PANCE Blueprint Cardiology (11%)

Cardiomyopathy

• Dilated cardiomyopathy: ventricles enlarge and weaken - inherited in about one-third of cases, may also result from alcohol, heavy metals, coronary artery disease, cocaine use, and viral infections.
• Hypertrophic cardiomyopathy: the heart muscle enlarges and thickens - inherited autosomal dominant
• Restrictive cardiomyopathy: ventricle stiffens - may be caused by amyloidosis, hemochromatosis, and some cancer treatments
• Arrhythmogenic right ventricular dysplasia (ARVD): fatty replacement of myocardium - genetic defect
• Takotsubo cardiomyopathy (broken heart syndrome): non-ischemic cardiomyopathy in which there is a sudden temporary weakening of the muscular portion of the heart -extreme emotional or physical stress

Dilated cardiomyopathy is the most common type (95%) of cardiomyopathy and is a condition in which an index event or process (such as an MI) damages the myocardium, weakening the heart muscle resulting in reduced strength of ventricular contraction, and dilation of the left ventricle

• Reduced contraction strength, large heart
• Causes include ischemia (CAD, MI, arrhythmia), genetics, excess alcohol, postpartum, chemotherapy, endocrine disorders, viral infections, cocaine use, heavy metals
  • Inherited in 1/3 of cases
• Physical exam: Dyspnea, S3 gallop, rales, cardiomegaly (displaced apical impulse), edema, jugular venous distention - systolic heart failure
• Can cause valve regurgitation and arrhythmias

"An S3 gallop signifies the end of rapid ventricular filling in the setting of fluid overload and is often associated with dilated cardiomyopathy."

DX: Echocardiography is the most definitive diagnosis - demonstrates left ventricular dilation and dysfunction and low cardiac output with poor EF (< 50%, but often less than 30%)

• EKG will show nonspecific ST/T wave changes.
• CXR often shows a balloon-like heart - will show cardiomegaly and pulmonary congestion

Dilated cardiomyopathy: enlarged ventricles with thin walls and reduced contraction. Image: BruceBlaus, CC BY 3.0, via Wikimedia Commons.

TX: βblocker + ACE + Loop Diuretic

• Use the mnemonic AABCD (anticoagulants, ACE-I, β-blockers, calcium channel blockers, and diuretics/ digoxin )
• Increase cardiac contractility - digitalis
• Treatment in extreme cases includes heart transplant or left ventricular assist device

• Abstain from alcohol, drug use

The hypertrophic portion of septum - LV outflow tract is narrowed - during systole and obstruction worsened with increased contractility

Hypertrophic cardiomyopathy with a thickened left ventricular wall. Image: BruceBlaus, CC BY 3.0, via Wikimedia Commons.

Presentation: young athlete with a positive family history has sudden death or syncopal episode

• Inherited autosomal dominant - screen family members
• Presents in early adulthood
• Not to be confused with hypertrophy of elite athlete

Physical Exam:

• Sustained PMI, bifid pulse, S4 gallop
• Murmur: High pitched mid-systolic murmur at LLSB. Increased with Valsalva and standing (less blood in the chamber)
  • Decreased with squatting (more blood in the chamber)

"The murmur due to HCM will increase in intensity with any maneuver that decreases the volume of blood in the left ventricle (such as standing abruptly or the strain phase of a Valsalva maneuver )."

DX: Diagnosis is by echocardiography or MRI

• Echo is the key to diagnosis and will show left ventricular hypertrophy with a thickened septum, small left ventricle, and diastolic dysfunction
• EKG will show nonspecific ST and T-wave changes and left ventricular hypertrophy

TX: β-blockers (metoprolol) and/or rate-limiting Ca channel blockers (usually verapamil) to decrease myocardial contractility and slow the heart rate and thus prolong diastolic filling and decrease outflow obstruction

• Avoid nitrates and other drugs that decrease preload (eg, diuretics, ACE inhibitors, angiotensin II receptor blockers) because these decrease LV size and worsen LV function
• Digoxin is contraindicated since it increases the force of contraction which can increase the obstruction
• Consider an implantable cardioverter-defibrillator for patients with syncope or sudden cardiac arrest
• Cessation of high-intensity athletics

• Surgical or alcohol ablation of the hypertrophied septum

Right heart failure with a history of an infiltrative process

• Etiology: Amyloidosis, sarcoidosis, hemochromatosis, scleroderma, fibrosis, and cancer (radiation and chemotherapy)
• Physical Exam:
  • Pulmonary HTN present
  • Normal ejection fraction, normal heart size, large atria, normal left ventricular wall, early diastolic filling

DX: Echocardiography shows a normal left ventricular ejection fraction. Common findings include dilated atria and myocardial hypertrophy

• The ECG is usually nonspecifically abnormal, showing ST-segment and T-wave abnormalities and sometimes low voltage
• If the diagnosis is still in doubt, MRI can show abnormal myocardial texture in disorders with myocardial infiltration
• Cardiac catheterization and myocardial biopsy are not often necessary. If done, catheterization detects high atrial pressure in RCM
• CXR: pulmonary vascular congestion with normal heart size

TX: often unsatisfactory unless the cause can be addressed

• Diuretics may benefit patients with edema or pulmonary vascular congestion but must be used cautiously to avoid lowering preload

Normal Sinus Rhythm

A normal sinus rhythm refers to both a normal heart rate and rhythm. Normal heart rates are from 60 to 100 beats per minute. The shape of the electrocardiogram (EKG) tracing will exhibit certain key attributes to be considered normal, as discussed below. With normal sinus rhythms, the heart beat's electrical impulse originates in the sinoatrial node (SA). The P waves are upright and appear before each QRS and have the same shape. The intervals between the P waves are regular although some variations can occur with respiration.

Sinus Arrhythmia

Sinus arrhythmia looks normal except for slight irregularities. A frequent cause of sinus arrhythmia can be rhythm variations caused by respiration.

Sinus Tachycardia

Sinus tachycardia is a normal sinus rhythm but with a heart rate over 100 bpm. It is a normal response to exercise, excitement and some illnesses.

Sinus Bradycardia

Sinus bradycardia is a sinus rhythm with a rate of 40-60 bpm.

Low-amplitude fibrillatory waves without discrete P waves and an irregularly irregular pattern of QRS complexes

Irritable sites in the atria fire very rapidly, between 400-600 bpm. This very rapid pacemaking caused the atria to quiver. The ventricles beat at a slower rate due to the AV node is blocking of some of the atrial impulses.

Atrial Flutter

There are two types of atrial flutter. Type I (also called classical or typical) has a rate of 250-350 bpm. Type II (also called non-typical) are faster, ranging from 350-450 bpm. EKG tracings will show tightly spaced waves or saw-tooth waveforms (F-waves).

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 than the PR Interval will be longer than normal (over 0.20 sec.).

• (PR interval longer than 1 big box 0.20 seconds)

Second degree AV block Type 1 (Wenckebach) and Type 2 (Mobitz)

Type I: Wenckebach block

Wenckebach (longer, 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. On an EKG tracing, PR Intervals will lengthen progressively with each beat until a QRS Complex is missing. After this blocked beat, the cycle of lengthening PR Intervals resumes. This heart block is also called a Wenckebach block.

Type II: Mobitz

MOBITZ 2 (some get dropped some get through now you've got mobitz 2)

With Mobitz Type II blocks, the impulse is blocked below the AV node (in the His bundle or bundle branches), so the QRS is often wide. Every few beats there will be a missing beat but the PR Interval will not lengthen.

Third degree AV block

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.

• There is no electrical communication between the atria and the ventricles complete AV dissociation. P wave do not match the QRS one for one

With this conduction block, either the left or right bundle branch is blocked intermittently or fixed. The QRS complex is wider than normal (> 0.12 sec.). Using a 12 lead EKG, blocks in either the left or right bundle branch may be diagnosed.

• Look at V1 and V2:
• Right BBB “R” = Rabbit Ears
• LBBB broad slurred R in V4 and V6

A faster than normal heart rate beginning above the heart's two lower chambers in the atria, AV junction or SA node

Wolff-Parkinson-White Syndrome

This occurs when the impulse travels between the atria and ventricles via an abnormal path, called the bundle of Kent. The impulse, not being delayed by the AV node, can cause the ventricles to contract prematurely. EKG characteristics include a shorter PR Interval, longer QRS complex, and a delta wave.

Multifocal Atrial Tachycardia

When multifocal atrial tachycardia occurs, multiple (non-SA) sites are firing impulses. The P waves will vary in shape and at least three different shapes can be observed. The PR Interval varies. Ventricular rhythm is irregular.

This occurs when an ectopic site within the atria fires an impulse before the next impulse from the SA node. If the ectopic site is near the SA node, the P wave will likely have a shape similar to a sinus rhythm. But this P wave will occur earlier than expected.

Premature junctional beats

Premature junctional complex (PJC) occurs when an irritable site within the AV node fires an impulse before the SA node. This impulse interrupts the sinus rhythm. The QRS complex will be narrow, usually measured at 0.10 sec or less.

Premature ventricular contractions

Premature ventricular complexes (PVCs) occur when a ventricular site generates an impulse. This happens before the next regular sinus beat. Look for a wide QRS complex, equal or greater than 0.12 sec. The QRS complex shape can be bizarre. The P wave will be absent.

Bradycardia or pauses alternating with atrial fibrillation or flutter (tachy-brady syndrome); permanent pacemaker when symptoms match the rhythm

Three or more consecutive ventricular beats in a row is ventricular tachycardia. The rate is usually 120–250 bpm; when in doubt, treat a wide-complex tachycardia as VT. Ventricular Tachycardia has two variations, monomorphic and polymorphic.

Ventricular Tachycardia Monomorphic

Monomorphic ventricular tachycardia occurs when the electrical impulse originates in one of the ventricles. The QRS complex is wide. Rate is above 100 bpm.

Ventricular Tachycardia Polymorphic

Polymorphic ventricular tachycardia has QRS complexes that vary in shape and size. If a polymorphic ventricular tachycardia has a long QT Interval, it could be Torsade de Pointes.

Ventricular fibrillation originates in the ventricles and is chaotic. No normal EKG waves are present. No heart rate can be observed. Ventricular fibrillation is an emergency requiring immediate CPR and defibrillation.

Torsade de Pointes is a special form of ventricular tachycardia. The QRS complexes vary in shape and amplitude and appear to wind around the baseline.

Atrial and ventricular pacing can be seen on the electrocardiogram (ECG) as a pacing stimulus (spike) followed by a P wave or QRS complex, respectively. The ECG has the ability to show normal and abnormal pacemaker function.

• The ductus arteriosus is a blood vessel which connects the pulmonary artery to the aorta. In utero this allows most of the blood to bypass the lungs. Prostaglandin E1 keeps it open; ibuprofen (preferred), acetaminophen, or indomethacin close it in preterm infants

** remember the patient got a patent for his machine!

Four features, "tet spells", baby with cyanosis and LOC with crying

• Right ventricular hypertrophy
• VSD
• Overriding aorta
• Right ventricular outflow obstruction

Tetralogy of Fallot

Systolic Left Heart Failure

• Systolic – S3 (Rapid ventricular filling during early diastole is the mechanism responsible for the S3)
• Dilated thin-walled weak left ventricle: Often due to CAD or heart attack which causes the muscle to die
• Dyspnea, PND, orthopnea, rales, crackles, displaced downward and to the left apical impulse
• Dilated left ventricle and a low ejection fraction (≤40%)
• Treat with the four GDMT pillars (ARNI or ACEi/ARB, evidence-based beta-blocker, MRA, SGLT2 inhibitor) + loop diuretic for congestion
• Systolic left heart failure is diagnosed and treated based on class: Class I, II, III and IV and patients can go from controlled class I to poorly controlled and worsening class II, III or IV and back.
• Acute worsening of heart failure: O2 + Ace + stop βblocker + start nitroglycerine and a double dose of diuretic IV (once stable go back on βblocker and PO loop diuretics)

Diastolic Left Heart Failure

• Diastolic - S4
• Hypertrophic thick walled left ventricle with impaired relaxation
• Increases over 55 years of age, commonly in patients with hypertension
• Patients will have problems when blood pressures increase, often when patients forget to take their medications
• Dyspnea and rales with an apical heave or lift
• Ejection fraction is usually normal
• Treat with: Ace inhibitor + βblocker or CCB (do not use diuretics in stable chronic diastolic failure)
• Never use digoxin for diastolic heart failure
• Acute = same as systolic left heart failure = Ace inhibitor + loop diuretic IV + NTG + O2

Right heart failure (Right ventricle)

• Cause: Pulmonary HTN – the right heart is unable to easily pump blood into the lungs. Most common cause of right heart failure is left heart failure.
• No rales, JVD, and leg edema
• Diagnose with echo and doppler, Gold Standard is right heart cardiac catheterization
• Treat the underlying condition

High output cardiac failure:

• Caused by increased metabolic demand – metabolic demand is higher than the heart can pump at maximum.
  • Hyperthyroidism
  • Severe anemia
  • Beriberi or thiamine deficiency
• Will have tachycardia at first but once the heart tires it will look like systolic failure because the heart will dilate and weaken
• Treat like heart failure and acute CHF, treat the underlying condition

• Goal <130/80 mm Hg for nearly all adults with hypertension (any age, including diabetes and CKD)
• Higher risk (CVD, CKD, diabetes, heart failure, PREVENT 10-year risk ≥7.5%, fit adults ≥65): also aim for systolic <120 mm Hg if tolerated
• Frail or limited life expectancy: individualize (the old JNC 8 targets of <140/90 and <150/90 are retired)

