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AMC FLASHCARDS > IM-Cardio > Flashcards

IM-Cardio Flashcards

1
Q
  1. What does each indicate:
    a. P wave:
    b. PR interval
    c. QRS complex:
    d. QT interval:
    e. T wave
    f. J point
    g. ST segment:
    h. U wave:
    i. RR interval:
A

a. Atrial depolarization.
b. Time from start of atrial dep to start of ventricular dep. <200 ms.
c. Vent. depolarization. <120 ms.
d. Vent. dep, mechanical heart contraction, vent. repolarization. e. Vent. repolarization. (inversion–>Ischemia or MI)
j. Junction between the end of QRS and the start of ST seg.
g. Isoelectric, ventricles depolarized.
h. Prominent in hypokalemia, and bradycardia.

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2
Q
  1. Indications of abnormal T wave:
A

a. Hyperkalemia
b. Wellen’s syndrome
c. Left Vent Hypertrophy with repolarization abnormalities
d. Pericarditis stage iii
e. ARVD: Arrhythmogenic right vent. Dysplasia
f. Hyper-acute T wave during MI

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3
Q

A wide QRS duration occurs in:

A
  • Right bundle branch block.
  • Left BBB.
  • Non-specific intraventricular conduction delay.
  • Ventricular arrhythmias eg. Vent. Tachyc.
  • Tricyclic antidepressant toxicity. Tx with Bicarbonate.
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4
Q

Indications for R/S wave ratio greater than 1 in lead V1:

A
  • Right BBB.
  • Wolff Parkinson White syndrome.
  • Acute posterior MI.
  • Right Vent. Hypertrophy.
  • Isolated Posterior Wall Hypertrophy (in Duchenne muscular dystrophy).
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5
Q

The causes of LAD are listed below. Note that the first three account for almost 90% of ECG tracings with LAD.

A
  • Normal variant
  • Left anterior fascicular block
  • Left ventricular hypertrophy (rarely with LVH; usually axis is normal)
  • Left bundle branch block (rarely with LBBB)
  • The mechanical shift of heart in the chest (lung disease, prior chest surgery, etc.)
  • Inferior myocardial infarction
  • Wolff-Parkinson-White syndrome with “pseudoinfarct” pattern
  • Ventricular rhythms (accelerated idioventricular or ventricular tachycardia)
  • Ostium primum atrial septal defect
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6
Q

The causes of RAD are:

A
  • Normal variant
  • Right bundle branch block
  • Right ventricular hypertrophy
  • Left posterior fascicular block
  • Dextrocardia
  • Ventricular rhythms (accelerated idioventricular or ventricular tachycardia)
  • Lateral wall myocardial infarction
  • Wolff-Parkinson-White syndrome
  • Acute right heart strain/pressure overload — also known as McGinn-White Sign or S1Q3T3 that occurs in pulmonary embolus
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7
Q

No P wave or abnormal P morphology indicates:

A
  • Atrial Fib.
  • Atrial flutter.
  • Ventricular fib.
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7
Q

ECG Leads placement:

A
  • II, III, aVF = Inferior
  • I, aVL, V5, V6, = Lateral
  • V1, V2 = Anterior
  • V3, V4 = Septal
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8
Q

Wolff-Parkinsons-White Syndrome:

  1. Characteristics
  2. Symptoms
  3. Diagnosis
  4. Tx
A
    • Abdnormal fast accessory conduction pathway from atria to the ventricle ( bindle of Kent)bypasses the rate-slowing AV Node–> early partial ventricular depolarization.
    • Delta wave
    • Widened QRS complex
    • Shortened PR interval.
    • Supraventricular tachycardia due to reentry circuit
  2. SOB, Dizziness, pounding heart beat, irregular HR

3.

  • Physical examination.
  • Medical history.
  • Electrocardiogram (ECG)
  • Exercise testing to assess whether the ECG abnormality persists with exercise.
  • An electrophysiology study

4.

  • Procainamide IV dose: class 1A antiarrhythmic, increases effective refractory period and reduces impulse conduction velocity and excitability in the atria, His-Purkinje fibers, ventricular muscle, and the AP of the heart.
  • Adenosine: it is important to be ready for DCCV when using adenosine for patients with WPW syndrome due to the cause of Atrial Fib leading to Vent. Fib.
  • Ablation.
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9
Q
  1. Identify Rhythm
  2. Causes
  3. Complication
  4. Tx
A
  1. Atrial Fib. No sinus rhythm. Irregularly irregular.
  2. HTN, CAD, Viral infx, Mitral valve disease, Congenital heart defect, binge drinking (holiday heart syndrome), Hyper/hypothyroidism, Pericarditis, and pericardial trauma, Pheochromocytoma.
  3. Stroke (Thromboembolic event)
  4. (for stable) Anticoagulation, Antiarrhythmic, Beta Blockers, Calcium Channel blockers, Ablation, rate control, rhythm control, and/or cardioversion (for hemodynamically unstable).

