Internal Medicine

Cardiology
Pt with chest pain…
• Substernal; radiates to arm, shoulder, or jaw; precipitated by exercise; relieved
by rest or nitro
• Coronary Artery Dz
• Sharp/stabbing pain; worse with inspiration
• Worse when lying flat ⇒ Pericarditis
• Hypoxia; respiratory distress ⇒ PE; Pneumothorax
• Sudden/severe tearing pain; radiates to back; elderly male; HTN
• Aortic Dz (eg, dissection, intramural hematoma)
• Non-exertional; epigastric or substernal; prolonged pain (>1hr); other GI sxs;
nocturnal pain
• GI & Esophageal Dz
• Persistent/prolonged pain; worse with movement or change in position; often
after repetitive activity
• MSK Dz
• Pt presents to ED with chest pain and suspected ACS (and low suspicion for
aortic dissection). What should you do immediately?
• Give aspirin
PVCs
• Although they can occur in healthy adults, what
population more commonly has them?
• Heart disease pts (e.g., MI, CHF)
• When is treatment indicated?
• When pt is symptomatic (e.g., palpitations, light headed)
• What is the first line treatment?
• Β-Blockers or CCBs
Coronary Artery Dz
• Tx of Stable Angina:
• β-blocker ⇒ ↓ myocardial O2 demands
• 2nd Line = verapamil, diltiazem
• ±Long-Acting Nitrates
• How do nitrates improve symptoms?
• Systemic vasodilation ⇒ ↓ Preload ⇒ ↓ LV EDV ⇒ ↓
Cardiac O2 demand
• Although nitrates primarily work via venodilation and
coronary artery dilation, their 1˚ anti-ischemic effects
are due to systemic vasodilation rather than coronary
artery dilation
Digitalis (Digoxin)
• When is it used?
• Toxicity:
• Most Specific Arrhythmia ⇒ Atrial Tachycardia w/ AV
Block
• Acute ⇒ GI sxs (anorexia, N/V), confusion, weakness
• Chronic ⇒ neuro sxs (confusion, disorientation, lethargy)
and vision changes (changes to color vision, scotomas,
blindness)
• What other cardiac drugs ↑ digoxin levels?
• Amiodarone, verapamil, quinidine, & propafenone
• Digoxin dose should be ↓ by 25-50%
SVTs
• What are SVTs?
• Any tachycardia (HR > 100) originating at or above the AV node
• Includes sinus tach, MAT, A Flutter, A Fib, AVRT, AVNRT, WPW
• How can you differentiate between A Tach and A Flutter?
• A Tach is slower (150-250 bpm) than A Flutter (250-350 bpm)
• What’s the classic presentation of SVTs?
• Abrupt onset of palpitations that resolves w/ vagal maneuvers
• What is the MC form of paroxysmal SVT?
• AVNRT (AV Nodal Reentrant Tachycardia)
• Best test for dx of SVTs?
• IV adenosine to unmask P-waves
• What is the initial tx for AVNRT? Explain how this works. 2nd line?
• 1st = vagal maneuvers (eg, carotid sinus massage, head in cold water, Valsalva)
• Maneuvers → ↑ vagal tone → ↓ conduction through AV node → termination
• 2nd = adenosine
• Would this work for AVRT? Why or why not?
• NO! Vagal maneuvers only work in AVNRT because the reentry pathway is at the AV node.
Heart Blocks
• 3rd Degree
• Managed with temporary pacemaker while reversible
causes are investigated
• If no reversible cause found, a permanent pacemaker is
warranted
WPW
• WPW is a subtype of AVRT
• What is the pathophysiology?
• Accessory pathway (Bundle of Kent) conducts depolarization directly from the
atria to ventricles, bypassing the AV node
• ECG findings?
• Delta waves
• Up to 30% of pts w/ WPW will develop A Fib. Why is this more serious
than other A Fib pts?
• A Fib viaBundle of Kent (bypassing AV node) → RVR (rate > 100) → potential
degeneration to V Tach or V Fib
• What is the tx for A Fib w/ RVR in WPW pts?
• Hemodynamically Stable ⇒ IV procainamide (or ibutilide) for rhythm control
• Hemodynamically Unstable ⇒ immediate electrical cardioversion
• What drugs are CI in WPW pts?
