Cardiology Flashcards

Question

Causes of Mobitz II?

Answer 1

Can be sign of high vagal /parasympathetic tone (e.g. athletes), can be consequence of myocardial infarct

Answer 2

Sinus P waves >100bpm w/ normal QRS.

Answer 3

3 ° = NO P waves conducted - need escape rhythm @ or below AVN Totally dissociated P-waves / QRS’s, therefore no relationship between atrium and ventricle

Answer 4

Occurs in normal subjects with increased sympathetic tone (e.g. exercise, anxiety, pain, pregnancy), alcohol use, caffeinated beverages, drugs (e.g. Œ≤-adrenergic agonists, anticholinergic drugs)

Answer 5

Treat underlying disease; consider B-blocker if symptomatic, calcium channel blocker if B-blockers contraindicated

Answer 6

- Atrial Premature Beat | - Junctional Premature Beat

Answer 7

Simple reassurance is appropriate, sometimes a beta-blocker

Answer 8

PACs are observed on the surface electrocardiogram as a P wave that occurs relatively early in the cardiac cycle (ie, prematurely before the next sinus P wave should occur) and has a different morphology and axis from the sinus P wave (inverted or biphasic).

Answer 9

Ectopic supraventricular beat that originates in the vicinity of the AV node. P wave is usually not seen or an inverted P wave is seen and may be before or closely follow the QRS complex (referred to as a retrograde, or “traveling backward” P wave)

Answer 10

Rapid, regular atrial depolarization from a macro re-entry circuit within the atrium (most commonly right atrium) The atria depolarize at a rate of 250 to 350 beats/minute (typically 300 beats/minute). Because the atrioventricular (AV) node cannot usually conduct at this rate, typically half of the impulses get through (2:1 block), resulting in a regular ventricular rate of 150 beats/minute.

Answer 11

Saw-tooth flutter waves

Answer 12

In atrial flutter with 2:1 block, carotid sinus massage (first check for bruits), Valsalva maneuver, or adenosine may decrease AV conduction and allow flutter waves to be more easily seen

Answer 13

- If unstable (e.g. hypotension, CHF, angina): electrical cardioversion - If stable: o 1. rate control: B-blocker, diltiazem, verapamil, or digoxin o 2. chemical cardioversion: sotalol, amiodarone, type I antiarrhythmics, or electrical cardioversion - Anticoagulation guidelines same as for patients with AFib

Answer 14

AFib includes antiarrhythmics and radiofrequency (RF) ablation (success rate dependent on site of origin of atrial flutter)

Answer 15

Irregular rhythm caused by presence of 3 or more atrial foci (may mimic AFib)

Answer 16

Occurs more commonly in patients with COPD and hypoxemia

Answer 17

Calcium channel blockers may be used (e.g. diltiazem, verapamil), B-blockers may be contraindicated because of severe pulmonary disease

Answer 18

Single circuit re-entry and/or ectopic foci, mostly arising from the pulmonary veins, act as aberrant generators producing atrial tachycardia (350-600 bpm), which leads to multiple re-entry circuity (microreentry). Impulses conduct irregularly across the atrial myocardium to give rise to fibrillation

Answer 19

Maintenance: The tachycardia causes atrial structural and electrophysiological remodelling changes that further promote AFib; the longer the patient is in AFib the more difficult it is to convert back to sinus rhythm

Answer 20

In atrial fibrillation, the atria do not contract, and the atrioventricular (AV) conduction system is bombarded with many electrical stimuli, causing inconsistent impulse transmission and an irregularly irregular ventricular rate, which is usually in the tachycardia rate range.

Answer 21

No organized P waves due to rapid atrial activity (350-600bpm) causing a chaotic fibrillatory baseline irregularly irregular ventricular response (typically 100-180 bpm), narrow QRS (unless aberrancy or previous BBB)

Answer 22

RACE - Rate control: Beta-blockers, Verapamil, Diltiazem, or Digoxin. In patients with heart failure: digoxin, amiodarone - Anticoagulation: NOAC - Cardioversion (electrical) If AFib <48 h, can usually cardiovert without anticoagulation If AFib >48 h, anticoagulate for 3 wk prior and 4 wk after cardioversion due to risk of unstable intra-atrial thrombus If patient unstable (hypotensive, active angina due to tachycardia, uncontrolled heart failure) should cardiovert immediately - Etiology

Answer 23

Usually initiated by a supraventricular or ventricular premature beat

Answer 24

Re-entrant circuit using dual pathways (fast conducting β-fibres and slow conducting α-fibres) within or near the AV node; often found in the absence of structural heart disease

Answer 25

Premature atrial beat might find fast pathway refractory - conduct down slow pathway - fires ventricle - now fast pathway recovered - retrograde conduction back up - fires atrium retrograde (hidden P’s) - repetitive ‘short circuit’

Answer 26

Congenital defect

Answer 27

- PR interval <120 msec - delta wave: slurred upstroke of the QRS (the leads with the delta wave vary with site of bypass) - widening of the QRS complex due to premature activation - secondary ST segment and T wave changes - tachyarrhythmias may occur - most often AVRT and AFib

Answer 28

- An accessory conduction tract (Bundle of Kent; can be in right or left atrium) abnormally allows early electrical activation of part of one ventricle - Impulses travel at a greater conduction velocity across the Bundle of Kent thereby effectively 'bypassing' AV node

Answer 29

Initiated by a premature atrial or ventricular complex

Answer 30

Stimulus from a premature complex travels up the bypass tract (V to A) and down the AV node (A to V) with narrow QRS complex (no delta wave because stimulus travels through normal conduction system)

Answer 31

Re-entrant loop via an accessory pathway

Answer 32

- Acute: similar to AVNRT except avoid long-acting AV nodal blockers (e.g. digoxin and verapamil) - Long-term: for recurrent arrhythmias ablation of the bypass tract is recommended

Answer 33

More rarely the stimulus goes up the AV node (V to A) and down the bypass tract (A to V); wide and abnormal QRS as ventricular activation is only via the bypass tract

Answer 34

Orthodromic AVRT comprises 95% of the reentrant tachycardias associated with WPW syndrome

Answer 35

Impulse travels from its ectopic site through the ventricles via slow cell-to-cell connections rather than through the normal rapidly conducting His– Purkinje system.

