Cardio Flashcards
CAD MCC, primary vs secondary prevention
*leading cause of mortality in the US
MCC: atherosclerosis
Primary prevention = risk factor reduction
*smoking cessation
*diet
*hypertension
– BP goal <140/90 for adults <60yo, <150/90 for ≥60yo
*hyperlipidemia
– LDL goal <130mg/dL
*diabetes
– A1c goal <7.0%
*ASA 81mg QD
– when 10yr CVD risk >20% in nondiabetics
– when 10yr CVD risk >10% in diabetics
Secondary prevention = pharmacologic therapy
*ASA 81mg QD
*clopidogrel & ticagrelor
*statins
*beta blockers
*ACEI
Stable Angina Pectoris definition and EKG findings
Myocardial ischemia: myocardial oxygen demand exceeds oxygen supply
*results when a fixed coronary plaque prevents sufficient blood supply through a coronary artery at times of increased O2 demand, resulting in predictable chest discomfort during times of physical or emotional stress
EKG Ischemia Findings:
*T wave flattening, hyperacute T waves (peaked)
*T wave inversions (TWI)
*ST depressions
Stable Angina sx, dx, tx
HX: man >50y or woman >60y; complains of episodic chest discomfort – heaviness, pressure, squeezing, smothering, choking (not sharp)
*pt often localizes pain over sternum
*typically lasts 2-30min
*may radiate to arms, back, jaw/neck, shoulders
Episodes caused by exertion/emotional upset & relieved by rest/NTG
Atypical angina, “anginal equivalents”
*dyspnea, N/V, fatigue, diaphoresis, faintness
*women, diabetics, elderly
dx
*total cholesterol, LDL, HDL, triglycerides, glucose (A1C), creatinine, hematocrit
UA: examine for DM & renal disease (including microalbuminuria)
CBC: anemia can aggravate angina
TFTs: hyperthyroidism can aggravate angina, hypothyroidism can lead to atherosclerosis
CRP >3mg/L is an independent risk factor for myocardial ischemia
EKG: +/- ST depressions, T wave inversions; normal in absence of symptoms
Stress testing: nuclear perfusion imaging, ECHO
Gold standard: cardiac catheterization, coronary CT angiography
Tx
Acute TX: sublingual nitroglycerin q5min up to 3x
RF TX: hyperlipidemia, HTN, DM, smoking cessation
Prevention Therapy:
1) beta blockers, first-line therapy
2) nitrates, take ~5min before activity
3) aspirin 75-325mg/d
4) high-intensity statin regardless of baseline LDL
ACEI/ARBs
CCBs: indicated if beta blockers are contraindicated, poorly tolerated, or ineffective
Coronary vasospasm: Vasospastic Angina (Prinzmetal or Variant Angina)
definition, sx, dx, tx
PATHO: focal or diffuse spasm of epicardial coronary artery resulting in dynamic high-grade obstruction
*vascular smooth muscle hyperreactivity
Cocaine: can induce ischemia & infarction by causing coronary artery vasoconstriction via alpha-1 receptor activation
sx
Chest pain/angina characteristics:
*CP indistinguishable from obstructive CAD
*occurs predominantly at rest, often 12am to early morning
*lasts 5-15 minutes, responds rapidly to NTG
dx
COVADIS Diagnostic Criteria:
1) nitrate-responsive angina
2) transient ischemic EKG changes
3) angiographic evidence of coronary artery spasm
EKG: normal between episodes
*transient ST-elevation/depression
If ⊕ EKG findings 🡪 cardiac troponins to r/o MI
*troponins ⊖ in vasospastic angina
Exercise stress test, ambulatory EKG monitoring
tx
*sublingual NTG
*smoking cessation
*ASCVD risk factor modification
CCBs: diltiazem, amlodipine, etc.
*prevent vasoconstriction & promote vasodilation in coronary vasculature
Beta Blocker MOA
MOA: beta-1 receptor antagonism; ↓ myocardial oxygen demand
*↓ HR (⊖chronotropy), ↓ contractility (⊖inotropy), ↓ LV wall tension (↓ preload)
Contraindications: vasospastic (variant) angina, acute HF, 2nd/3rd degree heart block
ADRs: bradycardia, hypotension, fatigue, dizziness, depression
Warning: can mask signs of hypoglycemia in pts w/ diabetes
BOXED WARNING: do not stop BB therapy abruptly = rebound angina
Nitrates MOA
MOA: nitrates release nitric oxide (NO) within smooth muscle cells which causes ↑ cGMP, leading to relaxation of vessels
*↓ myocardial O2 demand: ↓ venous return (↓ preload) which ↓ LV wall tension
*↑ myocardial O2 supply: ↑ blood flow through collateral arteries (non-atherosclerotic arteries)
Indications (short-acting): recommended for all patients w/ angina for immediate relief
Indications (long-acting): used when beta blockers are contraindicated or as add-on therapy
Contraindications: use w/ PDE-5 inhibitors
CCB MOA (DHP vs nonDHP)
MOA: inhibit calcium entry/release into myocardial cell, ↓ cardiac workload & O2 demand
*↑ myocardial blood supply
DHP
Indications: stable angina, Prinzmetal; preferred over non-DHP when used in combo w/ BB
Non-DHPs
Indications: unstable angina (Verapamil), stable angina
Contraindications: SBP <90, cardiogenic shock, 2nd/3rd degree AV block, acute MI, pulmonary congestion
Acute Coronary Syndrome (ACS) definition and types
ACS is spectrum of unstable cardiac ischemia
*UA ↔ NSTEMI ↔ STEMI
Unstable Angina (UA):
*ischemia w/o necrosis, partial obstruction
*+/- EKG findings, ⊖biomarkers
Non-ST Elevation Myocardial Infarction (NSTEMI):
*ischemia w/ necrosis, partial obstruction
*+/- EKG findings, ⊕biomarkers
ST-Elevation Myocardial Infarction (STEMI):
*ischemia w/ necrosis, complete obstruction
*⊕EKG findings, ⊕biomarkers
PATHO: insufficient O2 supply to cardiac muscle demands
*progressive growth of atherosclerotic lesions within the coronary arteries ⇢ decreased luminal diameter & coronary blood flow
*acute coronary plaque disruption ⇢ exposed thrombogenic endothelium ⇢ platelet aggregation & thrombus formation
Early Complications of MI:
*heart failure, cardiogenic shock, bradyarrhythmias, AV block, tachyarrhythmias
*LV free wall rupture, interventricular septum rupture, papillary muscle rupture
Late Complications of MI:
*LV thrombus, LV aneurysm
*Pleuropericarditis (Dressler Syndrome)
– 2-10wk post-MI fever, leukocytosis, friction rub
– pericardial or pleural effusion
Acute Coronary Syndrome (ACS) sx
UA: new-onset angina, angina w/ increasing frequency or duration, angina w/ minimal exertion or at rest
MC: substernal chest tightness/pressure
*radiates to L arm, neck/jaw, epigastrium
*occurs at rest, lasts >30min
Levine sign: clenched fist over chest
Associated S/SXS:
*dyspnea, diaphoresis, nausea
*sense of impending doom
Atypical, “silent” presentation: dyspnea, weakness, sweating, N/V, epigastric pain, palpitations, dizziness, fatigue
*women, elderly, diabetics
PE: often nonspecific
*pallor, diaphoresis, tachypnea
Cardiogenic Shock: hypotension, tachycardia, confusion, diaphoresis, pallor
Heart Failure: JVD, pulmonary crackles, S3/S4 gallop, MR murmur
RV Infarction:
➀ hypotension ➁ JVD ➂ clear lung fields
plus ⇨ evidence of inferior MI on EKG
Acute Coronary Syndrome (ACS) dx
EKG within 10mins of arrival, 1st often not diagnostic
*repeat q15-30mins until definitive diagnosis made
STEMI EKG Findings:
*ST elevations ≥1mm in 2 contiguous leads
*new LBBB, new Q waves
UA/NSTEMI EKG Findings:
*normal, T wave inversions, ST depressions
⊕EKG changes in inferior leads ⇢ think RV infarction!!
