Perelman School of Medicine at the University of Pennsylvania

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Cardiology Pearls

Acute Coronary Syndrome/Coronary Artery Disease

Describe the rise and fall of cardiac biomarkers in ischemia.

  • Order of biomarker rise: myoglobin, creatine kinase, troponin
  • Creatine kinase stays high for 3-4 days while troponin stays high for 7-10 days
  • If you are looking for a second ischemic event soon after, creatinine kinase is most likely to be helpful since it rises and falls faster than troponin
  • Review of the utility of troponin assays in acute coronary syndrome: http://www.ncbi.nlm.nih.gov/pubmed/26274536

What is the differential diagnosis for chest pain?

  • Cardiac: stable angina, acute coronary syndrome, coronary artery vasospasm, aortic stenosis, pericarditis, Takotsubo's cardiomyopathy
  • Pulmonary: pneumonia, pneumothorax, pulmonary embolism, pleuritis, rib fracture or metastases
  • GI: GERD, diffuse esophageal spasm, pill esophagitis, gastritis, peptic ulcer, Mallory Weiss tear, Boerhaave’s syndrome, pneumomediastinum
  • Psychiatry: panic attack, somatization disorder
  • JAMA Rational Clinical Examination on Does this Patient with Chest Pain Have Acute Coronary Syndrome? http://www.ncbi.nlm.nih.gov/pubmed/26547467  

What are common coronary vasospasm triggers?

  • Definition of coronary artery vasospasm: smooth muscle constriction severe enough to cause ischemia
  • Triggers: cocaine, tobacco, hyperventilation, also intentional administration of acetylcholine, ergonovine, serotonin, or histamine
  • NEJM video of coronary vasospasm on left heart catheterization: http://www.nejm.org/doi/full/10.1056/NEJMicm1503339

How is acute coronary syndrome defined?

  • ACS is generally associated with rupture of an atherosclerotic plaque or thrombosis of a coronary artery
  • Three classifications:
    • Unstable angina: new chest pain or chest pain not relieved with rest
    • NSTEMI: as above but with cardiac enzyme elevation but no ST elevation
    • STEMI: as above but with ST elevation
  • Review of acute coronary syndrome diagnosis and management: http://www.ncbi.nlm.nih.gov/pubmed/26380430

What are some causes of demand ischemia?

  • Physical exertion
  • Emotional stress
  • Physiologic demand stress from volume overload, hypotension/hypovlemia, infection, thyrotoxicosis, or surgical stress

What are the secondary causes of dyslipidemia?

  • High LDL: nephrotic syndrome, primary biliary cirrhosis, hypothyroidism, anorexia nervosa
  • Low HDL: diabetes mellitus, obesity, cigarette smoking
  • High triglycerides: diabetes mellitus, chronic kidney disease, hypothyroidism, alcoholism, pregnancy
  • Prevalence of dyslipidemia in different ethnic groups: http://www.ncbi.nlm.nih.gov/pubmed/26893006

Describe the Framingham Risk Score.

  • Assesses 10-year risk of coronary heart disease based on several risk factors
  • Components: age, total cholesterol, HDL, smoking status, systolic blood pressure and if currently being treated for hypertension
  • Ranges reported as 1% to >30%
  • Article on using the Framingham risk assessment four years after initial assessment: http://www.ncbi.nlm.nih.gov/pubmed/26895071

What are some non-ACS causes of ST elevations?

  • Left bundle branch block, right heart strain, pericarditis, cardiac contusion, vasopasm or Prinzmetal’s angina, Takotsubo’s, LV aneurysm, early repolarization
  • JAMA article on interpretation of ST elevations: http://www.ncbi.nlm.nih.gov/pubmed/26280655

What are the indications for a coronary stent?

  • Stable angina, NSTEMI, STEMI
  • Anginal equivalent: arrhythmias, shortness of breath, dizziness, syncope
  • Mildly symptomatic patients with moderate to severe ischemia on non-invasive testing
  • Review of acute coronary syndrome diagnosis and management: http://www.ncbi.nlm.nih.gov/pubmed/26380430

What antiplatelet therapy is needed in each kind of coronary stent?

  • Bare metal stent:
    • Metal in the form of a tubular mesh, coil, or slotted tube to increase coronary artery lumen size
    • Requires at least 1 month of dual antiplatelet therapy but preferably 1 year
  • Drug-eluting stent:
    • Scaffolds made of steel or a cobalt/chromium matrix with a polymer embedded with an antiproliferative drug
    • Requires at least 1 year of dual antiplatelet therapy
  • Review of dual antiplatelet therapy in older and newer stents: http://www.ncbi.nlm.nih.gov/pubmed/26858081

Which statin is safest in liver disease?

