF < 30-35%*.
Stable Angina
Section 6
Stable Angina HY
• If low pre-test probability with normal resing ECG:
• No further testing
• If intermediate pre-test probability with normal resting ECG:
• Best Next Step:
• Execise stress echocardiography
• Pharmacologic stress echocardiography
• If intermediate pre-test probability with abnormal stress testing:
• Best Next Step:
• Coronary Angiography
• If high pre-test probability:
• Best Next Step:
• Start pharmacologic therapy for CAD and refer to angiography
Stress Testing
Treatment of Stable Angina
Rapid Fire Ishcemic ECGs
Section 7
A 56F KTH a 10-year history of HTN on lisinopril and hydrochlorothiazide presents to the
ED with crushing new-onset chest pain for the past 2 hours.
A 55-year-old male is brought to the ED by EMS after experiencing 3 hours retrosternal
chest pain. He received 325 mg ASA on his way to the ED. On arrival, his ECG is shown
below:
A 65-year-old male is brought to the ED by EMS after experiencing 1 hour retrosternal
chest pain. His ECG is shown below:
Cardiomyopathies
Section 8
 Hypertrophic CM Dilated CM Restrictive CM ARVC
Etiology • Inherited in an • Mostly idiopathic • Mostly idiopathic • Autosomal
autosomal • Genetic • Systemic disorders recessive or
dominant predisposition (TTN) including dominant
(myosin- • Alcohol amyloidosis, • JUP (desmo
related genes) • Thiamine deficiency sarcoidosis, genes)
(Beriberi) hemochromatosis,
• Ischemic heart systemic sclerosis
disease • Post-radiation
• Infectious (Cox. B, fibrosis
Chagas, HIV)
• Systemic disorders
• Peripartum

Pathophysiology • Concentric • Eccentric hypertrophy • Profilation of • RV myocyte

hypertrophy => => decreased LV connective tissue apoptosis and
impaired contractiliy and EF => decreased replacement by
ventricular elasticity => leading fatty tissue
relaxation to severe diastolic
• Obstructive dysfunction
HCM
 Hypertrophic CM Dilated CM Restrictive CM ARVC
Distinctive • S4 gallop • S3 gallop • Si/sx of HF • Highly variable
Features • Frequently • Systolic murmur • Dspnea
asymptomatic • Si/sx of HF • Can lead to sudden
• Dyspnea, syncope death during or after
• Sudden death due exercise
to VT/VF not MI! • Epsilon wave on ECG

Echo findings • Decreased LV • Increased LV • Decreased LV size • RV enlargement

volume volume • Normal or • RV wall motion
• Normal EF • Decreased EF increased EF abnormality
• Increased wall • Normal or • Increased wall
thickness thinning of LV wall thickness
• SAM • Systolic • Dilated atria
• Dynamic dysfunction • Reduced diastolic
obstruction • Normal diastolic function
function
Physical Examination
HCM DCM RCM

• Systolic ejection murur which: • Systolic murmur due to • Si/Sx RHF

• increases with any mitral or tricuspid • S4 gallop
maneuver that decreases regurgitation • If carpal tunnel =>
EDV and as such increase • S3 gallop amyloidosis
obstruction (valsalva, • Peripheral edema • If bronze skin =>
standing, inotropes). hemochromatosis
• Decreases with hand grip, • If sacoidosis => erythema
squating, passive leg raise, nodosum
beta blockers
• Possible holosystolic murmur
at apex due to secondary MR.
• S4 gallop
• Paradoxial S2 split
Treatment