» get R-sided EKG
» ⊕RV infarction (RCA) = ST elevation in V4R
ST depression* in V1 & V2 = posterior infarction
Cardiac enzymes: initial, 3-6h later
*high sensitivity cardiac troponins I & T preferred
*CK-MB
» rise within 3-4h, peak 12-24h, normalize in 1-2d
*myoglobin
» rise within 1-2h, peak 4-6h, normalize in 24h
STEMI/NSTEMI = ⊕biomarkers, UA = ⊖biomarkers
Acute Coronary Syndrome (ACS) tx
AMI protocol: EKG within 10min, door to PCI within 90min (120min w/ travel to PCI facility)
IMMEDIATE MEASURES FOR ALL PTS: ANOM
*aspirin 162-325mg chewed (non-enteric-coated)
*0.4mg SL NTG q5min x3 dose MAX
*O2 (if SpO2 <90%), morphine (if refractory to NTG)
Initiate within first 24h:
*beta blocker
*ACEI/ARB
*high-intensity statin
ADDITIONAL THERAPIES FOR ALL ACS:
*antiplatelet drug (P2Y12) + AC (UFH, LMWH)
STEMI: reperfusion therapy, PCI preferred
» placement of drug-eluting stent (DES) MC
*fibrinolysis only recommended if PCI unavailable within 120min
UA/NSTEMI: TIMI score to assess need for PCI
*fibrinolysis NOT useful in UA/NSTEMI
DISHCARGE MEDS FOR ALL PTS:
*DAPT (ASA 81mg + P2Y12) continued ≥1y
» ASA 81mg indefinitely even after P2Y12 DC’d
*beta blocker + ACEI + statin continued indefinitely
Aspirin MOA
MOA: irreversibly binds to/inhibits COX-1/COX-2 enzymes, dose-related effects
*COX-1 inhibition = TXA2 inhibition = ↓ platelet activation/aggregation, ↓ vasodilation
– cardioprotective effects 75-160mg
CI: Reyes
ADP Receptor Antagonists (P2Y12 Inhibitors) aka clopidogrel MOA
MOA: bind ADP P2Y12 platelet receptor, inhibiting ADP-induced platelet aggregation
Indications: ACS
– Clopidogrel: ACS, secondary prevention of MI, stroke, & PAD
Indirect Thrombin Inhibitors aka enoxaparin MOA
MOA: bind to antithrombin III to accelerate its activity which enhances inactivation of thrombin & factor Xa, prevents new clot formation
Indications: ACS, VTE
Tissue Plasminogen Activators MOA
MOA: activate plasminogen to plasmin which degrades fibrin
Indications: STEMI ONLY, alternative if PCI unavailable within 120min & sxs onset ≤12h, less evidence if sxs onset 12-24h
Absolute Contraindications: active internal bleed, any hx of ICH, CVA in past 1y, known intracranial neoplasm, suspected aortic dissection or pericarditis
Sinus tachy defintion, sx, dx, tx
*HR 100 – (220 – age)bpm; *faster rates usually imply a different cause
*gradual onset/termination, P wave identical to NSR
S/SXS: usually only in patients w/ underlying cardiac disease
*SOB, CP
dx: EKG: HR >100bpm
tx
*treat underlying etiology if possible
*asymptomatic patients usually don’t require tx
*beta blockers, CCBs, possibly Ivabradine
Sinus Brady defintion, sx, dx, tx
*HR <55-60bpm, often normal finding in highly conditioned athletes
*incidence increases w/ age
S/SXS: dizziness, weakness, fatigue, & syncope
EKG: rate <60bpm
*treat underlying cause if possible
– Glucagon for beta blocker OD, calcium for CCB OD
Stable: DC any AV nodal blocking agents, monitor
Unstable: give atropine w/ escalation to dopamine or epinephrine drip (ACLS protocol)
*transcutaneous/transvenous pacing
Permanent pacemaker: consider for symptomatic patients, 3rd degree AV block, symptomatic ≥5sec pause in AFIB
Sinus Node Dysfunction (SND) “Sick Sinus Syndrome” definition, sx, dx, tx
SND: abnormality in SA node action potential generation or conduction
➀ Inappropriate sinus bradycardia
➁ Alternating bradycardia & atrial tachyarrhythmias (tachy-brady syndrome)
➂ Sinus pause/arrest: sinus pause >3s = sinus arrest (+/- escape rhythm)
➃ SA nodal exit block
▪︎Type I: progressively shorter P-P intervals followed by dropped P wave
▪︎Type II: pauses in sinus rhythm that are multiples of basic sinus rates
➄ Chronotropic incompetence: inability to ⇡ HR to match demand from ⇡ activity
MCC: sinus node degeneration & fibrosis; often involves other parts of conduction system
Often asymptomatic at first w/ symptoms developing over time
S/SXS: exercise intolerance, fatigue, dizziness, HA, nausea, palpitations, CP, SOB, syncope
tx
Unstable: urgent atropine, temporary cardiac pacing
First search for reversible causes
*beta blockers, CCBs, digoxin
*ischemia, autonomic imbalance
Asymptomatic: intermittent examinations
Symptomatic: permanent pacemaker
AV Blocks types, sx, dx, tx
Block occurs IN the AV node:
▪︎first-degree
▪︎second-degree Mobitz type I (Wenckebach)
Block occurs BELOW the AV node:
▪︎second-degree Mobitz type II
▪︎third-degree (complete heart block)
▪︎First-degree, Mobitz I: typically benign, rarely produces symptoms
▪︎Mobitz II, third-degree: almost always d/t pathologic disease involving the infranodal conduction system
» S/SXS: fatigue, dyspnea, presyncope, syncope
▪︎Third-degree (complete) AV block: “escape rhythms” drive the ventricle from below the block site; escape rhythm is slower than sinus (<50bpm) & MC has a narrow QRS
First-degree AV block: prolonged PR interval (>200ms)
Second-degree, Mobitz I (Wenckebach): progressively longer PR
▪︎ALL atrial impulses conducted interval followed by non-conducted P wave (dropped QRS)
Third-degree AV block: NO atrial impulses reach ventricles
Second-degree, Mobitz II: random dropped QRS, stable PR interval
tx
First-degree, Mobitz I:
*no treatment
Mobitz II: more serious
*can lead to complete
*permanent pacemaker often required
Third-degree (complete):
*permanent pacemaker imperative
Atrial Flutter definition, sx, dx, tx
Typical AFL (MC): isthmus-dependent *cavo-tricuspid isthmus
– Single reentrant circuit around tricuspid annulus (R atrium)
– Counterclockwise (MC) or clockwise
Atypical AFL: isthmus-INdependent, any area of R or L atria
*ONE irritable atrial focus causing atrial depolarization
– sudden onset/termination
*circuit usually initiated by PAC
*increased risk of thrombus formation; can lead to cerebral
or systemic embolization
S/SXS: asymptomatic, palpitations, fatigue, dyspnea, presyncope, s/sxs of HF
EKG Characteristics: atrial rate ~300bpm, ventricular rate ~150bpm
▪︎2:1 atrial-to-ventricular-rate ratio common
Typical AFL, counterclockwise: “sawtooth” pattern
▪︎flutter waves ⇢ ⊖ in inferior leads (II, III, aVF), ⊕ in V1 (resembles P waves
tx
Treatment very similar to AFIB
▪︎Unstable: cardioversion
▪︎Stable:
» Antiarrhythmics (ibutilide, flecainide, propafenone)
*Ibutilide very effective, but risk of Torsades d/t QT prolongation
» Rate control: non-DHP CCBs, beta blockers, digoxin
Definitive: radiofrequency ablation, highly effect
*pacemaker, long-term antiarrhythmics or rate control are alternatives,
anticoagulation usually required
AFib definition and types
*MC arrhythmia in the general population
– prevalence ⇡ w/ age
*MULTIPLE irritable atrial foci causing atrial depolarization
MCC: uncontrolled HTN & CAD
*valvular disease (mitral stenosis) & HF also common causes
*RISK OF THOMRBUS FORMATION/CEREBRAL OR SYSTEMIC EMBOLIZATION (e.g., stroke)
Types:
Paroxysmal: episodes last <7d, usually <24h
Persistent: lasts >7d but ≤1y; responds to cardioversion
Long-Standing Persistent: continuous AFIB that lasts >1y
Permanent: present >1y, no longer pursuing rhythm control
Lone: 1 episode in absence of structural heart disease
AFib sx and dx
S/SXS: palpitations, fatigue, dyspnea, dizziness, diaphoresis, HF SXS
dx: EKG: irregularly irregular rhythm,
▪︎absence of discrete P waves ⇢ replaced by small, rapid, continuously varying
fibrillatory waves oscillating at 350-600bpm
» coarse (≥1mm) or fine (<1mm), best seen in inferior leads/V1
▪︎ventricular rate
» normal, bradycardic (slow AFIB), or tachycardic (AFIB w/ RVR)
» most commonly 90-170bpm w/ higher rates in younger individuals
▪︎course fibrillatory waves in V1
▪︎fine fibrillatory waves in V1
▪︎AFIB w/ RVR
Additional Testing:
Holter monitor: help to screen & detect paroxysms
ECHO: should be performed in all newly diagnosed patients
▪︎MC abnormality ⇢ left atrial enlargement
AFib tx
SBP <90, ongoing MI/ischemia, pulmonary edema: immediate DCC
Stable, onset <48h: rhythm or rate control
Stable, onset ≥48h or unknown: consider rate control initially
▪︎defer consideration of electrical rhythm control until:
➀ anticoagulate x3wks, then cardiovert
➁ TEE to exclude LA thrombus
▪︎if ⊘ thrombus ⇢ cardiovert
▪︎if ⊕ thrombus ⇢ AC x3wks, then cardiovert
*Continue AC at least 4wks after cardioversion
▪︎Continuation >4wks based on RFs (CHADS-VASc)
Rate control *preferred in most
First-line: beta blockers, CCBs (verapamil, diltiazem)
▪︎MI, ischemia: beta blockers preferred (metoprolol, esmolol MC used)
▪︎Hypotension, LV dysfunction: diltiazem preferred
Rate control goals: ≤80bpm (symptomatic), ≤110bpm (asymptomatic)
Rhythm Control w/ Antiarrhythmic Drugs (AADs):
▪︎⊖ coronary or structural HD: flecainide, propafenone
▪︎⊕ LVH, CAD, systolic HF: amiodarone, dofetilide
Anticoagulation (AC) Therapy
AC of choice ⇢ DOAC: dabigatran, rivaroxaban, apixaban, edoxaban
▪︎First-line except: mod-to-severe MS, mechanical valve
▪︎When DOACs contraindicated ⇢ Warfarin
Long-term AFIB Therapy:
▪︎rhythm control should be attempted for most pts ⇢ Amiodarone
▪︎older patients w/ structural disease are less likely to remain in NSR &
more likely for SEs from AADs ⇢ rate control preferred (BBs, CCBs)
▪︎Refractory AFIB: catheter ablation
SVT: AV Nodal Reentrant Tachycardia (AVNRT) definition, sx, dx, tx
*HR 120-200bpm (can be faster); sudden onset/termination
*bimodal – initial presentation <20yo, reappears >50yo; MC in women
PATHO: reentry circuit via fast & slow pathways in AV node; often trigged by PAC
*PAC arrives at AV node when beta still in refractory period > down slow path > reaches ventricles when beta no longer in refractory > up fast path > reaches atria when alpha not in refractory > continuous reentry circuit
dx
EKG: HR 120-200bpm; P wave usually buried in QRS (retrograde IF visible)
*less common = pseudo-S wave (inferior leads) & pseudo-R’ wave (V1)
tx
*vagal maneuvers
– Valsalva, carotid massage
*IV adenosine first line pharmacotherapy
*catheter ablation**
Prevention: AV nodal blocking agents
*beta blockers, CCBs, digoxin
SVT: AV Reciprocating Tachycardia (AVRT) defintion, sx, dx, tx
*HR 140-250bpm, ectopic P wave; sudden onset/termination
*reentry mechanism via bypass tract between atria/ventricles, risk of VFIB
*only 5-10% of pts w/ bypass tracts have structural disease (Ebstein anomaly MC)
S/SXS: varies; palpitations, diaphoresis, SOB, dizziness, CP – syncope rare
PATHO: tachycardia usually initiated by PAC/PVC; reentry circuit develops
*Orthodromic (MC): anterograde over AV node, retrograde over accessory pathway
*NARROW QRS, retrograde P wave after QRS
*Antidromic: anterograde over accessory pathway, retrograde over AV node
*WIDE QRS, ⊕DELTA WAVE, P wave rare (retrograde before QRS if visible)
dx
*Orthodromic: narrow QRS, retrograde P wave after QRS, ⊖delta wave
*Antidromic: wide QRS, ⊕ delta wave, P wave rarely visible
tx
Asymptomatic w/ ⊕ delta wave:
*generally don’t require treatment
*vagal maneuvers
– Valsalva, carotid massage
*IV adenosine almost always works
*AVN blocking agents (BBs, CCBs, digoxin)
Refractory: catheter ablation
WAP vs MAT defintion, sx, dx, tx
*≥3 ectopic atrial foci generating impulses that are all conducted to the ventricles
*irregularly irregular rhythm w/ varying PR intervals
Wandering Atrial Pacemaker (“multifocal atrial rhythm”) = HR ≤100bpm
Multifocal Atrial Tachycardia = HR >100bpm
– MAT associated w/ COPD!
