Cardiology Flashcards
What elements of the history and physical steer you away from a diagnosis of MI?
Wrong age (under 40 without known heart disease, family history) Lack of risk factors Physical characteristics of pain (reproducible by palpation? sharp? well-localized? related to eating?)
What findings on EKG should make you suspect an MI?
Flipped or flattened T waves, ST-segment elevation (depression means ischemia; elevation means injury) and/or Q waves in segmental distribution
Describe the classic pattern of chest pain in an MI
Classically crushing or pressure sensation; poorly localized substernal pain that may radiate to the shoulder, arm, or jaw
Usually NOT reproducible on palpation and does not resolve with nitroglycerin (as it does in angina)
Lasts at least half an hour
What tests are used to diagnose an MI?
EKG, CK-MB, troponin I or T, or myoglobin (usually drawn Q8 3x before MI is ruled out)
Elevated LDH uncommonly used for late MI presentation (troponin stays elevated more than 24 hrs)
AST can be elevated but not used clinically
Radiographs - cardiomegaly +/- pulmonary congestion
Echo - ventricular wall motion abnormalities
Describe the classic physical exam findings in patients with MI
Diaphoretic, anxious, tachycardic, tachypneic, pale, may have nausea/vomiting
Large heart attacks causing HF: bilateral pulmonary rales, distended neck veins, S3 or S4 heart sound, new murmurs, hypotension, +/- shock
What historical points should steer you toward a diagnosis of MI?
History of angina or previous chest pain, murmurs, arrhythmias, risk factors for CAD, HTN, diabetes
What medications do you administer for an MI?
Morphine (pain control) Aspirin Nitroglycerin Beta blocker (reduce mortality rate of MI and incidence of second MI) Clopidogrel Unfractionated or LMW heparin ACEI or ARBC within 24 hrs HMG-Coa reductase inhibitor
When is reperfusion therapy indicated for an MI?
Reperfusion is indicated if the time from onset of symptoms is less than 12 hours. Early reperfusion (less than 4-6 hrs) is preferred to try to salvage myocardium.
Can be accomplished by fibrinolysis or percutaneous coronary intervention (i.e. balloon angioplasty/stent), coronary artery bypass grafting may be required.
True or false: With good management, patients with an MI will not die in the hospital.
False. Even with the best management, patients may die from an MI. May also have a second MI during hospitalization. Watch for sudden deterioration!
When is heparin indicated in the setting of chest pain and MI?
Heparin should be started if unstable angina is diagnosed, if the patient has a cardiac thrombus, or if severe congestive HF is seen on echo.
Do NOT give heparin to patients with contraindications to use (e.g. active bleeding)
What clues suggest GERD/peptic ulcer rather than MI chest pain?
Relation to certain foods (spicy, chocolate), smoking, caffeine, or lying down
Pain relieved by antacids or acid-reducing meds
Positive H. pylori test
What clues suggest chest wall (e.g. costochondritis, bruised or broken ribs) rather than MI chest pain?
Pain is well localized and reproducible on chest wall palpation
What clues suggest esophageal problems (e.g. achalasia, nutcracker esophagus, spasm) rather than MI chest pain?
Difficult differential!
Negative MI work-up or lack of atherosclerosis risk factors
Barium swallow abnormalities or esophageal manometry
What clues suggest pericarditis rather than MI chest pain?
Viral URI prodrome
EKG with diffuse ST-segment elevation, ESR elevated, low-grade fever
Pain relieved by sitting forward!
Most common cause is coxsackievirus (but also consider TB, uremia, malignancy, SLE)
What clues suggest pneumonia rather than MI chest pain?
Chest pain is due to pleuritis
Patients also have cough, fever, +/- sputum production
Ask about sick contacts
What clues suggest aortic dissection rather than MI chest pain?
Associated with severe tearing or ripping pain that may radiate to the back
Look for HTN or evidence of Marfan’s (tall, thin, hyperextensible joints)
Blunt chest trauma can cause aortic laceration and pseudoaneurysm
How can you recognize stable angina?