Cuff bladder should be 80% of arm circumference

• Average of two or more readings
• On two or more occasions
• No smoking or caffeine 30 minutes prior
• Up to 30% have white coat HTN - home BP monitor

Workup: EKG, U/A, BUN/CR, K+, Retinopathy, CVA/TIA/PAD, CBC, lipids, Ca++

Lifestyle Modification Goals

• Weight Reduction: Target BMI= 18.5-24.9
• DASH Diet: Fruit, veggies, low-fat dairy
• Sodium reduction <2.4G sodium/day
• Aerobic exercise 30 min/day (ideal)
• Decreased ETOH <2 drinks/daily

• Look for red flags: HTN at an early age <25 without family history, HTN first develops > 50, Previously controlled HTN now refractory

Aldosteronism:

• Most common treatable cause of HTN
• Most common presenting age 30-50
• Presents classically as HTN with hypokalemia (most patients actually have normal K+, so screen broadly — the Endocrine Society recommends ARR screening for all adults with HTN); aldosterone; renin
• 30-50% caused by aldosterone producing 50% caused by aldosterone producing adenomas;
• Best screening test: aldosterone/renin ratio
• Diagnose with CT or MRI of adrenal glands - shows: adrenal adenoma or hyperplasia

Chronic Kidney Disease

• Most common cause of secondary HTN
• HTN is present in more than 85% and is a major factor causing increased cardiovascular morbidity and mortality
• Mechanism: expanded plasma volume and peripheral vasoconstriction
• Screening tests: BUN/Cr, U/A,
  microalbuminuria
• Diagnose with Renal sonography

• Plus optic disc edema, progressive target organ complications and severe perioperative hypertension
• Must be reduced within a few hours
• Parenteral drug therapy is not required and goal is partial reduction of blood pressure with relief of symptoms
• TX with Clonidine

Hypertensive Emergency = ↑ BP + target organ damage DBP > 130

• BP must be reduced in 1 hour to avoid morbidity or death
• TX with Nicardipine IV - most potent and longest acting calcium channel blocker with potential to precipitate reflex tachycardia and should be used with a beta-blocker such as Labetalol (labetalol used in pregnancy)
• Reduce pressure by no more than 25% within 1-2 hours and then towards 160/100 within 2-6 hours
• If reduced too fast may precipitate coronary, renal or cerebral ischemia
• Avoid the use of sublingual or oral fast-acting nifedipine

Malignant Hypertension = Sustained elevated arterial blood pressure

• DBP ≥ 130
• SBP ≥ 200
• Characterized by encephalopathy or nephropathy with papilledema
• Treatment is identical to that of hypertensive emergencies

• Physical exam: Hypotension (SBP <90 mmHg), cyanosis, cool extremities, altered mental status, crackles
• ↑ capillary wedge pressure > 15mm
• Treatment: Fluid resuscitation, pressors (dopamine), and treat underlying cause

• autonomic dysfunction in DM common cause, medications, tilt table testing if autonomic dysfunction is suspected

Tx: Aspirin + P2Y12 inhibitor (usually given at PCI) + Heparin + high-intensity statin + beta-blocker + NTG; angiography within 24 hours for most NSTEMI; never fibrinolytics

EKG:

• ST elevation: acute ischemia
• T wave depression: myocardial injury
• Q wave: Infarct

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; high-sensitivity troponin rises within 1–3 hours, peaks at 12–24 hours, and lasts 7–14 days (draw at 0 and 1–3 hours)
• Myoglobin and CK-MB are no longer needed (CK-MB is only useful to detect reinfarction)

Tx: REPERFUSION + Aspirin + P2Y12 inhibitor (prasugrel or ticagrelor with PCI; clopidogrel with fibrinolysis) + Heparin + high-intensity statin + beta-blocker + ACEI

Aspirin and a P2Y12 inhibitor are given together. Immediate (within 90 minutes) coronary angiography and primary PCI. Fibrinolytic therapy (within 30 min of arrival, symptoms <12 h) if primary PCI cannot be done within 120 minutes, then transfer for angiography within 24 hours (typically 6 to 24 hours; rescue PCI right away if lysis fails).

• Relieved by rest

Stress test: Reversible wall motion abnormalities/ ST depression >1 mm

• Angiography- definitive diagnosis
• Treatment:
  • Beta blockers, nitroglycerin.
  • Severe: angioplasty and bypass.