HCM DCM RCM

• ICD in patients with • Treat underlying cause • Treat underlying cause

documented VT/VF or including alcohol • Refer to Heart
previous syncope abstinence Transplant
• First line: beta blockers • Treat CHF
• Second line: CCBs • If LVEF < 35% => ICD
• Septal reduction • Leading cause of Heart
therapy if severe and Transplant
heart transplant in end
stage HF
Rapid Fire Cardiomyopathies ECGs
Section 9
A 21-year-old healthy male presents to cardiology clinic prior to participation in a
football tournament.
A 21-year-old healthy male presents to cardiology clinic prior to participation in a
football tournament.
A 58-year-old female with a 30-year history of HTN and dyslipidemia presents to the
clinic for her annual check-up. She notes progressive fatigue and swelling in her legs. She
also notes that she sometimes feel fluttery sensations in her chest.
A 45-year-old female s/p chemotherapy and thoracic radiation for a PMHx of Hogkins
lymphoma presents to the clinic complaining of new onset orthopnea
A 24-year-old male with unknown history is rushed to the ED after collapsing on the
soccer field. EMS found him in VF and achieved ROSC after 1 defibrillatory shock. His
post-resuscitation ECG is shown below:
Heart Failure
Section 10
 Heart Failure Dictionary
• HF is a complex clinical syndrome caused
by structural or functional impairment
of ventricular filling and/or ejection of
blood.
• Congestive HF: HF w/ signs of fluid
overload.
• Left heart failure: structural or functional
dysfunction of left heart resulting in
increased pulmonary capillary pressures.
• Right heart failure: structural or functional
dysfunction of right heart resulting in
increased central venous pressures.
• Biventricular failure: LHF + RHF.
• Acute decompensated HF: AHF due to
decompensation.
• Systolic dysfunction: reduced ventricular
contractility resulting in ventricular
enlargement and reduced ejection fraction.
• Diastolic dysfunction: reduced ventricular
compliance characterized by elevated filling
pressures, abnormal relaxation, and
increased ventricular stiffness.
Left Heart Failure
• Presents as pulmonary findings (i.e., dyspnea, orthopnea, paroxysmal
nocturnal dyspnea).
• Left atrial pressure (LAP) = pulmonary capillary wedge pressure
(PCWP).
• Cardiogenic dyspnea => must have elevated LA pressures leading to elevated
PWCP
• If normal wedge pressure => LA is not sad.
• High PCWP + low BP => cardiogenic shock!
Right Heart Failure
• Presents as systemic findings – i.e., JVD and peripheral edema (CVP
elevated)
• Why doesn’t HTN cause peripheral edema => arterioles constrict preventing
blood flow into capillaries.
• Hepatosplenomegaly can also be seen in RHF
• Normal JVP is 3cm above the sternal angle. JVD is > 3 cm.
Congestive HF
• Both left- and right-heart failure findings.
• The most common cause of right heart failure is left heart failure.
• Patient will have dyspnea, JVD, and peripheral edema.
• PCWP is elevated in these patients.
Hemodynamics
HF Workup
• TTE is the best initial test.
• CXR and ECG useful.
• Right heart cath is most sensitive and
specific to confirm HFpEF but invasive
and expensive!
HF USMLE Treatment
1Indicatessurvival benefit in HF w/ systolic
dysfunction.

1. Start with ACEi, ARB, or sacubitril + ACEi/ARB.1

2. Make sure patient is euvolemic => use furosemide if volume
overloaded (does not decrease mortality)
3. Add beta-blocker (carvedilol, nebivolol, metoprolol, bisoprolol)
(mortality benefit)1
4. If EF still low => add MRA (spironolactone)1
5. If EF still low => add hydralazine + nitrates (“add isosorbide ditrate”)1
6. If EF still low => add digoxin (does not decrease mortality)
7. If EF still low => ICD
ADHF
HY Hyponatremia Notes in CHF
• Hyponatremia is an independent predictor of worse outcomes in CHF.
• Decreased perfusion at renal afferent arterioles => neurohumoral
activation and renin, NE and ADH secretion => ADH-promote free
water absorption, renin and NE increase proximal sodium and water
absorption and limit water delivery to distal tubule => free water
retention and dilutional hyponatremia
• Tx: Restrict water intake, ACEi and loop diuretics.
New Updates MAY BE INCLUDED on new
NBME*
Valvular Heart Diseases
Section 11
Murmurs 101
Aortic Stenosis
Etiology Presentation Pathophysiology Treatment

• Young • Si/Sx occur when LVOT • Concentric LV • Asymptomatic severe

• With mitral begins remodeling => (1-4-40 rule) with LVEF
involvement ± • Exertional dyspnea, impaired diastolic < 50%
fusion of angina, dizziness, and filling and increased • Symptomatic severe
commisures => syncope myocardial oxygen
rheumatic disease • Slow rising pulses demand
• Without fusion of • Crescendo- • Reduces coronary
commisures + decresendo murmur reserve
bicuspid leaflets => best heard at RUSB
BAV (assoc. with that radiates to
Turner syndrome) carotids
• Elderly • Soft S2 due to reduced
• Calcific A2 mobility, early
degeneration systolic ejection click
Aortic Stenosis Pathophysiology
Note on Williams Syndrome
• Supravalvular AS associated
with Williams Syndrome (Chr.
7). Findings include elfin
faces, intellectrual
disabilities, hypercalcemia,
very friendly, renal artery
stenosis.
Aortic Regurgitation
Etiology Presentation Pathophysiology Treatment