Begins with exertion or stress and remits with rest or calming down. Described as pressure or squeezing pain in substernal area and may radiate to shoulders, neck, and/or jaw.
Often accompanied by SOB, diaphoresis, +/- nausea. Usually relieved by nitroglycerin.
EKG - ST-segment depression during acute attack, otherwise normal
Pain lasts less than 20 minutes
Define unstable angina
Change from previously stable angina. If pt used to experience angina once a week and now has it once a day, technically that is unstable angina.
EKG shows ST depression, minimally elevated cardiac enzymes, prolonged chest pain that does not respond to nitro initially. Pain often begins at rest.
How do you treat unstable angina?
Similar to MI
O2, aspirin, nitro, beta-blocker, clopidogrel, heparin, glycoprotein IIb/IIIa receptor inhibitor, ACEI or ARB
Consider emergent PTCA if pain does not resolve
Describe variant (Prinzmetal angina)
Pain at rest (unrelated to exertion) and ST elevation; cardiac enzymes are normal.
Cause is coronary spasm.
Usually responds to nitro and it treated long-term with calcium channel blockers (reduce arterial spasm)
Define silent MI. How common is it?
Patients with silent MI do not develop chest pain
Present with CHF, shock, or confusion and delirium (esp. elderly patients)
Up to 25% of cases (esp. in diabetics with neuropathy)
What physical exam findings are associated with mitral stenosis?
Late diastolic blowing murmur (best heart at apex)
Opening snap, loud S1, a. fib, L atrial enlargement, pulmonary HTN
What physical exam findings are associated with mitral regurgitation?
Holosystolic murmur (radiates to axilla) Soft S1, L atrial enlargement, L ventricular hypertrophy, pulmonary HTN
What physical exam findings are associated with aortic stenosis?
Harsh systolic ejection murmur (best heard in aortic area, radiates to carotids)
Slow pulse upstroke, S3/S4, ejection click, L ventricular hypertrophy, cardiomegaly
*syncope, angina, HF
What physical exam findings are associated with aortic regurgitation?
Early diastolic decrescendo murmur (best heard at apex)
Widened pulse pressure, L ventricular hypertrophy, L ventricular dilatation, S3
What physical exam findings are associated with mitral prolapse?
Midsystolic click, late systolic murmur
*panic disorder
Who should receive endocarditis prophylaxis?
Cardiac conditions for which prophylaxis with dental procedures is recommended includes prosthetic cardiac valve, previous infectious endocarditis, congenital heart disease, and cardiac transplant recipients who develop valvulopathy
No longer recommended for GU or GI procedures.
Describe the protocols for endocarditis prophylaxis
Should be administered in single dose before procedure. Amoxicillin is preferred choice for oral therapy.
Cephalexin, clindamycin, azithromycin, or clarithromycin may be used for penicillin allergies.
Ampicillin, cefazolin, ceftriaxone, or clindamycin may be used if unable to take orals.
What is Virchow’s triad?
3 findings associated with DVT:
- endothelial damage
- venous stasis
- hypercoagulable state
Common clinical scenarios for development of DVT
Surgery (esp. orthopedic, pelvic, abdominal, or neurosurgery), malignancy, trauma, immobilization, pregnancy, birth control pills, DIC, thrombophilias
Describe the physical signs and symptoms of DVT. How is it diagnosed?
Unilateral leg swelling, pain or tenderness, +/- Homan sign (pain on dorsiflexion, present in 30%)
Best diagnosed by compression ultrasonography or impedance plethysmography of veins of extremity. Gold standard is venography but this is invasive, reserved for situations in which diagnosis is not clear.
True or false: Superficial thrombophlebitis is a risk factor for pulmonary embolus.
False. Superficial thrombophlebitis (erythema, tenderness, edema, palpable clot in superficial vein) affect superficial veins and does not cause PEs. It is considered a benign condition though if recurrent can be marker of malignancy (e.g. Trousseau syndrome - migratory thrombophlebitis - is classic marker for pancreatic cancer)
How should you treat patients with superficial thrombophlebitis?
NSAIDs and warm compresses
How is DVT treated? For how long?
