Cardiology Flashcards

1
Q

EKG findings with right atrial enlargement (RAE)

A
  • P wave peaked in V1 (> 1.5 mm) or lead II (> 2.5 mm)
  • This is caused by RA depolarization lasting longer than normal and waveform extends to end of LA depolarization. RA amplitude remains the same, though overlap with LA depolarization leads to taller p-wave.
  • Remember: P-wave is normal width.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

EKG findings in left atrial enlargement (LAE)

A
  • P-wave shaped like an “m” OR p-wave is > 3 mm in V1 OR lead II
  • LA depolarization takes longer –> LA/RA waves do not overlap as much (leading to dip in middle of p-wave) and combined depolarization of atria takes longer (i.e. increased width of p-wave)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Premature atrial complexes

A
  • Common in neonates
  • Mostly benign
  • If on DIGOXIN, PACs could be concerning (also look for N/V/D, anorexia, blurry vision, halos, palpitations, syncope, dyspnea, confusion, dizziness, delirium, fatigue)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Use of digoxin in children

A
  • Used for various heart conditions, including arrythmias and CHF.
  • Improves strength and efficiency of the heart and helps control the rate and rhythm of the heartbeat.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

EKG changes with HYPOkalemia

A
  • Prolonged QT
  • Flattened T-waves
  • ST segment depression
  • U-waves (think of empty glass of potassium [sitting in ST segment depression and/or on top of T-waves])
  • PVCs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

EKG changes with HYPERkalemia

A
  • Peaked T-waves (opposite of hypokalemia)
  • Absent or flat P-waves
  • Widened QRS
  • VTach
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Treatment of hyperkalemia

A
  • Calcium gluconate (to stabilize the heart rhythm - hyperkalemia can cause V-Tach)
  • Sodium polystyrene
  • Insulin (+ glucose to avoid hypoglycemia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

EKG findings with HYPOcalcemia

A
  • Prolonged QT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

EKG findings with HYPERcalcemia

A
  • Shortened ST segment –> shortened QT

- Widened T-wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

EKG findings with HYPOmagnesemia

A
  • Prolonged QT

- Prolonged PR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

EKG findings associated with sodium changes

A

NO EKG changes associated with hypo- or hypernatremia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Electrolyte disturbances associated with prolonged QT

A
  • HYPOkalemia
  • HYPOcalcemia
  • HYPOmagnesemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Causes of prolonged QT

A
  • MELT PC’s:
  • hypoMagnesemia
  • Erythromycin
  • Levofloxacin
  • TCAs
  • low Potassium
  • hypoCalcemia
  • *LOW electrolytes result in sLOW interval**
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Intrinsic rates of SA node, AV node and ventricles

A
  • SA node = 80 bpm
  • AV node = 60 bpm
  • Ventricular = 40 bpm
    • Think 8A node, then subtract 20 bpm as you move down the heart
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Brugada syndrome

A
  • RBBB + ST elevation in V1 -> V3 (precordial leads)
  • Usually found in adults, though can be found in children
  • May result in SUDDEN DEATH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Supraventricular tachycardia

A
  • HR usually > 240 bpm

- Typically diagnosed in children < 6 months old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

EKG findings with SVT

A
  • Regular, narrow complex tachycardia (usually > 240 bpm)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Treatment of SVT

A
  • Vagal maneuvers for 20 seconds (i.e. water or ice to the face, Valsalva if patient can cooperate)
  • If these tx do not work and patient stable, treat with ADENOSINE 0.1 mg/kg (may repeat x 1 @ 0.2 mg/kg - max 12 mg/dose)
  • If unstable or becoming unstable, use SYNCHRONIZED DC electrical cardioversion
  • If > 12 months, may also try diltizaem or verapamil - though DO NOT use these meds in children < 12 months!!!!
  • After patient in sinus rhythm, repeat EKG to assess for WPW
  • Maintenance therapy = beta blocker (propranolol) for 1 year to prevent recurrence. If resistant to tx, perform radiofrequency ablation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Wolff-Parkinson-White Syndrome

