Cardiology Flashcards
DDX for palpitations
Hypomagnesemia Hyperkalemia Anxiety Alcohol withdrawal Anemia Atrial septal defect Acute coronary syndrome Hypertrophic cardiomyopathy Mitral valve prolapse Hyperthyroidism Thyroid storm Hypoglycemia
DDX for DOE
Coarctation of the aorta
Mitral regurgitation
CHF
DDX for orthopnea
CHF (left)
Constrictive pericarditis
DDX for edema
CHF (right) Pericardial tamponade Dilated cardiomyopathy Restrictive cardiomyopathy Peripheral venous disease Chronic venous insufficiency
DDX for syncope
Hypocalcemia Anemia Ventricular septal defect Atrial septal defect Coarctation of the aorta Long QT syndrome Myocarditis Hypertrophic cardiomyopathy Aortic stenosis Mitral valve prolapse Abdominal aortic aneurysm Aortic dissection Pulmonary embolism
A new left bundle branch block should be treated as an _________
Infarction
Q waves are specific for ___________ but are a late finding
Necrosis
Cardiac enzymes
Myoglobin
CK-MB
Troponins (preferred)
Most pts with negative enzymes can have an MI excluded by _________, but for high risk pts, should continue serial labs for _________ hours
8 hours
12-24 hours
Reinfarction is diagnosed if troponin increases over ____%
20
Unstable angina will not have an elevation in:
Cardiac enzymes
Long PR interval > 0.2 seconds
Treatment?
First degree heart block
No treatment
PR progressively lengthens until it fails to produce a QRS complex.
Treatment?
Mobitz I / Wenckebach
No tx until pt is symptomatic.
Place pacemaker if symptoms are present.
Atropine if unstable
Patient will have continuously dropped QRS complex, however there won’t be lengthening of the PR interval.
Treatment?
Mobitz II
Pacemaker to prevent progression 3rd degree
Signal from atria does not reach ventricle. P waves are independent from QRS complex.
Treatment?
Third degree heart block
Pacemaker - may be fatal
Wide QRS, RSR pattern in leads V1/V2/V3, S wave wider than R wave in leads 1 and V6.
Treatment?
Right Bundle Branch Block
Asymptomatic does not need tx
Symptomatic: pacemaker
Wide QRS, notched R wave in leads I/aVL/V5/V6.
Treatment?
Left Bundle Branch Block
Must be treated as an MI if new
Patients will present with abrupt onset of palpitations and the EKG will show complex tachycardia.
QRS absorbs p waves.
Treatment?
Paroxysmal Supraventricular Tachycardia
If hemodynamic instability exists: cardiovert
If stable: vagal maneuvers - valsalva or carotid massage
If this does not work: adenosine - then CCB or BB
Wide complex QRS without P waves. Following wide complex QRS, will usually be a compensatory pause. Pts may present with palpitations
Treatment?
Premature ventricular contraction
Asymptomatic: no tx
Symptomatic: BB
P wave before expected and p wave morphology will differ
Treatment?
Premature atrial contraction
Asymptomatic: no tx
Symptomatic: BB
Treatment for wide complex tachycardia
Unstable: cardiovert
Stable: amiodarone, lidocaine or procainamide
If medication does not convert to sinus, cardiovert
Treatment for torsades de pointes
Magnesium sulfate is med of choice
Cardiac pacing if ineffective
Sawtooth waves at 250-300 bpm (no p waves)
Treatment?