• AV nodal blocking agents (e.g., adenosine, β-blockers, CCBs esp. verapamil, &
digoxin)
Acute STEMIs
• Initial Stabilization:
• O2 (if SaO2 < 90% or dyspnea)
• ASA 325 mg (antiplatelet)
• P2Y12 Inhibitor (clopidogrel)
• Sublingual Nitrates (systemic vasodilation)
• β-Blocker (unless CI; negative chronotrope/inotrope)
• High-Dose Statin (stabilization of plaque)
• Anticoagulation (depending on planned revascularization)
• Other Potential Drugs:
• If persistent pain, HTN, or HF ⇒ IV Nitroglycerin
• If persistent severe pain ⇒ IV Morphine
• If unstable sinus bradycardia ⇒ IV Atropine
• If “flash” pulmonary edema ⇒ IV Furosemide
• Reperfusion:
• PTCA (percutaneous transluminal coronary angioplasty) within 90 min
• Thrombolysis if PTCA not available within 120 min
Post-MI Complications…
• 43 y/o male w/ hx of allergic rhinitis and eczema
develops SOB and dry cough 1 day after presenting
with chest pain treated w/ ASA, clopidogrel,
metoprolol, LMWH, and lisinopril
• Likely bronchoconstriction 2/2 ASA and/or metoprolol in a pt
with undiagnosed asthma
• Cardiac cath and stenting POD 3: pt develops vague
abdominal pain, livedo reticularis, cyanotic toes w/
palpable pedal pulses, ↑ Cr
• Atheroembolism (cholesterol emboli) 2/2 large vessel
atherosclerotic plaque disruption during cardiac cath
• Acute or w/in 3-5 days: chest pain, new holosystolic
murmur, biventricular failure, shock, SOB
• Interventricular Septum Rupture
HOCM
• Inheritance pattern?
• AD
• Primary MV abnormality? How does this contribute?
• Systolic anterior motion of the mitral valve
• During systole, contact between mitral valve and thickened
interventricular septum leads to LVOT (LV outflow tract obstruction)
• Characteristic murmur?
• Crescendo-decrescendo systolic murmur along L sternal border
w/out radiation to the carotids
• What happens to the murmur when preload is decreased?
• Gets louder!
• ↓ preload → ↓ LV blood volume → ↓ obstruction → ↑ intensity
AV Fistulas
• AVFs can cause high-output HF by…
• Shunting blood past capillary beds, causing ↑ preload →
↑ contractility
• Best test for dx?
• Doppler of suspected AVF
• Tx?
• Surgery (for large AVF only)
Viral Myocarditis
• Typical presentation?
• S/s of decompensated heart failure (ie, dyspnea,
orthopnea, peripheral edema)
• Do patients always have a viral prodrome?
• NO! Most do (often for several weeks) but not all!
Carotid Artery Stenosis
• All patients with CAS ⇒ ASA + Statin
• Asymptomatic = CAS without recent TIA/stroke
• Medical management only
• Strict blood pressure control
• Symptomatic = CAS with TIA/stroke within 6 mos.
• Medical management ± Surgery
• Carotid endarterectomy (CEA) for 70%-99% occlusion
• CEA preferred to stenting
Valves
• Diastolic or continuous murmurs always warrant…
• TTE (b/c they are most likely 2/2 a pathological cause)
• MC cause of aortic stenosis in the elderly?
• Age-dependent idiopathic sclero-calcific changes to the valve
• MC cause of aortic stenosis in younger population?
• Bicuspid aortic valve
• In severe, chronic aortic regurgitation, the LV volume
overload is initially asymptomatic because…
• CO is first maintained via Frank-Starling (↑ LV stretch → ↑
SV)
• LV volume overload then leads to eccentric hypertrophy
• CO is later preserved via ↑ LV compliance and ↑ LV
contractility
Pericarditis
• Pleuritic chest pain; better with sitting up
• ECG ⇒ diffuse ST elevation & PR depression
• Uremic pericarditis
• Acute/chronic renal patients with BUN > 60
• Lacks typical ECG findings because of inflammation does
not involve myocardium
• 50% of these pts will also have a pericardial effusion
(rule out tamponade before starting dialysis)
• Tx with dialysis
Random
• S3
• Heard during rapid filling of ventricles in diastole (right after S2)
• Normal: children, young adults, pregnancy
• Abnormal: age > 40, heart failure, restrictive cardiomyopathy, high-output states
• S4
• Heard as blood is forced into stiff ventricle (right before S1)
• Normal: healthy older adults
• Abnormal: children, young adults, ventricular hypertrophy, acute MI
• Scaling, weeping, superficial erosions, pitting edema in lower extremities
• Stasis Dermatitis
• Dx based on clinical findings; can be confirmed with venous doppler, but not typically performed
• What is the immediate tx of PEA?