– hypoxia, electrolyte abnormalities (e.g., hypokalemia, hypomagnesemia)
dx
EKG: ≥3 distinct P wave morphologies in the same lead
▪︎irregularly irregular rhythm, varying PP/PR/RR intervals
▪isoelectric line between P waves (i.e., ⊘flutter waves)
Wandering Atrial Pacemaker: HR ≤100bpm
Multifocal Atrial Tachycardia (MAT): HR >100bpm
tx
WAP: benign, requires no treatment
Pharmacotherapy for MAT indicated if:
– Leads to sustained RVR that causes or
worsens myocardial ischemia, HF,
peripheral perfusion, or oxygenation
*Verapamil: COPD (d/t bronchospasm)
*Metoprolol
– AADs & cardioversion NOT usefulWolff-Parkinson White (WPW)
Wolff-Parkinson White (WPW) definition, sx, dx, tx
WPW Pattern: EKG findings w/o symptomatic arrhythmias
WPW Syndrome: congenital accessory pathway (Bundle of Kent) w/ associated SVT
S/SXS: if ⊕arrhythmia, may have palpitations, dizziness, or mild chest pain
dx
WPW: ➀ ⊕delta wave
➁ short PR interval (<120ms)
➂ wide QRS (>110ms)
▪︎secondary ST-T changes
AFIB in WPW: rate >200bpm, irregularly irregular rhythm
» occasional narrow QRS reflects AV node conduction
» wide QRS d/t anterograde conduction through accessory pathway (rates
close to 300bpm)
tx
Narrow complex tachycardia:
*implies conduction over AV node
*treat similar to AVNRT
Wide complex tachycardia:
*implies conduction over accessory path
– AVOID AVN-blocking agents
*may precipitate VFIB
– unstable: electrical cardioversion
– stable: IV procainamide or ibutilide
TOC: electrophysiologic study & catheter ablation of bypass tracts
Premature Atrial Contraction (PAC) defintion, sx, dx, tx
*typically a normal variant
dx
EKG Findings: premature beat followed by a normal QRS, P wave has different morphology from sinus P wave
S/SXS: +/- palpitations
tx
usually no treatment required
Complications: atrial tachycardia, AFIB/flutter
Premature Ventricular Contraction (PVC) definition, sx, dx, tx
*occasional PVCs occur in healthy adults
Other causes:
*stimulants (e.g., caffeine, nicotine, cocaine)
*catecholamine surge (e.g., pain), ischemia
*electrolyte abnormalities (e.g., hypokalemia)
*medication toxicity
dx
EKG Findings: premature wide QRS w/o preceding P wave
*followed by fully compensatory pause (interval between sinus beats before/after PVC is 2 RR intervals)
*≥3 PVCs = nonsustained VTACH
S/SXS: +/- palpitations
TX: usually no treatment required. can give BB
Ventricular Tachycardia (VT) types: sustained, non sustained, monomorphic, polymorphic, brugada
VT: ≥3 consecutive PVCs
– Nonsustained: lasts <30s & terminates spontaneously
– Sustained: no spontaneous termination, >100bpm
MCC: acute MI, dilated cardiomyopathy
Others Causes: chronic CAD, electrolyte abnormalities, drug toxicities
Monomorphic VT (MC):
*regular, broad complex tachycardia
*uniform QRS complexes within each lead (i.e., each QRS is identical)
*usually associated w/ myocardial scar
Polymorphic VT:
*QRS morphology continuously varies (requires >1 EKG lead to see variation)
*most often d/t ischemia in absence of QT prolongation
Brugada Syndrome: hereditary, characterized by structurally normal heart
*associated w/ ventricular dysrhythmias ⇢ syncope & sudden cardiac death
– d/t mutation in cardiac Na gene channel (“sodium channelopathy”)
*Asian men predominantly
Ventricular Tachycardia (VT) types: sustained, non sustained, monomorphic, polymorphic, brugada sx, dx and tx
S/SXS: CP, dyspnea, syncope, sudden cardiac death
dx
Monomorphic VT (MC): uniform QRS pattern, consistent morphology; rate 150-200bpm
Polymorphic VT: QRS morphology continuously varies
Brugada Pattern: pseudo-RBBB + persistent ST segment ⇡ (coved) in V1-V2
tx
Unstable: assume VT
*cardioversion
Stable VT: IV amiodarone first line
– DCC if VT fails to terminate/sxs worsen
Polymorphic: IV magnesium
Pulseless 🡪 ACLS
Recurrent, refractory: overdrive pacing
– Internal cardiac defibrillator (ICD)
Torsades de pointes *polymorphic VT: definition, sx, dx, tx
*paroxysmal form of polymorphic VT
*occurs secondary to QT prolongation, can be acquired (MC) or congenital
Acquired QT Prolongation:
– RX: haloperidol, TCAs, abx (e.g., macrolides), methadone, antihistamines,
antiemetics, anticonvulsants
– Electrolyte Abnormalities: hypokalemia, hypomagnesemia, hypocalcemia
dx
Torsades de pointes (“twisting of the points”):
▪︎paroxysmal form of polymorphic VT, sinusoidal; rates >200bpm
tx
*IV magnesium sulfate
Unstable: DCC
Refractory: ICD
Ventricular Fibrillation (VFIB) defintion, sx, dx, tx
*total disorganized ventricular depolarization
*ventricle impulse rates up to 500bpm
*total loss of synchronized ventricular contraction, complete loss of CO
dx
Ventricular Fibrillation: chaotic irregular zigzag pattern of varying amplitude
▪︎no identifiable P waves or QRS complexes, rates varying between 150-500bpm
▪︎as times passes, amplitude typically decreases (coarse ⇢ fine)
tx
ACLS Algorithm:
– CPR, defibrillation
– Epinephrine 1mg
– Amiodarone
Bundle Branch Blocks sx, dx, tx
2 key features of both left & right BBBs:
➀ prolonged QRS duration
➁ terminal conduction delay
▪︎Complete BBB: QRS ≥120ms
▪︎Incomplete BBB: QRS 110-120ms
Right Bundle Branch Block (RBBB): delay in depolarization of RV
*CAN occur in a healthy heart
Left Bundle Branch Block (LBBB): delay in depolarization of LV; entire sequence of ventricular activation is altered, affecting both the initial septal & subsequent ventricular forces
*does NOT occur in a healthy heart
dx
RBBB: QRS ≥120ms
▪︎terminal R wave in V1/V2 (rSR’) w/ discordant ST/T waves
» direct opposite of R’ (i.e., ST ⇣ or T wave inversion)
▪︎broad S waves in V5/V6
LBBB: QRS ≥120ms
▪︎broad, notched, or slurred R waves (rR’/RR’) in leads I, aVL, V5/V6
▪︎dominant S wave in lead V1
▪︎absence of Q waves in lateral leads, appropriate ST/T discordance
tx
Bundle Branch Blocks:
▪︎asymptomatic: no further tx
▪︎symptomatic: permanent pacemaker
Fascicular Block definition, sx, dx, tx
Fascicular Blocks: partial blocks in left bundle system (i.e., left anterior or posterior fascicular blocks)
▪︎generally do not prolong QRS substantially but instead cause left/right axis deviation
» Left Anterior Fascicular Block (LAFB): delay in depolarization of anterior & superior LV
▪︎QRS <120ms, LAD
» Left Posterior Fascicular Block (LPFB): delay in depolarization of inferior & posterior LV
▪︎QRS <120ms, RAD
dx
LAFB: QRS <120ms, LAD (lead I⊕, aVF⊖)
▪︎qR complexes in leads I & aVL, rS complexes in leads II, III, & aVF
LPFB: QRS <120ms, RAD (lead I⊖, aVF⊖)
▪︎rS complexes in leads I & aVL, qR complexes in leads II, III, & aVF
tx
Fascicular Blocks: no specific treatment
▪︎treat underlying disorder
Adenosine MOA
MOA: slows conduction through the AV node via activation of adenosine-I receptors; ⇣ conduction velocity, ⇡ ERP
Indications: rapid conversion to NSR in PSVT
Digoxin MOA
MOA: blocks at AV node = ⇣ conduction velocity, ⇡ nodal ERP
Indications: ventricular rate control in SVT; ineffective at controlling rate during exercise; used in combo w/ BB or CCB
Dilated Cardiomyopathy (DCM) definition, sx, dx, tx
Characterized by reduced strength of contraction & systolic dysfunction, results in right &/or left ventricular enlargement & progressive heart failure w/ increased risk for sudden cardiac death
HF SXS: exertional dyspnea, fatigue, edema, cough, hepatomegaly
PE: S3 gallop hallmark
▪︎cardiomegaly, elevated JVP, rales
▪︎mitral or tricuspid regurgitation
dx
ECHO:
▪︎left ventricular dilation, thin ventricular walls
▪︎⇣ EF, ventricular hypokinesis
CXR: cardiomegaly, pulmonary edema, pleural effusion
EKG: may show sinus tachycardia or arrhythmias
tx
HF TX: ACEI, BB, diuretics
▪︎automated implantable cardioverter/defibrillator if EF <35-30%
Hypertrophic Cardiomyopathy (HCM) definition, sx, dx, tx
▪︎Autosomal dominant genetic disorder of inappropriate
LV &/or RV hypertrophy w/ diastolic dysfunction
▪︎Subaortic outflow obstruction due to asymmetrical
septal hypertrophy & systolic anterior motion of the
mitral valve
The obstruction worsens w/:
⇡ contractility (exercise, Digoxin, beta agonists)
⇣ LV volume (dehydration, ⇣ venous return, Valsalva)
HF SXS: dyspnea MC, fatigue, angina, syncope, dizziness, arrhythmias; sudden cardiac death
PE: harsh systolic murmur best heart at LLSB
⇡ intensity:
⇣ venous return (Valsalva, standing)
⇣ intensity:
⇡ venous return (squatting, supine, leg raise)
handgrip (⇡ afterload)
+/- loud S4, mitral regurgitation, or pulsus biferiens
dx
ECHO:
▪︎asymmetric ventricular wall thickness (esp. septal)
▪︎systolic anterior motion of the mitral valve
▪︎small LV chamber size
EKG: LVH
tx
▪︎BBs, CCBs, disopyramide
▪︎myomectomy, alcohol septal ablation
