Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PANRE > Cardiology 16% > Flashcards

Cardiology 16% Flashcards

1
Q

Reduced contraction strength, large heart, systolic dysfunction

A

Dilated Cardiomyopathy

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

Dilated cardiomyopathy etiology

A

Genetics, excess alcohol, postpartum, chemotherapy, endocrine disorders

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

Dilated Cardiomyopathy physical exam

A

Dyspnea, S3 gallop, rales, jugular venous distention

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

Hypertrophic portion of septum - Young athlete with a positive family history has sudden death or syncopal episode

A

Hypertrophic Cardiomyopathy

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

Hypertrophic Cardiomyopathy physical exam

A

High pitched mid systolic murmur at LLSB. Increased with valsalva and standing (less blood in chamber). Decreased with squatting (more blood in chamber).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Right heart failure with a history of infiltrative process - stiff ventricles

A

Restrictive Cardiomyopathy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Restrictive cardiomyopathy etiologies

A

Amyloidosis, sarcoidosis, hemochromatosis, scleroderma, fibrosis, and cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

Atrial fibrillation

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

Regular, sawtooth pattern, atrial rate 250-350 BPM, narrow QRS complex

A

Atrial flutter

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

PR interval > .2 seconds.

Actually a delay rather than a block.

A

First degree AV block

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

First degree AV block caused by a ______

A

conduction delay at the AV node or bundle of His.

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

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

Second degree AV block Types

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe Second degree AV block Type 1 (Wenckebach)

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe Second degree AV block Type 2 (Mobitz)

A

Some get dropped some get through now you’ve got Mobitz 2.
With Mobitz Type II blocks, the impulse is blocked in the bundle of His. Every few beats there will be a missing beat but the PR Interval will not lengthen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

With this block, no atrial impulses are transmitted to the ventricles.

A

Third degree AV block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Describe Third degree AV block

A

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.

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

R and R’ (upward bunny ears) in V4-V6

A

Left bundle branch block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

R and R’ (upward bunny ears) in V1-V3

A

Right bundle branch block

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

SVT with abrupt onset and offset

A

Paroxysmal supraventricular tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Any tachydysrhythmia arising from above the level of the Bundle of His

A

Atrioventricular nodal reentrant tachycardia (AVNRT):

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles (Bundle of Kent fibers).

A

PWolff-Parkinson-White (WPW) syndrome

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

Wolff-Parkinson-White (WPW) syndrome on EKG

A

Shortened PR interval, widened QRS, and delta waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Premature beats

A

PVC, PAC, PJC

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

Early wide “bizarre” QRS, no p wave seen

A

PVC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Abnormally shaped P wave

A

PAC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

The QRS complex will be narrow, usually measured at 0.10 sec or less, no p wave or inverted p wave

A

PJC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Collective term used to describe dysfunction in the sinus node’s automaticity and impulse generation

A

Sick sinus syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Sinus bradycardia

A

Sinus rhythm with a resting heart rate of < 60 bpm in adults, or below the normal range for age in children

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

Sinus pause

A

pause < 3 seconds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Sinus arrest

A

pause > 3 seconds

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

Tachy-Brady Syndrome

A

Episodes of alternating sinus tachycardia and bradycardia

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

Wide complex tachycardia with three or more consecutive premature ventricular beats

A

Ventricular tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Stable ventricular tachycardia treatment

A

Amiodarone → lidocaine → procainamide (in this order)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Unstable ventricular tachycardia treatment

A

CPR and defibrillation (synchronized direct current (DC) cardioversion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

EKG: No discernible heart contractions

A

Ventricular fibrillation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Ventricular fibrillation treatment

A

CPR and defibrillation (AKA non-synchronized cardioversion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Polymorphic ventricular tachycardia that appears to be twisting around a baseline

A

Torsades de pointes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Torsades de pointes treatment

A

Magnesium sulfate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Foramen ovale fails to close

A

Atrial septal defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Atrial septal defect findings

A

Noncyanotic.
Wide fixed split second heart sound (S2). Systolic ejection murmur at second left intercostal space with an early to mid-systolic rumble.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Coarctation of the aorta findings

A

Noncyanotic

Higher blood pressures in the arms than in the legs and pulses are bounding in the arms but decreased in the legs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Patent ductus arteriosus findings

A

Noncyanotic

A continuous “machinery murmur” at the upper left sternal border

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Tetralogy of Fallot findings

A

Cyanotic

Four features “PROVe”: Pulmonary stenosis, Right ventricular hypertrophy, Overriding aorta, Ventricular septal defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

The most common pathologic murmur in childhood.