A
  • Accessory pathway bypasses AV node and connects atrium directly to ventricle
  • Normal short delay between A and V depolarization provided by AV node is not present –> pre-excitation leading to wave of depolarization that bypasses AV node
  • Most common form is forward through AV node, then retrograde through accessory pathway (orthodromic)
  • EKG = short PR (< 0.12 s) and widened QRS (> 0.10 s)
  • Prone to develop AV reetrant tachycardia (AVRT) NOT AVNRT
  • Tx tachycardia with vagal maneuvers and adenosine and prepare for cardioversion (if needed).
  • Generally avoid Ca channel and beta blockers, though DO NOT use if in Afib/flutter (do not affect refractory period of accessory pathways, which is typically shorter than AV node) –> may lead to Vfib and death!
  • If Afib/flutter present, tx with ibutilide or procainamide (increase refractory period of accessory pathway)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

AV node reentrant tachycardia (AVNRT)

A
  • Tachycardia originates at or near the AV node
  • Fast and slow conduction pathway around or in AV node
  • Typical AVNRT = “slow-fast”
  • EKG = (look at V1) retrograde or absent p-waves, R’ (bunny ears - similar to w/ RBBB, though with normal QRS duration).
  • Common cause of SVT - will respond to tx with vagal maneuvers and adenosine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What effect do vagal maneuvers and adenosine have?

A

Increase refractory period (or temporarily block) AV node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Atrial tachycardias

A
  • Includes atrial fibrillation or atrial flutter
  • DO NOT respond to adenosine or vagal maneuvers (these methods effect refractory period of AV node - with atrial tachycardias, the problem is in the atria, so blocking AV node further down the pathway won’t help).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

In which patients are atrial fibrillation and atrial flutter most likely to occur?

A

Patients with repaired structural heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Causes of ventricular tachycardia

A
  • Digoxin toxicity
  • Hyperkalemia
  • Prolonged QT interval
  • Treat with amiodarone (ONLY if absence of prolonged QT). May also tx with lidocaine or cardioversion.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Why is prolonged QT concerning?

A
  • Can lead to Torsades de Pointes (which may lead to Vfib!)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Prevention and treatment of Torsades de Pointes

A
  • Prevention = beta-blocker or defibrillator
  • Treat with magnesium sulfate
  • May also consider overdrive pacing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

When to consider prolonged QT

A
  • Loss of consciousness
  • Drowning
  • Syncope
  • Seizure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Treatment of Familial Prolonged QT Syndrome

A

Beta-blocker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Indications for pacemaker with complete heart block

A
  • Persists >7 days after surgery
  • Symptomatic
  • CHD AND HR < 75 bpm
  • WithOUT CHD + HR < 55 bpm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Common presentation of complete heart block on boards

A

Child with bradycardia except when crying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What maternal condition can predispose to complete heart block?

A

Systemic lupus erythematosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

EKG with right bundle branch block

A
  • RsR’ (“rabbit ears”) in V1 and V2

- COMMON in healthy individuals

33
Q

EKG with left bundle branch block

A
  • RsR’ in V5 and V6
34
Q

Situation in which left to right shunt may be helpful

A

In cyanotic heart disease. Blood on the right side has some oxygenated blood that needs to reach the periphery via a R -> L shunt.

35
Q

Exam findings with ASD

A
  • Fixed split S2
  • Parasternal impulse/heave
  • Soft LUSB midsystolic murmur
36
Q

Most common type of ASD

A

1) Ostium secundum (70%)

2) Ostium primum (20%)

37
Q

Indications for repair of ostium secundum ASD

A
  • Left to right shunt progresses to ratio of >1.7:1 (volume of blood going to pulmonary circulation: volume of blood going out of LV)
38
Q

Indications for repair of ostium primum ASD

A
  • Repair EARLY
  • May get pregnant is L -> R shunt < 2:1, but pregnancy is contraindicated if develops R -> L shunt!
  • R -> L shunt = Eisenmenger’s Syndrome
39
Q

