Aortic stenosis or HCM clues to diagnosis

exertional syncope, systolic murmur on PE

Treatment for hemodynamically unstable patients with torsades de pointes

immediate electrical defibrillation

Treatment for hemodynamically stable patients with torsades de pointes

IV magnesium sulfate

Treatment for cardiotoxicity due to hyperkalemia

calcium gluconate

First line therapy for monomorphic V tach

amiodarone

Treatment for acute termination of paroxysmal supraventricular tachycardia

adenosine

Wolff-Parkinson-White pathophys

ventricular preexcitation due to an accessory pathway that conducts depolarization directly from the atria to the ventricles; it competes with normal conduction through the AV node.

Most common arrhythmia seen with WPW

atrioventricular reentrant tachycardia

Procainamide

Class 1a antiarrythmic agent that inhibits cardiac sodium channels

Digoxin toxicity

atrial tachycardia due to increased automaticity of conduction in the atria

Mobitz type 1 AV block due to increased vagal tone causing slowed conduction through the AV node (you'll never see type 2 here)

Because digoxin competes with potassium to bind to the myocardium at the sodium-potassium ATPase

hypokalemia increases its binding and can worsen toxicity or cause it to occur at lower-than-expected serum levels

A wave

caused by right atrial contraction, closely followed by tricuspid valve closure

C wave

caused by right ventricular contraction against a closed tricuspid valve

V wave

representing the peak of right atrial filling, just prior to reopening of the tricuspid valve

Cannon A waves

intermittent prominent A waves caused by the surge in jugular venous pressure that occurs when the atria and ventricles happen to contract simultaneously; these waves can be seen with any arrhythmia involving atrioventricular dissociation, such as ventricular tachycardia, which is characterized by self-propagation within the ventricles without communication with the atria and is likely in a patient with recent MI. Can also be seen in complete AV block.

Symptoms associated with cannon A waves

headache, jaw pain, sensation of neck pulsation

Vasovagal syncope triggers

pain, anxiety, emotional stress, heat, prolonged standing

Situational syncope triggers

cough, micturition, defecation, eating, hair-combing

Vasovagal and situational syncope clinical presentation

prodome (warmth, pallor, nausea, diaphoresis)

rapid recovery of consciousness (<1-2 min)

Vasovagal and situational syncope diagnosis

mainly based on clinical history of event

upright tilt table testing sometimes indicated in uncertain cases

Vasovagal and situational syncope treatment

reassurance and avoidance of triggers

counterpressure techniques for recurrent episodes

Initial management of afib

usually focuses on rate control; a beta blocker (metoprolol) or nondihydropyridine calcium channel blocker (verapamil, diltiazem) is given initially. Emergency cardioversion is indicated only in patients who are hemodynamically unstab;e (severe hypotension)

First degree AV block

asymptomatic, PR interval prolongation, observation

Mobitz Type 1 second degree AV block

usually asymptomatic, progressive PR interval lengthening followed by dropped QRS complex, observation (rarely PPM placement)

Mobitz Type 2 second degree AV block

fatigue, light-headedness, syncope, constant PR interval with randomly dropped QRS complexes, PPM placement

Third degree (complete) AV block

fatigue-lightheadedness, syncope, complete dissociation of P waves and QRS complexes, PPM placement

Mobitz Type I AV block

level of block- AV node

ECG findings- progressive prolongation of PR interval followed by dropped QRS complex

QRS complexes- usually narrow

Decreased vagal tone (exercise, atropine)- block improves

Increased vagal tone (carotid massage/0- block worsens

Risk of complete block- low

Mobitz type II AV block

Level of block- Below AV node (His bundle)

ECG findings- constant PR interval with randomly dropped QRS complexes

QRS complexes- narrow or wide

Decreased vagal tone (exercise, atropine)- block worsens

Increased vagal tone (carotid massage)- block improves

Risk of complete block- high (indication for PPM)

Class 1a antiarrythmics

quinidine, procainamide, disopyramide

Class 1a antiarrythmics ECG effects

pronlonged QRS and QT intervals

Class 1b antiarrythmics

lidocaine, mexiletine, tocainide, phenytoin

Class 1b antiarrythmics ECG effects

none

Class 1c antiarrythmics

flecainide, propafenone, moricizine

Class 1c antiarrythmics ECG effects

prolonged QRS

Class II antiarrythmics

metoprolol, atenolol, bisoprolol, esmolol, nadolol, propranolol, acebutolol, timolol

