Cardiology 16% Flashcards
1
Q
Reduced contraction strength, large heart, systolic dysfunction
A
Dilated Cardiomyopathy
2
Q
Dilated cardiomyopathy etiology
A
Genetics, excess alcohol, postpartum, chemotherapy, endocrine disorders
3
Q
Dilated Cardiomyopathy physical exam
A
Dyspnea, S3 gallop, rales, jugular venous distention
4
Q
Hypertrophic portion of septum - Young athlete with a positive family history has sudden death or syncopal episode
A
Hypertrophic Cardiomyopathy
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).
6
Q
Right heart failure with a history of infiltrative process - stiff ventricles
A
Restrictive Cardiomyopathy
7
Q
Restrictive cardiomyopathy etiologies
A
Amyloidosis, sarcoidosis, hemochromatosis, scleroderma, fibrosis, and cancer
8
Q
Low-amplitude fibrillatory waves without discrete P waves and an irregularly irregular pattern of QRS complexes
A
Atrial fibrillation
9
Q
Regular, sawtooth pattern, atrial rate 250-350 BPM, narrow QRS complex
A
Atrial flutter
10
Q
PR interval > .2 seconds.
Actually a delay rather than a block.
A
First degree AV block
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.).
12
Q
Second degree AV block Types
A
Second degree AV block Type 1 (Wenckebach) and Type 2 (Mobitz)
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.
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.
15
Q
With this block, no atrial impulses are transmitted to the ventricles.
A
Third degree AV block
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.
17
Q
R and R’ (upward bunny ears) in V4-V6
A
Left bundle branch block
18
Q
R and R’ (upward bunny ears) in V1-V3
A
Right bundle branch block
19
Q
SVT with abrupt onset and offset
A
Paroxysmal supraventricular tachycardia
20
Q
Any tachydysrhythmia arising from above the level of the Bundle of His
A
Atrioventricular nodal reentrant tachycardia (AVNRT):
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
22
Q
Wolff-Parkinson-White (WPW) syndrome on EKG
A
Shortened PR interval, widened QRS, and delta waves
23
Q
Premature beats
A
PVC, PAC, PJC
24
Q
Early wide “bizarre” QRS, no p wave seen
A
PVC
25
Abnormally shaped P wave
PAC
26
The QRS complex will be narrow, usually measured at 0.10 sec or less, no p wave or inverted p wave
PJC
27
Collective term used to describe dysfunction in the sinus node's automaticity and impulse generation
Sick sinus syndrome
28
Sinus bradycardia
Sinus rhythm with a resting heart rate of < 60 bpm in adults, or below the normal range for age in children
29
Sinus pause
pause < 3 seconds
30
Sinus arrest
pause > 3 seconds
31
Tachy-Brady Syndrome
Episodes of alternating sinus tachycardia and bradycardia
32
Wide complex tachycardia with three or more consecutive premature ventricular beats
Ventricular tachycardia
33
Stable ventricular tachycardia treatment
Amiodarone → lidocaine → procainamide (in this order)
34
Unstable ventricular tachycardia treatment
CPR and defibrillation (synchronized direct current (DC) cardioversion)
35
EKG: No discernible heart contractions
Ventricular fibrillation
36
Ventricular fibrillation treatment
CPR and defibrillation (AKA non-synchronized cardioversion)
37
Polymorphic ventricular tachycardia that appears to be twisting around a baseline
Torsades de pointes
38
Torsades de pointes treatment
Magnesium sulfate
39
Foramen ovale fails to close
Atrial septal defect
40
Atrial septal defect findings
Noncyanotic.
Wide fixed split second heart sound (S2). Systolic ejection murmur at second left intercostal space with an early to mid-systolic rumble.
41
Coarctation of the aorta findings
Noncyanotic
| Higher blood pressures in the arms than in the legs and pulses are bounding in the arms but decreased in the legs.
42
Patent ductus arteriosus findings
Noncyanotic
| A continuous "machinery murmur" at the upper left sternal border
43
Tetralogy of Fallot findings
Cyanotic
| Four features "PROVe": Pulmonary stenosis, Right ventricular hypertrophy, Overriding aorta, Ventricular septal defect
44
The most common pathologic murmur in childhood.
Ventricular septal defect
45
Ventricular septal defect findings; treatment
Noncyanotic .
Loud, harsh, pansystolic murmur at the lower left sternal border.
Most close by age 6, surgery if large.
46
Heart failure types
Right sided
| Left sided: Systolic; Diastolic
47
Right sided heart failure findings
Peripheral and abdominal fluid accumulation = jugular venous distention, edema, hepatomegaly, no rales.