• Acute • Acute • Higher SBP due to higher • Surgery is the definitive

• Infective endocarditis • Sudden severe dyspnea preload from LA and Ao treatment
• Aortic dissection • Rapid decompensation • Lower DBP due to faster • In acute AR, surgery is
• Chronic • Pulmonary edema return of blood to the LV next best step
• Primary valvular • Chronic • Presentation depends if • In chronic AR, opimize
acute or chronic HTN and HF meds as initial
• Bicuspid AV • May be asymptomatic
despite progressive LV • Acute best step. Surgery is the
• Rheumatic AV definitive treatment.
dilation • Pulmonary edema
• Calcific AV*
• Symptoms of high PP • Chronic
• Aortic root
• S3 gallop • Increase in SV to
• Connective tissue
compensate =>
disorders
compensated HF =>
• Chronic HTN eccentric hypertrophy
• Aortitis => decompensated HF
• Thoracic aortic
aneurysm
Austin-Flint Murmur
AR Auscultation
Mitral Stenosis
Etiology Presentation Pathophysiology Treatment
• Rheumatic disease • Dyspnea, orthopnea, • Increased LA EDP and • Severe symptoms may
• Calcific MV in elderly AF (irregular), decreased LV EDV => develop due to
(rising etiology) thromboembolism, forward HF paroxysmal AF. Treat
• Don’t confuse with AR hoaresness • Cardiogenic AF directly!
with Austin Flint • Mitral facies (pink pulmonary edema • Symptomatic MS =>
murmur, LA myxoma, cheeks) surgery
endocardtitis • Loud S1, loud P2 if • New onset PH =>
vegetations. post-cap PH develops surgery
• ± Opening snap
• Mid-diastolic rumble
at apex
• S4 due to RV damage
Mitral Stenosis in Pregnancy
• Remember that a pregnant female with new-onset dyspnea during
the second trimester is alarming for a previously asymptomatic MS
that became symptmatic due to plasma expansion.
• Caution: late 3rd trimester dyspnea with peripheral edema =>
peripartum CM (anti-body mediated)
• UWorld: if patient is pre-conception and has significant MS =>
percutaneous intervention before pregnancy. If already pregnant,
surgery only if very severe symptoms refractory to medications.
Mitral Stenosis Music
Mitral Stenosis
Mitral Regurgitation
Etiology Presentation Pathophysiology Treatment
• Primary • Acute MR • Acute MR => rapid • Acute MR => surgery
• Degenerative MV • Si/Sx of LHF increase in LA volumes • Chronic MR:
• Rheumatic • Murmurs may not => pulmonary edema • HF management
• Endocarditis be heard • Chronic MR • Symptomatic
• Secondary • Chronic MR • Compensated by patients or those
• CAD • Dyspnea, eccentric with LVEF < 60%
palpitations, cough hypertrophy and (surgery)
• Dilated CM increase in SV
• Lateral displacement
of apical impulse • Decompensated
leads to elevated
• Holosystolic murmur
pressures and CHF
at apex radiating to
axilla
Very Imp. Table for Mitral Regurgitation
Chronic MR
Parameters Acute MR
Compensated Decompensated
Structual Normal Remodeling Remodeling
Remodeling
Hemodynamics Abnormal Normal Abnormal
Mitral Regurgitation
Note on MVP
• Mid-systolic click
• Main cause is myxomatous degeneration
• By itself => it is asymptomatic
• Mitral Valve Prolapse Syndrome: fleeting chest pain on the left chest
in a healthy 20-30 y/o => answer: no treatment required
• If patient presents for Y symptoms and the PE says mid-systolic click
=> ignore it (distractor) and not the cause of Y symptoms cause its
asymptomatic J
Tricuspid Regurgitation
• Holosystolic murmur that increases with inspiration (inspiRIGHT side)
• HY cause is pulmonary HTN. See TR => think PH