  • Liver disease (hepatitis, cirrhosis) is not a contraindication to using statins
  • Pravastatin usually has the lowest incidence of myopathies and is safest in liver disease
  • Safety profile of statins: http://www.ncbi.nlm.nih.gov/pubmed/16581329

What are the contraindications to cardiac stress testing?

  • Absolute contraindications: acute MI or unstable angina, uncontrolled cardiac arrhythmias or CHF, pulmonary embolism, symptomatic severe aortic stenosis, myocarditis/pericarditis, aortic dissection
  • Relative contraindications: left main coronary artery stenosis, BP above 200/110, moderate valvular stenosis, hypertrophic cardiomyopathy, high degree AV block

What are the types of cardiac stress tests?

  • Useful if a patient cannot exercise enough to tolerate a treadmill test or cannot achieve the target heart rate through exercise
  • Adenosine (and its analog regadenoson used in a Lexiscan) and dipyridamole (Persantine) are cardiac vasodilators which increase blood flow to normal vessels and decrease blood flow to stenotic vessels (thus the coronary steal)
  • Dobutamine increases inotropy and chronotropy mimicking exercise

What are the absolute contraindications to thrombolysis?

  • Absolute contraindications: prior intracranial hemorrhage, ischemic stroke within 3 months, known intracranial aneurysm/AV malformation, intracranial tumor, significant head or facial trauma within 3 months

Describe the TIMI Risk Score.

  • Used to estimate 14 day all-cause mortality, new or recurrent MI, or severe ischemia requiring urgent revascularization for patients with unstable angina or NSTEMI
  • 7 components: age > 65, 3 or more CAD risk factors, known CAD with >50% stenosis, ASA use in last 7 days, severe angina in last 24hrs, elevated enzymes, ST deviation greater than 0.5mm
  • On the lower side: 0-1 points is 3-5%, 2 points is 5-13%
  • On the higher side: 6-7 points is 19-41%
  • Comparison of the HEART and TIMI risk scores for acute coronary syndrome: http://www.ncbi.nlm.nih.gov/pubmed/26881812

What is the differential diagnosis for a troponin leak?

  • NSTEMI/STEMI, CHF exacerbation, Afib RVR, sepsis, Takotsubo’s cardiomyopathy, myocarditis, anthracycline cardiotoxicity, subendocardial wall stress, renal failure
  • Discussion of the differential diagnosis of a troponin leak: http://www.ncbi.nlm.nih.gov/pubmed/26777618

 

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Aortic Disease

How are aortic dissections classified?

  • Two classification systems: Stanford and DeBakey
  • Stanford classification:
    • Type A: involves the ascending aorta
    • Type B: does NOT involve the ascending aorta
  • DeBakey classification:
    • Type I: involves ascending aorta, aortic arch, and descending aorta
    • Type II: just the ascending aorta
    • Type IIIa: descending aorta distal to left subclavian artery but extend proximally and distally above the diaphragm
    • Type IIIb: descending aorta distal to left subclavian artery but extends distally and below the diaphragm
  • Radiology paper on dissections that don’t fit into current classifications: http://www.ncbi.nlm.nih.gov/pubmed/24617732

Describe the acute management of an aortic dissection.

  • BP control: use beta blockers or nitroprusside with goal SBP 100-120 to prevent shear forces (can use calcium channel blockers like nifedipine if BB contraindicated)
  • HR control: use beta blockers to bring HR to 60-80 bpm
  • Stanford Type A (DeBakey Type I/II): generally needs resection of the part of the aorta that has the intimal tear and replace with a graft
  • Stanford Type B (DeBakey Type III): if uncomplicated can do medical management of BP, usually only distal dissections that are leaking, ruptured, or causing poor perfusion to a vital organ get surgical intervention
  • ADSORB trial for the management of acute type B aortic dissection: http://www.ncbi.nlm.nih.gov/pubmed/25306065

What are some causes of aortic regurgitation?

  • Rheumatic fever/infective endocarditis
  • Degenerative aortic valve disease or collage vascular disease
  • Post-surgery
  • Traumatic

What are the pathognomonic physical exam findings for aortic regurgitation?

  • Corrigan’s pulse: rapid, forceful distension of the arterial pulse with quick collapse
  • De Musset’s sign: bobbing of the head with each heartbeat
  • Duroziez’s sign: gradual pressure over femoral artery leads to bruit
  • Hill’s sign: popliteal SBP 60mmHg greater than brachial SBP (most sensitive sign for aortic regurgitation)
  • Landolfi’s sign: systolic contraction and diastolic dilation of the pupil
  • Quincke’s sign: capillary pulsations on light compression of the nail bed
  • Shelly’s sign: pulsation of the cervix
  • Traube’s sign: systolic and diastolic “pistol shot” sounds over the femoral artery
  • JAMA Rational Clinical Examination on Does this Patient Have Aortic Regurgitation? http://www.ncbi.nlm.nih.gov/pubmed/10376577

What are the most common causes of aortic stenosis in young and old patients?

