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51 Cards in this Set

  • Front
  • Back
Stable Angina Pectoris
Coronary ischemia due to imbalance between blood supply and oxygen demand due to fixed atherosclerotic lesions in arteries

*Occurs with INCREASED OXYGEN DEMAND
Risk factors for Stable Angina Pectoris
1) DM
2) Hyperlipidemia - elevated LDL
3) HTN
4) Cigarette smoking
5) Age
6) Low HDL
7) Hyperhomocysteinemia
Normal cardiac ejection fraction
>50%
Clinical features of stable angina
1) Chest pain or substernal pressure lasting less than 10-15 minutes
2) Brought on by exertion or emotion
3) Relieved with rest or nitroglycerin
Diagnosis of coronary artery disease
1) Resting EKG
2) Stress EKG / Stress Echocardiogram
3) Pharmacologic stress test (if unable to exercise)
4) Holter monitoring (ambulatory EKG)
5) Cardiac catheterization with coronary angiography

*If stress studies +, proceed to catheterization
Metabolic Syndrome X
Obesity, plus any 2 of the following:
1) Hypercholesterolemia
2) Hypertriglyceridemia
3) DM
4) Hyperuricemia
5) HTN
Stress test considered positive with any of these findings...
1) S-T segment depression
2) Chest pain
3) HYPOtension
4) Significant arrhytmias
Syndrome X
Exertional angina with NORMAL coronary arteriogram
Exercise testing and nuclear imaging show evidence of MI

*Excellent prognosis
Medications used for pharmacologic stress test
1) IV adenosine
2) Dipyramidole
3) Dobutamine

*Adenosine and Dypyramidole cause generalized coronary vasodilation
*Dobutamine increases myocardial oxygen demand (HR, BP, contractility)
Treatment of CAD
1) Risk factor modification
2) Medical therapy (aspirin, beta-blockers, nitrates, Ca2+ channel blockers, ACEI [for CHF])
3) Revascularization (PTCA or CABG)
Coronary artery disease: Severe disease
1) Decreased ejection fraction (EF)
2) Three-vessel disease
3) Left main or LAD disease
Indications of Percutaneous Transluminal Coronary Angioplasty (PTCA)
Indicated with one- or two-vessel disease (proximal lesions)

*Restenosis occurs in 40% within 6 months --> rate reduced with stent placment
Unstable Angina Pectoris (USA)
Coronary artery blood supply is decreased secondary to reduced resting coronary flow

**Oxygen demand is unchanged --> Indicates stenosis that enlarged via thrombosis, hemorrhage, or plaque rupture**
Characteristics of USA
1) Chronic angina with increasing frequency, duration, or intensity of chest pain
2) New-onset angina that is severe and worsening
3) Angina at rest
First-line therapy for USA
1) Beta-blockers
2) Nitrates

*Aspirin, Low-molecular-weight heparin (LMWH), and Glycoprotein IIb/IIIa inhibitors helpful adjuncts
Variant (Prinzmetal's) Angina
Transient coronary vasospasm accompanied by fixed atherosclerotic lesion
Angina at rest, associated with ventricular dysrhythmias

*Transient S-T segment elevation
Coronary angiogram of variant angina
Displays coronary vasospasm

*Pt given Ergonovine (to provoke chest pain)
Treatment of variant angina
1) Calcium channel blockers
2) Nitrates
Myocardial Infarction (MI)
Necrosis of myocardium resulting from interruption of blood supply
Usually due to acute coronary thrombosis

*30% mortality rate
Clinical features of MI
1) Chest pain (substernal "crushing" pressure) that radiates to jaw, neck, arm on left side
2) May be asymptomatic
3) Dyspnea, Diaphoresis, Weakness / Fatigue, N/V, Syncope, Sense of impending doom
4) Sudden Cardiac Death (V-fib)
EKG markers for ischemia/infarction
1) Peaked T waves
2) S-T segment elevation (transmural injury)
3) Q waves
4) T wave inversion
Categories of cardiac infarcts
1) ST segment elevation - transmural (entire thickness of wall)
2) Non-ST segment elevation - subendocardial (inner one third to one half of wall)

*Types differentiated by cardiac enzymes
Cardiac enzymes
1) Creatine kinase-MB (CK-MB) - increases within 4-8 hrs of MI; returns to normal in 2-3 days
2) Troponins (I&T) - increases within 3-5 hrs; returns to normal in 5
-14 days

*Troponins are most important markers of MI
Medical therapy shown to reduce mortality after MI
1) Aspirin - inhibtis platelet aggregation on top of thrombus
2) Beta-blockers - blocks contractility and reduces afterload
3) ACE Inhibitors

*Statins, Nitrates, Morphine, Heparin & Oxygen used also
Complications of MI
1) Pump failure (CHF)
2) Arrhythmias
3) Recurrent infarction
4) Mechanical complications (rupture of free wall, interventricular septum, papillary muscle, etc)
5) Acute pericarditis
6) Dressler's Syndrome
MCC of in-hospital mortality post MI
Pump failure (CHF)

