Cardiology Flashcards
Risk factors for stabile angina pectoris (SAP)
Diabetes = worst risk factor Hypertension = most common risk factor Hyperlipidemia - elevated LDL Smoking Age (men > 45, women >55) Low HDL-levels Family history of CAD, especially 1st degree (Minor: obesity, lifestyle, stress, alcohol)
Prognostic indicators of CAD
1) Left ventricular function/Ejection fraction < 50% -> assoc. with increased mortality
2) Left main coronary artery - poor prognosis b.c it covers approx. 2/3 of the heart
3) Two- or three-vessel CAD - worse prognosis
What is the LDL goal in a patient with CAD?
LDL less than 100 mg/dL
Metabolic syndrome =
A cluster of conditions that occur together (hypercholesterolemia, hypertriglyceridemia, impaired glucose tolerance, diabetes, hyperuricemia, HTN), increasing your risk for CAD, stroke and Diabetes. Key underlying factor is insulin resistance (due to obesity).
Syndrome X =
Exertional angina with normal coronary arteriogram. Patients present with chest pain after exertion, but have no coronary stenosis at cardiac catherization. Excercise testing and nuclear imaging show evidence of myocardial ischemia.
Standard of care for stable angina
Aspirin and a B-blocker (only ones that lower mortality), and nitrates for chest pain.
Function of B-blockers
Block sympathetic stimulation of heart. First line choices include Atenolol and metoprolol. Reduces HR, BP and contractility, thereby decr. cardiac work(i.e oxygen consumption)
Management of mild stable angina (normal EF, mild angina, single-vessel disease)
1) Aspirin + Risk factor modification (Indicated in all)
2) B-blocker
3) Nitrates (for Sx and prophylaxis)
4) Consider calcium channel blockers if Sx continue despite nitrates and B-blockers.
Management of moderate stable angina (normal EF, moderate angina, two-vessel disease)
1) Aspirin + Risk factor modification (Indicated in all)
2) B-blocker
3) Nitrates (for Sx and prophylaxis)
4) Consider calcium channel blockers if Sx continue despite nitrates and B-blockers.
- If the above regimen does not control Sx, consider coronary angiography to assess suitability for revascularization (either PCI or CABG)
Management of severe stable angina (decreased EF, severe angina, three-vessel/left main or left anterior descending disease)
Coronary angiography and consider for CABG
“Acute Coronary Syndrome” =
The clinical manifestation of atherosclerotic plaque rupture and coronary occlusion. Term generally refers to USA, NSTEMI or STEMI.
What is the main difference between SA and USA?
With USA, oxygen demand is unchanged. Supply is decreased secondary to reduced resting coronary flow. This is in contrast to stable angina, which is due to increased demand.
What is the distinction between USA and NSTEMI?
The distinction between USA and NSTEMi is based entirely on cardiac enzymes. The latter has elevation of troponin or creatine kinase-MD (CK-MB). Both USA and NSTEMI lack ST-segment elevations and pathologic Q-waves.
Treatment of USA
Aggressive medical Mx is indicated - treat as in MI except for fibrinolysis.
A) Aspirin
B) Plavix/Clopidogrel
C) B-blockers - first line therapy if no contraindications
D) LMWH (Enoxaparin)- superior to unfractionated heparin - should be given for at least 2 days
E) Nitrates
F) O2
G) Glycoprotein IIb/IIIa inhibitors
H) Morphine (controversial bc can mask Sx)
I) Replacement of deficient electrolytes, espec. K+ and Mg2+
PS: Pts. w/USA should be treated w/Aspirin and Plavix for 9-12months, but may be altered according to bleeding-risk.
If no improvement of Sx or on ECG after 48h –> Catheterization/revascularization
After acute Tx: Aspirin/or other antiplatelet-therapy, B-blockers and nitrates + reduce RF
Variant (Prinzmetal) Angina =
Transient coronary vasospasm
Uually accompanied by a fixed atheroslerotic lesion, but can occur in normal coronary arteries.
Episodes occur at rest, often at night, and are assoc. w/ventricular dysrrhytmias.
Hallmark: Transient ST-segment elevation (not depression) on ECG during rest.
Def. test: Coronary angiography with given IV ergonovine or acetylcholine to provoke vasoconstriction.
Give vasodilators: Ca-channel blockers and nitrates.
Mechanism of MI
Necrosis of myocardium. Most cases are due to acute coronary thrombosis: Atheromatous plaque ruptures into the vessel lumen, and thrombus forms on top of this lesion, which causes occlusion of the vessel.
Markers for ischemia/infarction on ECG
- Peaked T-waves: Occur early and may be missed
- ST-segment Elevation: Indicates transmural injury and can be diagnostic of an acute infarct.
- Q-waves: Evidence for necrosis (specific) - Q-waves are usually seen late, typically not acutely
- T-wave inversion: sensitive, but not specific
- ST-segment depression: Subendocardial injury
ECG findings based on location of infarct
Anterior:
ST-segment elevation in V1-V4
Q-waves in leads V1-V4 (late change)
Posterior:
Large R-wave in V1 and V2
St segment depression in V1 and V2
Upright and prominent T-waves in V1 and V2
Lateral:
Q-waves in leads I and aVL (late change)
Inferior:
Q-waves in leads II, III and aVF (late change)
STEMI vs NSTEMI (location)
STEMI: Transmural (involves entire thickness of wall, tends to be larger.