  • Younger patient: bicuspid aortic valve
  • Older patient: senile calcification on aortic valve

How do we grade aortic stenosis severity?

  • Severity: (G=gradient, AVA=aortic valve area cm2)
  • Normal: 0, 3-4 (not bad until 2)
  • Mild: <25, 1.5-2
  • Moderate: 25-40, 1.0-1.5
  • Severe:  >40,  0.6-1.0
  • Critical: >60, <0.6

What physical exam findings suggest the severity of aortic stenosis?

  • Three physical exam findings that can suggest the severity of aortic stenosis
    • Timing of the murmur peak: worse if later in systole
    • Intensity of S2: worse if soft or absent
    • Pulsus parvus et tardus: worse if carotid upstroke is weak and late

What three symptoms or diagnoses increase the risk of aortic stenosis mortality?

  • Remember the sequelae in order as “ASH” since these are associated with a mortality increase
  • Once you develop the following sequelae of aortic stenosis your 50% mortality rate is:
    • Angina: 50% mortality in 5 years
    • Syncope: 50% mortality in 3 years
    • Heart Failure: 50% mortality in 2 years
  • Prognostic factors in elderly patients with severe aortic stenosis: http://www.ncbi.nlm.nih.gov/pubmed/25890579

What are the indications for aortic valve replacement?

  • Symptomatic severe aortic stenosis
  • Severe AS undergoing CABG
  • Severe AS undergoing aortic or other valvular surgery
  • Severe AS with LVEF<50%
  • 2014 AHA/ACC guidelines for valvular heart disease: http://www.ncbi.nlm.nih.gov/pubmed/24939033

 

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Atrial Fibrillation/Flutter

Describe the findings of the AFFIRM trial.

What are the causes of atrial fibrillation?

  • Remember “PIRATES” for the causes of Afib
  • P: pulmonary disease or PE
  • I: ischemia
  • R: rheumatic heart disease or mitral stenosis/regurgitation
  • A: alcohol
  • T: thyroid disease (hyperthyroidism)
  • E: elevated BP
  • S: sepsis or surgery

How do we define paroxysmal, persistent, and permanent atrial fibrillation?

  • Paroxysmal atrial fibrillation: episodes last for less than 7 days at a time (usually less than 1 day)
  • Persistent atrial fibrillation: episodes last for more than 7 days
  • Permanent atrial fibrillation: has lasted more than a year with or without cardioversion

How do you treat atrial fibrillation with rapid ventricular response?

  • Acute rate control: metoprolol, diltiazem (both can be IV or oral)
  • Acute rhythm control: IV amiodarone continuous infusion with IV/oral amiodarone load
  • If unstable then consider synchronized cardioversion

What are the CHADS2 Score/CHAD2DS2VASc Score?

  • CHADS2 Score:
    • CHF (1), Hypertension (1), Age >75 (1), Diabetes (1), Stroke/TIA (2)
  • CHA2DS2VASc Score:
    • CHF (1), Hypertension (1), Age >65 (1) or Age >75 (2), Diabetes (1), Stroke/TIA (2), Vascular disease (PAD, MI, aortic aneurysm atheroma) (1), Sex category-female (1)
  • Score 0-1: consider aspirin
  • Score >1: consider full anticoagulation (ex: warfarin, novel oral anticoagulant)
  • Paper introducing the CHA2DS2VASc score: http://www.ncbi.nlm.nih.gov/pubmed/20569748

 

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Cardiogenic Shock

How does each cardiac pressor affect inotropy and systemic vascular resistance?

  • Dopamine: increase inotropy, increase SVR
  • Dobutamine, increase inotropy, decrease SVR
  • Milrinone: increase inotropy, decrease SVR

 

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Congestive Heart Failure

What are the three main types of cardiomyopathy?

  • Dilated cardiomyopathy (systolic dysfunction with causes including alcohol, arrhythmias, idiopathic, viral, familial, etc)
  • Hypertrophic cardiomyopathy (HOCM)
  • Restrictive cardiomyopathy (severe diastolic dysfunction with causes including infiltrative disorders, amyloid, or familial)

What are the signs of digoxin toxicity?

  • Think of digoxin toxicity if a patient on digoxin has an acute kidney injury
  • Yellow vision changes (xanthopsia)
  • Almost every arrhythmia except for Afib RVR
  • Nausea/vomiting/abdominal pain
  • Altered mental status
  • Dizziness/weakness
  • Hyperkalemia (though digoxin toxicity can be potentiated by hypokalemia)
  • Reverse digoxin with Digibind (digoxin immune Fab fragments)
  • Review of digoxin toxicity: http://www.ncbi.nlm.nih.gov/pubmed/22444097

What is the conversion between diuretic dosages?

