PANCE Blueprint Cardiology (13%)

PANCE Blueprint Cardiology (13%)

PANCE Blueprint Cardiology (13%)

Follow along with the NCCPA™ PANCE and PANRE Cardiology Content Blueprint


  1. Cardiology System Exam (Members Only)

  2. Cardiology System Flashcards

    1. Cardiology Quick Cram Cards

    1. EKG Interpretation (Picmonic)

    2. EKG Cram Cards

    3. EKG Pearls and Pitfalls (video)

    1. Most common cardiomyopathy - reduced contraction strength, large heart, systolic dysfunction
      • Etiology: Genetics, excess alcohol, postpartum, chemotherapy, endocrine disorders
      • Physical exam: Dyspnea, S3 gallop, rales, jugular venous distention
    2. Hypertrophic Cardiomyopathy (HOCM)

      Hypertrophic portion of septum - Young athlete with a positive family history has sudden death or syncopal episode
      • High pitched mid systolic murmur at LLSB. Increased with valsalva and standing (less blood in chamber). Decreased with squatting (more blood in chamber)
    3. Restrictive Cardiomyopathy

      Right heart failure with a history of infiltrative process - stiff ventricles
      • Amyloidosis, sarcoidosis, hemochromatosis, scleroderma, fibrosis, and cancer
    1. Atrial fibrillation/flutter (ReelDx + Lecture)

      • Atrial Fibrillation: Low-amplitude fibrillatory waves without discrete P waves and an irregularly irregular pattern of QRS complexes
      • Atrial Flutter: Regular, sawtooth pattern, atrial rate 250-350 BPM, narrow QRS complex
    2. Atrioventricular block (lecture + ReelDx)

      First degree AV block: PR interval > .2 seconds.
      • First-degree heart block is actually a delay rather than a block. It is caused by a conduction delay at the AV node or bundle of His. This means that the PR Interval will be longer than normal (over 0.20 sec.).
      Second degree AV block Type 1 (Wenckebach) and Type 2 (Mobitz)
      • Second degree type 1 (Wenckebach)Longer, longer, drop now you've got a Wenckebach.
        • With second-degree heart block, Type I, some impulses are blocked but not all. More P waves can be observed vs QRS Complexes on a tracing. Each successive impulse undergoes a longer delay. After 3 or 4 beats the next impulse is blocked.
      • Second degree type 2 (Mobitz)Some get dropped some get through now you've got Mobitz 2.
        • With Mobitz Type II blocks, the impulse is blocked in the bundle of His. Every few beats there will be a missing beat but the PR Interval will not lengthen.
      Third degree AV block: P’s and Q’s don’t agree now the block is 3rd degree.
      • With this block, no atrial impulses are transmitted to the ventricles. As a result, the ventricles generate an escape impulse, which is independent of the atrial beat. In most cases, the atria will beat at 60-100 bpm while the ventricles asynchronously beat at 30-45 bpm.
    3. Bundle branch block

      • Left: R and R’ (upward bunny ears) in V4-V6
      • Right: R and R’ (upward bunny ears) in V1-V3
    4. Paroxysmal supraventricular tachycardia

      A SVT with abrupt onset and offset:
      • Atrioventricular nodal reentrant tachycardia (AVNRT): Any tachydysrhythmia arising from above the level of the Bundle of His
      • Wolff-Parkinson-White (WPW) syndrome: Caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles (Bundle of Kent fibers). hallmarks on EKG include a shortened PR interval, widened QRS, and delta waves
    5. Premature beats

      • PVC: Early wide "bizarre" QRS, no p wave seen
      • PAC: Abnormally shaped P wave
      • PJC: The QRS complex will be narrow, usually measured at 0.10 sec or less, no p wave or inverted p wave
    6. Sick sinus syndrome (sinus node dysfunction)