NOTE: same as Atrial flutter, except A flutter has a sawtooth appearance.

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10
Q
  1. +3 different looking P waves indicate:
  2. Diagnosis
  3. Management
A
  1. Multifocal Atrial Tachycardia associated with lung disease ( COPD, ASTHMA, SARCOIDOSIS..ETC). Similar to Wandering Atrial Pacemaker, except it has a stable heart rate.
  2. Diagnosis: History, Physical exam, Vagal maneuvers or Adenosine to show AV block. Also, the Abnormal Pulmonary Function test due to lung disease.
  3. Tx: Treat the underlying disease. Improve oxygenation and ventilation. If Left ventricular fxn preserved–> CCB, BB, Digoxin, Amiodarone, IV Flecainide, and IV Propafenone. If not preserved–> Digoxin, Diltiazem or Amiodarone. Don’t use cardioversion.
  4. If treatment is indicated, therapy should begin with first correcting underlying electrolyte abnormalities with repletion of potassium or magnesium. Studies have shown magnesium suppresses ectopic atrial activity and can be beneficial even if magnesium levels are within the normal range. Once electrolyte abnormalities have been corrected, possible treatment options include non-dihydropyridine calcium channel blockers, beta-blockers, and atrioventricular (AV) node ablation. Studies have found no role for antiarrhythmic agents, cardioversion, or anticoagulation.
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11
Q
  • Atria firing on its own.
  • Causes include Adrenergic excess, drugs, alcohol, tobacco, electrolyte imbalance, ischemia, and infection.
  • Early P wave that differs in morphology
  • QRS complex normal
  • Found in 50% normal adults who undergo HOLTER’S monitoring.
  • May cause palpitations or give rise to PSVT.
  • It doesn’t require Tx. B Blockers may be helpful.
A

Premature Atrial Complexes

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12
Q
  • Fires from the ventricles
  • This occurs with/without structural heart disease.
  • Causes: hypoxia, electrolyte abnormalities, stimulants, caffeine, medication, and structural heart disease.
  • Wide QRS, due to slow conduction.
  • P wave not usually seen.
  • Frequent PCV and underlying structural heart disease, are at high risk of sudden death due to arrhythmia.
  • Order Electrophysiology study because patients a=may benefit from an ICD.
A

Premature Ventricular Complexes.

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13
Q
  • AV nodal reentrant tachycardia ( within AV node)
  • Oethodromic AV reentrant tachycardia ( at distance from AV node)
  1. Lead to?
  2. Initiated or terminated by what?
  3. Causes?
  4. Treatment?
  5. Prevention?
A
  1. Paroxysmal Supraventricular Tachycardia. Narrow QRS complex due to short circuit and rapid conduction.
  2. AV node reentrant by PAC. Orthidromic by PAC or PVC.
  3. Ischemic HD, Digoxin Tox., AV node reentry, Excessive caffeine or alcohol, A flutter with a rapid ventricular response.
  4. Vagal maneuvers to block reentry mechanism: Valsalva maneuver, carotid massage, breath-holding, head immersion in cold water. Rx: IV adenosine (choice) to decrease sinoatrial and AV node activity. IV verapamil, IV esmolol or digoxin for pts with preserved left vent. fxn. DC Cardioversion if nothing works.
  5. Prevent with Verapamil or BB. Radiofrequency catheter ablation of the AV node or accessory tract if recurrent and symptomatic.
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14
Q
  1. Causes of Ventricular tachycardia?
  2. Symptoms?
  3. Types?
A
  1. CAD with Prior MI (common).Active ischemia, hypotension. Cardiomyopathies. Cong. defect. Prolonged QT syndrome. Drug toxicity.
  2. Palpitations, lightheadedness, angina, syncope or near syncope, sudden cardiac death, signs of cardiogenic shock, Cannon A wave in the neck and S1.
  3. Sustained ( longer than 30 s and symptomatic almost always) vs Nonsustained.
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15
Q

Drug-Induced long QT is due to:

A
  • Antiarrhythmics (Class IA, III)
  • Antibiotics (Macrolides)
  • Antipsychotics (Haloperidol)
  • Antidepressants (TCAs)
  • Antiemetics (Ondansteron)
16
Q

Torsades de Pointes

A
  • Shifting sinusoidal waveforms
  • Long QT
  • Decrease in K+, Mg+2, Ca2+
  • Congenital: Romano-Ward synd (AD)/ Jervell and Lange-Nielsen Synd (AR, sensorineural deafness).
  • Rx: Magnesium Sulfate
17
Q

Patients with underlying HD with nonsustained VT.

  • Management?
A

Implantable defibrillator!!