NSTEMI: Subendocardial (involves inner one-third to one-half of the wall), tends to be smaller, and presenttion is similar to USA, cardiac enzymes differentiate the two.
The Cardiac enzymes
- Troponins (Best)
Increases within 3-5h and returns to normal in 5-14d; reaches a peak in 24-48h. Obtain on admission and every 8h for 24h. - CK-MB
Increases within 4-8h and returns to normal in 48-72h, reaches a peak within 24h. Measure on admission and every 8h for 24h. More helpful in detecting recurrent infarction given quicker return to baseline than troponin.
Initial tx of MI
A) Aspirin B) B-blockers C) ACE-inhibitors D) Statins E) O2 F) Nitrates G) Morphine H) Heparin
Then Revascularization:
Benefits highest if performed early(within 90min of arrival)
Options include PCI, thrombolysis or CABG
PCI is the gold standard, but fibrinolysis alone may be the best option for delayed presentation. CABG if complicated MI(cardiogenic shock, life threatening v.tac, or after failure of PCI).
Dressler syndrome/Postmyocardial infarction syndrome =
Immunologically based syndrome consisting of fever, malaise, pericarditis, leukocytosis and peuritis. Occuring weeks to months after an MI. Aspirin as treatment.
Congestive Heart failure - what is the difference between systolic and diastolic dysfunction?
Systolic dysfunction: Owing to impaired contractility (i.e the abnormality is decr. EF).
Diastolic dysfunction: Owing to impaired ventricular filling during diastole.
Causes of systolic dysfunction CHF
Ischemic heart disease/after MI
HTN resulting in cardiomyopathy
Valvular heart disease
Myocarditis (postviral)
Causes of diastolic dysfunction CHF
HTN leadning to myocardial hypertrophy - mostcommon
Valvular diseases such as aortic stenosis, mitral stenosis
Restrictive cardiomyopathy (amyloidosis, sarcoidosis, hemochromatosis)
Sx of Left sided heart failure
Dyspnea - secondary to pulm congestion
Orthopnea - difficulty breathing in the recumbent position
Paroxysmal nocturnal dyspnea
Nocturnal cough
Confusion and memory impairment - result of inadequate brain perfusion
Diaphoresis and cool extremities at rest
Signs: Pathologic S3 S4 gallop Cracles/rales Dullness to percussion
Sx of Right sided heart failure
Peripheral pitting edema Nocturia - due to incr. venous return with elevation of legs Jugular venous distention Hepatomegaly/hepatojugular reflux Ascites Right ventricular heave
Diagnosis of CHF
Most important:
- Chest X ray
- Cardiomegaly
- Kerley B-lines (indicate pulm. congestion)
- Pleural effusion - Echocardiogram
- can differentiate between syst. or diast. failure
- Estimates EF (syst.failure: EF<40%).
- shows chamber dilation or hypertrophy
Treatment of CHF
Systolic dysfunction:
- Lifestyle modification
- Diuretics (Lasix/Loop diuretics most common)
- Spironolactone (only for advanced)
- ACE inhibitors (The combo of a diuretic and an ACE inhibitor should be the intitial tx in symptomatic pts.)
- B-blockers (Proven to decr. mortality in pts. with post-MI heart failure)
- Digitalis - (For patients with EF < 40%, who continue to have symptoms despite standard therapy)
Diastolic dysfunction:
- B-blockers
- Diuretics
- Spironolactone and Digoxin should NOT be used.
- NO medications have proven mortality benefit
Arrhytmias : Premature Complexes :
Premature Atrial Complexes
Early beat arising from atria, firing on its own. Found in 50% of people. Usually normal, may be a precursor of ischemia in diseased heart.
Causes: adrenergic excess, coffee, drugs, alcohol, electrolyte abn. etc.
ECG: Early P waves that differ in morphology from normal P wave. QRS normal.
Tx: Nothing. If very symptomatic - B-blockers.
Arrhytmias: Premature Complexes:
Premature Ventricular complexes
Early beat that fires on its own from a focus in the ventricle. Can occur in patients with or without structural heart disease. Can occur in 50% of people, presence of PVCs in pts with normal hearts is assoc. with incr. mortality. Workup is necessary. (Can cause arrhytmias)
Causes: hypoxia, electrolyte abn, stimulants, caffeine etc.
ECG: Wide, bizarre QRS complexes followed by a compensatory pause, P-wave often buried in the QRS-complex.
Tx: If symptomatic, B-blockers. If frequent PVCs: workup.
Tachyarrhytmias:
Atrial fibrillation
Multiple foci in atria fire continuously in a chaotic pattern -> irregular, rapid ventricular rate. Rate between 75 and 175. Markedly incr. risk of thromboembolism + hemodynamically compromise. Irregularly irregular pulse.
ECG: Irregular RR intervals, excessively rapid series of tiny, erratic spikes on ECG with a wavy baseline and no P-waves.
Treatment:
Unstable: Electrical cardioversion
Stable: 1) Rate control(B-blockers - target rate 60-100)
2) Anticoagulate pts. for 3 weeks OR TEE to check for thrombus in atrium then –> Cardioversion to sinus rhytm (after rate control achieved). INR of 2-3 is best.
