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