*pts should avoid dehydration, extreme exertion, & exercise; cautious use of digoxin, nitrates, & diuretics
Restrictive Cardiomyopathy (RCM) definition, sx, dx, tx
Diastolic dysfunction in a non-dilated ventricle, which impedes ventricular filling (⇣ compliance); stiff ventricle fills w/ great effort
Etiologies: infiltrative diseases: amyloidosis MC, sarcoidosis, hemochromatosis
sx:
R-sided HF > L-sided HF
▪︎R-sided HF: peripheral edema, JVD, hepatomegaly,
ascites, GI sxs
▪︎L-sided HF: dyspnea, fatigue
▪︎Kussmaul’s sign: ⇡ JVP w/ inspiration
dx
ECHO:
▪︎non-dilated ventricles w/ normal thickness
▪︎diastolic dysfunction
▪︎marked dilation of both atria
tx: underlying issue
Stress (Takotsubo) Cardiomyopathy definition, sx, dx, tx
Transient regional systolic dysfunction of the LV that can imitate MI but is associated w/ absence of significant obstructive CAD or evidence of plaque rupture
Risk Factors: postmenopausal women exposed to physical or emotional stress
PATHO: thought to be multifactorial, including catecholamine surge during physical or emotional stress, microvascular dysfunction, & coronary artery spasm
sx: Similar to ACS ⇢ substernal CP, dyspnea, syncope
dx
EKG: ST ⇡ (esp. in anterior leads); may have ST ⇣
Cardiac enzymes: often⊕
Coronary angiography: absence of acute plaque rupture or obstructive coronary disease
ECHO: transient regional LV systolic dysfunction, esp. apical left ventricular ballooning; usually performed after ACS has been r/o
tx
Initial: ASA, NTG, BB, heparin, coronary angiography
Short-term: conservative & supportive
- BBs
- ACEI for 3-6mo
- serial imaging to assess for improvement
- anticoagulation in some w/ severe LV dysfunction or if thrombus present
Acute vs Chronic HF
ACCF/AHA & HFSA: complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood leading to cardinal manifestations of dyspnea, fatigue, fluid retention
*Chronic HF: pts w/ longstanding (e.g., months-years) s/sxs of HF
*Acute HF: rapid onset or worsening of sxs of HF; most episodes result from worsening of chronic HF, but ~20% are due to new-onset HF that can occur in the setting of ACS, acute valvular dysfunction, hypertensive urgency, postcardiotomy syndrome
HFrEF vs HFmrEF vs HFpEF
*HFrEF: EF ≤40%
*HFmrEF: EF 40-50%
*HFpEF: EF ≥50%
R vs L sided HF
L-side sxs: pulmonary venous congestion (Lungs, L-sided)
*dyspnea MC
*exertional, orthopnea, paroxysmal nocturnal dyspnea
*fatigue
*rales/crackles (less likely in chronic HF)
R-side sxs: systemic venous congestion (SVC, IVC, hepatic)
*weight gain, lower extremity edema
*abdominal bloating, anorexia, early satiety
*RUQ pain w/ N/V
*hepatomegaly, splenomegaly, ↑ JVP
*hepatojugular reflux; ↑ JVP w/ liver compression
PE: S3 gallop (+/- S4)
*apical impulse displaced downward & to the left
*+/- pulsus alternans
Severe HF: anxious, diaphoretic, dyspneic, pallor, duskiness, cool extremities, cyanosis
NYHA Functional Classifications classes 1-4
NYHA Functional Classification:
*Class I: no limitation of activity, ordinary activity does not cause symptoms
*Class II: slight limitation; comfortable at rest, but ordinary activity causes symptoms
*Class III: marked limitation; only comfortable at rest, less than ordinary activity causes symptoms
*Class IV: symptoms at rest, unable to carry out any activity without symptoms
HF dx
DX: suspect if 1+ s/sxs of HF w/ no apparent non-cardiac cause
ECHO: assess LVEF
*LVEF ≥50% 🡪 workup for HFpEF
*LVEF <50% 🡪 workup for HFrEF
BNP >100pg/mL
NT-proBNP:
*<50y: >450pg/mL
*50-75y: >900pg/mL
*>75y: >1800pg/mL
EKG: can show AFIB, LA enlargement, LVH, pathologic Q waves
CXR: findings of pulmonary edema
*cephalization of pulmonary vessels
*Kerley B lines
*peribronchial cuffing
*pleural effusions
*cardiomegaly
Hemodynamic exercise test: RHC w/ PCWP assessed at rest & w/ exercise
*PCWP ≥15mmHg at rest
*PCWP ≥25mmHg w/ exercise
Labs: CMP, CBC, coagulation studies, UA
*elevated BUN/Cr
*hyponatremia, hypo/hyperkalemia
*anemia
HF tx
Lifestyle: smoking cessation, alcohol restriction, sodium ≤3g/d, fluid ≤1.5-2L/d, weight loss
Guideline-Directed Medical Therapy (GDMT):
*diuretic PLUS
*ARNI, ACEI, or ARB PLUS
*beta blocker
Diuretic Therapy: typically loop diuretic
*furosemide, torsemide
ARNI: sacubitril-valsartan
ACEI: if no hx of angioedema (“prils”)
ARB: for pts that cannot take ARNI or ACEI (“sartan”)
Beta blocker: carvedilol, metoprolol succinate, bisoprolol
ISDN-hydralazine: alternative to angiotensin blockers (ARNI, ACEI, ARB)
Secondary Therapy:
*MRA (spironolactone, eplerenone): for pts who are symptomatic (stages II-IV) + have EF ≤35% on optimal initial pharmacologic therapy
Other secondary therapies depend on indications: SGLT2-inhibitors, vericiguat, ivabradine, digoxin
Acute HF:
*loop diuretic: first line for volume overload w/ congestion
*vasodilators: used for pulmonary congestion for rapid relief of dyspnea
*IV NTG, sodium nitroprusside, nesiritide
*inotropic therapy: used for hypotension
*dobutamine, milrinone, dopamine
*position: sit pt up, have legs dangle over bed to decrease preload/venous return; positive pressure (ventilation)
Infective endocarditis definition, patho, valves effected
Mitral > aortic > (mitral & aortic) > tricuspid
*IVDU = tricuspid
PATHO: endocardial injury 🡪 focal adherence of platelets & fibrin 🡪 microorganisms circulating in blood infect platelet-fibrin nidus
*mature vegetation is a collection of fibrin, platelets, leukocytes, RBC debris, & dense clusters of bacteria
Acute: healthy hearts, rapidly progressive w/ high fevers, rigors, sepsis; S. aureus MCC
Subacute: pre-existing heart disease, non-specific symptoms, indolent; viridans streptococci MCC
Native Valve (NVE): S. aureus MCC, viridans strep, Enterococcus
Prosthetic Valve (PVE):
*<2mo: S. aureus, *CoNS, gram⊖ bacilli, Candida
*2-12mo: CoNS, S. aureus, streptococci, enterococci
*>12mo: streptococci & S. aureus, CoNS, enterococci
*CoNS: S. epidermis MC
IVDU: S. aureus MCC, unusual gram⊖, fungi
*tricuspid valve
Infective Endocarditis sx
MC S/SXS: FEVER, MURMURS
*chills, anorexia, weight loss, malaise, HA, *myalgias, arthralgias, night sweats
*abdominal pain, dyspnea, splenomegaly
*petechiae (palate, conjunctiva, extremities)
*splinter hemorrhages
Uncommon, but highly suggestive of IE:
*Janeway lesions: NONTENDER erythematous macules on palms/soles
*Osler nodes: TENDER nodules on finger/toe pads (“Osler, Ouch”)
*Roth spots: exudative, edematous, hemorrhagic lesions of retina w/ pale centers
Systemic complications at presentation:
*cardiac – valve regurgitation, HF
*neuro – embolic stroke, ICH, brain abscess
*septic arterial or pulmonary emboli
*vertebral osteomyelitis, septic arthritis
*glomerulonephritis (hematuria, proteinuria)
Infective Endocarditis dx
Labs: ↑ ESR, mild anemia, +RF, leukocytosis w/ left shift
*non-specific
EKG: +/- new or evolving conduction disease (1st/2nd degree AV block, BBB, complete heart block)
*consider perivalvular abscess if prolonged PR
CXR: evaluate for presence of septic pulmonary emboli, infiltrate (w/ or w/o cavitation), CHF
Blood cultures x3: different venipuncture sites, at least 1h between first & last, 3 sets ⊕>95% cases
*repeat q48-72h until clearance of bacteria
ECHO: ASAP (<12h after initial evaluation); TTE then TEE
*TTE insensitive in PVE, use TEE
*TEE superior for detecting complications (e.g., abscess, leaflet perforation, aortic pseudoaneurysm, fistula)
Major Criteria:
2 positive blood cultures
positive ECHO or new valvular regurg
Minor
RF: prosthetic valve, IVDU, valve lesion
Fever greater than 100.4
vascular phenomena
immunologic phenomena
Infective Endocarditis tx
Empiric antibiotic therapy warranted for any patient w/ signs of clinical instability
Empiric Antibiotic Therapy (IV):
NVE: Vancomycin + Ceftriaxone x4-6wks
PVE: Vancomycin + Rifampin x6wks
+ Gentamicin for first 2wks
*persistent fever after 1wk suggests a septic embolic focus or inadequate coverage
*reappearance of fever after initial resolution suggests septic emboli or drug fever
Common Surgical Indications:
*refractory HF, myocardial abscess
*valvular obstruction or dysfunction
*perivalvular extension (new conduction dz)
*persistent bacteremia, fungal endocarditis
*recurrent emboli
Hyperlipidemia defintion, causes, RF
High TC only = hypercholesterolemia
High TGs only = hypertriglyceridemia
High TC + TGs = hyperlipidemia
Primary Causes: familial genetic disorders
Secondary Causes: diabetes, alcohol, CKD, hypothyroidism, primary biliary cirrhosis/other liver disease, medications (e.g., thiazides, BBs, retinoids, antiretrovirals, cyclosporine, estrogen, steroids)
Traditional ASCVD Risk Factors: HTN, diabetes, family hx of premature ASCVD, cigarette smoking, CKD, obesity