*Mild: Tx with ACEI or diuretic
*Severe: Invasive hemodynamic monitoring
Management of 2nd degree (type 2) or 3rd degree AV block in setting of anterior MI
Emergent placement of temporary pacemaker, followed by placement of permanent pacemaker
Free wall rupture post MI
Occurs during first 2 weeks
90% mortality via hemopericardium and tamponade
Treated with hemodynamic stabilization, pericardiocentesis, and surgical repair
Valvular dysfunction caused by papillary muscle rupture
Mitral Regurgitation

*Valve replacement necessary
Ventricular Pseudoaneurysm
Incomplete free wall rupture

*Surgical emergency --> leads to free wall rupture
Treatment of post-MI acute pericarditis
Aspirin

*NSAIDS and corticosteroids contraindicated
Dressler's Syndrome
Fever, malaise, pericarditis, leukocytosis, and pleuritis occurring weeks to months after MI

*Aspirin is most effective therapy
Differential Diagnosis of Chest Pain: Heart
1) MI
2) Angina
3) Pericarditis
4) Aortic dissection
Differential Diagnosis of Chest Pain: Lungs
1) Pleuritis
2) Pulmonary embolism
3) Pneumothorax
4) Pneumonia
5) Status asthmaticus
Differential Diagnosis of Chest Pain: GI
1) GERD
2) Diffuse esophageal spasm
3) Peptic ulcer disease
4) Esophageal rupture
Differential Diagnosis of Chest Pain: Chest Wall
1) Costochondritis
2) Muscle strain
3) Rib fracture
4) Herpes zoster
5) Thoracic outlet syndrome
Differential Diagnosis of Chest Pain: Psychiatric / Drugs
1) Panic attacks
2) Anxiety
3) Somatization

*Cocaine use can cause angina
Systolic dysfunction in Congestive Heart Failure (CHF)
1) Impaired contractility
2) Cardiomyopathy
3) Myocarditis
Diastolic dysfunction in CHF
1) HTN leading to hypertrophy (MCC)
2) Valvular diseases
3) Restrictive cardiomyopathy (i.e., amyloidosis, sarcoidosis, hemochromatosis)
Clinical features of CHF
1) Dyspnea
2) Orthopnea
3) Paroxysmal nocturnal dyspnea
4) Nonproductive nocturnal cough
5) Confusion and memory impairment (inadequate brain perfusion)
6) Diaphoresis and cool extremities at rest
Orthopnea
Difficulty breathing in recumbent position

*Due to increased distribution of blood to the pulmonary circulation when laying down
Paroxysmal Nocturnal Dyspnea (PND)
Awakening after 1 -2 hours of sleep due to acute shortness of breath
Signs of left-sided heart failure
1) Displaced PMI
2) S3 gallop (best heard at apex with bell of stethoscope)
3) S4 gallop
4) Crackles / rales at lung bases
5) Dullness to percussion and decreased vocal fremitus (pleural effusion)
6) Increased intensity of pulomonic component of 2nd heart sound (left upper sternal border)
Signs/symptoms of right-sided heart failure
1) Peripheral pitting edema
2) Jugular venous distention
3) Nocturia (due to increased venous return w/ leg elevation
4) Hepatomegaly/hepatojugular reflex
5) Ascites
6) Right ventricular heave
Diagnosis of CHF
1) CXR
2) EKG
3) Stress testing
4) Cardiac catheterization
5) Echo (EF, r/o pericardial effusion)
6) Radionuclide ventriculography w/ technetium-99m
New York Heart Association (NYHA) Classification of CHF
Class I: Symptoms w/ vigorous activity; asymptomatic at rest
Class II: Symptoms w/ prolonged or moderate exertion; slight limitation of activities
Class III: Symptoms w/ usual daily activities; markedly limitation
Class IV: Symptoms at rest; incapacitating
Possible CXR findings in CHF
1) Cardiomegaly
2) Kerley B lines - short horizontal lines near periphery of lung
3) Prominent interstitial markings
4) Pleural effusion
Treatment options for CHF
1) Salt restriction (>4g /day)
2) Diuretics (symptomatic relief)
3) ACEI
4) Angiotensin II receptor blockers
5) Digitalis (+ inotropic agent; EF<30%)

*Hydralazine & Isosorbide dinitrates used in patients who cannot tolerate ACEI
6)
Signs of digoxin toxicity
1) GI: n/v, anorexia
2) Cardiac: AV block. AFib, ectopic ventricular beats
3) CNS: visual disturbances, disorientation
Carvedilol
Non-selective beta blocker/alpha-1 blocker
Used in tx of CHF

*Better improvement than Metoprolol
Useful in differentiating between dyspnea caused by CHF and COPD
B-type natriuretic peptide (BNP)

*Released from cardiac ventricles in response to volume expansion and pressure overload