Systemic anticoagulation is necessary. Use IV heparin or subcutaneous LMW heparin initially, followed by crossover to oral warfarin. Should be maintained on warfarin for at least 3-6 months - possibly for life if more than one episode of clotting occurs.
What is the best way to prevent DVT in patients undergoing surgery?
Early ambulation for low risk patients.
LMW heparin, low dose unfractioned heparin, or fondaparinux for moderate risk patients.
LMW heparin, fondaparinux, or oral vitamin K antagonist for high risk patients.
Moderate or high risk + high risk of bleeding = pneumatic compression stockings
In what clinical settings does PE occur? Describe the signs and symptoms.
Commonly follows DVT, delivery (amniotic fluid embolus), or fractures (fat emboli).
Tachypnea, dyspnea, chest pain, hemoptysis (if lung infarct occurred), and hypotension, syncope, or death in severe cases.
Rarely, CXR shows wedge-shaped defect due to pulmonary infarct.
True or false: DVT can lead to a stroke.
False - with one rare exception.
Embolization of L-sided heart clots (e.g. a. fib, ventricular wall aneurysm, severe CHF, endocarditis) causes arterial infarcts (stroke and renal, GI, or extremity infarcts) - NOT pulmonary emboli.
DVT (or R-sided heart clots) that embolize cause pulmonary emboli - NOT arterial emboli.
RARE Exception: Patient with R-to-L shunt (e.g. patent foramen ovale, atrial or ventricular septal defects, or pulmonary AV fistula)
How is PE diagnosed?
V/Q scan or CT pulmonary angiogram to screen. If test is positive, PE is diagnosed and treatment is started. If indeterminate, conventional pulmonary angiogram is used.
Conventional pulmonary angiography is gold standard but is invasive and carries high risk.
How is PE treated?
Initially with LMW heparin or IV unfractioned heparin to prevent further clots and emoboli. Then switch to oral warfarin, which must be taken for at least 3-6 months.
Recurrent clots on anticoagulation or contraindications to anticoagulation, IVC filter should be used.
Rare patients with massive PE, surgical embolectomy or pharmacologic thrombolysis (e.g. t-PA) may be attempted.
What is the most important side effect of heparin?
Thrombocytopenia that may be associated with arterial thrombosis. Measure CBC to monitor for this, usually occurs on days 3-7 of heparin administration. Discontinue heparin immediately if platelet counts begin to fall.
How are the effects of aspirin, heparin, and warfarin monitored?
Heparin - partial thromboplastin time (PTT), a measure of the internal coagulation pathway
Warfarin - prothrombin time (PT), a measure of the external coagulation pathway
Aspirin - bleeding time, a measure of platelet function
How are the effects of LMW heparin monitored?
LMW heparin does NOT affect any of the coagulation parameters and its effect is not clinically monitored. Rarely, a special type of factor X assay (anti-Xa) is used to measure the effect.
In an emergency, how can you reverse the effects of heparin, warfarin, and aspirin?
Heparin and LMW heparin - reversed with protamine
Warfarin - fresh frozen plasma (contains clotting factors; immediate effect) and/or Vitamin K (takes a few days to work)
Aspirin - platelet transfusions
How does Hemophilia A affect coagulation tests?
Prolongs PTT
Low levels of factor 8
Normal PT and bleeding time
X-linked
How does Hemophilia B affect coagulation tests?
Prolongs PTT
Low levels of factor 9
Normal PT and bleeding time
X-linked
How does vWF deficiency affect coagulation tests?
Prolongs bleeding time and PTT
Normal or low levels of factor 8
Normal PT
Autosomal dominant
How does DIC affect coagulation tests?
Prolongs PT, PTT, bleeding time
Positive D-dimer or fibrin degradation products
Postpartum, infection, malignancy
Schistocytes and fragmented cells on peripheral smear
How does liver disease affect coagulation tests?
Prolongs PT Normal or prolonged PTT All factors EXCEPT 8 are low Stigmata of liver disease NO correction with vitamin K
How does Vitamin K deficiency affect coagulation tests?