Eisenmenger’s Syndrome

A

Long-standing L -> R cardiac shunt leads to pulmonary hypertension, eventually causing R -> L shunt

40
Q

PE findings with VSD

A
  • LLSB holosystolic murmur
  • LLSB thrill
  • “Hyperdynamic precordium”
  • If VSD really large, may note NO murmur and a SINGLE S2
41
Q

CXR findings with VSD

A
  • Increased pulmonary vasculature

- Biventricular hypertrophy

42
Q

Syndromes associated with VSD

A
  • Cri-du-chat

- Major trisomies (13, 18 and 21)

43
Q

ASD in trisomies

A
  • Trisomies are more common in trisomies 13 and 18 than in 21
44
Q

Treatment of VSD

A
  • Diuretics
  • Afterload reduction (i.e. captopril) - think of decreased resistance to blood flow out of LV, so more blood will travel to the body)
  • Digoxin
  • Nutritional support
45
Q

Indications for repair of VSD

A
  • Pulmonary HTN
  • Failure to thrive
  • Shunt > 2:1
46
Q

Definition of AV canal defect

A
  • Presence of both ASD and VSD

- Left to right shunt

47
Q

Syndromes associated with AV canal defect

A
  • Down Syndrome

- DiGeorge Syndrome

48
Q

PE findings with AV canal defect

A
  • Loud S1 and S2

- Holosystolic apical murmur (due to associated mitral regurgitation or regurgitation at combine AV valve)

49
Q

Features of concerning murmurs

A
  • Click
  • Harsh
  • Grade III or “loud”
  • Diastolic
  • Pansystolic
  • Late systolic
  • S4 (4th heart sound)
  • S3 (3rd heart sound) that remains after changing position from supine to sitting)
50
Q

Feature of pulmonary stenosis

A
  • LUSB murmur
  • Single S1
  • Widely split S2 (think of pulmonic valve taking longer to close because it takes longer for blood to flow through pulmonic valve)
  • Rarely progressess. Low risk of sudden death.
51
Q

Features of mitral stenosis

A
  • Mid-DIASTOLIC murmur heard at the APEX (think of more intense flow from LA -> LV through stenotic mitral valve during diastole)
  • Associated with chronic rheumatic heart disease
52
Q

Features of tricuspid stenosis

A
  • Mid-DIASTOLIC murmur heard at LLSB (think of more intense flow from RA -> RV. B/C heart at an angle, flow shoots towards LLSB).
53
Q

Features of aortic stenosis

A
  • Mid-systolic murmur at RUSB
  • Thrill at suprasternal notch
  • Click or paradoxical split (i.e. S2 is single on inspiration and splits with expiration)
  • EKG = LVH
  • Progressive and associated with significant risk of SUDDEN DEATH, EXERTIONAL chest pain, SYNCOPE.
  • NO SPORTS until cleared by cardiologist
  • Tx with balloon dilatation
54
Q

Features of mitral regurgitation

A
  • Holosystolic, blowing apical murmur that may radiate to axilla
  • Associated with Marfan Syndrome and Ehlers-Danlos Syndrome
55
Q

What syndromes are associated with mitral regurgitation?

A
  • Marfan Syndrome

- Ehlers-Danlos Syndrome

56
Q

Features of mitral valve prolapse

A
  • Mid-systolic click + mid-late systolic murmur
57
Q

How to differentiate HOCM murmur from MVP murmur

A
  • BOTH associated with louder murmur with standing or Valsalva and decrease with squatting
  • Only MVP murmurs are preceded by a CLICK
  • Hand grip maneuver increases the MVP murmur and diminishes the HOCM murmur
58
Q

Features of aortic regurgitation/insufficiency

A
  • Apical, early-diastolic murmur (when AV closed during diastole, there is still backflow through the valve, resulting in a jet of blood hitting apex of heart and also impairing blood flow through MV).
  • BOUNDING PULSES
  • Associated with Marfan Syndrome
59
Q