Atrial flutter Stable: vagal, BB or CCB Unstable: synchronized cardioversion Definitive management: radiofrequency ablation Anticoagulation similar to AFib
Irregularly irregular rhythm with narrow QRS usually
Atrial fibrillation
Management of atrial fibrillation if stable
- Rate control: BB, CCB, digoxin
2. Rhythm control - cardioversion, radiofrequency ablation
Management of atrial fibrillation if unstable
Direct current (synchronized) cardioversion
Anticoagulation for atrial fibrillation
CHA2DS2-VASc score 2 - anticoagulants recommended Congestive heart failure Hypertension Age > 75 Diabetes mellitus Stroke, TIA, thrombus Vascular disease Age 65-74 Sex (female)
Increased BP + acute end organ damage
Hypertensive emergencies
Hypertensive emergencies are usually seen with systolic blood pressure > ______ and/or diastolic BP > _______
180
120
though, no specific threshold
4 types of damage seen with hypertensive emergencies
- Neurological damage
- Cardiac damage
- Renal damage
- Retinal damage
Ruling out neurological damage with hypertensive emergency
Neurological exam
May need CT to r/o stroke
Ruling out cardiac damage with hypertensive emergency
ECG
CXR to r/o dissection, look for pulmonary edema
CK-MB / troponin
Ruling out renal damage with hypertensive emergency
UA - proteinuria and/or hematuria
May need chemistries to look for increased BUN/Cr
Ruling out retinal damage with hypertensive emergency
Malignant HTN/Grade IV - papilledema
may present with blurred vision
Management of hypertensive emergency
Decrease BP by no more than 25% within the first hour and an additional 5-15% over the next 23 hours using IV agents
Signs/symptoms of shock (cardiogenic or hypovolemic)
Generally acutely ill AMS Decreased peripheral pulses Tachycardia Skin usually cool and mottled
Laboratory tests for shock (cardiogenic or hypovolemic)
- CBC
- BMP
- Lactate
- Coag studies
- Cultures (looking for sepsis)
- ABG
Etiologies of hypovolemic shock (hemorrhagic)
GI bleed, AAA rupture, massive hemoptysis, trauma, ectopic pregnancy, postpartum hemorrhage
Etiologies of hypovolemic shock (non-hemorrhagic)
Vomiting, bowel obstruction, pancreatitis, severe burns, diabetic ketoacidosis
Diagnosis of hypovolemic shock
Vasoconstriction (High SVR) Hypotension Low CO Decreased pulmonary capillary pressure CBC: high hgb, hct
Management of hypovolemic shock
- ABCDE’s - 2 large IV lines or central
- Volume resuscitation
- Control source of hemorrhage, +/- packed RBCs
- Prevention of hypothermia, treat any coagulopathies
Etiologies of cardiogenic shock
Cardiac disease - myocardial infarction, myocarditis, valve dysfunction, congenital heart disease, cardiomyopathy, arrhythmias
Management of cardiogenic shock
- Oxygen, isotonic fluids (not large amounts of fluid)
- Inotropic support - dobutamine, amrinone, intra aortic balloon pump
- Treat underlying cause
Most common cause of systolic congestive heart failure
Coronary artery disease
Most common cause of diastolic congestive heart failure
HTN
In diastolic dysfunction, ejection fracture is _________. In systolic dysfunction, ejection fraction is __________
Normal
< 50%
Fatigue, SOB, orthopnea, PND, chronic cough, pedal edema, JVD, S3 gallop, S4 gallop
Congestive heart failure
S3 gallop is seen with _______ heart failure
Systolic
S4 gallop is seen with _________ heart failure
Diastolic
Crackles, orthopnea, and PND are seen more with __________ heart dysfunction
Left sided
JvD, hepatojugular reflux, pedal edema, ascites are seen more with ________ heart dysfunction
Right sided
Diagnosis of congestive heart failure
- Clinical
- Echo with ejection fracture
- ECG
- CXR
- Stress testing
Treatment for diastolic dysfunction
Manage sx and treat comorbid conditions. No medications proven
Treatment for systolic dysfunction
ACEI/ARBs
BB
Never give _____ during an acute exacerbation of CHF and also be careful with _____
BB
CCB
Most acute exacerbations of CHF present with:;
Acute pulmonary edema
Treatment of acute exacerbation of CHF
LMNOP Loop diuretic Morphine Nitrates Oxygen Position (head up)
Substernal chest pain that is usually brought on by exertion (due to decreased supply and increased demand) - 4 different classes of severity
Angina pectoris
Levine’s sign
Clenched fist over chest
Diagnosis of angina pectoris
- ECG initial test
- Angiography gold standard
- Stress testing
- Stress echocardiogram
Classic ECG finding in angina pectoris
ST depression
50% have normal resting ECG
Management of angina pectoris
- PTCA - 1-2 vessel not including left main