Prolongs PT, PTT (slight) Normal bleeding time Low levels of factors 2, 7, 9, and 10 Low levels of protein C and S Look for neonate who did not receive vitamin K shot, malabsorption, alcoholism, prolonged antibiotic use (kills Vitamin K producing flora)
How does uremia affect platelets?
Causes QUALITATIVE platelet defect
How does Vitamin C deficiency and chronic corticosteroid therapy affect coagulation tests?
NORMAL coagulation tests but still have bleeding tendency
What are the general symptoms and signs of CHF?
Fatigue, ventricular hypertrophy on EKG, dyspnea, S3 or S4 on cardiac exam, cardiomegaly on CXR
Signs and symptoms of left-sided HF?
Orthopnea (SOB when lying down, pt sleeps on more than 1 pillow or even sitting up), paroxysmal nocturnal dyspnea, pulmonary congestion (rales), Kerley B lines on CXR, pulmonary vascular congestion and edema, bilateral pleural effusions
Signs and symptoms of right-sided HF?
Peripheral edema, jugular venous distention, hepatomegaly, ascites, underlying lung disease (cor pulmonale)
How is chronic CHF treated?
Sodium restriction, ACEI (first-line agents that reduce mortality), beat blockers (counter-intuitive but work), diuretics, spironolactone, digoxin (not for diastolic dysfunction, usually reserved for moderate-to-severe CHF with low EF or systolic dysfunction), vasodilators (arterial and venous)
How is acute CHF treated?
Inpatient basis with oxygen, diuretics, and positive inotropes. Digoxin may by used if patient is stable. IV sympathomimetics (dobutamine, dopamine, amrinone) are used for severe CHF.
What factors precipitate exacerbations in previously stable patients with CHF?
Most commonly noncompliance with diet or meds, but watch for MI, severe HTN, arrhythmias, infections and fever, pulmonary embolus, anemia, thyrotoxicosis, and myocarditis
Define cor pulmonale. With what clinical scenarios is it associated?
Right ventricular enlargement, hypertrophy, and failure due to primary lung disease. Common causes are COPD and PE.
In young woman with no other history/risk factors think of idiopathic pulmonary HTN (treat with prostacyclins - parenteral epoprostenol, antiendothelins - bosentant, PDE5 inhibitors, Ca channel blockers)
Sleep apnea (look for obese snorer who is sleepy during the day)
*Tachypnea, cyanosis, clubbing, parasternal heave, loud P2, and R-sided S4 in addition to pulmonary disease signs/symptoms
What causes restrictive cardiomyopathy?
Problem with the ventricles and usually is due to amyloidosis, sarcoidosis, hemochromatosis, or myocardial fibroelastosis. Ventricular biopsy is abnormal in all these conditions.
S4 (indicates stiff ventricles) and signs of R-sided HF (JVD and peripheral edema)
How is restrictive cardiomyopathy different from constrictive pericarditis?
Constrictive pericarditis can be fixed by removing an abnormal pericardium; look for pericardial knock on exam, calcifications of the pericardium, and a normal ventricular biopsy.
Both conditions can have S4 (indicates stiff ventricles) and signs of R-sided HF (JVD and peripheral edema).
What is the most common kind of cardiomyopathy? What causes it?
Dilated cardiomyopathy, most commonly caused by chronic CAD or ischemia, though by strict definition is not a true cardiomyopathy. Watch for alcohol, myocarditis, or doxorubicin as the cause.
Which cardiomyopathy is likely in a young person who passes our or dies while exercising and has a family history of sudden death?
Hypertrophic cardiomyopathy, which may be autosomal dominant. Causes an asymmetric ventricular hypertrophy that reduces cardiac output (diastolic dysfunction). Treat with beta-blockers, or disopyramide (to allow ventricle more time to fill). Competitive sports should be avoided. Positive inotropes (e.g. digoxin), diuretics, and vasodilators are CONTRAINDICATED because they worsen the condition.
How does atrial fibrillation look on EKG? How is it treated?