• Occurring at rest

• Preservation of exercise capacity

Flank pain, hypotension, pulsatile abdominal mass

Screening: Ultrasound, if male >65 and ever a smoker

Treatment:

• Immediate surgical repair (even if asymptomatic) if >5.5 cm or expands >0.6 cm per year
• Monitor annually if >3 cm. Monitor every 6 months if >4 cm
• Beta blocker

Aortic Dissection

Sudden onset tearing chest pain, between scapulas. Diminished pulses

Chest radiograph: Widened mediastinum

Treatment:

• Ascending aorta- Surgical emergency
• Descending aorta- Medical therapy (beta blockers) unless complications are present

Jaw claudication and headache, scalp pain elicited by touching the scalp or combing the hair, 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

• Lower extremity loss of hair, brittle nails, pallor, cyanosis, claudication, hypothermia
• Ulcers are pale to black, well circumscribed and painful, located laterally and distally
• Arteriography is gold standard for diagnosis

Treatment:

• Definitive treatment: Arterial bypass
• Medical treatment: Antiplatelets, anti lipids, manage risk factors, cilostazol Aspirin, Plavix,

• Presentation: Dull pain, erythema, induration of vein, palpable cord
• Venous duplex ultrasound Gold Standard for diagnosis
• Treatment: Symptomatic: NSAIDs, warm compress

Lower extremity pain after sitting/standing

• ABI, Trendelenburg tests, ultrasound

Treatment: Sclerotherapy, vein stripping, compression hose

Risk factors:

• Virchow’s triad: stasis, vascular injury, hypercoagulable state (OCP, cancer, surgery, factor V Leiden)
• Homan sign

Treatment: Heparin to Coumadin bridge

• Maneuver: Sitting leaning forward
• Chestpiece Position: Erb's-Point
• Chestpiece: Diaphragm

• Maneuver: Supine left side down
• Chestpiece Position: Mitral
• Chestpiece: Bell

• Left upper sternal border LUSB
• Maneuver: Sitting leaning forward
• Position: Pulmonic
• Chestpiece: Diaphragm

• Lower left sternal border (LLSB)
• Maneuver: Supine
• Position: Tricuspid
• Chestpiece: Bell

• Maneuver: Sitting
• Chestpiece Position: Aortic (RUSB)
• Chestpiece: Diaphragm

• Maneuver: Supine
• Chestpiece Position: Tricuspid
• Chestpiece: Bell

• S4 gallop and apical lift with thick, stiff left ventricle

• Maneuver: Supine
• Chestpiece Position: Mitral
• Chestpiece: Diaphragm

• Maneuver: Supine
• Position: Mitral
• Chestpiece: Diaphragm

• Maneuver: Supine
• Chestpiece Position: Mitral (Apex)
• Chestpiece: Diaphragm

• Maneuver: Supine
• Position: Tricuspid
• Chestpiece: Diaphragm

• Maneuver: Supine
• Chestpiece Position: Tricuspid (LLSB)
• Chestpiece: Diaphragm

Subacute bacterial endocarditis: Indolent infection of abnormal valves with less virulent organisms (S. viridans)

Duke's criteria, staph aureus in acute and IV drug users, and strep viridians in subacute

Classic signs of infective endocarditis

• Osler's nodes - tender (ouchie) nodules
• Janeway lesions - painless macules
• Roth spots on retina
• Splinter hemorrhages on nail bed
• Clubbing

The murmur:

• Pericardial friction rub heard best with patient upright and leaning forward
• Dressler's syndrome is pericarditis 2-5 days after an acute myocardial infarctions

Pericardial friction rub (listen and learn)

• Maneuver: Sitting leaning forward
• Position: Erb's-Point (middle left sternal border)
• Chestpiece: Diaphragm

EKG will demonstrate diffuse, ST segment elevations in the precordial leads

Diffuse ST elevation, without reciprocal ST depression, mostly in inferior limb leads and lateral precordial leads. This is very typical for pericarditis.

The 3 D's: Distant heart sounds, Distended jugular veins, and Decreased arterial pressure = Beck's triad

Beck’s triad:

1. Hypotension
2. muffled heart sounds
3. elevated neck veins (JVD)

Pulsus paradoxus is a classic finding for cardiac tamponade drop of BP > 10mm Hg of systolic BP with inspiration

• EKG will show electrical alternans and low voltage QRS complex
• Chest x-ray finding – water bottle heart: heart shaped like a canteen

Pericardial effusion with "water bottle sign"

• EKG showing low voltage QRS along with electric alternans (see media section)
• Echocardiogram with increased pericardial fluid

Electrical alternans as seen by changing QRS amplitudes best seen in lead II