Diagnose with echo and doppler, gold standard is right heart cardiac catheterization
48
Right sided heart failure diagnostics
Echo and doppler U/S.
| Gold standard is right heart cardiac catheterization
49
Left sided heart failure findings
Shortness of breath and fatigue - paroxysmal nocturnal dyspnea, cough, orthopnea, rales
50
Systolic heart failure findings
Decreased ejection fraction, S3 (rapid ventricular filling during early diastole is the mechanism responsible for the S3)
51
Diastolic heart failure findings
Ejection fraction is usually normal, S4
52
Heart failure CXR, lab test findings
Kerley B lines, ↑ BNP
53
Elevated blood pressure > 140/90 with no identifiable cause
Primary hypertension
54
Normal, prehypertension, Stage 1, Stage 2 blood pressure parameters
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
Systolic BP ≥ 140 diastolic BP ≥ 90 or both with an identifiable cause
Secondary hypertension
56
Secondary hypertension etiologies
Sleep apnea, pheochromocytoma, coarctation of the aorta, parenchymal renal disease, renal artery stenosis, Cushing syndrome, primary hyperaldosteronism (Conn’s disease)
57
Secondary hypertension treatments
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
Hypertensive emergency
BP usually >180/120 with impeding or progressing end organ damage
59
Hypertensive emergency end organ damage
Encephalopathy, nephropathy, intracranial hemorrhage, aortic dissection, pulmonary edema, unstable angina or MI (except papilledema which = malignant HTN)
60
Hypertensive emergency treatment
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
Hypertensive Urgency
BP usually 180/120 without signs of end organ damage
62
Hypertensive urgency treatment
Immediate BP reduction is not required.
| Treatment: oral antihypertensive Clonidine (drug of choice)
63
Malignant HTN
Diastolic reading >140 mm Hg associated with papilledema and either encephalopathy or nephropathy
64
Cardiogenic shock findings
Hypotension (SBP <90mmg), cyanosis, cool extremities, altered mental status, and crackles.
65
Cardiogenic shock etilogies
acute MI, heart failure, cardiac tamponade
66
Cardiogenic shock treatment
Fluid resuscitation, pressors (dopamine), and treat underlying cause.
67
Orthostatic hypotension
Drop of > 20 mm Hg systolic, 10 mmHg diastolic, or both 2-5 minutes after change from supine to standing
68
Non-ST-Segment Elevation MI (NSTEMI) EKG and lab findings
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
ST-Segment Elevation Myocardial Infarction (STEMI)
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
ST elevation =
Acute ischemia
71
T wave depression =
Myocardial injury
72
Q wave =
Infarct
73
Lateral STEMI
I, aVL, V5, V6: Left circumflex
74
Anterior STEMI
V2-V4: Left anterior descending
75
Septal STEMI
V1, V2: Left anterior descending
76
Anterolateral STEMI
V4, V5, V6: Left main
77
Posterior STEMI
V1, V2: ST depression: Right coronary artery
78
Inferior STEMI
II, III, aVF: Right coronary artery
79
Serial cardiac enzymes
Troponins, myoglobin, CK-MB
80
Troponins results
Most specific test, appears at 4-8 hours, peaks 12-24 hours and lasts for 7-10 days
81
Myoglobin results
Elevate in 1-4 hours
82
CK-MB results
Appears at 4-6 hours, peaks at 12-24 hours and lasts for 3-4 days
83
Previously stable and predictable symptoms of angina that are now more frequent, increasing or present at rest.
Unstable angina
84
Coronary artery vasospasms causing transient ST segment elevations, not associated with clot
Prinzmetal variant angina
85
Prinzmetal variant angina risk factors
History of smoking (#1 risk factor) or cocaine abuse
86
Prinzmetal variant angina EKG findings
May show inverted U waves
87
Abdominal Aortic Aneurysm signs/symptoms
Flank pain, hypotension, pulsatile abdominal mass
88
Aortic Dissection
Sudden onset tearing chest pain, between scapulas.
| Diminished pulses
89
Aortic Dissection signs/symptoms
Sudden onset tearing chest pain, between scapulae. Diminished pulses
90
Aortic dissection x-ray findings
Chest radiograph: Widened mediastinum
91
Aortic Dissection treatment
Ascending aorta - Surgical emergency
| Descending aorta - Medical therapy (beta blockers) unless complications are present
92
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.