Erratic ventricular rate and atrial waves are not identical from segment to segment
In symptomatic patients, first slow ventricular rate with beta-blocker, Ca channel blocker, or digoxin:
- If acute (onset <24 hrs), cardiovert with amiodarone, procainamide, or DC cardioversion
- If chronic, first anticoagulate, then cardiovert; if this fails leave patient on rate control meds and warfarin
How does atrial flutter look on EKG? How is it treated?
Atrial waves are identical (“sawtooth”)
Treat like atrial fibrillation. May try to stop arrhythmia with vagal maneuvers (e.g. carotid massage)
How does first-degree heart block look on EKG? How do you treat it?
PR interval prolonged (more than 0.20 seconds)
No treatment, avoid beta-blockers and Ca channel blockers, both of which slow conduction
How does second-degree Mobitz type I heart block look on EKG? How do you treat it?
Progression of PR interval before impulse is completely blocked
Treat with pacemaker or atropine only in symptomatic patients
How does second-degree Mobitz type II heart block look on EKG? How do you treat it?
Every alternate P wave is blocked
Treat with pacemaker
How does WPW look on EKG? How is it treated?
Shortened PR interval and delta wave (slurred upstroke of QRS complex)
Treat with procainamide or quinidine; avoid digoxin and verapamil
How does WPW syndrome classically present?
Child becomes dizzy or dyspneic or passes out after playing, then recovers and has no other symptoms. The cause is a transient arrhythmia via the accessory pathway.
How is ventricular tachycardia treated?
If pulseless, treat with immediate defibrillation followed by epinephrine, vasopressin, amiodarone, or lidocaine
If pulse is present, treat with amiodarone and synchronized cardioversion
How is ventricular fibrillation treated?
Immediate defibrillation
How are premature ventricular complexes treated?
Usually not treated; if severe and symptomatic, consider beta-blockers or amiodarone
How is sinus bradycardia treated?
Usually not treated; use atropine if severe and symptomatic (e.g. after MI)
Avoid beta-blockers, Ca channel blockers, and other conduction-slowing medications
How is sinus tachycardia treated?
Usually not treated; correct underlying cause
Use beta-blocker or Ca channel blocker if symptomatic
What endocrine disease is suggested when a patient presents with sinus tachycardia or atrial fibrillation?
Hyperthyroidism, check TSH level as screening test
Describe patent ductus arteriosus
Constant, machine-like murmur in upper L sternal border
Dyspnea and possible CHF
Close with indomethacin or surgery (if indomethacin fails)
Keep open with PGE1
Associated with congenital rubella and high altitudes
Describe ventricular septal defect
Holosystolic mumur next to sternum
Most cases resolve on their own
Watch for fetal alcohol, Down syndrome, or TORCH
What is the most common congenital heart defect?
Ventricular septal defect
Describe atrial septal defect
Often asymptomatic until adulthood
Fixed, split S2, and palpitations
Most defects do not require correction (unless very large)
Describe Tetralogy of Fallot
Four anomalies: VSD, RVH, pulmonary stenosis, overriding aorta
Look for “tet” spells (squatting after exertion)
What is the most common cyanotic congenital heart defect?
Tetralogy of Fallot
Describe coarctation of aorta
Upper extremity HTN only, radiofemoral delay, systolic murmur heard best over mid-upper back
Rib notching on CXR
Associated with Turner syndrome
What is most important to remember about tachycardia in children?
Heart rates over 100 bpm may be noral in a child, as may respiratory rates greater than 20 per minutes
In the fetal circulation, where is the highest and lowest oxygen content?
Higher oxygen content in umbilical vein (blood coming from the mother)
Lowest in umbilical arteries
Remember that oxygen content is higher in blood going to the upper extremities than in blood going to lower extremities
What changes occur in the circulation as an infant goes from intrauterine to extrauterine life?
First breaths inflate lungs and cause decreased pulmonary vascular resistance, which increases blood flow to pulmonary arteries. This and clamping of cord increases L-sided heart pressures, causing functional closure of foramen ovale. Increased oxygen concentration shuts off prostaglandin production in ductus arteriosus, causing gradual closure.