Class II antiarrythmics ECG effects

prolonged PR interval

Class III antiarrythmics

amiodarone, bretylium, dofetilide, dronedarone, ibutilide, sotalol

Amiodarone ECG effects

prolonged PR, QRS, and QT intervals

Sotalol ECG effects

prolonged PR and QT intervals

Other class III antiarrythmic ECG effects

prolonged QT interval

Class IV antiarrythmics

diltiazem, verapamil

Class IV antiarrythmics ECG effects

prolonged PR interval

Patients with prior MI complicated by left ventricular systolic dysfunction with EF no greater than 30% are at an increased risk of SCD due to

ventricular arrhythmia (v tach, v fib). Following a trial of optimal medical therapy, primary prevention with placement of an implantable cardioverter-defibrillator is indicated in these patients

Westermark sign

peripheral hyperlucency of the pulmonary arterial tree resulting from blood flow being cut off by the pulmonary embolism

Hampton Hump

peripheral, wedge-shaped lung opacity representing pulmonary infarction. An ipsilateral pleural effusion in also commonly present with this sign (pulm infarction is the typical cause of pulmonary embolism-associated pleural effusion)

Fleischner sign

enlargement of the pulmonary artery resulting from increased pressure proximal to the pulmonary embolism

Gold standard for ruling out or confirming pulmonary embolism

Chest CT angiography

Peptic ulcer perforation presents with

acute abdominal pain with radiation to the back or right shoulder and signs of peritonitis. Upright chest x-ray may reveal pneumoperitoneum with free air under the diaphragm

Vagal maneuvers (carotid massage, cold-water immersion of diving reflex, valsalva maneuver, eyeball pressure)

increases parasympathetic tone in the heart and result in a temporary slowing of conduction of the AV node and an increase in the AV node refractory period, leading to termination of AVNRT

Cardiac sarcoidosis should be suspected in any young patient younger than the age of 55 with

unexplained second or third degree heart block or when ECF changes occur in a patient with known or suspected systemic disease. A disease of noncaseating granuloma infiltration of the myocardium and can result in serious arrhythmia, cardiomyopathy, heart failure, and SCD

What should be used to reduce the risk of systemic thromboembolism in patients with afib and a high risk of thromboembolic events?

an anticoagulation agent, such as a direct oral anticoagulant (apixaban) or warfarin

Sick sinus syndrome clinical features

elderly patients

bradycardia: fatigue, dyspnea, dizziness, syncope

bradycardia-tachycardia syndrome: atrial arrythmias (afib), plapitations

Sick sinus syndrome ECG findings

sinus bradycardia, sinus pauses (delayed P waves), sinoatrial nodal exit block (dropped P waves)

Sick sinus syndrome treatment

pacemaker, +/- rate-control medication (if tachyarrhythmias)

Sick sinus syndrome

inability of the sinoatrial node to generate an adequate heart rate. Age-related degeneration of the cardiac conduction system with fibrosis of the sinus node is the most common cause.

IV adenosine

useful in the initial diagnosis and management of patients with narrow-QRS-complex tachycardia. It slows the sinus rate, increases atrioventricular (AV) nodal conduction delay, or can cause a transient block in AV node conduction. It can be useful in identifying P waves to clarify diagnosis or atrial flutter or atrial tachycardia. It can also terminate paroxysmal supraventricular tachycardias by interrupting the AV nodal reentry circuit.

Hypertrophic cardiomyopathy pathophysiology

genetic mutations affecting cardiac sarcomere proteins, AD, variable phenotypic penetrance

Hypertrophic cardiomyopathy clinical features

many patients are asymptomatic, exertional dyspnea, fatigue, angina, light-headedness, syncope, systolic ejection murmur accentuated by decreased LV blood volume, diastolic dysfunction with audible S4, increased risk for afib and v tach

Hypertrophic cardiomyopathy diagnosis

ECG: left axis deviation, abnormalities of depolarization (Q waves) or repolarization (inverted T waves)