  • Oral: Bumetanide 1mg PO = Furosemide 40mg PO = Torsemide 20mg PO
  • IV: Bumetanide 1mg IV = Furosemide 20mg IV = Torsemide 10mg IV
  • Website for converting diuretic doses: http://www.globalrph.com/diuretics.htm

Name some causes of CHF exacerbations.

  • Medication noncompliance
  • Fluid/sodium restriction noncompliance
  • Arrhythmia (example: Afib with RVR)
  • Ischemia
  • Progression of valvular disease

What are the NYHA and ACC/AHA classifications in CHF?

  • Classification: NYHA Class: 1 (CHF no symptoms), 2 (slight limit), 3 (marked limit), 4 (significant limit).
  • Classification: ACC/AHA Stage: A (at risk of CHF, no symptoms), B (structural disease but no signs of CHF), C (structural with prior/current symptoms), D (refractory needing advanced therapies)

Which medications provide mortality in CHF?

  • 5 classes of CHF medications with mortality benefit
  • ACE inhibitor: captopril, enalapril, lisinopril
  • Beta blocker: only bisoprolol, carvedilol, metoprolol succinate (XL)
  • Hydralazine: proven in African Americans with isosorbide dinitrate
  • Isosorbide dinitrate: proven in African Americans with hydralazine
  • Spironolactone: for NYHA Class II-IV CHF with EF<35%)
  • 1987 paper that was the first to show ACE inhibitors as a mortality benefit (CONSENSUS I): http://www.ncbi.nlm.nih.gov/pubmed/2883575

Which medications only provide symptom relief and hospitalization decrease in CHF?

  • These medications only improve symptoms and reduce hospitalizations but do not improve mortality
  • Furosemide (or other diuretics)
  • Digoxin

How do you diurese a patient with a sulfa allergy?

 

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EKG Findings

What are the most common EKG findings in hyperkalemia?

  • Peaked T waves (across different vascular territories)
  • P wave widening and flattening
  • PR segment lengthening
  • QRS complex widening
  • Sinusoidal wave

What does each of the following pathognomonic EKG findings suggest?

  • Delta wave: Wolff-Parkinson White
  • Osborne wave (J-wave): hypothermia or hypercalcemia
  • U wave: hypokalemia

How on an EKG can you differentiate pericarditis from a STEMI?

  • Pericarditis: ST elevations in every lead crossing vascular territories (sometimes not aVR), rarely has reciprocal depressions, can have PR depressions
  • STEMI: in contiguous leads indicating a particular vascular territory, often has reciprocal ST depression
  • Review of pericarditis: http://www.ncbi.nlm.nih.gov/pubmed/25517707

What are the EKG findings in pulmonary embolism?

  • Sinus tachycardia is the most common
  • S1Q3T3 (large downward S wave in I, deep Q wave in III, downward T wave in III) is pathognomonic but can also occur in anything that causes right heart strain such as pulmonary disease
  • Also consider atrial fibrillation with rapid ventricular response especially post-surgery
  • Role of EKG findings in diagnosing pulmonary embolism: http://www.ncbi.nlm.nih.gov/pubmed/26512143

What are the causes of prolonged QT?

  • Medications (antiarrhythmics, antipsychotics, fluoroquinolones, macrolides, etc)
  • Electrolyte abnormalities (hypokalemia, hypocalcemia, hypomagnesemia)
  • Genetic or idiopathic long QTc syndromes
  • QT prolongation puts patients at risk of Torsades de Pointes (polymorphic ventricular tachycardia)
  • Review of antipsychotics and QT prolongation: http://www.ncbi.nlm.nih.gov/pubmed/26649027

What are some non-ACS causes of ST elevations?

  • Left bundle branch block, right heart strain, pericarditis, cardiac contusion, vasopasm or Prinzmetal’s angina, Takotsubo’s, LV aneurysm, early repolarization
  • JAMA article on interpretation of ST elevations: http://www.ncbi.nlm.nih.gov/pubmed/26280655

Describe the EKG vascular territories.

  • I/AVL/V5/V6: lateral (left circumflex artery)
  • II/III/AVF: inferior (right coronary artery)
  • V1/V2: septal (left anterior descending artery and left circumflex artery)
  • V1-V4: anterior (left anterior descending artery)

 

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Endocarditis

What are the classifications of infective endocarditis?

  • Native valve versus prosthetic valve
  • Short incubation (acute) versus long incubation (subacute)
  • Culture negative versus culture positive
  • Right sided versus left sided

What are the Duke Criteria for infective endocarditis?