• IV Drug User => holosystolic murmur increase with respiration =>
Tricuspid valve endocarditis
• Don’t forget carcinoid can cause this (think of it when you see
serotonin symptoms)
Pulmonary HTN Recap
• Definition: mPAP > 20 mmHg
• Focus on:
• Group 2 PH due to Left-sided valvular heart disease (increased pulmonary
venous pressures => increased PCWP (post-cap))
• Causes increased TR velocity
• Any elevation of RA pressure => enlargement of coronary sinus
Important Imaging for Valvular
Heart Disease
Section 12
ECGs in valvular heart diseases
• Any disease
leading to LVH due
to pressure
overload (mostly
AS):
• (S V1 or V2 + R V5
or V6 > 35) ± non-
specific T wave
abnormalities
• R in aVL > 11 mm
ECGs in valvular heart diseases
• If left atrial
enlargement alone
=> MS
• If lAAE + LVH =>
MR
Pulmonary
Edema
Aortic Stenosis Echo - HY
Endocarditis
Section 13
Classifications
• Native Valve Endocarditis
• Acute: rapid progression, high grade fever, affects healthy native valves
• Subacute: slow progression, low grade fever, affects diseased (prior injury or
congenital) native valves
• Prosthetic Valve Endocarditis
• Early onset <1 year
• Late onset >1 year
Pathogenesis
• Acute bacterial endocarditis: Staph. aureus causing large vegetations that
damage the valve(coagulase positive)
• Affects left-sided valves (mitral > aortic) more frequently due to higher blood
turbulence
• Affects tricuspid valve if IV drug user (HIV increases risk) (S. aureus most common,
Candida common with heroin).
• Subacute bacterial endocarditis: Streptococcus viridans causing small
vegetations that do not destroy the valve (alpha hemolytic) (Can be further
broken down into: S. sanguinis, S. mutans, and S. mitis.)
• Prior dental procedures is a HY cause
• Prosthetic valve endocarditis:
• Early: gram negative bacilli
• Late: Viridans group Strep
• If S. Bovis cause of endocarditis => next best step is colonoscopy!
Presentation
• New-onset murmur + fever = endocarditis
• Malaise, weight loss, night sweats etc.
• Sometimes you would see reactive thrombocytosis w/ endocarditis
• Hematuria if thrombus ends up in kidneys
• Endocarditis + stroke-like episode can lead to focal neurologic deficits
• Can lead to glomerulonephritis
Diagnosis & Treatment
• Dx:
• Blood cultures prior to ABX
• TEE not TTE for diagnostic confirmation
• Tx:
• Vancomycin + gentamycin or ampicillin/sulbactam
• Surgery consult if: prosthetic valve, mobile vegitation > 10-20mm, heart failure
• Prophylaxis (ampicillin or cefoxitin) prior to dental procedures if:
• Hx of endocarditis
• Prosthetic valves
• Hx of heart transplant with regurgitant valves
• Do not give prophylaxis prior to dental procedures for any native stenotic or regurgitant
lesion including MVP!
Noninfective Endocarditis
• Sterile Platelet Thrombus
• Libman Sacks (verrucous) Endocaritis: endocarditis on both sides of
the mitral vave in pt with SLE or Antiphospholipid Syndrome.
• Etiologies:
• Malignancy (pancreatic adenocarcinoma), hypercoagulable state, chronic
infections
• Embolization is more common here, usually asymptomatic till the
thrombus dislodges
• Sterile cultures
• Treat with heparin
Perivalvular Abscess
• Develops secondary to aortic valve endocarditis
• If diastolic murmur at erb’s point + fever + development of AV
conduction block => Perivalvular abscess
Cardiac Electrophysiolgy
Section 14
HY Arrhythmias for USMLE

