Cardiology Flashcards
What is your job when the Step 2 examination describes a patient with chest pain?
Make sure that the chest pain is not because of any life-threatening condition (ie MI)
What elements of the history and physical examination steer you away from a diagnosis of myocardial infarction (MI)?
Wrong age: patient < 40 yo is extremely unlikely to have an MI.
Lack of risk factors: strong family history, or multiple risk factors for coronary artery disease (high LDL)
Physical characteristics of pain: pain associated with MI is usually not sharp or well localized; If pain is reproducible, it is of MSK origin; may also be related to certain foods or eating.
Get at least an electrocardiogram (ECG) and possibly one or more sets of cardiac enzyme levels. For the Step 2 examination, however, these clues should steer you toward an alternative diagnosis.
What 3 findings on ECG should make you suspect an MI?
- flipped or flattened T waves
- ST segment elevation (depression means ischemia; elevation means injury)
- Q waves in a segmental distribution (e.g., leads II, III, and aVF for an inferior infarct)
Note: ST-segment elevation is seen in leads I, aVL, and V2 through V6 in image
What historical points should steer you toward a diagnosis of MI?
history of angina or previous chest pain, murmurs, arrhythmias, risk factors for coronary artery disease, hypertension, or diabetes.
may be taking digoxin, furosemide, or cholesterol, antihypertensives, or cardiac medications.
11 treatment for an MI
- Early reperfusion indicated if time from onset of symptoms is < 12 hours; accomplished by fibrinolysis, percutaneous coronary intervention (i.e., balloon angioplasty/stent), or coronary artery bypass grafting
- ECG monitoring - if ventricular tachycardia occurs, use amiodarone.
- Give O2 - maintain an oxygen saturation > 90%.
- Morphine for pain; may improve pulmonary edema, if present.
- Aspirin.
- Nitroglycerin.
- ß blockers
- Clopidogrel.
- Heparin (unfractionated or low-molecular-weight)
- ACEi or ARB - started within 24 hours.
- Statin (HMG-CoA reductase inhibitor)
MI - BRANCHES MAG
True or false: With good management, patients with an MI will not die in the hospital.
False
Even with the best of medical management, patients may die from an MI. They also may have a second heart attack during hospitalization. Watch for sudden deterioration.
When is heparin indicated in the setting of chest pain and MI? 3
if unstable angina is diagnosed
if the patient has a cardiac thrombus
if severe CHF is seen on echocardiogram
What clues suggest GERD/PUD instead of cardiac causes of chest pain?
GERD pain:
- relation to certain foods (spicy foods, chocolate), smoking, caffeine, or lying down.
- Pain is relieved by antacids or acid-reducing medications.
- test positive for Helicobacter pylori if PUD
What clues suggest chest wall pain (costochondritis, bruised or broken ribs) instead of cardiac causes of chest pain?
well localized and reproducible on chest wall palpation
What clues suggest esophageal problems (achalasia, nutcracker esophagus, or esophageal spasm) instead of cardiac causes of chest pain?
- negative workup for MI
- lack of atherosclerosis risk factors
- abnormalities with barium swallow or esophageal manometry
Treat achalasia with pneumatic dilatation or botulism toxin administration
Treat nutcracker esophagus or esophageal spasm with calcium channel blockers.
If medical treatments are ineffective, surgical myotomy may be needed.
What clues suggest pericarditis instead of cardiac causes of chest pain?
What is a common cause of pericarditis?
evidence of viral URI
low grade fever
ECG shows diffuse STE
elevated ESR
pain relieved by sitting up and forward
common cause: coxackievirus, TB, uremia, malignancy, lupus erythematosus, autoimmune disease
What clues suggest pneumonia instead of cardiac causes of chest pain?
- pleuritis - chest pain that worsens when breathing, coughing or sneezing
- cough
- fever
- sputum production
- possible sick contacts
What clues suggest aortic dissection instead of cardiac causes of chest pain?
- severe tearing or ripping pain that may radiate to the back
- hypertension
- evidence of Marfan syndrome (tall, thin patient with hyperextensible joints)
How can you recognize stable angina?
- begins with exertion or stress and remits with rest or calming down
- pain last <20 min, described as a pressure or squeezing pain in the substernal area and may radiate to the shoulders, neck, and/or jaw; usually relieved by NTG
- often accompanied by SOB, diaphoresis, and/or N
- pain is usually relieved by nitroglycerin.
- ECG during an acute attack often shows ST depression, but in the absence of pain, the ECG is often normal.
- may be progression to unstable angina or MI
Define unstable angina. How is it diagnosed and treated?
- defined as a change from previously stable angina
- normal or only minimally elevated cardiac enzymes
- ECG changes (ST depression)
- chest pain that often begins with rest, is prolonged, and does not respond to nitroglycerin initially (like a heart attack)
- history of stable angina or coronary artery disease risk factor
treatment similar to that of an MI
Describe variant (Prinzmetal) angina.
How is this treated?
caused by coronary artery spasms
pain at rest (unrelated to exertion) and ST-elevation
normal cardiac enzymes
acute treatment: NTG
long-term treatment: Ca channel blockers (reduces arterial spasms)
Define silent MI. How does it present instead? How common is it?
Patients with a silent MI do not develop chest pain
Their symptoms include CHF, shock, or confusion and delirium (especially elderly patients).
MIs are silent in up to 25% of cases (especially in diabetic patients with neuropathy).
What are the physical features of mitral stenosis?