Answer 36

QRS width >120msec, no preceding P wave, bizarre QRS morphology

Answer 37

3 or more consecutive ectopic ventricular complexes. Often >160ms

Answer 38

Ventricular flutter: if rate >200 bpm and complexes resemble a sinusoidal pattern

Answer 39

"sustained VT" if it lasts longer than 30s

Answer 40

Left axis or right axis deviation, nonspecific intraventricular block pattern, monophasic or biphasic QRS in V1 with RBBB, QRS concordance in V1-V6

Answer 41

Identical complexes with uniform morphology. Typically result from intraventricular re-entry circuit, may be idiopathic without any structural heart disease

Answer 42

Monomorphic VT more common than polymorphic VT

Answer 43

Complexes with constantly changing morphology, amplitude, and polarity

Answer 44

- Sustained VT (>30 s) is an emergency requiring immediate treatment - Hemodynamic compromise: electrical cardioversion - No hemodynamic compromise: electrical cardioversion, amiodarone, type Ia agents (procainamide, quinidine)

Answer 45

Polymorhpic VT is more frequently associated with hemodynamic instability due to faster rates (typically 200-250 bpm) vs. monomorphic VT

Answer 46

Treatment: IV magnesium, temporary pacing, isoproterenol and correcting the underlying cause of prolonged QT, electrical cardioversion if hemodynamic compromise Sometimes an implanted defibrillator

Answer 47

Predisposition in patients with prolonged QT intervals

Answer 48

* Congenital long QT syndromes * Drugs: e.g. class IA (quinidine), class III (sotalol), phenothiazines (TCAs), erythromycin, quinolones, antihistamines * Electrolyte disturbances: hypokalemia, hypomagnesemia * Nutritional deficiencies causing above electrolyte abnormalities

Answer 49

A variant of polymorphic VT that occurs in patients with baseline QT prolongation – “twisting of the points”

Answer 50

Ventricles look like a ‘bag of worms’

Answer 51

Chaotic, random, colliding wave fronts of electrical activity  CARDIAC ARREST

Answer 52

Only treatment = immediate electrical DEFIBRILLATION

Answer 53

1. Increased capillary hydrostatic pressure - Increased plasma volume due to renal sodium retention • Heart failure • Reduced systemic vascular resistance (e.g., cirrhosis) • Primary renal sodium retention (e.g., renal disease, drugs) • Pregnancy • Premenstrual edema - Decreased arteriolar resistance (e.g., calcium channel blockers, idiopathic) 2. Decreased oncotic pressure (hypoalbuminemia) - Protein loss (e.g., nephrotic syndrome) - Reduced albumin synthesis (e.g., liver disease/cirrhosis, malnutrition) 3. Increased capillary permeability (e.g., burns, inflammation) 4. Increased interstitial oncotic pressure (e.g., myxedema)

Answer 54

- Venous insufficiency (including postphlebitic syndrome) - Deep venous thrombosis (DVT) - Trauma - Lymphedema (e.g., malignancy, primary) - Infection (cellulitis/soft tissue/bone) - Inflammation (e.g., ruptured Baker cyst, chronic dermatitis)

Answer 55

- SOB (PE, HF), sx of hypothyroidism (slow mental and physical activity, weakness, or fatigue - Meds - PMHx: HTN, diabetes, thyroid disease, COPD, sleep apnea - Social: alcohol use, liver disease

Answer 56

- Unilateral or bilateral - Dependency of edema - Timing of edema

Answer 57

Local compression Obstruction of vein Lymphatic drainage

Answer 58

Venous insufficiency

Answer 59

Decreased plasma oncotic pressure

Answer 60

Deep venous thrombosis, cellulitis, ruptured popliteal cyst, acute compartment syndrome due to trauma, or use of a recent new medication (especially calcium channel blockers)

Answer 61

Normal pregnancy

Answer 62

CHF, renal disease, or hepatic disease

Answer 63

- Vitals: fever (cellulitis, hypotension (HF or cirrhosis, hypertension (renal disease), JVP (elevated = heart failure, constrictive pericarditis) - Skin: Warmth (cellulitis), Signs of chronic venous insufficiency, Signs of myxedema - HEENT: Nonpitting periorbital edema - myxedema (due to hypothyroidism) or nephrotic syndrome - Cardiac: Valvular heart disease or S3 gallop indicative of low ejection fraction - Lungs: SOB - pulmonary edema and/or heart failure - Abdomen: Signs of liver failure - Extremities: Pitting edema - found in dependent areas such as lower extremities (or sacrum if at bed rest). Nonpitting edema – lymphedema, myxedema, lipedema

Answer 64

Brawny, reddish coloration of skin, especially at medial ankle/calf. Progression to lipodermatosclerosis, characterized by fibrosis, hemosiderin deposition, and/or ulceration or erosions (especially over malleolus)

Answer 65

Due to hypothyroidism - generalized dry, thick skin, yellow to orange skin discoloration over knees, elbows, palms, and soles

Answer 66

Enlarged or shrunken liver, which may suggest scarring. Other signs suggestive of cirrhosis such as jaundice, spider angiomata, and caput medusae. Presence of ascites may suggest advanced liver disease, right heart failure, or constrictive pericarditis

Answer 67

- Blood chemistry panel including serum creatinine and liver function tests to assess kidney and liver function - Serum albumin to assess for nephrotic syndrome, liver disease, protein-losing enteropathy and malnutrition states - Plasma B-type natriuretic peptide (BNP) - Urinalysis to look for albuminuria and other signs of renal disease - Chest x-ray to assess for heart failure and chronic obstructive pulmonary disease (COPD) - Electrocardiogram to detect ischemic heart disease or pericardial disease - Thyroid-stimulating hormone levels to rule out hypothyroidism

