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58 Cards in this Set
- Front
- Back
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What are the structural diseases of the heart? |
CHF Valves Cardiomyopathy |
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What are the electrical parts of the heart? |
Arrythmias EKG Pacemakers |
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What is are the diseases due to the plumbing of the heart? |
Coronary artery disease Acute Myocardial Infarction |
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What is the most common, serious, chronic, and life-threading illness in the US? |
Coronary Artery Disease |
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ACS - Acute Coronary Syndrome includes what? |
Unstable Angina (UA) Non-ST elevation Myocardial Infarction (NSTEMI) ST elevated Myocardial Infarction (STEMI) |
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CAD is Coronary artery disease. It is also known as what? |
Ischemic Heart disease (IHC) Atherosclerotic Coronary Heart Disease (ASCHD) |
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CAD is a condition in which what occurs? |
There is an inadequate supply of blood and oxygen to a portion of the myocardium; Its oxygen supply and demand |
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Patients with CAD most commonly present with what? |
Stable Angina |
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What are the layers of the arterial vasculature? |
Intima Media Adventetia |
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UA is defined as what? |
Angina pectoris or equivalent ischemic discomfort with at least one of 3 features. - It occurs at rest (or with minimal exertion) usually lasting > 10 minutes - It is severe and new onset (within the prior 4-6 weeks) - It occurs with a crescendo pattern (distinctly more severe, prolonged, or more frequent then previously) |
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The diagnosis of NSTEMI is established if a patient with the clinical features of UA develops evidence of myocardial necrosis, as reflective in what? |
Elevated cardiac biomarkers |
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Non-STEMI Is how much occluded? Must have elevated what? What may the EKG show? |
Sub-totally occlusive thrombus Elevated cardiac enzymes - troponin - CPK - CK-MB May have non-specific EKG changes - ST-segment depression - T-wave inversion (30-50%) |
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STEMI is how much occluded? What will the EKG show? |
Completely occlusive thrombus. EKG - ST segment elevation - Most develop Q-wave MI on EKG. |
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Where will an EKG show an anterior infarct? Which vessels is this? |
ST elevation in: - Lead I - Lead AVL - Leads V2, V4, V6 Left anterior descending artery |
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Where will an EKG show and inferior infarct? Which vessel is this? |
ST elevation in: - Lead II - Lead III - Lead AVF Right coronary artery or Left coronary Artery |
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UA/NSTEMI - caused by what? |
- reduction in oxygen supply and/or by - an increase in myocardial demand - superimiposed on an atherosclerotic coronary plaque, with varying degrees of obstruction. |
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What are possible causes of obstruction in UA/NSTEMI? |
- Plaque rupture with non-occlusive thrombus - Coronary spasm - Prnzmetals variant angina - Rapidly progressive atherosclerosis or restenosis following coronary stent or CABG - Marked increase in O2 demand/supply as in anemia, metabolic stress, sepsis - White platelet thrombus (rather than RBC-rich red clot of STEMI) **often multiple sites of disruption |
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There are 5 types of MI, What is Type I? |
Spontaneous MI related to ischemia caused by a primary coronary event such as plaque erosion and/or rupture, fissuring, or dissection. |
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What is Type II? |
MI secondary to ischemia resulting from an imbalance between oxygen demand and supply, troponin elevated secondary to sepsis, trauma, hypoxia, etc. |
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What is Type III? |
Sudden death from cardiac disease (before blood samples can be obtained) with symptoms of MI accompanied by new ST elevations or left bundle branch, or coronary thrombus verified by angiography. |
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What is Type IV? |
MI associated with primary percutaneous coronary intervention. |
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What is Type V? |