      Collective term used to describe dysfunction in the sinus node's automaticity and impulse generation
      • Sinus bradycardia: Sinus rhythm with a resting heart rate of < 60 bpm in adults, or below the normal range for age in children
      • Sinus pause: pause < 3 seconds
      • Sinus arrest: pause > 3 seconds
      • Tachy-Brady Syndrome: Episodes of alternating sinus tachycardia and bradycardia
    7. Sinus arrhythmia

      Sinus arrhythmia represents normal, minimal variations in the SA Node's pacing rate in association with the phases of respiration. Heart rate frequently increases with inspiration, decreases with expiration
    8. Torsade de pointes (Lecture)

      EKG: Polymorphic ventricular tachycardia that appears to be twisting around a baseline
      • Treatment: IV Magnesium sulfate
    9. Ventricular fibrillation (Lecture)

      EKG: No discernible heart contractions
      • Treatment: CPR and defibrillation (AKA non-synchronized cardioversion)
    10. Ventricular tachycardia (ReelDx + Lecture)

      EKG: Wide complex tachycardia with three or more consecutive ventricular premature beats
      • Stable: Treat with amiodarone → lidocaine → procainamide (in this order)
      • Unstable: Treat with CPR and defibrillation synchronized direct current (DC) cardioversion
    1. Atrial septal defect

      Noncyanotic - Foramen ovale fails to close. Wide fixed split second heart sound (S2). Systolic ejection murmur at second left intercostals space with an early to mid-systolic rumble
    2. Coarctation of the aorta

      Noncyanotic - Higher blood pressures in the arms than in the legs and pulses are bounding in the arms but decreased in the legs.
    3. Patent ductus arteriosus

      Noncyanotic - A continuous "machinery murmur" at the upper left sternal border
    4. Failure to thrive. "tet spells", baby with cyanosis and loss of consciousness with crying
      • Cyanotic - Four features "PROVe":Pulmonary Stenosis, Right ventricular hypertrophy, Overriding aorta, Ventricular septal defect
    5. Ventricular septal defect

      Noncyanotic - VSD is the most common pathologic murmur in childhood.
      • Loud, harsh, pansystolic murmur at the lower left sternal border.
      • Most close by age 6, surgery if large.
  3. Coronary Heart Disease (PEARLS)

    1. Acute myocardial infarction (PEARLS)

      1. Non-ST-Segment Elevation MI (NSTEMI) ReelDx

        Evidence of myocardial necrosis (cardiac markers in blood; troponin I or troponin T and elevated CK) without acute ST-segment elevation or Q waves
        • ECG changes such as ST-segment depression, T-wave inversion, or both may be present
      2. ST-Segment Elevation Myocardial Infarction (Lecture)

        ST segment elevations > 1 mm in > 2 contiguous leads on ECG and evidence of myocardial necrosis (cardiac markers in blood; troponin I or troponin T and elevated CK)
        • ST elevation: acute ischemia
        • T wave depression: myocardial injury
        • Q wave: Infarct
        Characteristic symptoms of myocardial infarction include pain in the substernal region of the chest that radiates to the left armshortness of breath, and diaphoresis
        • The underlying pathologic process of myocardial infarction is plaque rupture with the adhesion of platelets and platelet aggregation
        Location of heart:
        • Lateral (I, aVL, V5, V6): Left circumflex
        • Anterior (V2-V4): Left anterior descending
        • Septal (V1, V2): Left anterior descending
        • Anterolateral (V4, V5, V6): Left main
        • Posterior (V1, V2: ST depression): Right coronary artery
        • Inferior (II, III, aVF): Right coronary artery
        Serial cardiac enzymes:
        • Troponins: Most specific test, appears at 4-8 hours, peaks at 12-24 hours, and lasts for 7-10 days
        • Myoglobin: Elevate in 1- 4 hours
        • CK-MB: Appears at 4-6 hours, peaks at 12-24 hours, and lasts for 3-4 days
        Treatment includes Beta Blockers + NTG + Aspirin + Heparin + ACEI + REPERFUSION
        • PCI (Percutaneous Coronary Intervention) GOLD STANDARD - best if within 3 hours of sx onset (especially 90 minutes), PCI is superior to thrombolytics
        • Thrombolytic therapy - Done if no access to cath lab or surgery is contraindicated
          • TPA
          • Streptokinase
        Absolute contraindications for fibrinolytic use in STEMI include the following:
        • Prior intracranial hemorrhage (ICH)
        • Known structural cerebral vascular lesion
        • Known malignant intracranial neoplasm
        • Ischemic stroke within 3 months
        • Suspected aortic dissection
        • Active bleeding or bleeding diathesis (excluding menses)
        Upon discharge - ACE inhibitors have been shown to decrease left ventricular hypertrophy and remodeling to allow for a greater ejection fraction.
    2. Angina pectoris (PEARLS)