Answer 68

D-dimer, duplex US

Answer 69

Chronic venous insufficiency: duplex ultrasonography, ankle-brachial index to evaluate for arterial insufficiency

Answer 70

- If patient has history of cancer, pelvic surgery, or trauma, perform pelvic magnetic resonance venography to detect tumor or obstruction - If clinical exam suggests lymphedema, confirm with lymphoscintigraphy and/or T1-weighted magnetic resonance lymphangiography

Answer 71

DDDD – Diet low salt < 2,000 mg/day, fluid restriction (1.5 2 L/day), diuretics (furosemide 20-80 mg/d), vasodilator (ACEi - first line therapy in HF and hypertension. ARB if ACEi not tolerated), B Blockers, digitalis digoxin

Answer 72

- Dietary sodium restriction to < 2,000 mg/day - Diuretics • Loop diuretics (such as furosemide) • Spironolactone commonly used in patients with cirrhosis who have secondary hyperaldosteronism

Answer 73

- Leg elevation and exercise | - Compression stockings

Answer 74

- Rapid diuresis should be avoided (500 mL per day is suggested), especially in those with primarily ascites (without much peripheral edema), to reduce risk of hepatorenal syndrome and hemodynamic collapse - Large-volume paracenteses may be used to reduce need for high dose diuretics in selected patients

Answer 75

- Treat acute thrombotic events with anticoagulation therapy (unfractionated or low molecular weight heparin or warfarin [Coumadin]) to prevent progression of clot or development of postthrombotic syndrome - Consider thrombolysis in select patients

Answer 76

- Maintenance treatment is compression stockings at 30-40 mm Hg - Surgical debulking or bypass procedures should be limited to severe, refractory cases

Answer 77

Mild to moderate mitral stenosis, tachycardia or high cardiac output, shortened PR interval

Answer 78

Occurs just after the beginning of systole and is predominantly due to mitral closure but may also include tricuspid closure components

Answer 79

Clicks occur only during systole; they are distinguished from S1 and S2 by their higher pitch and briefer duration.

Answer 80

Severe MS , severe AS , mitral regurgitation, prolonged PR interval

Answer 81

Early systole – Congenital aortic stenosis or pulmonic stenosis are thought to result from abnormal ventricular wall tension

Answer 82

Occurs at the beginning of diastole, due to aortic and pulmonic valve closure

Answer 83

Aortic valve closure (A2)

Answer 84

Pulmonary hypertension (loud P2) or systemic hypertension (loud A2)

Answer 85

RBBB, pulmonary stenosis (PS), pulmonary hypertension

Answer 86

Atrial septal defect, RV failure

Answer 87

It occurs during passive diastolic ventricular filling and usually indicates serious ventricular dysfunction in adults

Answer 88

Low-pitched, early diastolic sound, usually heard at apex (MON-TRE-al). Abnormal in most adults; suggest heart failure and/or volume overload.

Answer 89

May be normal in some children and pregnant woman

Answer 90

Produced by augmented ventricular filling, caused by atrial contraction

Answer 91

A summation gallop occurs when S3 and S4 are present in a patient with tachycardia, which shortens diastole so that the 2 sounds merge. Loud S3 and S4 may be palpable at the apex when the patient is in the left lateral decubitus position

Answer 92

Low pitched, late diastolic sound, usually heard at apex (tor-ON-to). Caused by atrial contraction into a non-compliant ventricle. Suggested ventricular hypertrophy. Almost always present in active myocardial ischemia or soon after myocardial infarction.

Answer 93

Murmurs are produced by blood flow turbulence and are more prolonged than heart sounds; they may be systolic, diastolic, or continuous. They are graded by intensity and are described by their location and when they occur within the cardiac cycle

Answer 94

Due to turbulent forward flow through narrowed or irregular valves or outflow tracts

Answer 95

Crescendo-diminuendo character that usually becomes louder and longer as flow becomes more obstructed. The greater the stenosis and turbulence, the longer the crescendo phase and the shorter the diminuendo phase.

Answer 96

- Outflow obstruction (aortic sclerosis, aortic stenosis, coarctation of the aorta, hypertrophic cardiomyopathy, subvalvular stenosis, supravalvular stenosis) - Dilation of ascending aorta (aneurysm of aorta, aortitis, atheroma ) - Dilation of pulmonary artery - Increased blood flow across the aortic valve (aortic regurgitation, hyperkinetic states) - Increased blood flow across the pulmonic valve (hyperkinetic states, left-to-right shunt due to atrial septal defect, ventricular septal defect) - Pulmonic obstruction (infundibular stenosis, pulmonic stenosis, supravalvular pulmonary artery stenosis)

Answer 97

- Mitral valve prolapse | - Papillary muscle dysfunction

Answer 98

- Mitral regurgitation - Tricuspid regurgitation - Ventricular septal defect

Answer 99

- Aortic regurgitation | - Pulmonic regurgitation

Answer 100

- Atrial ball-valve thrombi - Increased blood flow across nonstenotic mitral valve (eg, mitral regurgitation, ventricular septal defect, patent ductus arteriosus, high-output states, complete heart block) - Increased blood flow across nonstenotic tricuspid valve (eg, tricuspid regurgitation, atrial septal defect, anomalous pulmonary venous return) - Left or right atrial tumors - Mitral stenosis (eg, due to rheumatic fever, congenital stenosis, cor triatriatum) - Tricuspid stenosis

Answer 101

- Pericardial friction rub - Patent ductus arteriosus - loudest in late systole obscuring obscuring S2, best heard in 2nd ICS LSB - sounds like ‘machinery’ - Venous hum - best heard in 1st or 2nd ICS

Answer 102

A pericardial friction rub is caused by movement of inflammatory adhesions between visceral and parietal pericardial layers. It is a high-pitched or squeaking sound; it may be systolic, diastolic and systolic, or triphasic (when atrial contraction accentuates the diastolic component during late diastole).