MI associated with coronary artery bypass graft (CABG) |
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What are the clinical hallmark symptoms upon examination for a UA/NSTEMI? |
- Chest pain - typically substernal - Pain radiates to the neck, left shoulder, arm - New onset (4-6 weeks) - Longer duration of pain - More frequent episodes |
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How does atypical angina present? |
Dyspnea or abdominal pain |
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How will typical angina present? |
- Chest Pain - Radiates to neck, jaw, back, or L arm - Diaphoresis and/or dyspnea - Worse with exertion - Relieved with rest or nitro |
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What may be present on physical exam during a UA/NSTEMI? |
May be normal - Pale or cool skin - Sinus tachycardia - 3rd and 4th heart sounds - basilar rales (crackles in chest) |
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How will an EKG appear in a UA/NSTEMI? |
ST segment depression Transient ST segment elevated T wave inversions (occur in 30-50% of patients) |
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How can a UA be distinguished from a NSTEMI? |
Cardiac Biomarkers Elevated cardiac biomarkers - troponin - CPK - CK-MB Will be elevated in NSTEMI, NOT elevated in UA |
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Patients with initial negative biomarkers must have what done? |
Be remeasured within 8-12 hours |
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There is a direct relationship between elevated troponin and what? |
Mortality |
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What is the most specific and sensitive marker of myocardial necrosis? |
Troponin |
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Which will elevate faster - troponin or CK-MB? Which will stay elevated longer? Which can be used to distinguish a new event from a previous event occurrence? |
CK-MB Troponin CK-MB - it will go away faster and re-elevated if a new event has occurred within a few days of a prior event. The troponin may still be elevated from a previous event. |
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What are the risk factors for UA/NSTEMI? |
- Clinical history of typical angina or angina equivalent symptoms - Established diagnosis of CAD (seen on prior imaging - Prior MI - CHF - New EKG changes - Elevated cardiac biomarkers - >70 years in age - Male - Diabetes - Known PAD or CVD (its a systemic disease) - Old EKG abnormalities |
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What are some differential diagnosis for UA/NSTEMI? |
- Acute Myocardial Infarction (my upgrade to STEMI) - Acute Aortic Dissection (back pain/CT scan) - Acute Pericarditis (diffuse ST seg elevation) - Acute Pulmonary Embolism (pleuritic pain with dyspnea) (elevated d-dimer/CT) - GI cause of pain - PUD, esophageal spasm, hiatal hernia, cholecystitis, acute pancreatitis |
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What is the medical treatment for UA/NSTEMI? |
- IV access - O2 by nasal cannula - Continuous telemetry monitoring - repeat 12 lead EKG upon admission - lab work Nitrates - sublingual nitro (up to 3 doses 5 min apart) - or cont. IV gtt if pain persists Beta-blockers - metoprolol or carvedilol - to target heart rate of 50-60 bpm - helps relax heart and increase C.O. Morphine Calcium channel blockers - diltiazem or verapamil - used in patients who have persistent or recurrent symptoms after full dose of nitrates and beta-blockers or in patients with contra-indications to B-blockers Ace Inhibitor (or ARBs) - for long term secondary prevention HMG-CoA reductase inhibitors (statins) - for long term secondary prevention. (regardless of cholesterol levels) |
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What is the Anti-Thrombotic therapy for UA/NSTEMI? |
Oral anti-platelet med - Aspirin (ASA) - recommended long-term - Clopidogrel (Plavix), Prasugrel (Effient), Ticagrelor (Brilinta) - IV-anti-platelet meds (used usually post-PCI) Heparin or Unfractionated Heparin (UFH) - associated with Heparin Induced Thrombocytopenia (HIT) - measure platelet levels Enoxaprin or Low Molecular Weight Heparin (LMWH) Lovenox - safer, but more costly. Decreased risk of HIT. - will take off heparin if platelet levels decrease |
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What is the treatment for UA/NSTEMI? |
Heart Catheterization - Percutaneous Transluminal Coronary Angioplasty (PTCA). If troponin is elevated - pt will go to heart cath - not have stress tests done. Nuclear stress test Stress Echo Treadmill EKG |
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What are the Class I Recommendations for Use of an Early Invasive Strategy (heart cath) |
