NUR 146 - Week 8 - Coronary Artery Disease Flashcards

1
Q

Define atherosclerosis

A

an abnormal accumulation of lipid and fibrous tissue in the lining of arterial blood vessels

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2
Q

What is metabolic syndrome?

A

Defined as a cluster of metabolic abnormalities

Diagnosis is made if a person has 3 of the following 5 risk factors

1) Enlarged waist circumference >40” in men, >35” in women​

2) Elevated triglycerides >175mg/dl​

3) Reduced HDL <40mg/dl in males, <50g/dl in females​

4) Hypertension ​

5) Elevated fasting blood glucose​

  • Metabolic Syndrome is considered a major risk factor for CAD
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3
Q

How can CAD be prevented?

A

Controlling modifiable risk factors:
- Manage cholesterol via medication, diet, exercise
- Tobacco cessation
- Manage hypertension with meds, diet, exercise
- Manage diabetes with meds, diet, exercise

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4
Q

Discuss Low Density Lipoproteins in regard to CAD

A

“Bad cholesterol”
Promotes production of atheroma

  • Primarily made of cholesterol
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5
Q

Discuss High Density Lipoproteins in regard to CAd

A
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6
Q

Lipid level recommendations for:

Total
LDL
HDL
Triglycerides

A

Total: <200 mg/dl
LDL: <100 mg/dl or <70mg/dl if high risk
HDL: > 40mg/dl in males, >50 mg/dl in females
Triglycerides: <150 mg/dl

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7
Q

Hyperlipidemia:

Management

A

Dietary

  • High fiber
  • Emphasis on plant-based foods, whole grains
  • Fish
  • Low intake of red meat

Physical Activity
- weight reduction
- Increased physical activity can increase HDL and lower triglycerides
- Goal is 150 min/week

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8
Q

Hyperlipidemia:

Pharmacologic therapy

A

Used in conjunction with diet and exercise

6 categories:
- Statins
- Nicotinic Acids
- Bile acid sequestrants
- Cholesterol absorption inhibitors
- Omega-3 Acid Ethyl Ester

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9
Q

Statins

What do they do?
Adverse Effects?

A

First line medication to treat increased LDL levels; results in lower total cholesterol, LDL and triglyceride AND increase HDL levels

Adverse effects:
Common = Myalgia, Arthralgia (Muscle pain, joint pain)
Serious = Myopathy, rhabdomyolysis (breakdown of muscle)

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10
Q

What should you monitor for a patient on Statins?

A

LFTS

  • Statins are contraindicated in patients with liver disease
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11
Q

What time do you administer statins? Why?

A

In the evening

  • Body produces cholesterol at night
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12
Q

Bile Acid Sequestrants:

How are they used?
Mechanism of action
Nursing Considerations
Side effects

A

Cholestyramine, colestipol

Used in adjunct therapy with statins; results in decreased LDL, may slightly increase HDL

Mechanism of action: Decreased fat absorption

Nursing considerations:
- Take before meals
- May decrease absorption of meds

Side effects:
- Constipation
- Abdominal pain
- GI bleed

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13
Q

Cholesterol Absorption Inhibitors:
What does it do?
Side effects
Nursing considerations

A

Ezetimibe
- Inhibits absorption of cholesterol in small intestine = lower LDL levels
Side effects:
- Abdominal pain
- Myalgia, athralgia (muscle pain, joint pain)
Nursing Considerations:
- Contraindicated in liver disease; monitor LFTs
- May cause increased fasting glucose & Hgb A1c
- May cause increased AST, ALT
- May cause hyperkalemia

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14
Q

Risk factors for CAD

A

Modifiable:
- Hyperlipidemia
- HTN
- smoking
- diabetes
- obesity
- sedentary lifestyle
- metabolic syndrome

Nonmodifiable:
- Male gender
- Family hx
- hx of hypercholesterolemia
- male >45 yo, female >55 yo
- African american

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15
Q

Effects of tobacco use in regards to CAD

A

Effects of tobacco use:
- HTN
- Coronary vasoconstriction
- Increased LDL oxidation –> damages endothelium, causing thrombus formation
- Smoke inhalation increased CO2 levels = decreased oxygen to myocardium

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16
Q

Describe the relationship of diabetes and CAD

A

Hyperglycemia accelerates development of CAD

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17
Q

Angina Pectoris:

What is it?
Cause?
Types?