18
Q

Atropine and cardiac pacemaker (transcutanous/ transvenous):

A

Sinus Bradycardia

19
Q

Causes of Valvular dysfx:

A
  • Disease (bacterial, viral), RF, and inflammation
  • Congenital heart defects
  • Ischemic heart disease
  • Cardiac hypertrophy or dilation
  • as occurs in heart failure
  • Ruptured chordae tendineae
20
Q

Mitral Stenosis:

  1. Characteristics
  2. SS
  3. Dxn
  4. Tx
A
  1. Due to RHF in the early years “wear and tear” cross-activity of streptococcal antigens and valve tissue. Common in immigrants and pregnancy.
    - Leads to Pulmonary congestion due to increased left atrial and pulmonary venous pressure. It leads to Pulmonary HTN and RVF.
  2. Exertional dyspnea, orthopnea, angina, hemoptysis, dysphagia, palpitations, Afib(thromboembolism), ascites&edema (RVF). Signs: S2 followed by an opening snap followed by a low-pitched diastolic rumble. Loud S1.
    - Heard with the bell at the left lateral decubitus position.
    - Squatting and leg raise will increase murmur.
  3. Dxn: Echocardiogram (first initial test)- TEE (more accurate) OR TTF (best initial).
    - Catheterization ( 2nd most accurate)
  4. Tx:
    - SURGERY!- Percutaneous balloon valvuloplasty, Replacement.
    - Medical: Diuretics and BB- alone do not improve case.
21
Q

Aortic Stenosis

  1. Chx
  2. SS
  3. Dxn
  4. Tx
A
  1. Aging is a leading factor. LV dilatation>> LFH. It also causes MR due to pulling the valve annulus apart.
    - Due to calcification of a congenitally abnormal bicuspid valve or tricuspid aorta valve in the elderly. RF.
    - Angina( most common feature), Syncope, HF are signs of poor prognosis and high mortality rate.
  2. Murmur: Crescendo-decrescendo systolic murmur.
    - Radiates tp carotid. S2 is soft. S4( pathology). Parvus et tradus (diminished and delayed carotid upstrokes).
    - Valsalva and standing: decrease murmur.
    - Handgrip: Softens murmur.
  3. Dxn: ECHO ( diagnostic in most cases), Catheterization ( definitive diagnosis).
    - CXR: LV/LA enlarged. Heart size is >50% of the transthoracic diameter. LVH (ECG: S in V1 and R in V5 >35 mm)
  4. Tx:
    - VALVE REPLACEMENT! Balloon valvuloplasty isn’t effective with calcification.
22
Q

Aortic Regurgitation

  1. Chx
  2. SS
  3. Dx
  4. Tx
A
  1. Increase in the left vent. end-diastolic pressure.
    - LVH occurs. The survival rate is 75%, 5 years. After angina, death occurs 4 years later. 2 years after HF.
    - Acute causes: Inf. Endocarditis. Trauma, aortic dissection or iatrogenic.
    - Chronic: RF, Marfan syndrome, Bicuspid aortic valve, Ehler-Danlos syn. Ankylosing Sp., SLE [primary valvular].

Syphilitic aortitis, osteogenesis imp., aortic dissection, behcet synd., reiter synd., systemin HTN. [aortic root diseases].

  1. Cyanosis and shock in the acute phase. Same in CHF.
    - Widened pulse pressure- markedly increased systolic BP, and decreased diastolic BP.
    - Water hammer pulse (corigan). Austin flint murmur. Hill sign, quincke pulse, de musset sign, muller sign, duriziez sign.
  2. Dx: echo and catheterization. CXR: LVH, dilated aorta. ECG.
  3. Tx: Conservative management if stable and asymptomatic: salt restriction, duiretics, vasodilators(mainly-ACE/ARB)
    - SURGERY! Acute AR post MI is a medical emergency. Replacement.
23
Q

Always suspect Pericarditis in patients with:

A
  • A new heart murmur.
  • Fever or unexplained bacteremia.
24
Q
  • Acute pericarditis by:
  • Subacute by:
A
  1. S. aureus. (virulent)
  2. Strep. viridans and Enterocuccus. (less virulent)
25
Q

Native Valve Endocarditis:

Prosthetic Valve Endo:

A
  • S. viridans ( most common)
  • Others: Staph aureus more than epidermidis. Enterococci.
  • HACEK:
  • Hemophilus
  • Actinobacillus
  • Cardiobacterium
  • Eikenella
  • Kingella
  • Staph. epidermidis more common than aureus. for early onset
  • For late onset: Streptococcus
26
Q

Duke Criteria of Endocarditis:

A
  1. Major:
  • Sustained bacteremia.
  • Endocardial involvement: Vegetation, abscess, valve perforation, prosthetic dehiscence or clearly established new valvular regurgitation.
  1. Minor:
  • Predisposing condition
  • Fever
  • Vascular phenomena: septic arterial or pulmonary emboli, mycotic aneurysm, intracranial hem., Janeway lesions ( painless erythematous lesions on palms and soles.)
  • Immune phenomena: Glomerulonephritis, Osler nodes, Roth spots (oval, retinal hem. with a clear, pale center), Rheumatoid factor.
  • Positive blood culture
  • Positive Echo not meeting criteria.

AMC FLASHCARDS (2 decks)

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