      1. Prinzmetal variant angina (vasospastic angina)

        Coronary artery vasospasms causing transient ST segment elevations, not associated with clot
        • Look for a history of smoking (#1 risk factor) or cocaine abuse
        • EKG may show inverted U waves
      2. Stable angina

        Predictable, relieved by rest and/or nitroglycerine
      3. Unstable angina (ReelDx)

        Previously stable and predictable symptoms of angina that are now more frequent, increasing or present at rest
  4. Heart Failure (ReelDx)

    Right sided: causes peripheral and abdominal fluid accumulation -  jugular venous distention, edema, hepatomegaly, no rales
    • Diagnose with echo and doppler, gold standard is right heart cardiac catheterization
    Left sided: causes shortness of breath and fatigue - paroxysmal nocturnal dyspnea, cough, orthopnea, rales
    • Systolic: Decreased ejection fraction, S3 (Rapid ventricular filling during early diastole is the mechanism responsible for the S3)
    • Diastolic: Ejection fraction is usually normal, S4
    Chest radiograph: Kerley B lines, ↑ BNP
  5. Hypertension (PEARLS)

    1. Essential hypertension

      Primary hypertension is defined as a resting systolic BP ≥ 130 or diastolic BP ≥ 80  on at least two readings on at least two separate visits with no identifiable cause
      • Normal: < 120/80 mmHg and < 80 mmHg
      • Elevated: 120–129 mmHg and < 80 mmHg
      • Stage 1: 130–139 mmHg or 80-89 mm Hg
      • Stage 2:  ≥ 140 mm Hg or ≥ 90 mm Hg
    2. Hypertensive emergencies (ReelDx)

      Hypertensive emergency: 
      • BP usually >180/120 with impending or progressing end organ damage
        • End organ damage: encephalopathy, nephropathy, intracranial hemorrhage, aortic dissection, pulmonary edema, unstable angina or MI (except papilledema which = malignant HTN)
      • BP must be reduced within 1 hour to prevent progression of end organ damage or death
      • Treatment: IV labetalol or calcium channel blocker (dihydropyridine), Sodium Nitroprusside (drug of choice) 
      Hypertensive Urgency: 
      • BP usually > 180/120 without signs of end organ damage
      • Immediate BP reduction is not required
      • Treatment: oral antihypertensive Clonidine (drug of choice)
      Malignant HTN
      • Characterized by diastolic reading > 140 mm Hg associated with papilledema and either encephalopathy or nephropathy
    3. Secondary hypertension

      Systolic BP ≥ 140 diastolic BP ≥ 90 or both with an identifiable cause
      • Sleep apnea, pheochromocytoma, coarctation of the aorta, parenchymal renal disease, renal artery stenosis, Cushing syndrome, primary hyperaldosteronism (Conn’s disease)
      • Reduce BP to < 140/90 mm Hg for everyone < 60, including those with a kidney disorder or diabetes
      • Reduce BP to < 150/90 mm Hg for everyone ≥ 60
  6. Hypotension (PEARLS)

    1. Cardiogenic shock

      Common causes include acute MI, heart failure, cardiac tamponade.
      • Hypotension (SBP <90mmg), cyanosis, cool extremities, altered mental status, and crackles.
      • Treatment includes fluid resuscitation, pressors (dopamine), and treat underlying cause.
    2. Orthostatic hypotension (ReelDx)