A

Ventricular septal defect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Ventricular septal defect findings; treatment

A

Noncyanotic .
Loud, harsh, pansystolic murmur at the lower left sternal border.
Most close by age 6, surgery if large.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Heart failure types

A

Right sided

Left sided: Systolic; Diastolic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Right sided heart failure findings

A

Peripheral and abdominal fluid accumulation = jugular venous distention, edema, hepatomegaly, no rales.
Diagnose with echo and doppler, gold standard is right heart cardiac catheterization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Right sided heart failure diagnostics

A

Echo and doppler U/S.

Gold standard is right heart cardiac catheterization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Left sided heart failure findings

A

Shortness of breath and fatigue - paroxysmal nocturnal dyspnea, cough, orthopnea, rales

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Systolic heart failure findings

A

Decreased ejection fraction, S3 (rapid ventricular filling during early diastole is the mechanism responsible for the S3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Diastolic heart failure findings

A

Ejection fraction is usually normal, S4

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Heart failure CXR, lab test findings

A

Kerley B lines, ↑ BNP

53
Q

Elevated blood pressure > 140/90 with no identifiable cause

A

Primary hypertension

54
Q

Normal, prehypertension, Stage 1, Stage 2 blood pressure parameters

A

Normal: < 120/80 mmHg
Prehypertension: 120–139/80–89 mmHg
Stage 1: 140–159 mmHg (systolic) or 90–99 mm Hg (diastolic)
Stage 2: ≥ 160 mm Hg (systolic) or ≥ 100 mm Hg (diastolic)

55
Q

Systolic BP ≥ 140 diastolic BP ≥ 90 or both with an identifiable cause

A

Secondary hypertension

56
Q

Secondary hypertension etiologies

A

Sleep apnea, pheochromocytoma, coarctation of the aorta, parenchymal renal disease, renal artery stenosis, Cushing syndrome, primary hyperaldosteronism (Conn’s disease)

57
Q

Secondary hypertension treatments

A

Reduce BP to < 140/90 mm Hg for everyone < 60, including those with a kidney disorder or diabetes
Reduce BP to < 150/90 mm Hg for everyone ≥ 60

58
Q

Hypertensive emergency

A

BP usually >180/120 with impeding or progressing end organ damage

59
Q

Hypertensive emergency end organ damage

A

Encephalopathy, nephropathy, intracranial hemorrhage, aortic dissection, pulmonary edema, unstable angina or MI (except papilledema which = malignant HTN)

60
Q

Hypertensive emergency treatment

A

BP must be reduced within 1 hour to prevent progression of end organ damage or death.
Treatment: IV labetalol or calcium channel blocker (dihydropyridine), Sodium Nitroprusside (drug of choice)

61
Q

Hypertensive Urgency

A

BP usually 180/120 without signs of end organ damage

62
Q

Hypertensive urgency treatment

A

Immediate BP reduction is not required.

Treatment: oral antihypertensive Clonidine (drug of choice)

63
Q

Malignant HTN

A

Diastolic reading >140 mm Hg associated with papilledema and either encephalopathy or nephropathy

64
Q

Cardiogenic shock findings

A

Hypotension (SBP <90mmg), cyanosis, cool extremities, altered mental status, and crackles.

65
Q

Cardiogenic shock etilogies

A

acute MI, heart failure, cardiac tamponade

66
Q

Cardiogenic shock treatment

A

Fluid resuscitation, pressors (dopamine), and treat underlying cause.

67
Q

Orthostatic hypotension

A

Drop of > 20 mm Hg systolic, 10 mmHg diastolic, or both 2-5 minutes after change from supine to standing

68
Q

Non-ST-Segment Elevation MI (NSTEMI) EKG and lab findings

A

ECG changes such as ST-segment depression, T-wave inversion, or both may be present.
Evidence of myocardial necrosis (cardiac markers in blood; troponin I or troponin T and elevated CK) WITHOUT acute ST-segment elevation or Q waves.