  • Pathologic Criteria:
    • Positive culture of vegetation
    • Vegetation or abscess confirmed
  • Major Clinical Criteria:
    • Positive blood cultures commonly associated with endocarditis
    • Echocardiogram evidence of endocarditis
  • Minor Clinical Criteria:
    • Predisposing heart condition or IV drug use
    • Fever
    • Vascular phenomena (emboli, infarcts, Janeway lesions)
    • Immunologic phenomena (Osler’s nodes, Roth’s spots, glomerulonephritis)
    • Positive blood culture but not meeting major criteria.
  • Requirements for diagnosis: 2 major, 1 major and 3 minor, or 5 minor
  • The original 1994 paper introducing the Duke criteria for endocarditis: http://www.ncbi.nlm.nih.gov/pubmed?term=8154507

How sensitive is echocardiogram for detecting vegetations?

What are the HACEK organisms in endocarditis?

  • Haemophilus aphrophilus
  • Actinobacillus actinomycetemcomitans
  • Cardiobacterium hominis
  • Eikenella corrodens
  • Kingella kingae
  • Prospective cohort study on the causative organisms of infective endocarditis (http://www.ncbi.nlm.nih.gov/pubmed?term=19273776)

What are the complications of septic emboli?

  • Cardiac: coronary artery embolism (myocardial infarction)
  • CNS: embolic stroke, retinal artery embolism, subdural hemorrhage (mycotic aneurysms)
  • Pulmonary: pulmonary embolism for right sided endocarditis, pleural effusion/empyema
  • Renal: renal emboli
  • Spleen: splenic infarction
  • A 2008 paper found 30% of patients with left-sided infective endocarditis had clinically silent strokes on MRI (http://www.ncbi.nlm.nih.gov/pubmed/?term=18491965)

 

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Heart Block

How is each type of heart block managed?

  • 1st degree heart block: no treatment unless symptomatic
  • 2nd degree heart block:
    • Mobitz Type I aka Wenckebach: no treatment unless symptomatic
    • Mobitz Type II: usually needs temporary and/or permanent pacing
  • 3rd degree heart block: usually needs temporary and/or permanent pacing
  • 2016 meta-analysis of adverse cardiac events related to first-degree heart block: http://www.ncbi.nlm.nih.gov/pubmed/26879241

What are the types of heart block?

  • 1st degree heart block: PR prolongation > 200 milliseconds
  • 2nd degree heart block:
    • Mobitz Type I aka Wenckebach: progressive PR prolongation until a P wave doesn’t get conducted to the ventricles (dropped beat)
    • Mobitz Type II: constant PR interval then a P wave that doesn’t get conducted to the ventricles (dropped beat)
  • 3rd degree heart block: P waves and QRS complexes occur at fixed intervals but are not coordinated together

 

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Heart Transplantation

What are some contraindications to heart transplant?

  • Age > 65 (though this is a relative contraindication, differs based on institution)
  • Pulmonary vascular resistance > 4 Woods units even after pulmonary HTN meds
  • Active malignancy (some exceptions can be made for 3-5 year disease-free periods)
  • Active infection or systemic disease (collagen vascular disease)
  • Psychosocial instability (substance use, non-compliance)

 

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Hypertension

What are some considerations in ACE inhibitor initiation?

  • Expected/tolerable creatinine rise: 30% rise
  • Generally okay to use ACE inhibitor up to creatinine of 3 (but no absolute contraindication based on creatinine)
  • Cough, angioedema can occur at any point while taking an ACE inhibitor
  • Monitor for hyperkalemia (about 5% of patients will go above K 5.7, usually if already with kidney disease or diabetes, usually not in renocompetent patients)

What are examples of end-organ damage in hypertensive emergency?

  • Cardiac: MI or angina, aortic dissection, acute left ventricular dysfunction or acute pulmonary edema
  • Neurologic: stroke, hemorrhage, encephalopathy, retinopathy
  • Other: acute kidney injury, eclampsia
  • Review article of hypertensive emergency: http://www.ncbi.nlm.nih.gov/pubmed/26893930

What are the causes of secondary hypertension?

  • Most common: obstructive sleep apnea, then renal artery stenosis
  • Medications/Toxins (alcohol, oral contraceptives/estrogens, NSAIDs, nasal decongestants)
  • Endocrine disorders: hyperaldosteronism (Conn’s syndrome), Cushing’s syndrome, pheochromocytoma, acromegaly
  • Cardiac abnormalities: coarctation

What are the stages of hypertension?

 

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Implantable Cardiac Defibrillator

What are the Class I indications for an ICD?

  • Structural heart disease
  • Sustained VT
  • Inducible VT/VF in setting of syncope
  • LVEF <35% NYHA Class II or III
  • LVEF <30% due to MI at least 40 days ago
  • LVEF <40% due to MI but also with inducible VT/VF

How do you turn off a pacemaker/ICD?