      Drop of > 20 mm Hg systolic, 10 mmHg diastolic, or both 2-5 minutes after change from supine to standing
    3. A sudden drop in heart rate and blood pressure leading to fainting, often in reaction to a stressful trigger
      • Upright tilt-table study can reproduce the symptoms in susceptible people
      • Treatment usually involves trigger avoidance, but may on rare occasions include β-blockers and disopyramide or a pacemaker
    1. Hypercholesterolemia

      Four groups most likely to benefit from statin therapy are identified:
      • Patients with any form of clinical atherosclerotic cardiovascular disease (ASCVD)
      • Patients with primary LDL-C levels of 190 mg per dL or greater.
      • Patients with diabetes mellitus, 40 to 75 years of age, with LDL-C levels of 70 to 189 mg per dL.
      • Patients without diabetes, 40 to 75 years of age, with an estimated 10-year ASCVD risk ≥ 7.5%
    2. Hypertriglyceridemia

      Obtain fasting lipid panel beginning at age 20 and repeated every 5 years
      • Normal <150 mg/dL
      • Mild hypertriglyceridemia  150 to 499 mg/dL
      • Moderate hypertriglyceridemia 500 to 886 mg/dL
      • Very high or severe hypertriglyceridemia 886 mg/dL
      • Triglyceride level should be reduced to < 500 mg/dL to prevent this pancreatitis
      • Isolated triglycerides are treated with Fibrates (gemfibrozil and fenofibrate) and Niacin
      • Niacin may cause hyperglycemia so caution in patients with DM
      • Flushing treated with daily aspirin, will have a beneficial effect on HDL cholesterol
  7. Traumatic, infectious, and inflammatory heart conditions (PEARLS)

    1. Acute bacterial endocarditis: Infection of normal valves with a virulent organism (S. aureus) Subacute bacterial endocarditis: Indolent infection of abnormal valves with less virulent organisms (S. viridans)
    2. Acute pericarditis (ReelDx)

      Chest pain that is relieved by sitting and/or leaning forward worse when lying down
      • Dressler's syndrome is pericarditis 2-5 days after an acute myocardial infarctions
      • Pericardial friction rub heard best with patient upright and leaning forward
      • EKG will demonstrate diffuse, ST segment elevations in the precordial leads
    3. Cardiac tamponade (ReelDx)

      Beck’s triad on physical exam: jugular venous distention, hypotension, muffled heart sounds
      • Pulsus paradoxus is a classic finding (drop 10 mmHg in systolic pressure on inspiration), narrow pulse pressure
      • EKG will show electrical alternans (when consecutive, normally-conducted QRS complexes alternate in height) and low voltage QRS complex
      • Chest x-ray finding – water bottle heart - heart shaped like a canteen
      • Treatment: Pericardiocentesis
    4. Pericardial effusion (ReelDx)

      Same symptoms as acute pericarditis except patient will now have signs of fluid buildup around the heart which include low voltage QRS complexes, electrical alternans, distant heart sounds and an echocardiogram showing a collection of pericardial fluid.
    5. Acute myocarditis

  8. Valvular Disorders (PEARLS)

    1. Aortic stenosis (ReelDx)

      Harsh systolic ejection crescendo-decrescendo murmur at the right upper sternal border (aortic area) with radiation to the neck and apex heard best by leaning forward with expiration
    2. Aortic regurgitation (Diastolic)

      Soft, early diastolic blowing murmur along the left sternal border with the patient sitting leaning forward after exhaling
    3. Mitral stenosis (Diastolic)

      Diastolic low pitched decrescendo rumbling murmur with opening snap heard best at the apex (mitral area) with patient in lateral decubitus position
    4. Mitral regurgitation

      Holosystolic high-pitched blowing murmur at apex (mitral area) that radiates to axilla with a split S2
    5. Mitral valve prolapse

      Midsystolic ejection click heard best at the apex (mitral area)
    6. Tricuspid stenosis (Diastolic)