- Recurrent angina at rest/low-level activity despite RX. - Elevated T-T or T-I - New ST-segment depression - Rec. angina/ischemia with CHF symptoms, rales, MR - Positive stress test - EF < .40 (new onset heart failure is most often due to ischemia/infarct of the heart) - Decreased BP - Sustained VT - Longer than 30 seconds - PCI < 6 months, prior CABG |
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What is the long term pharmacological management for UA/NSTEMI? |
Beta-Blockers - metoprolol, cardivelol - relax heart to improved C.O., prevent CHF ACE inhibitors (or ARBs) - lisinopril, enalopril, losartan Statins - check liver enzymes before starting them Anti-platelet meds - ASA for life - Clopidogrel (Plavix) for 1 year - 1 month (depending on type of stent placed) Nitrates - PRN |
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Which cardiac drugs cannot be given during pregnancy? |
ACE/ARBs |
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What patient education is given for long term management following UA/NSTEMI? |
- smoking cessation - weight control - daily exercise and appropriate diet - blood pressure control - control cholesterol - control hyperglycemia - compliance with medications |
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What can heart disease risk factors can we not control? |
Age and Genetics (family history) |
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What is the mortality rate from AMI (STEMI)? |
30% - 30 day mortality rate - more than 1/2 of patients done reach hospital |
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What is survival of an AMI (STEMI) improving due to? |
- Improved BLS and ACLS - Transportation to cardiac cath lab (door to balloon within 90 minutes) - Revascularization - Secondary prevention of CAD |
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When does a STEMI occur? |
When coronary blood flow decreases abruptly after a thrombotic occlusion of a coronary artery previously affected by atherosclerosis A mural thrombus forms at the site of plaque disruption, and the involved coronary artery becomes occluded |
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Pathology is _______ thickness MI due to ____________ occlusion of major epicardial vessel secondary to ___________ rupture and "red clot". |
Full thickness Complete occlusion Plaque |
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AMI (STEMI) is NOT due to progression of chronic stenosis - why? |
these develop regional collaterals |
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How does a patient present with STEMI? What does an EKG show? How will biomarkers appear? |
Ischemic resting pain ST segment elevation (this will show before troponin) Elevated cardiac enzymes - CK-MB - CPK - Troponin |
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If a patient presents as NSTEMI what may it progress on to? |
Platelets may propagate more thrombosis and lead to complete occlusion. |
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What are the risk factor for STEMI? |
Same as UA/NSTEMI with the addition of: Cocaine Use Hypercoagulability |
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What is the presentation of physical exam for a STEMI? |
Same as UA/NSTEMI - pale or cool skin - sinus tachycardia - 3rd or 4th heart sound - basilar rales With the addition of: - S4 - increased intensity of S1 - murmur or frictional rub - arrhythmia - pulmonary edema (depending on size, location, and extent of infarct - Elevated JVP (jugular venous pressure) |
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Where will an Anterior MI present on an EKG? |
ST Elevation V1, V2, V3, V4 Left Anterior Descending Artery |
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Where will an Inferior MI present on an EKG? |
ST Elevation II III AVF Right Coronary Artery (RCA) |
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Where will a Lateral MI present on an EKG? |
ST Elevation I AVL V5 V6 Left Circumflex Artery |
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Where will a Posterior MI present on an EKG? |
ST Depression V1 V2 RCA/ LCX |
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Where will a subendocardial infarct present on an EKG? |
Diffuse or Localized Change Non Q-wave |
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What is the diagnosis for STEMI? |
ST Elevation on EKG
Ischemic chest pain or equivalent Elevated cardiac biomarkers |
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What are the goals of therapy for STEMI? |
Salavge as much myocardium as possible by decreasing O2 demand Minimize extension of infarct Reestablish flow through or around occluded artery Keep pt alive by treating arrhythmias and avoiding complications of therapy. |