Risk-Enhancing Factors:
– family hx of premature ASCVD (M <55yo, F <65yo)
– primary hypercholesterolemia (LDL ≥160mg/dL)
– persistently elevated TGs ≥175mg/dL
– CKD
– metabolic syndrome
– inflammatory disorders (e.g., RA, SLE, psoriasis, HIV)
– high-risk race/ethnicity (e.g., South Asian ancestry)
– hx of premature menopause (<40yo)
HLD sx, screening and dx
S/SXS: most are asymptomatic
– High LDL 🡪 xanthomas
*tendinous (e.g., Achilles, patellar, back of hand)
*palmar (yellowish plaques), tuberous (located over joints)
*eruptive (reddish papules all over body)
– High LDL 🡪 xanthelasma (smaller than xanthoma)
*yellow collection of cholesterol under skin, usually on/around eyelids
– Hypertriglyceridemia
*lipemia retinalis (cream-colored blood vessels in fundus)
*pancreatitis (>500mg/dL)
Screening Guidelines: determine if 1+ traditional RFs present & obtain baseline fasting lipid profile for individuals ≥20yo, reassess risk q4-6y
*if 1+ traditional RF (HTN, obesity, diabetes, etc.):
– f/u lipid screening at 25-30yo for males, 30-35yo for females
*if Ø other traditional RF:
– start regular lipid screening at 35yo for males, 45yo for female
Lipid profile ranges of total cholesterol, triglyceride, HDL, LDL, VLDL
TC: less than 200
TG: less than 150
HDL: greater than 50 F or 40 M
LDL: less than 130
VLDL: 2-30
HLD tx
TX: lower LDL ▶︎ statins
TX: lower triglycerides ▶︎ fibrates
Initiate statin therapy for:
1) anyone w/ ASCVD (MI, stable/unstable angina, stroke, PAD, etc.)
2) anyone w/ LDL ≥190mg/dL
3) adults 40-75yo w/ ⊕diabetes regardless of LDL
4) adults 40-75yo w/ LDL 70-189mg/dL & ≥7.5% 10y ASCVD risk
Treatment goals:
– ≥50% LDL reduction for high-intensity statin
– ≥30% LDL reduction for moderate-intensity statin
Statin Therapy Monitoring:
*baseline CK & aminotransferases, only repeat if sxs develop
*repeat lipid profile 4-12wks after statin initiation/dosage change
*monitor lipid profile q12mo thereafter
*more frequent monitoring if concern for noncompliance
High vs moderate intensity statins
High
Atorvastatin 40-80 mg
Rosuvastatin 20-40 mg
Moderate
Atorvastatin 10-20 mg
Rosuvastatin 5-10 mg
Simvastatin 20-40 mg
Pravastatin 40-80 mg
Lovastatin 40 mg
HMG-CoA Reductase Inhibitors (Statins) MOA
MOA: inhibit the rate-limiting step in hepatic cholesterol synthesis via inhibition of the enzyme HMG-CoA reductase
*increase LDL receptors, promoting LDL clearance; reduce triglycerides
Indications:
*best drug to decrease LDL
*have been shown to decrease cardiovascular complications
Muscle damage (myositis, rhabdomyolysis)
↑ LFTs, hepatitis
GI sxs, DM
Contraindications: active hepatic disease, persistent elevated LFTs, pregnancy/breastfeeding
Fibrates
2nd line for HLD
MOA: increases HDL (delays HDL clearance); decreases hepatic production of LDL & its precursor VLDL; decreases triglycerides
Indications: best drug to increase HDL levels
Increased PGs (flushing, warm sensation, pruritis)
*NSAIDs/aspirin can be given 30min before
Dry skin, hyperuricemia, hyperglycemia
Hepatotoxicity, GI (N/V, dyspepsia)
Contraindications: active PUD, active liver disease, arterial bleeding
Bile Acid Sequestrants MOA
MOA: binds bile acids in the intestine, blocking enterohepatic reabsorption of bile acids; reduces cholesterol pool, lowers intrahepatic cholesterol
*because the liver has to make new bile acids, it increases its LDL receptors, decreasing LDL levels
Indications: often used in combo w/ statin to reduce LDL levels; mild to moderate increase in HDL
*SAFE IN PREGNANCY
*Cholestyramine used to treat pruritis associated w/ biliary obstruction
Ezetimibe MOA
MOA: inhibits intestinal cholesterol absorption
Indications: often used in combo w/ a statin to reduce LDL levels
Hypertension MCC, primary vs secondary
*HTN associated w/ MI, HF, stroke, & CKD
*↑ prevalence in ethnic minorities, ♀︎, & ↑ age
Primary Essential HTN (MCC, 95%)
*onset usually 25-50yo
PATHO: sympathetic/RAAS overactivation, defect in natriuresis, variations in cardiovascular/renal development, ↑ intracellular Na/Ca levels
Secondary HTN (5%), i.e., identifiable cause
*suspect if HTN develops <25yo or >50yo
*resistant to max doses of 3 drugs is another clue
MCC: renal parenchymal disease
HTN sx, dx, tx
MC SXS: headache
Fundoscopic exam: +/- hemorrhage, papilledema, cotton wool spots, arteriolar narrowing, AV nicking (hypertensive retinopathy)
dx
DX: BP ≥130/80 when averaged from 2+ readings obtained on 2+ occasions
LABS: CBC, CMP (GFR, creatinine, Na/K/Ca), fasting blood glucose, lipid profile, uric acid, UA, TSH
EKG: LVH
tx
Nonpharmacologic interventions:
*weight loss, DASH diet, smoking cessation
*salt restriction ≤1500mg/d (optimal)
*potassium 3500-5000mg/d
*aerobic exercise 90-150min/wk
*≤2drink/d for men, ≤1drink/d for women
Monotherapy vs Combination Drug Therapy:
*stage 2 HTN & >20/10mmHg above goal
– combo, fixed-dose combination preferred
Initial TX w/ Monotherapy:
*ACEI/ARB or CCB or thiazide-like diuretic
Initial TX w/ Combo Therapy:
*ACEI + DHP CCB single-pill combo
– Amlodipine-Benazepril (Lotrel)
– Perindopril-Amlodipine (Prestalia)
F/u q4wks until BP controlled, then q3-6mo
*if BP uncontrolled, escalate doses on current drugs to at least half max dose before adding additional agent
Additional RX needed:
– add agent from among 3 preferred classes
*ACEI/ARB, CCB, thiazide-like diuretic
Hypertensive Urgency definition, sx, dx, tx
*BP ≥180/120, Ø signs of end-organ damage
S/SXS: asymptomatic
EXAM: should look for the s/sxs suggestive of end-organ damage
*neuro sxs (e.g., seizures, vision changes, AMS), N/V, CP, tearing back pain, dyspnea
*flame hemorrhages, exudates (cotton-wool spots), papilledema (fundoscopy)
tx
BP target <160/100, but MAP should not be lowered >25-30% over the first 2-4hrs, rapid lowering of BP can be harmful
*Clonidine, Captopril, CCB, beta blocker, ACEI/ARB
Hypertensive Emergency definition and tx
*BP ≥180/120 + acute signs of end-organ damage
“Malignant Hypertension”
– encephalopathy or nephropathy + hypertensive retinopathy
tx
*IV Nicardipine (SBP ≥160), IV Labetalol (SBP <160)
– Immediately reduce SBP <220
– Subsequent treatment over first 1-2h to ↓ SBP to 140-160
Thiazides MOA
MOA: inhibit Na reabsorption in distal convoluted tubule, ↓ plasma volume, BP, & edema
Indications: first-line agent, but ACEI/ARB or CCB generally preferred
*useful in pts w/ osteoporosis or edema
ACE MOA
MOA: cardioprotective, synergistic effect when used w/ thiazides; ↓preload/afterload, (↓ synthesis or AG II/aldosterone production), potentiates other vasodilators (bradykinin, PGs, NO); increases exercise tolerance; improves insulin’s actions
Indications: first-line HTN agent (esp. for CKD, HFrEF, post-MI)
ARBs MOA
MOA: similar actions as ACEI but binds & blocks the angiotensin II receptor – does not increase bradykinin production
Indications: first-line HTN agent, good for use in pts who cannot take ACEI
GCA definition, sx, dx, tx
*large & medium vessel granulomatous vasculitis of the extracranial branches of the carotid artery (temporal artery, occipital artery, ophthalmic artery, posterior ciliary artery)
sx
*HA
*jaw claudication w/ mastication
*visual changes (anterior ischemic optic neuritis MC)
+/- scalp tenderness
Temporal artery 🡪 tender, pulseless, or normal
Constitutional sxs: fever, fatigue, weight loss, night sweats, malaise
dx
Clinical
Labs:
*increased ESR & CRP
*normocytic normochromic anemia
Temporal biopsy – definitive
tx: high-dose corticosteroids to prevent blindness (MC complication)
Myocarditis definition, MCC, sx, dx, tx
Inflammation of the heart muscle; MC in young adults
PATHO: myocellular damage leads to myocardial necrosis & dysfunction, leading to HF
Etiologies:
*infectious: viral MC (enteroviruses – Coxsackievirus B)
sx
Viral prodrome – fever, myalgias, malaise for several days followed by sxs of systolic dysfunction (dilated cardiomyopathy)
HF sxs: dyspnea, fatigue, exercise intolerance, S3 gallop
dx
CXR: cardiomegaly
EKG: non-specific – sinus tachycardia MC
Labs: may have + cardiac enzymes, ↑ ESR
Echo: ventricular systolic dysfunction
Endomyocardial bx: gold standard – infiltration of lymphocytes w/ myocardial tissue necrosis
tx: Supportive
Pericarditis definition, sx, dx, tx
Inflammation of the pericardium, the outer layer of the heart
Fibrinous or serofibrinous: e.g., post-MI, infectious
Etiologies:
*2 MCC – idiopathic, viral (Coxsackievirus & echovirus)
*Dressler syndrome (post MI pericarditis + fever + pleural effusion)
sx
Chest pain: sudden onset
*pleuritic (sharp, worse w/ inspiration)
*persistent
*postural (worse when supine & improved w/ sitting forward)
*pain may radiate to back, shoulder, neck, arm, or epigastric area