      Diastolic rumbling murmur at the LLSB (tricuspid area) with an opening snap
    7. Tricuspid regurgitation

      High pitched holosystolic murmur at LLSB (tricuspid area) radiates to the sternum and increases with inspiration
    8. Pulmonary stenosis

      Harsh, loud, medium pitched systolic murmur heard best at the 2nd /3rd left intercostal space (pulmonic area) that may decrease with inspiration
    9. Pulmonary regurgitation (diastolic)

      High pitched early diastolic decrescendo murmur at the LUSB (pulmonic area) that increases with inspiration
  9. Vascular Disease (PEARLS)

    1. Aortic aneurysm/dissection

      Abdominal Aortic Aneurysm: Flank pain, hypotension, pulsatile abdominal mass

      • Surgical repair if >5.5 cm or expands >0.6 cm per year
      • Monitor annually if >3 cm. Monitor every 6 months if >4 cm
      • Beta blockers
      Aortic Dissection: Sudden onset tearing chest pain, between scapulas.Diminished pulses
      • Chest radiograph: Widened mediastinum
      • Ascending aorta- Surgical emergency
      • Descending aorta- Medical therapy (beta blockers) unless complications are present
    2. Arterial embolism/thrombosis

      Caused by a sudden arterial occlusion - The P's of arterial emboli: PAIN, PALLOR, PULSELESSNESS, PARESTHESIA, PARALYSIS, POIKILOTHERMIA
      • Atrial fibrillation and mitral stenosis are common causes of thrombus formation
      • Angiography is considered the gold standard for diagnosis
      • Treat with IV heparin then call vascular surgeon
    3. Arteriovenous malformation is an abnormal connection between arteries and veins, bypassing the capillary system.
      • In about half of all brain AVMs, intracranial hemorrhage is the first sign
      • Signs and symptoms may also include seizure, headache and focal neurologic deficit
      • Angiography is the diagnostic gold standard
      • Surgical excision is the mainstay of treatment along with radiosurgery and endovascular embolization
    4. Giant cell arteritis

      Inflammation of large and medium vessels: Jaw claudication and headache, thickened temporal artery scalp pain elicited by touching the scalp or combing the hair, acute vision disturbances  Amaurosis fugax (temporary monocular blindness) secondary to anterior ischemic optic neuritis
      • ESR > 100
      • Diagnosed with Temporal artery biopsy
      • Treat with high dose prednisone – do urgently to prevent blindness (Do not wait for biopsy results)
      • Associated with polymyalgia rheumatica
    5. Peripheral artery disease

      Intermittent claudication, atrophic skin, rubor, hair loss, decreased pulses or non healing ulcers
      • Diagnosis with ankle/brachial index (< 0.9)
      • angiography is gold standard
      • βblockers are contraindicated in isolated PAD – it will worsen claudication
    6. Phlebitis/thrombophlebitis

      Spontaneous or after trauma, IV/PICC lines - dull pain, erythema, induration of vein, palpable cord
      • Venous duplex ultrasound Gold Standard for diagnosis
      • NSAIDs, warm compress
    7. Varicose veins

      Presentation: Dilated tortuous superficial veins, venous stasis ulcers, ankle edema, lower extremity pain after sitting/standing
      • Treatment: leg elevation and compression stockings
    8. Venous insufficiency (ReelDx)

      Edema, atrophic shiny skin, brawny induration, stasis dermatitis, brown hyperpigmentation, varicosities, and venous stasis ulcers above medial malleolus.
      • ABI, Trendelenburg tests, ultrasound.
      • Treatment: Sclerotherapy, vein stripping, compression hose.
    9. Venous thrombosis (ReelDx)

      Unilateral (ASYMMETRICAL) swelling of lower extremity
      • Virchow’s triad: stasis, vascular injury, hypercoagulable state (OCP, cancer, surgery, factor V Leiden)
      • D-dimer, venous duplex ultrasound first line imaging, venography gold standard
      • Homan signdiscomfort behind the knee on forced dorsiflexion of the foot

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