ECHO: septal LV hypertrophy, dynamic LVOT obstruction, LA dilation

Hypertrophic cardiomyopathy management

beta blocker or nondihydropyridine CCB (facilitate increased LV volume), avoidance of dehydration and vasodilators (avoid decreased LV blood volume), ICD placement for increased risk for SCD, septal ablation, cardiac transplantation

Where in the heart does afib come from?

pulmonary veins

Where in the heart does atrial tachycardia come from? (single focus)

ectopic pacemaker

Where in the heart does AVNRT come from?

atrioventricular node

Where in the heart does atrial flutter come from?

cavotricuspid isthmus

Where in the heart does WPW come from?

accessory pathway (bundle of kent)

Most common arrhythmia causing syncope

v tach

Conditions that increase risk of atrial fibrillation, triggers of increased automaticity

hyperthyroidism, excessive alcohol use, increased sympathetic tone: acute illness (sepsis, PE, MI), cardiac surgery, sympathomimetic drugs (cocaine)

Conditions that increase the risk of a fib (precipitants of atrial dilation and/or conduction remodeling

advanced age, systemic HTN, mitral valve dysfunction, left ventricular failure, coronary artery disease and related factors (DM, smoking), obesity and obstructive sleep apnea, chronic hypoxic lung disease (COPD)

Patients to screen for fibromuscular dysplasia

Women under age 50 with 1 of the following:

severe or resistant HTN, onset of HTN before age 35, sudden increase in BP from baseline, increase in creatinine after starting ACEI or ARB and without significant effect on BP, systolic-diastolic epigastric bruit

Clinical presentation of fibromuscular dysplasia

resistant HYN from renal artery involvement, cerebrovascular FMD with symptoms of brain ischemia (amaurosis fugax, Horner's syndrome, transient ischemic attack, stroke), nonspecific symptoms (headache, pulsatile tinnitus, dizziness) from carotid or vertebral artery involvement, can also involve iliac, subclavian, and visceral arteries

Diagnosis and follow up for fibromuscular dysplasia

noninvasive testing preferred (CT angiography, duplex US), catheter-based digital subtraction arteriography for pts with inconclusive noninvasive testing, medically treated patients need follow-up BP and creatinine every 3-4 months and renal US every 6-12 months

HTN-related clues to renovascular disease

resistant HTN (uncontrolled despite 3-drug regimen), malignant HTN (with end-organ damage), onset of severe HTN (>180/120 mmHg) after age 55, severe HTN with diffuse atherosclerosis, recurrent flash pulmonary edema with severe HTN

Supportive evidence of renovascular disease

PE- asymmetric renal size (>1.5 cm), abdominal bruit

Lab results- unexplained rise in serum creatinine (>30%) after starting aCEIs or ARBs

Imaging results- unexplained atrophic kidney

ADPKD clinical presentation

most patients asymptomatic until age 30-40, flank pain, hematuria, HTN, palpable abdominal masses (usually bilateral), CKD

ADPKD extrarenal features

cerebral aneurysms, hepatic and pancreatic cysts, mitral valve prolapse, aortic regurgitation, colonic diverticulosis, ventral and inguinal hernias

ADPKD diagnosis

US showing multiple renal cysts

ADPKD management

aggressive control of risk factors for CV and CVD, ACEIs preferred for HTN, hemodialysis, renal transplant for ESRD

Sacubitril-valsartan

a neprilysin inhibitor combined with an angiotensin II receptor blocker. They cause increased levels of bradykinin and increase the risk of angioedema.

Pulmonary edema in patients with acute decompensated heart failure should be treated with

preload reduction using an IV diuretic

Primary manifestations of Chagas disease

megacolon/megaesophagus, cardiac disease

Hyponatremia in chronic decompensated heart failure with reduced ejection fraction

Common, parallels disease severity and predicts mortality. It likely results primarily from ongoing and profound nonosmotic stimulation for antidiuretic hormone secretion in the setting of reduced renal perfusion

Cyanide poisoning clinical features

HTN, tachycardia, tachypnea --> circulatory collapse, death, headache, confusion, anxiety --> seizures, coma, cherry-red skin, elevated anion gap metabolic acidosis with increased lactic acid

Cyanide poisoning treatment

decontamination, supportive care, empiric treatment with hydroxocobalamin +/- sodium thiosulfate

Cyanide poisoning pathophysiology

inhibits oxidative phosphorylation and forces anaerobic meatbolism, rapidly lethal if untreated