Pericardial friction rub: best heard at end expiration while upright & leaning forward
dx
EKG: diffuse ST elevations in the precordial leads w/ associated PR depressions in those leads
tx
Anti-inflammatory meds: NSAIDs or ASA x7-14d
- colchicine second line
Dressler Syndrome: ASA or colchicine
- avoid NSAIDs because they can interfere w/ myocardial scar formation
Pericardial Effusion definition, sx, dx, tx
Accumulation of fluid in the pericardial space
sx
*chest pain (if associated w/ acute pericarditis)
*dyspnea, fatigue
PE: decreased (muffled) heart sounds (due to fluid)
dx
Echo: test of choice – increased fluid in pericardial space
EKG: electrical alternans (alternating amplitudes of the QRS complexes); low QRS voltage
CXR: “water bottle” heart
tx
Treat the underlying cause (acute pericarditis)
Serial echo if needed
Large effusions may need pericardiocentesis for symptomatic relief
Cardiac Tamponade definition, sx, dx, tx
Pericardial effusion causing significant pressure on the heart, impeding cardiac filling, leading to decreased CO & shock
sx
Beck’s triad:
*distant (muffled) heart sounds
*↑ JVP
*systemic hypotension
Pulsus paradoxus: exaggerated (>10mmHg) ↓ in systolic pressure w/ inspiration
Dyspnea, fatigue, peripheral edema, shock, reflex tachycardia, cool extremities
dx
Echo: pericardial effusion + diastolic collapse of cardiac chambers
EKG: low voltage QRS complexes, electrical alternans
CXR: may show enlarged cardiac silhouette
Right heart catheterization: equalization of pressures in diastole
tx
IMMEDIATE PERICARDIOCENTESIS to remove the pressure
- volume resuscitation & pressor support if needed
- pericardial window drainage if recurrent
Constrictive Pericarditis definition, sx, dx, tx
Loss of pericardial elasticity (thickening, fibrosis, calcification) leading to restriction of ventricular diastolic filling
PATHO: fibrosis limits ventricular filling, decreased stroke volume & cardiac output
sx
*dyspnea (MC), fatigue, orthopnea
Right-sided HF signs:
*↑ JVD, peripheral edema, N/V
*↑ hepatojugular reflex
*Kussmaul’s sign (the lack of an inspiratory decline or an ↑ in jugular vein pressure w/ inspiration)
Pericardial knock: high pitched diastolic sound similar to S3 (sudden cessation of ventricular filling)
dx
CXR: pericardial calcification may be seen esp. on lateral view, clear lung fields
*normal or slightly increased heart size
*square root sign on cardiac catheterization
Echo: pericardial thickening &/or calcification (also used to r/o restrictive cardiomyopathy)
*”square root” sign – early diastolic dip followed by a plateau if diastasis
CT scan/MRI: pericardial thickening or calcification
tx
Diuretics for symptom relief as well as reduction of edema & venous pressure
Definitive: pericardiectomy
Peripheral Arterial Disease definition, sx, dx, tx
Atherosclerotic disease of the arteries of the lower extremities
sx
Intermittent claudication – MC sxs (lower extremity pain w/ ambulation)
*Leriche’s Syndrome: triad of buttock/thigh claudication + impotence + ↓ femoral pulses
Ischemic rest pain: in advanced disease; MC at night & relieved w/ foot dependency
PE:
*pulses: decreased or absent; bruits (>50% occlusion), decreased capillary refill
*skin: atrophic changes – muscle atrophy, thin/shiny skin, hair loss, thickened nails cool limbs, areas of necrosis; usually no edema
LATERAL MALLEOLUS ULCERS
*color: pale on elevation, dependent rubor (dusky red w/ dependency)
dx
ABI: most useful screening test
*+ PAD if <0.90 (0.50 is severe); rest pain if <0.4 (normal is 1-1.2)
*>1.2 🡪 possible noncompressible (calcified) vessels – may lead to a false reading
Arteriography: gold standard – usually only performed if revascularization is planned
tx
Supportive: first line therapy – exercise (fixed distance walking), decreasing RF (smoking cessation associated w/ greatest benefit, hyperlipidemia, DM), foot care
Platelet inhibitors: cilostazol most effective medical therapy; aspirin, clopidogrel, pentoxifylline
Revascularization: percutaneous transluminal angioplasty (first line revascularization procedure) bypass grafts, endarterectomy (last line)
Acute Arterial Occlusion definition, sx, dx, tx
Acute limb ischemia – rapidly developing or sudden decrease in limb perfusion
sx
6 Ps: paresthesias (often early), pain, pallor, pulselessness, poikilothermia, paralysis (late finding associated w/ a worse prognosis); sxs usually distal to the occlusion
Decreased capillary refill, decreased or absent pulses, cool temperature
dx
Bedside arterial doppler to assess for pulses
CT angiography or catheter angiography
An immediately threatened limb may undergo further evaluation & treatment in a surgical suite
tx
Reperfusion mainstay of tx – surgical bypass, surgical or catheter based thromboembolectomy, endarterectomy; thrombolytic therapy or percutaneous angioplasty
Thromboangiitis Obliterans (Buerger’s Disease) definition, sx, dx, tx
*nonatherosclerotic inflammatory small & medium vessel vasculitis, leading to vasocclusive phenomena
*suspect in young smokers/tobacco users w/ distal extremity ischemia/ischemic ulcers or gangrene of the digits
sx
Triad: distal extremity ischemia both upper & lower extremities (claudication in the lower calf or arch of the foot, ischemic ulcers), Raynaud’s phenomenon, & superficial migratory thrombophlebitis – due to decreased blood flow in the medium & small arteries and veins
dx
Abnormal Allen test: delayed perfusion of the radial ulnar arteries
Aortography: corkscrew collaterals
Biopsy: segmental vascular inflammation
tx
Smoking/tobacco cessation cornerstone of management
Wound care—debridement, moist dressings, negative pressure wound therapy
Amputation if gangrene occurs or to avoid the spread of infection in severe ischemic cases
Iloprost: PG analog that may help w/ critical limb ischemia while smoking cessation is in progress
CCBs for Raynaud’s phenomenon
Superficial Thrombophlebitis definition, sx, dx, tx
*inflammation &/or thrombosis of a superficial vein
*MC associated w/ IV catheterization, pregnancy, varicose veins, venous stasis
sx
Local phlebitis: tenderness, pain, induration, edema, & erythema along the course of the vein under the skin; may feel a palpable cord
Trosseau sign: migratory thrombophlebitis associated w/ malignancy (e.g., pancreatic cancer); may be seen w/ other vasculitic disorders
dx
Mainly a clinical diagnosis
Venous duplex U/S: noncompressible vein w/ clot & wall thickening
Hypercoagulability workup: factor V Leiden (MC cause), prothrombin gene mutations, protein C & S, antiphospholipid antibodies, lupus anticoagulant, factor VII, homocysteine
Migratory phlebitis: malignancy workup: carcinoembryonic antigen (CEA), prostate specific antigen (PSA), colonoscopy, CT scan, mammography (as indicated based on suspicion)
tx
Supportive mainstay – NSAIDs, extremity elevation, warm compresses
Vein ligation/excision (phlebectomy): if extensive varicose veins, septic phlebitis, or persistent sxs despite supportive measures
Varicose Veins definition, sx, tx
Dilation of superficial veins due to failure of the venous valves in the saphenous veins, leading to retrograde flow, venous stasis, & pooling of blood
sx
Most are asymptomatic but may present due to cosmetic issues
Dull ache or pressure sensation; pain is worse w/ prolonged standing or sitting w/ the leg dependent & is relieved w/ elevation
PE: dilated visible veins, telangiectasias, swelling, discoloration, venous stasis ulcers: severe varicosities resulting in skin ulcerations; +/- mild ankle edema
tx
Conservative: compression stockings, leg elevation, pain control
Ablation: catheter-based endovenous thermal ablation (laser or radiofrequency)
Ligation & stripping, sclerotherapy
Chronic Venous Insufficiency definition, sx, tx
Changes due to venous HTN of the lower extremities as a result of venous valvular incompetency
MC occurs after superficial thrombophlebitis, after DVT or trauma to the affected leg
sx
Leg pain worsened w/ prolonged standing, prolonged sitting w/ the feet dependent
Leg pain improved w/ ambulation & leg elevation
Pain classically described as a burning, aching, throbbing, cramping, or “heavy leg”
PE:
*stasis dermatitis: itchy eczematous rash (inflammatory papules, crusts, or scales), excoriations, weeping erosions & brownish or dark purple hyperpigmentation of the skin (hemosiderin deposition)
*venous stasis ulcers
MEDIAL MALLEOLUS ULCERS
*dependent pitting leg edema, increased leg circumference, varicosities & erythema w/ normal pulse & temperature
*atrophic blanche: atrophic, hypopigmented areas w/ telangiectasias & punctate red dots
tx