Atrial fibrillation

Sinus arrhythmias

SVT
• AVNRT
• AVRT
Atrial flutter • Focal
tachycardia
Ventricular ectopies • MAT
VT
VF
Don’t Forget Your Sinus Arrhythmias!
• If sinus tachycardia => treat non-cardiac cause. If very symptomatic
and no identifiable cause => beta blocker, then if didn’t work
ivabradine.
• If sinus bradycardia (sick sinus, MI, hypothyroidism, increased ICP):
• If asymptomatic and athletic => bravo
• If symptomatic and elderly (Acute episode) => 1) treat reversible cause, 2) IV
atropine, 3) either transcutaneous pacing, dopamine or epinephrine.
• If symptomatic and elderly => diagnosis of sick sinus syndrome => PPM
Atrial Fibrillation HY
• You think of this when you see elderly or young patient with mitral stenosis
presenting w/ irregular heart rhythm.
• Pulmonary veins most common origin for ectopic beats.
• Most important complication is emboli => mainly formed in left atrial
appendage.
• Check TSH in young patients with AF.
• If suspecting AF but now patient sinus in ER, put a 24-hour holter monitor.
• Severe abdominal pain in a pt with hyperthryoidism or AF should raise the
suspicion for acute mesenteric ischemia => next step is mesenteric
angiography or if unstable directly laparotomy.
• If acute limb ischemia => embolectomy
• AF + unstable patient => DC cardioversion
Atrial Fibrillation Management
• All should be either on
antiarrhythmics or rate
control meds (beta
blockers, diltiazem,
digoxin)
• If pt older than 65 with
any CV risk factor =>
give anticoagulation
(warfarin or DOACs
work)
Atrial Flutter
• Origin is the cavotricuspid isthmus
• Treatment is same for AF BUT if
asked about the best treatment to
cure the patient => ablation of the
isthmus.
SVT (Regular) for USMLE
• Any tachycardia coming from level of the AV node or above
• Most common regular SVT seen on USMLE is AVNRT
• Think of that differential in a young patient with palpitations + regular
tachycardiac rhythm
• ED Management
• Unstable => DC cardioversion NOT defibrillation
• Stable => 1) vagal maneuvers, 2) adenosine, 3) DC cardioversion
• Long-term Management:
• Vagal Maneuvers if mild and not frequent for AVNRT
• Most regular narrow complex SVT can be ablated as first-line
Wolf Parkinson White Syndrome
• Accessary pathway that
predisposes to SVT
• Short PR => pre-excitation
• Wide QRS
• Definitive treatment: catheter
ablation to accessory pathway
Ventricular Tachycardia
• Ischemic heart disease is most common
cause
• Drug-induced toxicity and electrolyte
abnormalities can cause VT
• If no pulse => CPR + defibrillation if
polymorphic (or synchronize if
monomorphic)
• If pulse:
• First line: antiarrhythmics
(amiodarone, sotalol)
• If refractory: Shock!
Torsade de Pointes
• Patients at increased risk if receive class IA or class III AAD.
• QT prolongation is risk factor for development of TdP. Agents such as
anti- psychotics, macrolides, and metoclopramide prolong the QT.
• If unstable => CPR + defibrillate
• If stable => IV magnesium sulfate
Long QT Syndrome
• Jervell-Lange-Nielsen syndrome:
• FHx of SCA
• Sensorineural hearing loss
• Prolonged QTc
• Treat with propranolol or nadolol
• If PMHx of syncope => insert ICD
AV Blocks
• First and Second Mobitz I Degree:
nothing
• Second Mobitz II and Third Degree:
implant a permanent pacemaker
Congenital Heart Diseases
Section 15
ASD
• Female > Male • Widely split S2 which is fixed
• Associated with Down Syndrome, Fetal • ECG hint is IRBBB
Alcohol Syndrome • Confirmed with TTE
• Ostium secundum most common type • Rarely treated, may cause embolic
• Asymptomatic stroke
• Systolic ejection murmur can be heard
due to relatively stenotic pulmonary
valve compared to the increased flow
VSD
• Most common CHD • Babies born asymptomatic due to
• Most common genetic association is elevated pulmonary vascular
Downs Syndrome resistance
• Most common maternal risk factor is • Small VSDs close alone, large ones
Diabetes require surgical cosure
• Most commonly affect the • Do not treat if Eisenmenger Syndrome
membranous part of the ventricle
• Harsh holosystolic murmur heard at
LLSB, increases with increased
afterload, and is louder in smaller
defects
PFO
• Failure of the atrial septum primum to fuse with the septum
secundum following birth → persistence of foramen
ovale → mild left-to-right shunt
• Dx with agitated saline TTE (first line), TEE is second line if initially