Answer 103

- Grade 1: very faint, heard only after ‘tuning in’, may not be heard in all positions - Grade 2: quiet, but heard immediately after placing stethoscope on chest - Grade 3: moderately loud without thrill - Grade 4: loud, with palpable thrill - Grade 5: very loud, with palpable thrill - may be heard when partly off the chest - Grade 6: very loud, with palpable thrill - heard when completely off the chest

Answer 104

1. Degenerative calcification – wear and tear on normal valve 2. Calcification of a congenital bicuspid aortic valve – fusion of two leaflets – most common cause under 65 3. Rheumatic

Answer 105

Increase LVP to drive blood across stenotic aortic valve results in hypertrophy (concentric) - increased LV wall thickness, LV cavity reduces (restores nearly normal afterload. However you have a price to pay - concentric LVH increases muscle stiffness, therefore LA pressures must increase to drive blood into LV and more oxygen supply. This increases the need of atrial kick. If they lose the atrial kick, they go into atrial fibrillation and require left atrium pressures more. End stage - increases LV wall tension = afterload - decreases LV systolic function (eventually) and thus the LV starts to enlarge (dilate) which increases the diastole LVP

Answer 106

- Angina – Discomfort, usually squeezing, crushing, brought on by lack of O2 in cardiac tissue. Coronary Perfusion Pressure = Aortic P - LV P. In systole, LVP ~ AoP, therefore, it occurs in diastole. AS LVH - increasing the cardiac tissue to perfuse. The increase in LV diastolic pressure decreases the pressure gradient between aortic and LV - Dyspnea – The increase in diastolic pressures can increase LA pressures, increasing pulmonary pressures = dyspnea - Syncope – During exertion (decreased vascular resistance), the LV can’t increase CO because of the fixed stenotic aortic orifice with AS, no major increase output - decreases BP - decreases brain perfusion -syncope

Answer 107

- LVH - apex usually still in normal position, when LV fails and dilates - diffuse, displaced apex - Palpation (apical beat): Normal location, normal size, sustained apical beat >1/2 of systole - Carotid pulse - ‘low and slow’ pulse (parvus et tardus) - Peripheral pulses: Brachioradial delay - JVP: Normal, A wave dominant in asymptomatic patient. Elevated only if decompensation of LV - Aortic part of S2 (A2) may decrease intensity, or even disappear - A2 comes later, even after P2 (pulmonic S2) = Paradoxical splitting of S2 - S4 - low-pitched sound made as increase atrial kick empties into stiff LV

Answer 108

Loudest RUSB, early systole, peaks later as AS progresses, holosystolic in severe AS. Crescendo-decrescendo, may radiate to clavicle or carotids

Answer 109

- ECG – LVH - Echo – examine leaflets - Cardiac catheterization - can measure both LV and Ao pressures  estimate severity of AS

Answer 110

Only definitive treatment is valve replacement, can fix coronary disease at time of surgery

Answer 111

1. Leaflet problems: - Leaflets ↓ mobile = scarred, thickened = improper closing - Bicuspid aortic valve - Leaflets fail to close / coapt well due to distorted cusps (predominates over AS) - Leaflets normal mobility = perforated / eroded = leakage - Leaflets ↑mobile / flail (partly detached) 2. Aortic annulus problems - Support structures of leaflets abnormal = dilated aortic root - pulls leaflets open - Hypertension - Genetic defects - weak fibrous tissue in aorta - Bicuspid aortic valve

Answer 112

- LV volume increases and therefore diastolic pressure which backs up into the LA – backs up into the lungs – pulmonary edema - There’s no time for the LV to dilate

Answer 113

- Similar to MR, LV undergoes compensatory adaptation, chronic dilation – eccentric hypertrophy with some increased thickness - Slight increase in LV diastolic pressure because of compliant LV. Decrease in aortic diastolic pressure - Increased flow ejected needs increased LV systolic P = pressure load - Long-standing LV volume / pressure load = slow decreased LV systolic function - 5 x ↑↑↑ stroke volume = ↑↑ aortic systolic pressures (Aorta cannot stretch that much* with each systole!). Therefore, widened pulse pressure.

Answer 114

- Long asymptomatic time course - Gradual onset of symptoms: - Palpitations - common sensation of forceful heart beat and increased pulse pressure - Angina – LVH, increased LV size, increased O2 demand. Due to the decreased aortic diastolic pressure and increased LV diastolic pressures results in decreased perfusion pressure which reduces myocardial oxygen supply. - Dyspnea

Answer 115

- Vital Signs: BP may see wide pulse pressure, Resp (AR – pulmonary edema – dyspnea) - Hands: May have signs of infective endocarditis, cyanosis, quincke’s sign, water hammer pulse (increase pulse pressure (systolic – diastolic BP)) - Face: de Musset’s sign, cyanosis - Carotid: Pulsus bisferiens, hyperkinetic pulse and large pulse pressure - Palpation: Systolic apical thrill (late AR). Apical beat: May be displaced inferolaterally, sustained, diffuse - S3 - S4 = sign of high end-diastolic LV pressure, atrial ‘kick’ emptying into LV

Answer 116

Systolic Flow Murmur: RUSB, early-mid systolic, high (blowing), crescendo-decrescendo

Answer 117

- ECG – may show LVH - CXR – enlarged LV - Echo - can define leaflet and root anatomy

Answer 118

- AR may hit anterior mitral leaflet - partially close the MV - functional mitral stenosis = Austin-Flint murmur - Apex S, mid diastolic, low rumbling

Answer 119

- BP drugs - lower BP - especially vaso-dilating calcium channel blocker = Nifedipine - No beta-blockers - Diuretics - may help alleviate heart failure symptoms from excessive LV volume loading - Surgery once symptoms start and Asymptomatic patients with progressive bad LV dilation or dysfunction

Answer 120

L parasternal; 3rd-4th intercostal space, early diastolic, high, decrescendo, along L sternal border