Conservative: initial management of choice – leg elevation, compression stockings, exercise, weight management
Treat the underlying cause
Acute Rheumatic Fever definition, sx, dx, tx
*acute autoimmune inflammatory multi-systemic illness mainly affecting children 5-15yrs
PATHO:
*symptomatic or asymptomatic infectious w/ group A strep stimulates antibody production to host tissues & damages organs directly
sx
Polyarthritis
*2 or more joints affected or migratory (lower 🡪 upper)
*medium/large joints MC affected (knees, hips, wrists, elbows, shoulders)
*heat, redness, swelling, & severe joint pain must be present
*usually lasts 3-4wks
Active carditis
*can affect valves (esp. mitral/aortic), myocardium (myocarditis), &/or pericardium (pericarditis)
Sydenham’s Chorea: “Saint Vitus Dance” may occur 1-8mo after initial infection
*sudden involuntary, jerky, non-rhythmic purposeless movements esp. involving the head/arms
Erythema marginatum: often accompanies carditis
*macular, erythematous, non-pruritic annular rash w/ rounded, sharply demarcated borders (may have central clearing)
*MC seen on trunk/extremities (not on face)
Subcutaneous nodules: rare
*seen over joints (extensor surfaces), scalp, & spinal column
Other findings: abdominal pain, facial tics/grimaces, epistaxis
dx
JONES CRITERIA: 2 major OR 1 major + 2 minor
MAJOR CRITERIA:
*J – Joint (migratory polyarthritis)
*O – Oh my heart (active carditis)
*N – Nodules (subcutaneous)
*E – Erythema marginatum
*S – Sydenham’s chorea
MINOR CRITERIA:
Clinical
*fever (≥101.3F)
*arthralgia (joint pain)
Laboratory
*↑ ESR, CRP, leukocytosis
*EKG: prolonged PR interval
PLUS supportive evidence of a recent group A strep infection
*⊕throat culture for GAS or
*rapid streptococcal antigen or
*⇡ streptococcal Ab titers (e.g., antideoxynuclease B or antistreptolysin O)
tx
Anti-inflammatory:
*Aspirin (2-6wks w/ taper) +/- corticosteroids
Complications:
*rheumatic valvular disease (MC mitral/aortic)
Heart Disease definition, sx, dx, tx
Consequence of rheumatic fever characterized by inflammation & scarring of the heart valves
*MC affects mitral valve > A > T
Etiology: at least 1 episode of acute rheumatic fever from group A streptococci
sx
Early stage: valve regurgitation (MC mitral valve)
Later stage: valve stenosis
*early stage may last for years & may be asymptomatic
*onset of sxs usually occurs 10-20yrs after acute rheumatic fever
*palpitations, dyspnea, mitral regurgitation
*mitral stenosis, aortic stenosis, aortic regurgitation
dx
Based on clinical presentation & confirmed w/ echo
Echo: valvular abnormalities, including regurgitation or stenosis
Labs:
*↑ anti-streptolysin O (ASO) titers
Histology: Aschoff bodies (granulomas w/ giant cells) on heart valves
tx: Penicillin
Abdominal Aortic Aneurysm (AAA) definition, sx, dx, tx
Focal aortic dilation >1.5 normal (>3.0 considered aneurysmal) – infrarenal MC site
Risk Factors:
*smoking (main modifiable), >60yrs, Caucasians, males
sx
Most pts are asymptomatic – may be found incidentally on imaging or in pts w/ an abdominal bruit or a palpable abdominal mass
Symptomatic (unruptured):
*abdominal, flank, or back pain
*on exam, an abdominal bruit may be auscultated & a palpable abdominal mass may be palpated
Symptomatic (ruptured):
*abdominal, flank, or back pain
*abdominal bruit
*pulsatile mass
*hypotension or syncope
*flank ecchymosis
dx
CT w/ contrast: best initial test in symptomatic, hemodynamically stable pts to deter presence, size, & extent
Focused bedside U/S: may be initial study of choice in hemodynamically unstable pts w/ suspected AAA
Pts w/ known AAA who present w/ classic sxs or signs of rupture can be taken to the operative room for surgical repair w/o preoperative imaging
Asymptomatic w/ suspected AAA:
*abdominal U/S: initial test in asymptomatic pts & to monitor progression
tx
Symptomatic or ruptured:
*IMMEDIATE SURGICAL REPAIR
-endovascular stent graft
-open repair
*BBs reduce shearing forces, decreases expansion & rupture risk
AAA Screening: one-time screening via abdominal U/S in men 65-75yrs who ever smoked
Aortic Dissection definition, sx, dx, tx
Tear through the innermost layer of the aorta (intima) due to cystic medial necrosis
Ascending MC near the aortic arch or left subclavian
*descending
*aortic arch
Risk Factors:
*HTN (most important)
*age >50yrs
*men, vasculitis, trauma, family hx
*Turner’s syndrome
*collagen d/o (Marfan, Ehlers-Danlos), pregnancy
sx
Chest pain: sudden onset severe, tearing (ripping, knife-like) chest/upper back pain; may radiate between the scapulae
*ascending: anterior chest pain
*aortic arch: neck/jaw pain
*descending: interscapular pain
Unequal BP in both arms
dx
CT angiogram, MR angiogram, TEE
CXR: widened mediastinum
tx
Acute proximal: surgical
- preoperative BP control
Descending/distal: medical
- non-selective BBs (labetalol)
+/- sodium nitroprusside
- SBP rapidly lowered to a goal of 100-120 within 20min
DVT definition, RF, causes
MC Prothrombotic States:
*Factor V Leiden mutation
*Prothrombin gene mutation
Risk Factors:
*hx of immobilization (e.g., travel)
*recent surgery/trauma (~12wks)
*previous VTE, family history of VTE
*obesity, >65yo, malignancy, smoker
*pregnancy, postpartum, OCPs, HRT
*heart failure, IBD
Provoked DVT: ⊕identifiable RF
Unprovoked DVT: ⊖identifiable RF
DVT sx, dx, tx
sx
S/SXS: LE swelling (unilateral), pain, warmth, & erythema
*isolated distal DVT: symptoms confined to calf
*proximal DVT: calf or whole leg symptoms
*Homans’ sign (calf pain on passive foot dorsiflexion) is UNRELIABLE for presence of DVT
dx
D-dimer (✓sensitivity, ✗specificity) *useful to r/o DVT
*high ⊖predictive value for low/moderate PTP
DVT unlikely (low/moderate PTP) ⇢ D-dimer
⊖ = <500ng/mL ⇢ DVT ruled out, no further testing
⊕ = ≥500ng/mL ⇢ compression U/S w/ Doppler
DVT likely (high PTP) ⇢ compression U/S w/ Doppler
*NO D-DIMER FIRST
Compression U/S w/ Doppler:
⊖ = full compressibility of all imaged veins
⊕ = non-compressibility of imaged vein w/ pressure
Ascending contrast venography
*CT/MR venography previously gold standard, now rarely used
tx
AC choice ⇢ DOACs *avoid use if CrCl ≤30
Proximal DVT ⇢ AC alone > thrombolytic + AC
IVC filter only recommended if CI to AC
Primary Treatment (at least 3mo)
➀ Provoked by transient/chronic RF, unprovoked
⇢ shorter AC course (3-6mo) recommended
Secondary Prevention (after primary treatment)
➀ DC anticoagulation vs continue indefinitely
Systolic heart sounds: S1 and S2
S1: closure of the mitral & tricuspid valves – comprised of M1 & T1: M1 is mitral valve closing, T1 is tricuspid valve closing
S2: closure of the aortic & pulmonic valves – comprised of A2 (first) & P2 (second): A2 is aortic valve closing, P2 is pulmonic valve closing
S2 splitting
Physiologic: splitting of S2 into A2 & P2 w/ INSPIRATION – increased venous return to the right side of the heart delays the closure of the pulmonic valve (major effect), & decreased return to the left side of the heart speeds the closing of the aortic valve (minor effect)
Ejection Click: MVP (chordae tendineae abruptly pulls the MV tight)
Diastolic Heart Sounds: S3 and S4
S3: vigorous LV filling – normal in pts <40yrs; >40 🡪 decreased LV contractility, myocardial failure, volume overload
(Kentucky)
after S2
S4: dull, low pitch sound caused by increased resistance to LV filling after an atrial contraction (no S4 in atrial fibrillation)
Stiffening of the myocardium can occur from CAD, hypertension, cardiomyopathy, or aortic stenosis
Opening Snap: opening of stenotic MV = MS; best heard at apex
(Tennessee)
before S1
Harsh rumble vs blow sounds (murmur)
Harsh/rumble sounds = think STENOSIS: AS, MS – abnormal forward flow of blood through (stenotic) valve that should be open; stenotic lesions lead to pressure overload; regurgitation leads to volume overload
Blow sound = think REGURGITATION: AR, MR – abnormal backflow of blood (regurgitation) through an incompletely closed valve; regurgitation leads to volume overload
Aortic stenosis definition, sx, dx, tx
PATHO: LV outflow obstruction leads to a fixed CO, ↑ afterload, LVH, & eventually LV failure
MC VALVULAR DISEASE – sxs usually occur when Aov <1cm2
sx
Once symptomatic, lifespan is dramatically reduced
*dyspnea
*angina
*syncope
*CHF
Systolic crescendo-decrescendo murmur
*location: RUSB, radiates to carotid artery
↑ intensity:
*sitting while leaning forward
*↑ venous return (squatting, supine, leg raise)
*expiration
↓ intensity:
*↓ venous return (Valsalva, standing)
*inspiration
*handgrip (d/t ↓ ejection of blood)
dx
Echo:
*small aortic orifice
*LVH
*calcified aortic valve
tx
Surgical therapy: replacement only effective treatment