Giant cell arteritis
93
Giant cell arteritis testing
ESR > 100
| Diagnosed with temporal artery biopsy
94
Giant cell arteritis treatment
Treat with high dose prednisone – do urgently to prevent blindness (Do not wait for biopsy results)
95
Peripheral artery disease presentation
Intermittent claudication, atrophic skin, rubor, hair loss, decreased pulses or non healing ulcers
96
Peripheral artery disease diagnosis
Ankle/brachial index (< 0.9).
| Angiography is gold standard.
97
Peripheral artery disease contraindicated treatment
β-blockers are contraindicated in isolated PAD – it will worsen claudication
98
Phlebitis/thrombophlebitis
Dull pain, erythema, induration of vein, palpable cord.
| May be spontaneous or after trauma, IV/PICC lines.
99
Phlebitis/thrombophlebitis diagnosis/treatment
Venous duplex ultrasound - gold standard for diagnosis.
| NSAIDs, warm compress.
100
Varicose veins presentation
Dilated tortuous superficial veins, venous stasis ulcers, ankle edema, lower extremity pain after sitting/standing
101
Varicose veins treatment
Leg elevation and compression stockings
102
Venous insufficiency presentation
Edema, atrophic shiny skin, brawny induration, stasis dermatitis, brown hyperpigmentation, varicosities, and venous stasis ulcers above medial malleolus.
103
Venous insufficiency dianosis/treatment
ABI, Trendelenburg tests, ultrasound.
| Treatment: Sclerotherapy, vein stripping, compression hose.
104
Unilateral (ASYMMETRICAL) swelling of lower extremity
Venous thrombosis
105
Virchow’s triad
stasis, vascular injury, hypercoagulable state (OCP, cancer, surgery, factor V Leiden)
106
Homans' sign
Discomfort behind the knee on forced dorsiflexion of the foot - consider venous thrombosis
107
Venous thrombosis testing
D-dimer, venous duplex ultrasound first line imaging, venography gold standard
108
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
Aortic stenosis (systolic)
109
Soft early diastolic blowing murmur along left sternal border with patient sitting leaning forward after exhaling
Aortic regurgitation (diastolic)
110
Diastolic low pitched decrescendo rumbling murmur with opening snap heard best at the apex (mitral area) with patient in lateral decubitus position
Mitral stenosis (diastolic)
111
Holosystolic high-pitched blowing murmur at apex (mitral area) that radiates to axilla with a split S2
Mitral regurgitation
112
Midsystolic ejection click heard best at the apex (mitral area)
Mitral valve prolapse
113
Diastolic rumbling murmur at the LLSB (tricuspid area) with an opening snap
Tricuspid stenosis (Diastolic)
114
High pitched holosystolic murmur at LLSB (tricuspid area) radiates to the sternum and increases with inspiration
Tricuspid regurgitation
115
Harsh, loud, medium pitched systolic murmur heard best at the 2nd /3rd left intercostal space (pulmonic area) that may decrease with inspiration
Pulmonary stenosis
116
High pitched early diastolic decrescendo murmur at the LUSB (pulmonic area) that increases with inspiration
Pulmonary regurgitation (diastolic)
117
Infection of normal valves with a virulent organism (S. aureus); IV drug users
Acute bacterial endocarditis
118
Indolent infection of abnormal valves with less virulent organisms (S. viridans)
Subacute bacterial endocarditis
119
Classic signs of infective endocarditis
```
Osler's nodes - tender (ouchy) nodules
Janeway lesions - painless macules
Roth spots on retina
Splinter hemorrhages on nail bed
Clubbing
```
120
Chest pain that is relieved by sitting and/or leaning forward; worse when lying downe
Acute pericarditis
121
Dressler's syndrome
Pericarditis 2-5 days after an acute myocardial infarction
122
Acute pericarditis on physical exam; EKG findings
Pericardial friction rub heard best with patient upright and leaning forward
Diffuse, ST segment elevations in the precordial leads
123
Beck’s triad on physical exam; signs of ________
Jugular venous distention, hypotension, muffled heart sounds;
Cardiac tamponade
124
Pulsus paradoxus (define) is a classic finding of ________, also ______;
Drop of 10 mmHg in systolic pressure on inspiration
Cardiac tamponade
Narrow pulse pressure
125
Cardiac tamponade diagnosis
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
Cardiac tamponade treatment
Pericardiocentesis
127
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.
Pericardial effusion
128
Pericardial effusion diagnosis
EKG: low voltage QRS along with electric alternans.
Echocardiogram: increased pericardial fluid.
CXR: Water bottle heart
129
Pericardial effusion treatment
Treat underlying cause.
| Pericardiocentesis if effusion is large.