Features of Still’s murmur

A
  • Buzzing/musical
  • Mid-systolic
  • Non-radiating
  • Possibly best heard at apex
  • DIMINISHES with STANDING (HOCM worsens with standing)
60
Q

Murmur heard at left subclavicular region

A

PDA

61
Q

Features of venous hum

A
  • Continuous
  • Vibratory
  • Right subclavicular region
  • Present when sitting
  • Resolves when supine or head is turned
62
Q

Causes of bounding pulse

A
  • Aortic regurgitation
  • Large L -> R shunt
  • *Think of rapid decrease in blood flow through aorta (due to backflow with AR or due to lack of blood flow with L -> R shunts)**
63
Q

Causes of wide pulse pressure

A
  • Aortic regurgitation
  • PDA
  • *Backflow occurs during diastole -> lower diastolic blood pressure**
64
Q

Cranial bruits

A
  • Can be due to intracranial AV malformations

- Watch for signs of high-output CHF!!

65
Q

Carotid bruits

A

Benign in children

66
Q

Fixed split S2

A

Almost always 2/2 ASD (due to L -> R shunting, leading to higher volumes through pulmonic valve and delayed closure of the valve)

67
Q

Causes of widely split S2

A
  • RBBB
  • Pulmonic stenosis
  • *Delayed closure of pulmonic valve –> normal A2–P2 becomes A2———P2)**
68
Q

Causes of paradoxical split of S2

A
  • LBBB
  • Aortic stenosis
  • *A2 is delayed and therefore overlies P2 -> single S2 on inspiration. S2 then splits on expiration**
69
Q

Most common causes of endocarditis

A
  • Endocarditis = infected heart valve

- Strep viridans -> Staph aureus -> Staph epidermidis most likely causes.

70
Q

Major and minor criteria for diagnosis of Acute Rheumatic Fever

A
  • Major:
  • Asymmetric, migratory polyarthritis of large joints
  • Signs of carditis (new murmur, CHF, cardiomegaly, pericarditis)
  • Painless, firm subQ nodules (wrists, elbows, knees)
  • Syndenham’s Chorea
  • Minor:
  • Arthralgias (pain without inflammation)
  • Elevated ESR or CRP
  • Fever
  • Prolonged PR
71
Q

Diagnosis of Acute Rheumatic Fever

A
  • 2 Major criteria
  • 1 Major and 2 Minor criteria
  • History of ARF or rheumatic heart disease + 3 Minor criteria
72
Q

Mneumonic for ARF

A

JONES:

  • Joints = asymmetric, migratory, polyarthritis of large joints
  • O (like a heart) = carditis (new murmur, CHF, cardiomegaly, pericarditis)
  • N = nodules (painless, firm subQ nodules on wrists, elbows, knees)
  • E = erythema marginatum
  • S = Syndenham’s Chorea
73
Q

Exceptions to JONES criteria for diagnosis of ARF

A
  • Syndenham’s Chorea + recent Strep throat

- “Indolent” carditis (carditis may be the only manifestation months after Strep infection)

74
Q

Treatment of ARF

A
  • Penicillin VK (PO) x 10 days or Benzathine Penicillin (IM/IV) x 1
  • If carditis present, also give ASA and prednisone
75
Q

Recurrence of ARF

A
  • High chance of recurrence
  • Tx with monthly injections of penicillin to PREVENT GAS pharyngitis.
  • Discontinue maintenance therapy after 21 years of age
76
Q

Aschoff Bodies

A
  • Nodules on the heart or in the aorta
  • On biopsy -> inflammatory cells arranged in ROSETTE pattern around fibrinoid core
  • Pathognomonic for ARF
77
Q

Valves affected with ARF

A
  • Mitral, tricuspid and aortic valves may be affected, leading to stenosis or regurgitation
  • Mitral regurgitation is most common murmur of rheumatic fever (holosystolic, blowing apical murmur that may radiate to axilla)
78
Q

Most common murmur associated with ARF

A

Mitral regurgitation (holosystolic, blowing apical murmur that may radiate to axilla)