What are the physical features of mitral regurgitation?
What are the physical features of aortic stenosis?
What are the physical features of aortic regurgitation?
What are the physical features of mitral prolapse?
What are the causes of mitral stenosis and what features of the history would clue you into this?
What are the causes mitral regurgitation and what features of the history would clue you into this?
What are the causes of aortic stenosis and what features of the history would clue you into this?
What are the causes of aortic regurgitation and what features of the history would clue you into this?
What is the treatment for the following valvular disorders?
mitral stenosis?
mitral regurgitation?
aortic stenosis?
aortic regurgitation?
Mitral stenosis - balloon valvotomy or surgery if it becomes severe; diuretics, digoxin, ß blockers are adjunctive therapies
Mitral regurgitation - corrective surgery if there is flail leaflet or severe regurgitation, vasodilators (nitroprusside, hydralazine) if symptomatic
- anticoagulation if a-fib is present
Aortic stenosis - aortic valve replacement if symptomatic
Aortic regurgitation - aortic valve replacement if symptomatic or if there is progressive LV enlargement
Who should receive endocarditis prophylaxis?
patients with
- prosthetic cardiac valves
- prior infectious endocarditis
- congenital heart disease
- cardiac transplant who developed valvulopathy
should receive a single dose of antibiotic prophylaxis, usually amoxicillin), prior dental procedures
What is the Virchow triad?
endothelial damage, venous stasis, and hypercoagulable state
Common clinical scenarios for development of DVT
- Surgery (especially orthopedic, pelvic, abdominal, or neurosurgery)
- Malignancy
- Trauma
- Immobilization
- Pregnancy
- Use of birth control pills
- DIC
- Hypercoagulable states
- factor V (Leiden)
- antithrombin III deficiency
- protein C/S deficiency
- prothrombin G20210A mutation
- hyperhomocysteinemia
- antiphospholipid antibodies
Describe the physical signs and symptoms of DVT.
How is it diagnosed?
Physical signs
- unilateral leg swelling
- pain or tenderness
- Homan sign (present in 30% of cases).
- note: superficial palpable cords imply superficial thrombophlebitis rather than DVT
DVT is best diagnosed by Doppler compression US or impedance plethysmography of the veins of the extremity. The gold standard is venography, but this invasive test is reserved for situations when the diagnosis is not clear.
True or false: Superficial thrombophlebitis is a risk factor for pulmonary embolus (PE).
Treatment for superficial thrombophlebitis? 2
False
Superficial thrombophlebitis (erythema, tenderness, edema, and palpable clot in a superficial vein) affects superficial veins and is considered a benign condition.
However, recurrent superficial thrombophlebitis can be a marker for underlying malignancy (e.g., Trousseau syndrome, or migratory thrombophlebitis, is a classic marker for pancreatic cancer).
Treat affected patients with NSAIDs and warm compresses.
How is a-fib treated if it’s acute in onset? chronic? symptomatic?
If symptomatic: first slow the ventricular rate with ß blockers, Ca channel blockers, or digoxin
if acute (onset < 24 hr): cardiovert with amiodarone, procainamide, or DC cardioversion.
If chronic: first anticoagulate, then cardiovert
if this approach fails or atrial fibrillation recurs, leave the patient on rate control medications (beta blocker, calcium channel blocker, or digoxin) and warfarin.
How is a-flutter treated?
Try to stop the arrhythmia with vagal maneuvers (e.g., carotid massage) but otherwise treat as a-fib
- If symptomatic: first slow the ventricular rate with ß blockers, Ca channel blockers, or digoxin
- if acute (onset < 24 hr): cardiovert with amiodarone, procainamide, or DC cardioversion.
- If chronic: first anticoagulate, then cardiovert
- if this approach fails or if it recurs, leave the patient on rate control medications (beta blocker, calcium channel blocker, or digoxin) and warfarin.
How is first-degree heart block treated?
What should you avoid?
No treatment
Avoid ß blockers and Ca channel blockers, both of which slow conduction.
How is 2nd degree Mobitz I heart block treated?
use pacemaker or atropine only in symptomatic patients
How is 2nd degree Mobitz II heart block treated?
pacemaker in all patients
How is 3rd degree heart block treated?
pacemaker
How is WPW syndrome treated?
What should you avoid?
procainamide or quinidine
avoid digoxin and verapamil.
How is ventricular tachycardia treated?
If pulseless: immediate defibrillation followed by epinephrine, vasopressin, amiodarone, or lidocaine.
If a pulse is present: amiodarone and synchronized cardioversion.
How is ventricular fib treated?
Immediate defibrillation followed by epinephrine, vasopressin, amiodarone, or lidocaine.
How are PVC’s treated?
Usually not treated
If severe and symptomatic, consider beta blockers or amiodarone.
How is sinus bradycardia treated?
What should you avoid in these patients?
Usually not treated; use atropine or pacing if severe and symptomatic (e.g., after heart attack).
Avoid ß blockers, Ca channel blockers, and other conduction-slowing medications.
How is sinus tachycardia treated?
Usually none; correct the underlying cause. Use beta blocker or calcium channel blocker if symptomatic.
Which patients with atrial fibrillation should receive anticoagulation?
CHADS2 score
- A score of 0 is low risk for stroke, so aspirin can be used.
- A score of 1 is moderate risk, so aspirin or warfarin can be used.
- A score of 2 or greater is moderate or high risk, so warfarin should be used unless contraindicated (e.g., significant fall risk).