inconclusive
• May cause stroke
• Tx:
• Usually not required for asymptomatic patients
• May close PFO post-stroke
PDA
• Failure of ductus arteriosus to close (6th aortic arch embryologically)
• Etiology: Rubella, alcohol
• Small PDAs are usually asymptomatic
• Large PDAs result in a loud machinary murmur best heard at the left
infraclavicular region, leads to widening of PP, failure to thrive and HF in
infancy.
• Mixing of blood post-PDA (SpO2 difference between RA and lower limbs)!
• Echo confirms it
• Tx in pre-term infants with indomethacin and ibuprofen.
Coarctation of the Aorta
• Male > Females
• Associated with Turner Syndrome and
bicuspid AV
• Secondary HTN in children
• Brachial-femoral delay
• Relative to subclavian:
• If coarctation proximal to subclavian: BP
in right arm > BP in left arm
• If coarctation distal to subclavian: BP
both arms > BP both legs
• Treat the coarctation surgically
Tetralogy of Fallot
• 1) Pulmonary stenosis, 2) RVH, 3) VSD, 4)
overriding aorta.
• Harsh systolic murmur at LUSB that disappears
during Tet spells.
• Degree of symptoms dictated by degree of
pulmonary stenosis (RVOT obstruction)
• Cyanotic CHD (acyanotic at birth, becomes
cyanotic when develops Eisenmenger
Syndrome => around school age => these
children tend to squat to improve their
symptoms).
• Squatting increases afterload, which LV
pressure, which decreases the pressure
gradient of the R-to-L shunt.
• If severe RVOT obstruction, PGE1 infusion tills
surgery.
Transposition of Great Vessels
• Maternal risk factor: diabetes
• Associated with DiGeoge Syndrome
• Caused by failed spiraling of the aorticopulmonary
septum
• Fatal unless you have a shunt
• SpO2 is low
• Causes an egg-on-a-string appearance on CXR
• Infusion of PGE1 to maintain PDA till surgey w/in 2
weeks of life
Ebstein Anomaly
• Malformed tricuspid valve leaflets causing its distal
displacement (RV atrialization) => Tricuspid
regurgitation.
• PFO/ASD seen in most patients. Associated with
WPW syndrome.
• Associated with prenatal lithium exposure.
• Infusion of PGE1 to maintain PDA followed by
surgical repaire. Bundle of Kent may require
ablation.
Total Anomalous Pulmonary Venous Return
• All four pulmonary veins
drain into the systemic
venous circulation rather
than the LA.
• Associated with ASD
usually.
• Snowman sign on CXR
• Tx with surgical repair
Truncus Arteriosus
§ There is a common arterial trunk.
§ Most patients have a VSD.
§ The truncal valve is often very abnormal.
§ Presents with cyanosis and heart failure in the first few weeks, as
pulmonary vascular resistance falls.
§ Absent ectodermal neural crest cells during development is the
cause.
Vascular Disorders
Section 15
Thoracic Aneurysm
• Peak incidence at 60-65 y/o
• Risk factors: HTN, smoking, BAV, connective
tissue disorders, tertiary syphilis.
• Most common location at ascending aorta
due to cystic medial degeneration => may
lead to AR
• Mostly are asymptomatic
• First initial test: CXR
• Best confirmatory test: CTA
• Tx:
• Unstable => emergency repair
• Symptomatic stable => urgent repair
• Asymptomatic stable => follow-up + optimal risk
factors control => repair when thresholds reached
(~5cm)
Abdominal Aortic Aneurysm
• Smoking most important risk factors (screen any smoker at 65+ y/o w/ Abdo US)
• Due to inflammation and proteolytic destruction of connective tissue
• Diabetes is a protective factor against AAA
• Mainly infrarenal
• Can present as a visible pulsation; can have a bruit on auscultation
• Best initial and confirmatory step: Abdominal ultrasound (POCUS)
• For Surgery, AAA repair is indicated if the aneurysm is >5.5 cm or the rate of change of
size increase is >0.5cm/month for 6 months
• Regular monitoring is important for size progression surveillance
Aortic Dissection
• Most common risk factor is HTN; trauma or vasculitis
• Also associated with Connective tissue disorders and BAV
• Clinical features: ripping tearing pain, asymmetric BP/pulses
• Dx:
• Stable: CTA
• Unstable: TEE not TTE!
• Stanford Classification:
• Type A: involves ascending aorta => IV labetalol + surgery
• Type B: does not involve the ascending aorta => 1) IV labetalol, 2) nitroprusside
Traumatic Aortic Rupture
• Most common cause of death due to car accident or fall.
• Most commonly at aortic isthmus, distal to origin of left subclavian artery.