69
Q

ST-Segment Elevation Myocardial Infarction (STEMI)

A

ST segment elevations > 1mm in > 2 contiguous leads on ECG.

Evidence of myocardial necrosis (cardiac markers in blood; troponin I or troponin T and elevated CK)

70
Q

ST elevation =

A

Acute ischemia

71
Q

T wave depression =

A

Myocardial injury

72
Q

Q wave =

A

Infarct

73
Q

Lateral STEMI

A

I, aVL, V5, V6: Left circumflex

74
Q

Anterior STEMI

A

V2-V4: Left anterior descending

75
Q

Septal STEMI

A

V1, V2: Left anterior descending

76
Q

Anterolateral STEMI

A

V4, V5, V6: Left main

77
Q

Posterior STEMI

A

V1, V2: ST depression: Right coronary artery

78
Q

Inferior STEMI

A

II, III, aVF: Right coronary artery

79
Q

Serial cardiac enzymes

A

Troponins, myoglobin, CK-MB

80
Q

Troponins results

A

Most specific test, appears at 4-8 hours, peaks 12-24 hours and lasts for 7-10 days

81
Q

Myoglobin results

A

Elevate in 1-4 hours

82
Q

CK-MB results

A

Appears at 4-6 hours, peaks at 12-24 hours and lasts for 3-4 days

83
Q

Previously stable and predictable symptoms of angina that are now more frequent, increasing or present at rest.

A

Unstable angina

84
Q

Coronary artery vasospasms causing transient ST segment elevations, not associated with clot

A

Prinzmetal variant angina

85
Q

Prinzmetal variant angina risk factors

A

History of smoking (#1 risk factor) or cocaine abuse

86
Q

Prinzmetal variant angina EKG findings

A

May show inverted U waves

87
Q

Abdominal Aortic Aneurysm signs/symptoms

A

Flank pain, hypotension, pulsatile abdominal mass

88
Q

Aortic Dissection

A

Sudden onset tearing chest pain, between scapulas.

Diminished pulses

89
Q

Aortic Dissection signs/symptoms

A

Sudden onset tearing chest pain, between scapulae. Diminished pulses

90
Q

Aortic dissection x-ray findings

A

Chest radiograph: Widened mediastinum

91
Q

Aortic Dissection treatment

A

Ascending aorta - Surgical emergency

Descending aorta - Medical therapy (beta blockers) unless complications are present

92
Q

Inflammation of large and medium vessels: jaw claudication and headache, thickened temporal artery scalp pain elicited by touching the scalp or combing the hair, acute vision disturbances – Amaurosis fugax (temporary monocular blindness) secondary to anterior ischemic optic neuritis. Associated with polymyalgia rheumatica.

A

Giant cell arteritis

93
Q

Giant cell arteritis testing

A

ESR > 100

Diagnosed with temporal artery biopsy

94
Q

Giant cell arteritis treatment

A

Treat with high dose prednisone – do urgently to prevent blindness (Do not wait for biopsy results)

95
Q

Peripheral artery disease presentation

A

Intermittent claudication, atrophic skin, rubor, hair loss, decreased pulses or non healing ulcers

96
Q

Peripheral artery disease diagnosis

A

Ankle/brachial index (< 0.9).

Angiography is gold standard.

97
Q

Peripheral artery disease contraindicated treatment

A

β-blockers are contraindicated in isolated PAD – it will worsen claudication

98
Q

Phlebitis/thrombophlebitis

A

Dull pain, erythema, induration of vein, palpable cord.

May be spontaneous or after trauma, IV/PICC lines.

99
Q

Phlebitis/thrombophlebitis diagnosis/treatment

A

Venous duplex ultrasound - gold standard for diagnosis.

NSAIDs, warm compress.

100
Q

Varicose veins presentation

A

Dilated tortuous superficial veins, venous stasis ulcers, ankle edema, lower extremity pain after sitting/standing

101
Q

Varicose veins treatment

A

Leg elevation and compression stockings

102
Q

Venous insufficiency presentation

A

Edema, atrophic shiny skin, brawny induration, stasis dermatitis, brown hyperpigmentation, varicosities, and venous stasis ulcers above medial malleolus.