2. CABG - left main, >70% stenosis, 3 vessel disease, decreased ejection fraction
Coronary spasms leading to transient ST elevations usually without MI
Variant (Prinzmetal) Angina
Signs/symptoms of variant (prinzmetal) angina
CP usually nonexertional, often occurring at rest. Often occurs in morning, with hyperventilation, emotional stress or cold weather
Diagnosis of variant (prinzmetal) angina
- ECG - +/- transient ST elevation
- Angiography - vasospasms
- Symptoms + ST elevations resolve with CCB or nitro
Management of variant (prinzmetal) angina
CCB - drug of choice
Nitrates as needed
ECG and cardiac enzymes with stable angina
Normal
Treatment for stable angina
Lifestyle modifications Control HTN, diabetes, hyperlipidemia Statin, Aspirin, Beta blocker Nitroglycerin PCI or CABG if cannot be controlled with medications
__________ is a very specific predictor of ACS (ST segment elevation)
Diaphoresis
Do not want to give pts with a right sided MI _______ as this will cause a severe drop in BP
Nitrates
Inferior MI
Leads II, III, and aVF
Anterior MI
Leads V1-V4
Lateral MI
Leads I, aVL, and V5-V6
Myoglobin begins to rise after _______ and stays elevated for a couple of days
1 hour
CK-MB will rise after _________ and will stay elevated for a couple of days
4 hours
Troponins rises after _____ and will stay elevated for up to 2 weeks
4 hours
Unstable angina _______ have elevation in cardiac enzymes
will not
NSTEMI and STEMI ______ have elevation in cardiac enzymes
will
Treatment for acute coronary syndrome (unstable angina, NSTEMI, STEMI)
MONA morphine oxygen nitrates aspirin (chewed) All pts should also get loading dose of a P2Y12 drug (clopidogrel, prasugrel, ticagrelor)
Treatment if pt has inferior MI:
Avoid nitrates (causes severe drop in BP) -give pts fluids instead
All patients with a STEMI should receive:
Heparin
PCI is preferred to thrombolytics, but must be done within ___________ of arrival to hospital
90 minutes
Thrombolytics should be given within ________ of hospital arrival - indicated if chest pain has been present < 12 hours and lacks CI
30 minutes
Most common cause of death within first few days after an MI is _______________, therefore continuous rhythm monitoring is required
Ventricular tachycardia or ventricular fibrillation
Dressler syndrome
Autoimmune mediated pericarditis - pts present with pericarditis, fever, malaise, and leukocytosis 2-10 weeks post MI. Give an aspirin
All pts post MI should be continued on:
Beta blocker
ACE
Statin
Dual antiplatelet therapy (clopidogrel and aspirin) is used for one year
In order to be considered aneurysmal, an AAA must be at least > _______
3 cm
Risk factors for AAA
Atherosclerosis (MC)
Age > 60 y/o
Smoking
Males, Caucasians
Classic presentation of AAA (when not asymptomatic)
Older male > 60 y/o Severe back or abdominal pain presents with hypotension/syncope Tender, pulsatile abdominal mass May complain of unilateral groin/hip pain
Diagnosis of AAA
- Abdominal ultrasound - initial test of choice
- CT scan - especially for thoracic aneurysm
- Angiography - gold standard
- MRI/MRA
- Abdominal radiograph
Management of AAA > 5.5 cm
Immediate surgical repair even if asymptomatic
Management of an AAA with expansion of > 0.5 cm in 6 months
Immediate surgical repair even if asymptomatic
Management of AAA > 4.5 cm
Vascular surgeon referral
Management of AAA 4-4.5 cm
Monitor by US every 6 months
Management of AAA 3-4 cm
Monitor by US every year
Medicational management of AAA
Beta blockers
Also decrease risk factors
65% of aortic dissections are ________
Ascending
_________ aortic dissections are associated with a high mortality
Ascending
Most important risk factor for aortic dissection
HTN
Risk factors for aortic dissection
HTN Marfan Syndrome Age 50+ Men Cocaine use
Signs/symptoms of aortic dissection
Chest pain - severe, tearing, ripping, knife-life
N/V
Diaphoresis
Physical exam sign of aortic dissection
Decreased peripheral pulses - radial, carotid or femoral
Diagnosis of aortic dissection
- CT scan with contrast - TOC
- MRI angiography - gold standard
- TEE
- CXR
What will show on CXR with aortic dissection?
Widening of the mediastinum
Management of Stanford A / DeBakey I and II aortic dissections, or type III with complications
Involve the ascending aorta / aortic arch
Surgery
Management of Stanford / DeBakey III aortic dissections
Are limited to descending aorta
Esmolol, Labetalol -1st line
Sodium nitroprusside, nicardipine if needed
How often should aortic dissection be imaged if not surgically fixed?