  • Once a patient with an ICD has decided that an ICD shock is not consistent with the goals of care, you must disable the ICD to prevent inappropriate shocks
  • Place a magnet over the ICD which will prevent an ICD discharge but does NOT turn off the pacemaker
  • Patient’s perspectives on deactivating ICDs at end of life: http://www.ncbi.nlm.nih.gov/pubmed/23490027

 

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IVC Filter

 What are the indications for an IVC filter?

  • DVT or PE with contraindication or s/p complication of anticoagulation
  • Failure of anticoagulation therapy (new embolic event while on anticoagulation)
  • Free-floating iliofemoral or IVC thrombus

What are the complications of an IVC filter?

  • From jugular access: pneumothorax, access site thrombosis, bleeding
  • From filter itself: IVC trauma/penetration, filter fracture/migration/infection, IVC thrombus, death
  • Feasibility of removing two types of IVC filters: http://www.ncbi.nlm.nih.gov/pubmed/26486152

 

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Mitral Valve Disease

Name some causes of mitral regurgitation.

  • Functional: from cardiomyopathy or left atrial dilation
  • Organic: myxomatous or collagen/vascular changes, papillary muscle dysfunction or chordal rupture related to ischemia, rheumatic heart disease, endocarditis

How do you manage mitral regurgitation?

  • Afterload reduction (includes beta blockers, ACE inhibitors, hydralazine)
  • Diuretics
  • Consideration of intra-aortic balloon pump
  • Consideration of mitral valve surgery if severe mitral regurgitation
  • 2014 AHA/ACC guidelines for valvular heart disease: http://www.ncbi.nlm.nih.gov/pubmed/24939033

How do we classify mitral stenosis based on valve size?

  • Normal mitral valve area: 4-6 cm2
  • Symptomatic mitral stenosis: about 2-2.5 cm2
  • Severe mitral stenosis: < 1 cm2

 

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Multifocal Atrial Tachycardia

What is the definition of multifocal atrial tachycardia?

  • Arrhythmia caused by multiple sites of atrial activity
  • Atrial rate irregular and greater than 100 bpm
  • 3 morphologically different P waves
  • Isoelectric baseline between P waves

 

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Murmurs

What causes of a holosystolic murmur?

  • Mitral regurgitation, tricuspid regurgitation, VSD (ventricular septal defect)

Which murmurs get louder with inspiration?

  • Tricuspid regurgitation (called Carvallo’s sign) and pulmonic regurgitation

Which murmurs get louder with squatting?

  • Aortic stenosis

Which murmurs get louder with Valsalva?

  • HOCM (hypertrophic obstructive cardiomyopathy)
  • Valsalva decreases left ventricular filling which allows the thick septum in HOCM to bulge into the LV causing more outflow obstruction

What causes an S3 or S4 sound?

  • Order of heart sounds: S1, S2, S3, S4 (thus S4 happens right before S1 and S3 happens right after S2)
  • S3: can be in systolic heart failure or normal hearts
  • S4: can be in diastolic heart failure

 

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Pacemaker

What are the absolute indications for pacemakers?

  • Sick sinus syndrome or tachycardia/bradycardia syndrome
  • Symptomatic sinus bradycardia
  • Complete AV block
  • Chronotropic incompetence (can’t raise heart rate during exercise)
  • Prolonged QT syndrome
  • Cardiac resynchronization therapy

How do you turn off a pacemaker/ICD?

  • Once a patient with an ICD has decided that an ICD shock is not consistent with the goals of care, you must disable the ICD to prevent inappropriate shocks
  • Place a magnet over the ICD which will prevent an ICD discharge but does NOT turn off the pacemaker
  • Patient’s perspectives on deactivating ICDs at end of life: http://www.ncbi.nlm.nih.gov/pubmed/23490027

 

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Pericarditis

What is a normal amount of pericardial fluid?

  • Normal pericardial fluid: 15-50mL
  • Quick accumulation of around 150mL can cause tamponade physiology
  • Larger amounts up to 2L can occur if accumulated slowly
  • Post-cardiac surgery, you can have a loculated pericardial effusion next to only one chamber that also causes tamponade physiology

What are the causes of pericarditis?

  • Idiopathic, infectious (viral, bacterial, tuberculous), inflammatory (rheumatologic causes), metabolic (renal failure or hypothyroidism), post-MI/Dressler’s syndrome, neoplastic, post-surgical, drug-induced lupus, radiation
  • Review of pericarditis: http://www.ncbi.nlm.nih.gov/pubmed/25517707

How do you differentiate pericarditis from a STEMI on EKG?

  • Pericarditis: ST elevations in every lead crossing vascular territories (sometimes not aVR), rarely has reciprocal depressions, can have PR depressions
  • STEMI: in contiguous leads indicating a particular vascular territory, often has reciprocal ST depression
  • Review of pericarditis: http://www.ncbi.nlm.nih.gov/pubmed/25517707

How do you treat pericarditis?

  • If appropriate, treat the underlying cause (antibiotics, chemotherapy, immunosuppressants)
  • NSAIDs (can include aspirin and ibuprofen)
  • Steroids
  • Anti-inflammatory agents (colchicine)
  • 2015 JAMA review of evaluation and treatment of pericarditis: http://www.ncbi.nlm.nih.gov/pubmed/26461998

What are the physical exam findings of cardiac tamponade?

  • Exam
    • Beck’s triad: hypotension, soft/muffled heart sounds, elevated JVP
    • Pulsus paradoxus: > 12mmHg

What are the radiology findings of cardiac tamponade?

  • Radiology
    • Water bottle heart on CXR
    • Pericardial effusion on echo (can be circumferential or adjacent to one chamber especially post-surgery)

How do you treat cardiac tamponade?

  • Treat the underlying cause (ex: systemic inflammation, coagulopathy, infection, perforation)
  • IV fluids to increase preload and prevent right ventricular collapse
  • Consider pericardiocentesis (in an emergency can do subxiphoid percutaneous drainage)
  • Misconceptions about pericardial effusions and tamponade: http://www.ncbi.nlm.nih.gov/pubmed/23891285

 

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Pharmacology in Cardiology

What are the toxicities of amiodarone?

  • Remember to check PFTs, TFTs, LFTs
  • Pulmonary function tests: can lead to interstitial lung disease
  • Thyroid function tests: check TSH every 6 months for hypo- or hyper-thyroidism
  • Liver function tests: no routine testing recommended
  • Can also lead to bradycardia and hypotension especially for IV amiodarone

What are the classes of antiarrhythmics?

  • Class IA: quinidine, amiodarone, procainamide, disopyrimide
  • Class IB: lidocaine, mexiletine
  • Class IC: flecainide, propafenone
  • Class II: beta blockers
  • Class III: sotalol, amiodarone (again), dronedarone, dofetilide
  • Class IV: calcium channel blockers (verapamil, diltiazem)

Which beta blockers are lipid soluble and why does this matter?

  • Lipid soluble beta blockers, such as propranolol and metoprolol, can cross the blood-brain barrier
  • Thus these are often used for migraines and panic attacks or stage fright

What are the signs of digoxin toxicity?

  • Think of digoxin toxicity if a patient on digoxin has an acute kidney injury
  • Yellow vision changes (xanthopsia)
  • Almost every arrhythmia except for Afib RVR
  • Nausea/vomiting/abdominal pain
  • Altered mental status
  • Dizziness/weakness
  • Hyperkalemia (though digoxin toxicity can be potentiated by hypokalemia)
  • Reverse digoxin with Digibind (digoxin immune Fab fragments)
  • Review of digoxin toxicity: http://www.ncbi.nlm.nih.gov/pubmed/22444097

Which statin is safest in liver disease?

  • Liver disease (hepatitis, cirrhosis) is not a contraindication to using statins
  • Pravastatin usually has the lowest incidence of myopathies and is safest in liver disease
  • Safety profile of statins: http://www.ncbi.nlm.nih.gov/pubmed/16581329

What are the absolute contraindications of thrombolysis?

  • Absolute contraindications: prior intracranial hemorrhage, ischemic stroke within 3 months, known intracranial aneurysm/AV malformation, intracranial tumor, significant head or facial trauma within 3 months

 

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Pregnancy in Cardiology

Which types of pregnant patients with cardiac conditions warrant a Maternal Fetal Medicine consult?

  • The following are high-risk cardiac conditions which prompt consideration of a Maternal Fetal Medicine consult:
    • Any valvular disease with NYHA Class III or IV symptoms (MR, MS, AR) or severe aortic stenosis regardless of symptoms
    • Aortic and/or mitral valve disease with LV ejection fraction < 40% or pulmonary pressures > 75% of systemic pressures
    • Cardiac complications with prior births
  • Approaches to treating peripartum cardiomyopathy: http://www.ncbi.nlm.nih.gov/pubmed/25927492

How does pregnancy affect cardiac output, BP HR, and hematocrit?

  • Cardiac output increases by 30-50%
  • BP decreases by 10-15 mmHg
  • HR increases by 10-15 bpm
  • Hematocrit decreases due to increased plasma volume

 

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Pulmonary Hypertension

What are the WHO groups in pulmonary hypertension?

  • WHO Group 1: pulmonary arterial hypertension (idiopathic or inherited)
  • WHO Group 2: pulmonary hypertension due to left heart disease
  • WHO Group 3: pulmonary hypertension due to lung disease
  • WHO Group 4: pulmonary hypertension due to chronic thromboembolic disease
  • WHO Group 5: pulmonary hypertension from other causes (includes hematologic, systemic diseases, and metabolic disorders)

How does treatment of pulmonary hypertension vary by WHO Group?

  • Diuretics indicated if volume overload in any Group
  • Anticoagulation indicated in Group 1 and 4
  • Mechanical thrombectomy potentially curable for Group 4
  • Advanced therapies for Group 1 and potentially Groups 3-5 if evidence of vasodilator response
    • Prostacyclins (Epoprostenol aka Flolan)
    • Endothelin Receptor Antagonists (Bosentan)
    • PDE-5 Inhibitors (Sildenafil)

 

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Pulseless Electrical Activity

What are the 6 H’s and T’s of pulseless electrical activity

  • H’s: hypovolemia, hypoxia, hypothermia, hypo/hyperkalemia, hypoglycemia, hydrogen ion (acidosis)
  • T’s: toxins, tamponade, tension pneumothorax, thrombosis (coronary), thrombosis (pulmonary embolism), trauma

 

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Tamponade/Pericardial Effusion

What is a normal amount of pericardial fluid?

  • Normal pericardial fluid: 15-50mL
  • Quick accumulation of around 150mL can cause tamponade physiology
  • Larger amounts up to 2L can occur if accumulated slowly
  • Post-cardiac surgery, you can have a loculated pericardial effusion next to only one chamber that also causes tamponade physiology

What are the physical exam findings of cardiac tamponade?

  • Exam
    • Beck’s triad: hypotension, soft/muffled heart sounds, elevated JVP
    • Pulsus paradoxus: > 12mmHg

What are the radiology findings of cardiac tamponade?

  • Radiology
    • Water bottle heart on CXR
    • Pericardial effusion on echo (can be circumferential or adjacent to one chamber especially post-surgery)

How do you treat cardiac tamponade?

  • Treat the underlying cause (ex: systemic inflammation, coagulopathy, infection, perforation)
  • IV fluids to increase preload and prevent right ventricular collapse
  • Consider pericardiocentesis (in an emergency can do subxiphoid percutaneous drainage)
  • Misconceptions about pericardial effusions and tamponade: http://www.ncbi.nlm.nih.gov/pubmed/23891285

 

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Torsades de Pointes

How do you treat Torsades de Pointes?

  • Magnesium sulfate (IV): can be repeated or given as a drip, but monitor closely to prevent magnesium toxicity
  • Isoproterenol (IV infusion): if bradycardia-dependent Torsades (increasing heart rate decreases QT interval)
  • Temporary transcutaneous/transvenous pacing: again, to increase heart rate and decrease QT interval
  • Unstable or in extremis: cardioversion
  • Pharmacologic treatment of Torsades de Pointes: http://www.ncbi.nlm.nih.gov/pubmed/26183037

What are some causes of QT prolongation?

  • Medications (antiarrhythmics, antipsychotics, fluoroquinolones, macrolides, etc)
  • Electrolyte abnormalities (hypokalemia, hypocalcemia, hypomagnesemia)
  • Genetic or idiopathic long QTc syndromes
  • QT prolongation puts patients at risk of Torsades de Pointes (polymorphic ventricular tachycardia)
  • Review of antipsychotics and QT prolongation: http://www.ncbi.nlm.nih.gov/pubmed/26649027

 

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Tricuspid Valve Disease

What are the causes of tricuspid regurgitation?

  • Cardiac: rheumatic heart disease, endocarditis, tricuspid valve prolapsed, papillary muscle dysfunction, trauma, right ventricular dilation, Ebstein anomaly
  • Systemic: connective tissue diseases (includes Marfan syndrome, osteogenesis imperfect, Ehlers-Danlos syndrome), carcinoid
  • Pharmacologic: medications acting on serotonergic receptors

 

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Ventricular Tachycardia

What are the causes of ventricular tachycardia?

  • Ischemia
  • Electrolyte imbalances
  • Structural heart disease (includes CHF, hypertrophic cardiomyopathy, infiltrative diseases like sarcoid/amyloid)
  • Drug-induced (includes cocaine, methamphetamine, digitalis, other antiarrhythmics)
  • Inherited channelopathies (includes  long QT syndrome)

 

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Wolff-Parkinson-White Syndrome

What are the EKG findings in Wolff-Parkinson-White syndrome?

  • Shortened PR interval
  • Wide QRS
  • Slurred and slow rise of upstroke of QRS complex (delta wave)
  • ST changes in opposite direction of delta wave
  • How do you acutely treat Wolff-Parkinson-White syndrome?
    • Vagal maneuvers (splashing cold water on face, Valsalva, carotid sinus massage)
    • IV adenosine
    • IV verapamil or diltiazem
    • If unstable then synchronized cardioversion
    • Consider radiofrequency ablation
    • Long-term antiarrhythmic medications

 

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