• CPR
• Vasopressors (epi)
• Attempt to identify and tx the reversible causes of PEA (the 5H’s and T’s)
• Pt w/ prolonged tachyarrhythmia w/ RVR presents with 1 month hx of dyspnea, exercise intolerance, fatigue; previously no issues
• Tachycardia-Mediated Cardiomyopathy
• Initial tx aimed at restoration of normal sinus rhythm or aggressive control of ventricular rate
• What’s the difference between cardioversion and defibrillation?
• Cardioversion is synchronized to the QRS complex (minimizes likelihood of shock being delivered during repolarization, potentially
precipitating V Fib)
• Defibrillation is delivered at a random moment during the cardiac cycle (indicated for V Fib or pulseless V Tach)
Atrial Fibrillation
• MC location of ectopic foci?
• Pulmonary veins
Peripheral Artery Dz
• Main cause of M&M in pts w/ PAD?
• CV disease
• Pt with PAD and intermittent claudication:
• 20% 5-year risk of nonfatal MI or stroke
• 15-30% 5-year risk of death due to CV causes
• <2% of pts will develop critical limb ischemia requiring
amputation
Heart Failure
• Inotrope ⇒ affects contractility
• Chronotrope ⇒ affects rate
• Dobutamine
• Strong β1 receptor agonist (weak β2 and α1 activity)
• Potent inotropic agent → ↑ Cardiac contractility → ↑
EF (↓ LV ESV) → symptomatic improvement of
decompensated HF
• CHF due to LV Systolic Dysfunction
• ↓ CO/CI; ↑ SVR; ↑ LV EDV
• Cardiac Index (CI) = CO / body surface area
Aortic Dissection
• What is the strongest overall RF?
• Hypertension, especially in pts > 60 y/o
• What is an important RF in pts < 40 y/o?
• Marfan S/D
• What is the medical management?
• IV β-blockers (ie, labetalol, esmolol, propranolol) to ↓ SBP and ↓ LV
contractility
• Pain control (morphine)
• ±Sodium Nitroprusside if SBP > 120
• What is Type A?
• When ascending aorta is involved
• What is Type B?
• When ascending aorta is NOT involved
• Why is this important?
• Type A is a surgical emergency!
Hyperlipidemia
• What are the 2 types of lipids found in our blood?
• Cholesterols & Triglycerides
• What are the complications of hyperTG?
• If TGs > 150 ⇒ increased risk of CV events
• If TGs > 1000 ⇒ pancreatitis
• What is the tx of hyperTG?
• If 150-500 ⇒ lifestyle modifications (minimal EtOH intake, wt loss, exercise) ± statin (if at
risk for CV event)
• If >1000 ⇒ fibrates, fish oil, abstinence from EtOH (all for goal of pancreatitis prevention)
• What’s the mechanism behind high-dose niacin’s major adverse effect?
• Prostaglandin-induced peripheral vasodilation ⇒ flushing; pruritus
• Preventable with low-dose ASA
• Statin Therapy Guidelines:
• Clinically significant ASCVD
• LDL ≥ 190
• Age 40-75 w/ DM
• Estimated 10-yr ASCVD risk ≥ 7.5%
 Hypertension
• Pt with new diagnosis of HTN… What happens during initial evaluation?
• Initial Evaluation ⇒ Identify any complications of HTN or any comorbidities; screen for major ASCVD risk factors
• Renal Labs: BMP, CBC, U/A
• Endocrine Labs: TSH, A1C or fasting glucose, lipid panel
• Cardiac Tests: ECG, echo (optional)
• Isolated Systolic HTN
• 2/2 increased stiffness and decreased elasticity of arterial walls
• Tx is similar to essential HTn
• Young female with persistently elevated HTN
• Fibromuscular Dysplasia
• Noninflammatory and nonatherosclerotic
• Presentation based on which arteries are involved
• ↓ Renal perfusion → ↑ Renin & ↑ Aldosterone → Secondary Hyperaldosteronism
• Confirm dx with CT angiography of the abdomen
• Renal Parenchymal Dz
• Renovascular Dz
• Primary Aldosteronism
• Pheochromocytoma
• Cushing S/D
• Hypothyroidism
• Primary Hyperparathyroidism
• HyperCa, kidney stones, neuropsychiatric presentation
• “Stones, bones, groans, psychiatric overtones”
• Coarctation of the Aorta
Pulmonology
• What medications are common triggers for
asthmatics?
• ASA and nonselective β-blockers (both commonly used
in MI therapy)