Answer 121

1. Leaflet / Chords abnormal = 1° mitral valve problem - Reduced mobility – rheumatic mitral valve, leaflets scar and can’t close properly - Normal mobility – perforation almost always due to endocarditis Increased mobility: Prolapse of leaflet = MVP, Flail leaflet due to rupture of chord 2. LV distorted - pulls mitral valve apart = 2° mitral regurgitation - Ischemic papillary muscle - Papillary muscle fails to ‘pull’ on chords - Ischemic scarred LV – scarred papillary muscle pulls leaflet open - LV dilation – increase/dilates annulus

Answer 122

- Fibrous tissue (collagen) of the leaflets are replaced with myxomatous soft tissue - Could be due to a genetic connective tissue disease - Usually no symptoms, benign, could have vague chest pains, palpitations

Answer 123

Produces a mid-systolic click: - If volume in the LV decreases – click and murmur move closer to S1 - If volume in the LV increases – click and murmur move further from S1

Answer 124

- No time for LA or LV to dilate (still ‘stiff’) - Since the LAP will increase dramatically, severe pulmonary edema and poor forward output - Compensate - Since LA filled by MR and pulmonary veins, increase LV filling in diastole. LV accommodates by stretching its myofibers to increase stroke volume. However, the LV stiffness limits amount of increase in volume.

Answer 125

- LA & LV dilate (decreases stiff) without increase pressure - LV - accepts increases LV volume with no increase in diastolic LVP - Compensate - Increase wall thickness – lengthening and thickening of fibers – eccentric hypertrophy - Worsens with increase aortic BP, and aortic stenosis

Answer 126

- Long asymptomatic time course - Increased back pressure will result in left heart failure - Long-standing ↑↑LA back-pressure – atrial fibrillation - Late – right heart failure – peripheral edema + ascites

Answer 127

- Carotid pulse: Severe MR - Hyperkinetic (but NO wide pulse pressure; normal diastolic P - Severe MR - LV apex enlarged, displaced, diffuse, hyperdynamic - Palpable MR ‘thrill’ - S1 variable, wide S2 split (A2 closes early) - Chronic decompensated MR: L S3 - Acute MR: L S4

Answer 128

Apex, early-mid systolic, high-pitched blowing, decrescendo, radiates to L axilla

Answer 129

Apex, holosystolic, high-pitched blowing, radiates to L axilla, isometric hand grip ↑intenisty

Answer 130

- ECG – enlarged LV, LA | - CXR

Answer 131

- Diuretics, could use rate-slowing drugs if a fib - Timing of surgery – LV dysfunction – measure Ejection fraction (at rest or with exercise) or End-systolic volume. Once symptoms start or progressive LV dilation

Answer 132

Rheumatic fever

Answer 133

Mitral valve is tight – increases LA pressure creates a backflow all the way to the systemic tissues

Answer 134

- Dyspnea (especially during exercise), orthopnea, PND - Hemoptysis (rupture of bronchial veins) - Fatigue (pressure backs up into the RV which will dilate and fail causing insufficient forward input) - Arrhythmias - increasing LA pressure – increases LA enlargement which increases likelihood of short circuits – fibrillation. The atrial doesn’t contract nicely (loss of atrial kick) and thus you need higher pressures to fill the LV. Creates sluggish flow resulting in blood clots – emboli (20%/yr in MS) – need to put on anticoagulant. almost always Afib - ↑↑HR (AV node filters out ~ 2/3rds of atrial signals bombarding it) - need HR control drugs

Answer 135

- S1 will sound louder – thickened leaflets, however in late stage disease when rigid S1 intensity gradually decrease - Opening snap – sound from MV opening, also disappears as valve becomes rigid. If it opens soon after S2, severity of MS increased - RV overload - enlarged, hypertrophied RV causes palpable lift underneath sternum = ‘parasternal lift’ or ‘RV heave’ - Dilated RV = stretches tricuspid annulus  leaky tricuspid valve = tricuspid regurgitation

Answer 136

Diastolic murmur – diastolic rumble – turbulent flow across the valve. the worse the MS, the longer into diastole the murmur lasts (longer time for pressure gradient to disappear). Presystolic accentuation

Answer 137

- ECG – enlarged LA, RV hypertrophy - CX – calcified MV, Kerley B lines - Echo – see valve in action

Answer 138

- Diuretics, rate-slowing drugs, beta blockers, anticoagulant - Balloon valvuloplasty – cracks open the fused MV - Valve replacement – tissue or metal valve – clot risk (warfarin)

Answer 139

"Four Ts" (Thymoma, Thyroid enlargement (goitre), Teratoma, Tumours (lymphoma, parathyroid, esophageal, angiomatous))

Answer 140

Pericardial cyst, bronchogenic cyst/tumour, lymphoma, lymph node enlargement (metastatic disease, SCLC), aortic aneurysm

Answer 141

Neurogenic tumours, meningocele, enteric cysts, lymphoma, diaphragmatic hernias, esophageal tumour, aortic aneurysm. Mostly home of tumors of neural origin

Answer 142

Substernal thyroids

Answer 143

Radioisotope thyroid scans are the study of first choice

Answer 144

Lymphadenopathy, whether from lymphoma, metastatic carcinoma, sarcoid, or tuberculosis

Answer 145

Bilateral and asymmetric

Answer 146

Myasthenia gravis

Answer 147

Thymic Hyperplasia

Answer 148

Klinefelter syndrome

Answer 149

- 50% asymptomatic (mainly benign); when symptomatic, 50% are malignant - Chest pain, cough, SOB, dyspnea, recurrent respiratory infections - Hoarseness, dysphagia, Horner's syndrome (ptosis, miosis, anhydrosis), facial/upper extremity edema (SVC compression) - Paraneoplastic syndromes (e.g.myasthenia gravis [thymomas]) - Gynecomastia (teratoma), hypercalcemia sx (parathyroid adenoma), HTN (thyroid disorder)

Answer 150

- CXR (compare to previous) - CT with contrast (anatomic location, density, relation to mediastinal vascular structures) - MRI: specifically indicated in the evaluation of neurogenic tumours - Radionuclide scanning: 131I (for thyroid), gallium (for lymphoma) - Biochemical studies: thyroid function, serum calcium, phosphate, PTH, AFP, B-hCG - Biopsy (mediastinoscopy, percutaneous needle aspiration)