103
Q

Venous insufficiency dianosis/treatment

A

ABI, Trendelenburg tests, ultrasound.

Treatment: Sclerotherapy, vein stripping, compression hose.

104
Q

Unilateral (ASYMMETRICAL) swelling of lower extremity

A

Venous thrombosis

105
Q

Virchow’s triad

A

stasis, vascular injury, hypercoagulable state (OCP, cancer, surgery, factor V Leiden)

106
Q

Homans’ sign

A

Discomfort behind the knee on forced dorsiflexion of the foot - consider venous thrombosis

107
Q

Venous thrombosis testing

A

D-dimer, venous duplex ultrasound first line imaging, venography gold standard

108
Q

Harsh systolic ejection crescendo-decrescendo murmur at the right upper sternal border (aortic area) with radiation to the neck and apex heard best by leaning forward with expiration

A

Aortic stenosis (systolic)

109
Q

Soft early diastolic blowing murmur along left sternal border with patient sitting leaning forward after exhaling

A

Aortic regurgitation (diastolic)

110
Q

Diastolic low pitched decrescendo rumbling murmur with opening snap heard best at the apex (mitral area) with patient in lateral decubitus position

A

Mitral stenosis (diastolic)

111
Q

Holosystolic high-pitched blowing murmur at apex (mitral area) that radiates to axilla with a split S2

A

Mitral regurgitation

112
Q

Midsystolic ejection click heard best at the apex (mitral area)

A

Mitral valve prolapse

113
Q

Diastolic rumbling murmur at the LLSB (tricuspid area) with an opening snap

A

Tricuspid stenosis (Diastolic)

114
Q

High pitched holosystolic murmur at LLSB (tricuspid area) radiates to the sternum and increases with inspiration

A

Tricuspid regurgitation

115
Q

Harsh, loud, medium pitched systolic murmur heard best at the 2nd /3rd left intercostal space (pulmonic area) that may decrease with inspiration

A

Pulmonary stenosis

116
Q

High pitched early diastolic decrescendo murmur at the LUSB (pulmonic area) that increases with inspiration

A

Pulmonary regurgitation (diastolic)

117
Q

Infection of normal valves with a virulent organism (S. aureus); IV drug users

A

Acute bacterial endocarditis

118
Q

Indolent infection of abnormal valves with less virulent organisms (S. viridans)

A

Subacute bacterial endocarditis

119
Q

Classic signs of infective endocarditis

A 
Osler's nodes - tender (ouchy) nodules
Janeway lesions - painless macules
Roth spots on retina
Splinter hemorrhages on nail bed
Clubbing
120
Q

Chest pain that is relieved by sitting and/or leaning forward; worse when lying downe

A

Acute pericarditis

121
Q

Dressler’s syndrome

A

Pericarditis 2-5 days after an acute myocardial infarction

122
Q

Acute pericarditis on physical exam; EKG findings

A

Pericardial friction rub heard best with patient upright and leaning forward
Diffuse, ST segment elevations in the precordial leads

123
Q

Beck’s triad on physical exam; signs of ________

A

Jugular venous distention, hypotension, muffled heart sounds;
Cardiac tamponade

124
Q

Pulsus paradoxus (define) is a classic finding of ________, also ______;

A

Drop of 10 mmHg in systolic pressure on inspiration
Cardiac tamponade
Narrow pulse pressure

125
Q

Cardiac tamponade diagnosis

A

EKG: electrical alternans (when consecutive, normally-conducted QRS complexes alternate in height) and low voltage QRS complex.
CXR: Water bottle heart - heart shaped like a canteen

126
Q

Cardiac tamponade treatment

A

Pericardiocentesis

127
Q

Same symptoms as acute pericarditis except patient will now have signs of fluid buildup around the heart which include low voltage QRS complexes, electrical alternans, distant heart sounds and an echocardiogram showing a collection of pericardial fluid.

A

Pericardial effusion

128
Q

Pericardial effusion diagnosis

A

EKG: low voltage QRS along with electric alternans.
Echocardiogram: increased pericardial fluid.
CXR: Water bottle heart

129
Q

Pericardial effusion treatment

A

Treat underlying cause.

Pericardiocentesis if effusion is large.

PANRE (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions