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Cardiology Pearls

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

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?

What are common coronary vasospasm triggers?

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

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

Describe the Framingham Risk Score.

What are some non-ACS causes of ST elevations?

What are the indications for a coronary stent?

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

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

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

What is the differential diagnosis for a troponin leak?

 

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

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

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?

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

What are the indications for aortic valve replacement?

 

Describe the findings of the AFFIRM trial.

  • There was no survival difference between rate or rhythm controlling in atrial fibrillation
  • There were more adverse medication complications in the rhythm control group
  • 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

 

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

 

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

What is the conversion between diuretic dosages?

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)

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?

 

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?

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

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

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

What are some non-ACS causes of ST elevations?

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)

 

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: 

How sensitive is echocardiogram for detecting vegetations?

What are the HACEK organisms in endocarditis?

What are the complications of septic emboli?

 

How is each type of heart block managed?

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

 

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)

 

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

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?

 

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

 

 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?

 

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?

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

 

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

 

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

 

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

 

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

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

How do you treat pericarditis?

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

 

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

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

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

 

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

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

 

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)

 

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

 

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

 

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

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

 

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

 

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)

 

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