Percutaneous aortic valvuloplasty (PAV)
Pulmonic Stenosis (PS) definition, sx, dx, tx
*right ventricular outflow obstruction of blood across the pulmonic valve
Almost always congenital & a disease of the young (congenital rubella syndrome)
sx
Harsh mid-systolic crescendo-decrescendo murmur
*location: LUSB, radiates to neck
↑ intensity: inspiration
*longer murmur duration = ↑ stenosis
*systolic ejection click (often buried in S1)
*wide split S2 (delayed P2), +/- S4
dx: echo
tx: Balloon valvuloplasty
Mitral Regurgitation (MR) definition, sx, dx, tx
Etiologies:
*leaflet abnormalities: MVP MCC in US, rheumatic fever MCC in developing countries
-endocarditis, valvulitis, LV dilation
-Marfan syndrome
*papillary muscle dysfunction
sx
Chronic:
*HF sxs – dyspnea, fatigue
*AFIB
*hemoptysis, HTN
Acute:
*pulmonary edema
*hypotension
Blowing holosystolic murmur
*location: apex, radiates to axilla
↑ intensity:
*left lateral decubitus, expiration, exercise
*↑ venous return (squatting, supine, leg raise)
*handgrip
↓ intensity:
*↓ venous return (Valsalva, standing)
*inspiration, amyl nitrate
dx
Echo:
*hyperdynamic LV, regurgitant jet
EKG: nonspecific
*left atrial enlargement, LVH
*AFIB
CXR: nonspecific
*left atrial enlargement, LVH
*pulmonary edema
tx
Medical: sxs control w/ afterload reducers or diuretics
*ACEI, ARBs, hydralazine, nitrates
Surgical: repair > replacement
*indications: EF ≤60%, refractory to medical therapy
Tricuspid Regurgitation (TR) definition, sx, dx, tx
PATHO: right-sided pressure overload 🡪 right-sided HF
Etiologies:
*functional overload: pulm HTN, RV dilation
*structural leaflet abnormalities: endocarditis, Ebstein anomaly
sx
Asymptomatic
+/- pulsatile liver
JVD
Holosystolic, blowing, high-pitched murmur
*location: L mid-sternal border
↑ intensity:
*↑ venous return (squatting, supine, leg raise)
*inspiration
Carvallo’s Sign: ↑ intensity w/ inspiration
*helps to distinguish TR from MR
tx
Medical:
*diuretics (for volume overload & congestion)
*LV dysfunction: standard HF therapy
Surgical: suggested for pts w/ severe TR despite medical therapy
*repair > replacement
Mitral Valve Prolapse (MVP) definition, sx, dx, tx
*leaflets of the mitral valve bulge (prolapse) into the left atrium during systole
*MVP MCC of MR in the US
*MC in young women (15-35yrs)
sx
Most are asymptomatic
Autonomic dysfunction:
*anxiety, atypical chest pain
*panic attacks, palpitations
*syncope, dizziness, fatigue
Mid-late systolic ejection click
*location: apex
dx
Echo: posterior bulging leaflets w/ tissue redundancy
tx
Reassurance in most pts (good prognosis)
Autonomic dysfunction: beta blockers
Repair/replacement
*reserved for MVP w/ severe MR to prevent CHF
Aortic Regurgitation (AR) definition, sx, dx, tx
Incomplete aortic valve closure leads to LV volume overload w/ eventual LV dilation & HF
sx
Signs of widened pulse pressure (seen in chronic)
Water Hammer pulse: swift upstroke & rapid fall of radial pulse accentuated w/ wrist elevation
Corrigan’s pulse (carotid)
Hill’s sign (most sensitive)
*popliteal > brachial BP by 60mmHg
*bounding pulses, pulsus bisferiens
Diastolic blowing decrescendo murmur
*location: LUSB
↑ intensity:
*sitting while leaning forward
*↑ venous return (squatting, supine, leg raise)
*expiration, handgrip
↓ intensity:
*↓ venous return (Valsalva, standing)
*inspiration, amyl nitrate
Austin-Flint Murmur: mid-late diastolic rumble @ apex secondary to retrograde regurgitant jet competing w/ antegrade flow from LA into LV
dx
Echo: regurgitant jet
Cardiac catheterization: definitive
tx
Medical therapy: afterload reduction
*ACEI, ARBs, nifedipine, hydralazine
Surgical: definitive
*indications: acute or symptomatic, asymptomatic w/ LV decompensation (EF <55%)
Pulmonic Regurgitation (PR) definition, sx, dx, tx
PATHO: retrograde blood flow from pulmonary artery into RV 🡪 R-sided volume overload
sx
IF symptomatic: R-sided HF sxs
Graham-Steell Murmur: brief decrescendo early diastolic murmur
*location: LUSB w/ full inspiration
*severe pulm. HTN ↑ velocity of regurgitation
↑ intensity:
*↑ venous return (squatting, supine, leg raise)
*inspiration
↓ intensity:
*↓ venous return (Valsalva, standing)
*expiration
tx: No tx needed in most (well tolerated)
Tricuspid Stenosis (TS) definition, sx, dx, tx
Blood backs up into the right atrium 🡪 increased right atrial enlargement 🡪 right sided HF
sx
Mid-diastolic murmur
*location: LLSB
↑ intensity:
*↑ venous return (squatting, supine, leg raise)
*inspiration
*opening snap (usually later than snap of MS)
tx
Medical: ↓ RA volume overload
*diuretics
*Na restriction
Surgical: commissurotomy or replacement if R-HF or ↓ CO
Mitral Stenosis (MS) definition, sx, dx, tx
PATHO:
*obstruction of flow from LA to LV secondary to narrowed mitral orifice 🡪 blood backs up into the left atrium
*↑ L-atrial pressure/volume overload 🡪 pulmonary congestion 🡪 pulmonary HTN 🡪 CHF
Etiologies:
*rheumatic heart disease almost always the cause – MC in 3rd/4th decade
sx
*dyspnea, hemoptysis
*pulm. HTN
*AFIB *enlarged atria
*right-sided HF
Mitral facies = flushed cheeks w/ facial pallor
Ortner’s Syndrome: laryngeal nerve compression 🡪 hoarse
Low-pitched, mid-diastolic rumbling murmur
*location: apex
*prominent S1, opening snap
↑ intensity:
*left lateral decubitus, expiration, exercise
*↑ venous return (squatting, supine, leg raise)
↓ intensity:
*↓ venous return (Valsalva, standing)
*inspiration
dx
EKG:
*left atrial enlargement
*AFIB
*pulmonary HTN
Echo
CXR: left atrial enlargement
Cardiac catheterization
tx
Percutaneous balloon valvuloplasty:
*best tx for symptomatic MS in younger pts w/ noncalcified valves or if refractory to medical therapy
Mitral valve replacement: reserved if mitral valvuloplasty is contraindicated or w/ unfavorable valve morphology
Medical:
*diuretics & sodium restriction for edema & volume overload
*rate control of AFIB w/ BBs, CCBs, or digoxin (anticoag. for AFIB – warfarin)
Syncope: reflex, orthostatic, cardiac
Loss of Consciousness (LOC): a cognitive state of loss of awareness of self & situation w/ an inability to response to stimuli
Transient Loss of Consciousness (TLOC): rapid onset, self-limited LOC w/ complete recovery
Presyncope (near-syncope): prodromal symptoms of syncope (e.g., lightheadedness, N/V, diaphoresis, blurry vision)
Syncope: transient, self-limited LOC caused by transient, self-terminating, inadequate nutrient flow to the brain
Reflex Syncope (neurally-mediated): neural reflexes inappropriately modify HR & BP
▪︎Vasovagal syncope (VVS):
» emotional stress (e.g., fear/pain, sight of blood)
» orthostatic stress (e.g., prolonged standing, usually in a warm environment)
▪︎Situational syncope: coughing, swallowing, micturition/defecation
▪︎Carotid sinus syndrome/syncope (CSS): occurs w/ pressure on carotid sinus d/t carotid sinus hypersensitivity (CSH)
» ⊕ = HR (ventricular) pause ≥3s &/or SBP ⇣ ≥50mmHg when pressure applied
Orthostatic (postural) Hypotension (OH): SBP ⇣ ≥20mmHg or DBP ⇣ ≥10mmHg w/ upright posture
▪︎Medication-related: antidepressants (e.g., TCAs, phenothiazine APs), antihypertensive agents (e.g., β/⍺ blockers,
hydralazine, ACEI), vasodilators (e.g., CCBs, nitrates), opiates, bromocriptine
▪︎Volume depletion: inadequate fluid intake, excessive loss (e.g., sweating, hemorrhage), vomiting/diarrhea
▪︎Autonomic failure
» Primary: pure autonomic failure, multiple system atrophy, Parkinson
» Secondary: diabetes, amyloidosis, spinal cord injuries, autoimmune neuropathy (Guillain-Barré)
Cardiac:
▪︎Arrhythmias: tachyarrhythmias (e.g., VTACH, SVT), bradyarrhythmias (e.g., AV block, prolonged sinus pause)
▪︎Structural disease: severe aortic stenosis, HCM, cardiac tamponade, atrial myxoma
▪︎Cardiopulmonary/vascular: pulmonary embolism, acute MI/ischemia, severe pulmonary HTN, aortic dissection
Syncope management
Initial evaluation: detailed H&P, EKG, risk assessment, ECHO if structural heart disease suspected
S/SXS:
▪︎Vasovagal
▪︎⊕prodromal SXS (e.g., dizziness, nausea, sweating)
▪︎clinical
▪︎recovery prompt but not immediate (5-15m)
▪︎precipitant apparent, reproducible
▪︎Orthostatic
▪︎SXS develop within several minutes of being upright
▪︎Arrhythmia
▪︎sudden onset w/o warning, unprovoked
Dx
▪︎clinical +/- tilt table testing
⊕orthostatic vitals
▪︎Holter monitor
▪︎recovery immediate on awakening
▪︎may occur in any position
▪︎Structural
▪︎exertional syncope, prompt recovery ▪︎ECHO
High risk arrhythmic causes:
▪︎persistent bradycardia <40bpm or sinus pauses >3s ▪︎3rd degree (complete) AV block
▪︎second degree, Mobitz II ▪︎pre-excited QRS complexes suggesting WPW
▪︎alternating L/RBBB ▪︎VT or PSVT w/ RVR
▪︎long or short QT intervals ▪︎Brugada syndrome