Answer 151

- Excision - symptomatic benign mass that is enlarging or a mass with concerns for malignancy - Resect bronchogenic cysts and localized neurogenic tumours via minimally invasive video assisted procedures - Exploration via sternotomy or thoracotomy - ± post-operative radiotherapy/chemotherapy if malignant

Answer 152

Rifle approach – a bullet goes through all these layers: - Skin - Bites, burns, Herpes, zoster - Sub Q – cellulitis, abscess - MSK - Sprains or strains, fractures, Costochondritis - Pleura: Pneumothorax, Pneumonia, Pleural effusion, Pulmonary cancer, Pleurisy, PE - Pericardium - Pericarditis - Heart - MI, Myocarditis, stable angina, valvular heart disease - Esophagus - GERD, esophagus spasm, mallory-weiss, esophagitis - Trachea - perforation, tracheitis - Aorta - Dissection, aneurysm - Psych - Panic attack

Answer 153

Sudden onset, sharp pleuritic pain, unilateral hyperresonance, decreased breath sounds

Answer 154

Increased w/ respiration, decreased w/ sitting forward or sitting up +/- pericardial friction rub. Also radiates to trapezius

Answer 155

Sudden onset pleuritic pain, increased RR and HR, decreased S2O2, ECG changes

Answer 156

1. Substernal Pressure 2. Exertional Chest Pain 3. Chest Pain relieved with rest (nitroglycerin). - Typical Angina: 3 criteria from above - Atypical Angina: 2 criteria from above - Non-Anginal Chest Pain: 1 criteria from above

Answer 157

Pleuritic, dyspnea, fever, cough, sputum, increased RR, crackles, CXR infiltrate

Answer 158

GI cocktail (Lidocaine)

Answer 159

Substernal burning, acid taste in mouth, water brash. Increased with meals and recumbency, decreased by antacids

Answer 160

Sudden severe tearing pain +/- asymmetric BP, neurological symptoms (cerebral hypoperfusion or occlusion of carotid, vertebral, or spinal arteries)

Answer 161

- 12-lead ECG - CXR, CT - Troponin – At baseline and 3-6 h after symptom onset, repeat 6h later if clinical or ECG changes - D-dimer (PE) - BNP (acute heart failure) - CBC (infections)

Answer 162

The most common finding is sinus tachycardia. The classically described finding "S1Q3T3" (ie, prominent S wave in lead I, Q wave in lead III, and inverted T wave in lead III).

Answer 163

- OPQRST - Associated symptoms - Pain quality and location - Risk Factors (ACS, PE, pneumothroax)

Answer 164

- VS - BP in both arms (aortic dissection) - Cardiac - Gallops (rapid rate of ventricular filling), murmurs (aortic insufficiency – aortic dissection), rubs (pericarditis), signs of vascular disease (carotid/femoral bruits, decreased pulses) - Abdomen exam - epigastric tenderness (GI) - MSK exam - Chest wall for reproducibility (costochondritis) - Pulmonary - unilateral decreased breath sounds (pneumothorax), crackles (left ventricular dysfunction - ACS)

Answer 165

Recent history of prolonged immobilization (eg, long distance travel), surgery (particularly an orthopedic procedure of the lower extremity lasting more than 30 minutes), central venous catheterization, or trauma.

Answer 166

Male sex, age over 55 years, family history of coronary artery disease, diabetes mellitus, hypercholesterolemia, hypertension, and tobacco use.

Answer 167

- Stable angina, discomfort occurs only when activity creates an oxygen demand that outstrips supply limitations imposed by a fixed atherosclerotic lesion. This occurs at relatively predictable points and changes slowly over time. - Unstable angina represents an abrupt change from baseline functioning, which may manifest as discomfort that begins at lower levels of exercise or at rest.

Answer 168

Low voltage and electrical alternans

Answer 169

Intense substernal pain. Increased by swallowing, decreased by NTG.

Answer 170

Localized sharp pain, increased w/ movement. Reproduced with palpation

Answer 171

Costochondritis

Answer 172

Pericarditis

Answer 173

Discomfort/chest pain associated with disturbance in myocardial function but without necrosis. 70% stenosis – inadequate coronary vasodilation reserve if over-exert – myocardial ischemia – sensation of angina

Answer 174

Predicts 10yr risk of non-fatal MI or coronary death (age, FHx, gender, smoking, HDL level, systolic BP, DM)

Answer 175

No critical blockage during rest and therefore normal ECG

Answer 176

Exercise causing stress and perhaps ischemia of myocardium (usually sub-endocardium) ST depression - If seen on BOTH stress & rest = scar = infarct - If defect with stress, OK rest = reversible = ischemia

Answer 177

- High risk EST (Exercise Stress Test) - High clinical suspicion with equivocal non-invasive testing - Unresponsive to maximal medical therapy - Heart failure with ischemia - Multiple ischemic areas on myocardial perfusion scanning - Gold standard for diagnosing where / how bad coronary stenoses are + Identifies patients who may benefit from revascularization

Answer 178

1. Coronary balloons/stents using PCI - Balloon angioplasty - Stents: Bare metal Stents, Drug-eluting stents - Anti-proliferative drug inside stent - prevents intimal scarring. Cuts re-stenosis rate > 50% compared to similar bare metal stent. However, it impairs endothelial healing, or ‘chew away’ at underlying vessel wall tissue and increases risk of clots - CABG: Long patency with IMA, saphenous vein not as good patency

Answer 179

BB (best option), CaCB, nitrates

Answer 180

- Stable CAD aspirin 81mg forever – secondary prevention - Unstable CAD add P2Y12 receptor antagonist (eg Clopidogrel, Ticagrelor) for 1 year if not longer - Bare metal stent – ASA + Clopidogrel for 1 month then ASA forever - Drug eluting stents - ASA + Clopidogrel for at least 3 months, (at least 12-36 months in ACS) then ASA forever. - Never stop the dual therapy!