• MVA + CXR showing widened mediastinum => CTA is the best next step.
• Even if hypotensive, in rupture, IV labetalol is used to decrease wall stress.
Peripheral Artery Disease
• Etiology mainly due to atherosclerosis => decreased perfusion
• Most are asymptomatic
• Intermittent claudication
• Rest pain indicates progressive disease
• Physical exam shows hair loss, decreased temp, atrophied muscles, ulcers etc. May show
foot pallor on elevation.
• First line for non acute PAD: ABI (<0.9 is abnormal)
• To assess prior to surgery: MRA is first-line. If contrast contraindicated => duplex US
• Tx: 1) Structured exercise program + ASA + high-intensity statins, 2) cilostazol, 3)
revascularization
Leriche syndrome
• At the level of the aortic bifurcation or bilateral occlusion of the iliac arteries.
• Triad of bilateral buttock, hip, or thigh claudication, erectile dysfunction, and
absent/diminished femoral pulses.
• Impotence is almost always present in men and absence should lead to other diagnosis.
Cholesterol Embolization Syndrome
• Mostly occurs after cardiac cath; may occur from atherosclerotic
plaque from aorta
• Usually causes AKI, livedo reticularis, blue-toe syndrome, CNS and GI
symptoms
• Pathology: Amorphous, eosinophilic material in the vessel lumen with
spindle shaped vacuoles.
• Dx with angiography and tx with angioplasty
Acute Limb Ischemia
• Occurs from arterial occlusion caused by cardiac emboli, thrombosis (eg vascular stents,
hypercoagulable state) or trauma.
• 6Ps: pain, pallor, poikilothermia, paresthesia, pulselessness and paralysis.
• Best initial test: arterial and venous Doppler
• Confirmatory test: Angiography
• Tx: IV Heparin followed by either revascularization, or amputation
Pericardial Diseases
Section 16
Acute Pericarditis
• Etiologies:
• Serous: post-viral (Coxsackie B), secondary to autoimmune disease (RA or SLE),
cocaine use
• Fibrinous: Post-MI complications
• Uremic: occurs in renal failure. pericarditis + very high BUN (>60) and Cr
• Clinical Features: chest pain worse when lying down and during inspiration and improves
while leaning forward.
• Pericardial friction rub ± low-grade fever
• ECG shows diffuse ST elevations.
• Echocardiography is first line for pericardial disease evaluation.
• Tx with NSAID. May consider colchicine. For uremic pericarditis => dialysis.
Constrictive Pericarditis
• Chronic type of pericarditis that usually presents in TB patients.
• TB + heart filling impairment = constrictive pericarditis.
• Symptoms of fluid overload + reduced CO.
• Kussmaul sign is present contary to tamponade due to the rigid
pericardium.
• An increase in JVP during inspiration rather than in expiration!
Purulent Pericarditis
• Most commonly caused by Staph, Strep, or Mycobacterium TB
• High fever, tachycardia, chest pain, pericardial friction rub
• Pericardial effusion on echo
• Tx: pericardiocentesis + IV ABX
Cardiac Tamponade
• Tamponade = Pericardial effusion + low BP
• It is dictated by the rate of fluid accumulation rather than the volume accumulated
• Beck’s triad: hypotension, muffled heart sounds, and JVD
• Pulsus paradoxus = drop in SBP > 10 mmHg during inspiration
• ECG shows alternans
• Management flow: ECG => Echo => pericardiocentesis or pericardial window
Shock
Section 17
Very HY
Miscellanous
Section 18
Pharmacology Side-Effects
• Dihydropridine CCBs => lower limb edema
• Verapamil => constipation
• Beta blockers => sexual dysfunction and depression
• Amiodarone => greyish skin discoloration, thryoiditis
• Quinidine => headache + tinnitus
• Digoxin => yellow vision
• Procainamide => drug induced Lupus
• Flecainide => shouldn’t be used in structurally abnormal hearts
Toxicities
• Beta blocker: Bradycardia, hypotension, AV block, cardiogenic shock,
wheezes, hypoglycemia, neurologic symptoms.
• Tx: 1)Secure airway, 2) IV fluids and IV atropine, 3) IV glucagon to increase
cAMP
• Cyanide toxicity: Altered mental status, lactic acidosis, seizures and
coma.
Myxomas
• 80% located in LA
• Histologically: scattered mesenchymal cells with gelatinous material surrounded by
glycosaminoglycans
• Constitutional symptoms due to IL-6 production
• CV complications (mid diastolic murmur at apex
• Embolization (TIA etc.)
• Echo is diagnostic followed by surgical resection.
Kawasaki Disease
Good luck!