3, 6 and 12 mo to look for progression, redissection and/or new aneurysm formation
Definitive diagnosis for all valvular disease is reached with:
Echocardiogram
Most symptoms of valvular disease are similar to that of CHF
SOB and chest discomfort
Holosystolic murmurs
Mitral regurgitation
Tricuspid regurgitation
VSD
Increases sound of all murmurs, except mitral valve prolapse and HOCM (decreases)
Squatting
Leg raise
Handgrip
Systolic crescendo-decrescendo murmur heard best at the second right intercostal space - radiates to the neck
Aortic stenosis
Heard best at the left upper sternal border with an ejection click
Pulmonic Stenosis
Holosystolic murmur heard best over the apex that radiates to the axilla
Mitral regurgitation
Mid systolic click with a possible late systolic murmur
Mitral valve prolapse
Holosystolic murmur heard best at the left mid sternal border
Tricuspid regurgitation
Decrescendo murmur with a blowing quality heart best at the left sternal border
Aortic regurgitation
Decrescendo murmur
Pulmonic regurgitation
Low pitch rumble heard best at the apex
Mitral stenosis
Heard best at the 4th intercostal space at the left loewr sternal border
Tricuspid stenosis
Infection of the endocardial surface of the heart, which extends to the heart valves
Endocarditis
Risk factors for endocarditis
Valvular heart disease Congenital heart disease Prosthetic heart valves Immunosuppression Age > 60 y/o Injection drug users
Most common etiology of endocarditis in native valves
Streptococci viridans
Most common etiology of endocarditis in those who are injection drug users
Staphylococcus aureus
Most common etiology of endocarditis in those with prosthetic valve endocarditis
Staphylococcus epidermidis
Fever, anorexia, weight loss, fatigue, ECG conduction abnormalities
Endocarditis
Painless erythematous macules on the palms and soles
Janeway Lesions
Endocarditis
Retinal hemorrhages with pale centers. Petechiae (conjunctiva and palate)
Roth spots
Endocarditis
Tender nodules on the pads of the digits
Osler’s Nodes
Endocarditis
Splinter hemorrhages of proximal nail bed, clubbing, hepatosplenomegaly
Endocarditis
Diagnostic studies for endocarditis
- Blood cultures - before abx initiation - 3 sets at least 1 hour apart if pt is stable
- ECG
- Echo
- Labs - leukocytosis, anemia, increased ESR, rheumatoid factor
Major Duke Criteria
- Sustained bacteremia (2 blood cultures)
- Endocardial involvement on echo
- New aortic or mitral regurg
Minor Duke Criteria
- Predisposing condition
- Fever
- Janeway lesions, etc.
- blood culture
- echo not meeting major criteria
Clinical criteria for infective endocarditis based on Duke’’s Criteria
2 major or
1 major + 3 minor or
5 minor
Indications for surgery with endocarditis
Refractory CHF Persistent or refractory infxn Invasive infection Prosthetic valve Recurrent systemic emboli Fungal infxns
Management of endocarditis (acute)
Nafcillin + gentamicin OR
Vanco + gentamicin
Management of endocarditis (prosthetic valve)
Vancomycin + gentamicin + rifampin
Management of endocarditis (fungal)
Amphotericin B
Pericardial effusion causing significant pressure on the heart leading to cardiac output
Cardiac tamponade
Signs/symptoms of cardiac tamponade
Beck’s triad
Pulsus paradoxus
Pulsus paradoxus
Cardiac tamponade
Exaggerated > 10 mmHg decrease in systolic BP with inspiration
Decreased pulses with inspiration
Beck’s triad
Cardiac tamponade
- Distant (muffled) heart sounds
- Hypotension
- JVD
Diagnosis of cardiac tamponade
- Echocardiogram - presence of effusion + diastolic collapse of cardiac chambers
Management of cardiac tamponade
Pericardiocentesis (immediate!)
Increased fluid in pericardial space
Pericardial effusion
Etiologies of pericardial effusion
Same as acute pericarditis (viral and idiopathic)
Signs/symptoms of pericardial effusion
Distant (muffled) heart sounds
+/- symptoms of pericarditis
Diagnosis of pericardial effusion
- ECG - low voltage
2. Echocardiogram - pericardial fluid, no hemodynamic compromise
Management of pericardial effusion
Treat underlying cause
Pericardial window if recurrent
Presentation is that of angina in the legs (leg pain with exertion and relieved with rest). Lower extremities may show pallor, ulcerations, diminished pulses, and hair loss
Peripheral vascular disease
Diagnosis of peripheral vascular disease
ABI - positive if ratio is < 0.9
All pts with peripheral vascular disease should receive, however first step is a:
Aspirin
Supervised 12 week exercise regimen