Answer 181

1. Antiplatelets 2. ACEi 3. B Blockers: First line chronic therapy for acute coronary syndrome and LV dysfunction, decrease the rates of recurrent infarction 4. CaCB: slow heart rate, decrease BP, and dilate coronary arteries 5. Blood Pressure Control: <140/90 mm Hg or <130/80 mm Hg (perhaps lower) if patient has diabetes or chronic kidney disease 6. Cholesterol Management: Consider statin therapy for all CAD patients–high potency, even if low LDL. Target: LDL-C ≤ 2.0 mM (or at least 50% decrease in LDL) 7. Diabetes Management: NO TZD medications (pioglitazone) s/e increases Na reabsorption 8. Diet 9. Exercise 10. End Pain: Discontinue all COX-2 inhibitors and NSAIDs, EXCEPT aspirin or Acetaminophen 11. Vaccines: Annual influenza + pneumococcal polysaccharide vaccinations (prevent complications

Answer 182

Heart failure, or LVEF ≤ 40%, large myocardial infarcts, diabetes, severe left ventricular hypertrophy

Answer 183

If plaque ruptures-->blood meets cholesterol--> thombrogenic stimuli--> clots--> ischemia. Includes STEMI, NSTEMI and unstable angina

Answer 184

- Onset – typically gradual in onset - Provocation and palliation – Ischemic pain is generally provoked by an activity, such as exercise, which increases cardiac oxygen demand. Ischemic pain does not change with respiration or position. It may or may not respond to nitroglycerin and, if there is improvement, this may only be temporary. - Quality – Ischemic pain is often characterized more as a discomfort than pain - Radiation – Ischemic pain often radiates to other parts of the body including the upper abdomen (epigastrium), shoulders, arms (upper and forearm), wrist, fingers, neck and throat, lower jaw and teeth (but not upper jaw). - Time course – Angina is usually brief (two to five minutes) and is relieved by rest or with nitroglycerin. In comparison, patients with an acute coronary syndrome (ACS) may have chest pain at rest, and the duration is variable but generally lasts longer than 30 minutes. - Associated symptoms: The most common is shortness of breath, which may reflect mild pulmonary congestion resulting from ischemia-mediated diastolic dysfunction. Other symptoms may include belching, nausea, indigestion, vomiting, diaphoresis, dizziness, lightheadedness, clamminess, and fatigue.

Answer 185

When the chest pain occurs at rest, is new, is increasing in frequency, or when its onset is triggered with a lower level of exertion. Unstable angina is caused by an unstable plaque that has ruptured and caused a non-occlusive thrombus - NO myocardial damage ie. necrosis (no rise in blood enzymes)

Answer 186

Non-exertional, often early morning angina, from spontaneous severe coronary vasospasm - major drop in O2 supply. Classically without major coronary plaques. Treatment = very high dose anti-spasm drugs

Answer 187

Myocardial Infarct = severe enough mismatch in myocardial blood / O2 supply relative to demands - myocardial necrosis = myocardial death. No ST elevation - usually NOT transmural ischemia

Answer 188

Myocardial Infarct = severe enough mismatch in myocardial blood / O2 supply relative to demands - myocardial necrosis = myocardial death. ST elevation - usually transmural ischemia. Usually 100% blockage for 100% of time! After 6 hrs you’ll get full thickness necrosis

Answer 189

- Admit: to CCU - Diagnosis: acute myocardial infarction - Diet: cardiac diet (<2g Na/d) - Activity: bed rest (with bathroom privileges) - Vitals: CCU vitals - Ins/Outs: fluid restriction if CHF - IV: TKVO DK5 or SL IV - Investigations - Drugs (MONA + DVT Prophylaxis + Other): morphine 4mg IV q4h PRN + oxygen by nasal prongs (2-4L) to bring saturation >92% + nitroglycern 0.4mg SL q5min x 3 + ASA 325mg chewed STAT then 81-325mg PO OD + LMWH IV to keep PTT at 1.5-2x normal + metoprolol or atenolol 5mg IV q5min x 3 doses (not in HR < 50, SBP < 90, CHF, severe asthma/COPD, 2nd or 3rd degree heart block

Answer 190

Continuous cardiac monitoring + ECG qdaily and PRN with chest pain + CXR + Cardiac Enzymes (CK + Troponin + CK-MB q8h x 3) + Fasting Lipids (total cholesterol, LDL-C, HDL-C, TG) + Fasting Glucose + (CBCd + Urea + Creatinine + INR/PTT) qDaily + Echocardiogram + Exercise Tolerance Test or MIBI +/- Angio)

Answer 191

- Select reperfusion strategy: Primary PCI for pt <12 hours chest pain, especially for high risk patients with cardiogenic shock, heart failure, late presentation, or contraindications to fibrinolysis. - Activate cardiac catheterization team as indicated. For patients with symptoms of >12 hours, fibrinolytic therapy is NOT indicated, but emergent PCI may be considered, particularly for patients with evidence of ongoing ischemia or those at high risk of death. - Treat with fibrinolysis within 30 min of first medical contact, symptoms <12 hours, and no contraindications – use if delay to cath >90min of ECG diagnosis - Give antiplatelet (clopidogrel 300mg PO x1 dose, or 75mg if age >75) and anticoagulant (ASA 160) therapy to all patients - Morphine for pain control

Answer 192

Absolute Contraindications of fibrinolysis – prior intracranial hemorrhage, recent stroke or head trauma <3months, head trauma, active internal bleeding, aortic dissection

Answer 193

- Give antiplatelet and anticoagulant therapy to all patients (aspirin) - Enoxaparin 1mg/kg SC BID for 48 hours - BB, nitrates (if current pain), statins, heparin - Cardiac cath and revascularization

Answer 194

ABCN: ASA (81mg PO OD) + ACEi (Ramipril 2.5-5mg PO OD) + Beta Blocker (Carvedalol 6.25mg PO BID) + Cholesterol Drug (Lipitor 10mg PO OD) + Clopidogrel (Plavix 75mg PO OD) + Nitroglycerin 0.3mg SL q5min x 3 PRN

Answer 195

Cardiac arrest is the cessation of cardiac mechanical activity resulting in the absence of circulating blood flow. Cardiac arrest stops blood from flowing to vital organs, depriving them of oxygen, and, if left untreated, results in death

Answer 196

- Coronary artery disease - Cardiac conduction abnormalities - Myocardial abnormalities - Non-cardiac causes (e.g., pulmonary embolus)

Answer 197

- Ischemia secondary to atherosclerotic heart disease - Anomalous coronary circulation - Coronary vasospasm - Ischemic cardiomyopathy

Answer 198

- Congenital long QT syndrome - Acquired long QT syndrome - congenital short QT syndrome - Brugada syndrome - catecholaminergic polymorphic ventricular tachycardia (CPVT) - Wolff-Parkinson White (WPW) syndrome - idiopathic ventricular tachycardia

Answer 199

- dilated cardiomyopathy - hypertrophic cardiomyopathy - takotsubo cardiomyopathy - infiltrative, such as cardiac sarcoidosis, amyloid heart disease - arrhythmogenic right ventricular cardiomyopathy - left ventricular noncompaction - myocarditis

Answer 200

- Metabolic imbalance causes include: hyperkalemia, hypokalemia, hypocalcemia, hypomagnesemia, severe acidosis - Neurological causes include: intracerebral hemorrhage, epilepsy - Massive pulmonary embolism (PE) - Opioid overdose - Other noncardiac causes include: digoxin, antiarrhythmic drugs, antidepressants, drugs prolonging QT interval

Answer 201

- Trigger catalyzes an anatomic or electrophysiological substrate (can be genetic or acquired) and results in ventricular fibrillation or ventricular tachycardia that degenerates to ventricular fibrillation - Ventricular fibrillation results in hemodynamic collapse, cessation of cardiac mechanical activity, and loss of cerebral perfusion  Asystole or pulseless electrical activity following acute event (PE)

Answer 202

- General physical: unresponsiveness and absence of blood pressure, pulse, and/or breathing - Skin: pallor, mottling, or cyanosis - HEENT: look for vomitus or blood, dilated and unresponsive pupils - Cardiac: absent heartbeat - Lungs: absent or agonal breathing - Extremities: absent pulses

Answer 203

o Obtain detailed history from both patients (post arrest history) and any witnesses as patient often has retrograde amnesia and unable to recall event o Ventricular fibrillation most common initial rhythm when cardiac disease is cause of arrest o Ask about possible exertion trigger event, if applicable, including less common inherited conditions that are triggered by exertion o Medication history o Past medical history (PMH): chest pain, syncope, chronic ischemic heart disease, myocardial infarction, hypertrophic cardiomyopathy, ventricular tachycardia, long QT syndrome o Family history (FH): sudden cardiac arrest or death

Answer 204

- 12-lead electrocardiogram (ECG) - echocardiography - coronary angiography in patients with ischemic electrocardiogram (ST-elevation or ST-segment depression with T-wave inversion), history of chest pain, or known coronary artery disease risk factors - Stress testing - Cardiac magnetic resonance imaging - Blood tests: obtain blood gases (VBG), pH, and electrolytes - Measure markers of cardiac injury (cardiac troponins) and screen for toxins and/or drugs

Answer 205

Step 1: Assess scene safety. Step 2: Assess patient responsiveness -shake shoulders Step 3: Call for help – 911, retreieve AED Step 4: Assess for signs of life - Check pulse and respiration simultaneously - Head-tilt/chin-lift maneuver, jaw-thrust maneuver. Start CPR immediately if any of the following are identified: No palpable pulse, Apnea, Agonal respirations Step 5: Perform CPR and defibrillate as needed. - Single-rescuer CPR - Perform 30 chest compressions followed by two rescue breaths (30:2) per cycle - Compression-only CPR is reasonable if mouth-to-mouthbreathing is deemed too risky and BMV equipment is unavailable. AED

Answer 206

Consider advanced imaging in patients with nondiagnostic electrocardiogram, coronary angiography, and echocardiography if suspect any - arrhythmogenic right ventricular dysplasia - cardiac sarcoidosis - myocarditis - myocardial injury from coronary spasm

Answer 207

1. Priority 1: CPR: Perform CPR for at least 2 minutes before the first rhythm check. Do not interrupt CPR, except for rhythm and pulse checks 2. Priority 2: Rhythm and pulse check. - If either of the following shockable rhythms is identified, proceed first to "Priority 3": Ventricular fibrillation, Ventricular tachycardia - If either of the following nonshockable rhythms is identified, proceed directly to "Priority 4": PEA, Asystole 3. Priority 3: Defibrillation (shockable rhythms only): Deliver shock as soon as a shockable rhythm is recognized (do not defibrillate nonshockable rhythms). 4. Priority 4: Resuscitation Medications 5. Priority 5: Hs and Ts - Treat Hs and Ts - IV fluids - Rewarming - Medications: e.g., calcium chloride, - Thrombolytics

Answer 208

Epinephrine 1 mg IV/IO as soon as possible; repeat every 3-5 minutes as needed

Answer 209

- After 2nd cycle of defibrillation: epinephrine 1 mg IV/IO - After 3rd unsuccessful cycle of defibrillation - Amiodarone 300 mg IV/IO; then 150 mg IV/IO once after 3-5 minutes OR - lidocaine 1-1.5 mg/kg IV/IO once, then 0.5-0.75 mg/kg IV/IO once after 3-5 minutes - Repeat epinephrine every 3-5 minutes as needed

Answer 210

Hs - Hypovolemia - Hypoxia - Hypokalemia - Hyperkalemia - Hydrogen ion (acidosis) - Hypothermia Ts - Tension pneumothorax - Tamponade (cardiac) - Toxins - Thrombosis (pulmonary embolism) - Thrombosis (myocardial infarction)

Cardiology Flashcards

(238 cards)