A

Clinical syndrome characterized by episodes of pain or pressure in anterior chest

Cause: Insufficient coronary blood flow which = decreased oxygen supply in the setting of increased myocardial oxygen demands

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18
Q

Angina:

Pathophysiology

A

Supply vs. Demand; usually caused by underlying atherosclerotic disease

  • Often associated with obstruction of at least one major coronary artery
  • When myocardium (cardiac muscle) has increased demands, it must increase blood flow through coronary arteries

Results in ischemia = chest pain

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19
Q

Precipitating Factors of Angina:

The 4 E’s
Explain the patho for each “E”

A

physical Exertion, cold Exposure, Eating heavy meal, Emotional stress

physical Exertion:
- Increases myocardial oxygen demand

Exposure to cold:
- Vasoconstriction and elevated BP
- Increases oxygen demands

Eating a heavy meal:
- Increases blood flow to GI tract for digestion
- Results in reduced blood flow to heart

Emotional stressors:
- Results in catecholamine (epinephrine, norepinephrine) release
- Results in increased BP, HR and myocardial workload

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20
Q

Angina:

Clinical manifestations

A

Anginal Pain

Quality: Described as tightness, choking or heavy sensation

Location: Often retrosternal, may radiate to neck, jaw, shoulders

Often associated with anxiety or impending doom

Associated symptoms:
- N/V, dyspnea, SOB, dizziness, diaphoresis

Physical assessment may show as normal

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21
Q

Types of Angina:

Stable

A

Predictable pattern; “If I do this, I will feel pain”

  • Pain occurs on exertion
  • Symptoms are similar between episodes
  • Pain is relieved by rest and/or nitroglycerin
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22
Q

Types of Angina:

Unstable

A

Unpredictable pattern

  • Pain may occur at rest
  • Pain lasts longer than the previous episode
  • Seen as high risk of MI

Requires medical intervention!

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23
Q

Types of Angina:

Variant / Prinzmetal’s

What is it
Patho
Cause/Trigger

A

Chest pain occurring at rest

Patho: Coronary Vasospasm (Blood vessels spasm)

  • Pain is caused by decreased blood supply during spasm
  • Pain is NOT a result of increased Myocardial oxygen demand

Triggered by autonomic stimulation, smoking, cocaine use

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24
Q

Variant / Prinzmetal’s Angina:

Treatment

A
  • Isosorbide Mononitrate
  • Calcium channel blockers
  • May also be treated with cardiac stent to decrease spasms
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25
Isosorbide Mononitrate: What is it used for / Indications? Mechanism of action Side effects Nursing Considerations
Purpose: Prevention of recurrent angina (will NOT treat anginal attack once it has begun) Mechanism of Action: Vasodilator, relaxes blood vessels, increasing oxygen delivery Side effects: Headache, hypotension, dizziness, redness of face/neck Nursing Considerations: - Monitor blood pressure - Assess for fall risk - Report any rhythm disturbances - Report any palpitations, chest pain, SOB, fainting
26
Types of Angina: Intractable / Refractory Angina What is it? Relieved by?
Severely incapacitating chest pain. forcing patient to stop and sit Pain may last for long periods of time Relieved by: - Rest - Nitroglycerin - Removal of precipitating factors
27
Silent Ischemia
Objective evidence of ischemia (EKG Changes) but with no reported symptoms Patient does not experience pain
28
CAD: Gerontologic Considerations
Older patients may not experience typical symptoms due to diminished pain sensation May experience silent ischemia
29
Angina: Assessment
Patient interview and history is key Determine characteristics of pain: - Location - Character - Severity - Onset - Duration - Radiation - Precipitating factors - Relieving factors
30
Angina: Diagnostics
12-Lead EKG - * **T wave inversion** * - ST abnormalities - Abnormal Q-wave Lab studies: - Cardiac biomarkers: troponin, CKMB Stress Test: - Exercise stress test - Pharmacologic stress test Nuclear Scan Cardiac Catheterization
31
Angina: Treatment Goals
Decrease oxygen demands of heart: - Rest - Medications Increase oxygen supply to heart: - Oxygen - Medications - Reperfusion (Open blood vessel) procedures Prevent angina from progressing to MI: - Identify and manage risk factors
32
Nitroglycerin: Purpose Mechanism of action Side effects Patient Education
Purpose: - Vasodilator; improves blood flow to myocardium Mechanism of action: - Decreases preload and afterload - Decreases oxygen demands of myocardium Side effects: - Flushing - Headache - Hypotension - Tachycardia Patient Education: - Renew and check expiration frequently; store in sealed dark bottle - Call EMS if no relief after 3 sublingual doses
33
Angiotensin converting enzymes (ACE) Inhibitors, (Pril's): Mechanism of action What does it do? Side effects
Lisinopril, enalapril, captopril Block the conversion of Angiotensin I to Angiotensin II, results in moderate vasodilation and decreased sodium reabsorption in kidneys What does it do: "Lowers demand" - Results in decreased BP and decreased cardiac workload - Reduction of preload & afterload, increasing stroke volume Side effects: - **Angioedema**, life threatening - Hypotension - Dry cough - Hyperkalemia
34
Beta Adrenergic Blockers (lol's): Mechanism of action What does it do Side effects Contraindications
Metoprolol, propanolol, atenolol Mechanism of action: "Lowers demand" - Blocks effect of beta receptors - Decreased preload, contractility and afterload What does it do: - Decreased sympathetic activity on the heart - Decreased heart rate - Decreased BP - Reduced myocardial oxygen demands Side effects: - Hypotension - Bradycardia - Depressed mood - Fatigue Contraindications: - Hypotension - Bradycardia - Hx of heart block, heart failure - Asthma
35
Calcium Channel Blockers: Mechanism of Action What does it do Side effects Nursing Considerations
Amlodipine, Diltiazem Mechanism: - Decrease SA node automaticity (decreases amount of time SA node fires = slows heart rate) - Decrease AV nodal conduction What does it do: "Decrease workload of heart" - Decreased HR - Decreases strength of myocardial contractility - Vasodilates of coronary arterioles Side effects: - Hypotension - Bradycardia - Constipation Nursing Considerations: - Administer slowly when given IV, can cause hypotension - Monitor blood pressure - Do not crush sustained release meds
36
Antiplatelet Agents: Acetylsalicylic Acid (Aspirin) Mechanism of action What does it do Side effects
Mechanism of action: - Prevents platelet aggregations What does it do: - Reduces incidence of MI and Death in patients with CAD - Works immediately - Prescribed daily for patients with angina Side Effect: - Risk for GI bled
37
Antiplatelets Agents: Adenosine Diphosphate Receptor Antagonists / Ticagrelor, clopidogrel What does it do?
Block platelet aggregation along a different pathway than Acetylsalicylic Acid; less platelet activity May take a few days to be effective
38
Heparin:
May be used to treat unstable angina Labs to monitor: - aPTT
39
Low Molecular Weight Heparin: Function? Indication?
Provides stable anticoagulation Indications: - Unstable angina, NSTEMI - No need to monitor aPTT Administration: - SubQ Nursing considerations: - Patient should be on bleeding precautions
40
Angina: Nursing Interventions
Treat Angina: - Obtain EKG - Administer meds as ordered - Administer oxygen as ordered Reduce anxiety: - Speak in a calm manner - Stress reducing techniques
41
Acute Coronary Syndrome (ACS)
Acute onset of myocardial ischemia; emergency situation - a sudden reduction in blood flow to the heart muscle, leading to chest pain or discomfort - May lead to myocardial death if ischemia is left untreated Unstable angina NSTEMI STEMI
42
Acute Coronary Syndrome: Patho of Unstable Angina
Reduced blood flow in a coronary artery usually secondary to rupture of an atherosclerotic plaque Clot forms over ruptured lesions
43
ACS: PATHO OF MI
Imbalance of myocardial oxygen supply and demand; most commonly d/t plaque rupture and thombus formation Other less common causes: - Vasospasm of coronary artery - Significant hypoxemia (Anemia, blood less, hypotension) - Increased demand for oxygen (tachycardia, thyrotoxicosis, cocaine)
44
Myocardial Infarction: Causes
Caused by imbalance of myocardial oxygen supply and demand Most common: - Plaque rupture - Thrombus formation Less common: - Vasospasm of coronary artery - Significant hypoxemia: Anemia, blood loss - Increased demand for oxygen: Tachycardia, thyrotoxicosis
45
Acute Coronary Syndrome: Clinical Manifestations
Chest pain occurring suddenly and continues despite rest and medications Symptoms of unstable angina and MI may be identical - Diagnostic testing required to differentiate
46
Acute Coronary Syndrome: Diagnostic Tests
EKG = standard 12-lead EKG performed within 10 minutes of complaint of pain Abnormal EKG findings: - T-wave inversion - ST segment depression (usually ischemia) - ST segment elevation (Usually STEMI)
47
Acute Coronary Syndorme: Abnormal EKG findings: Signs of ischemia Signs of active infarction Signs of past infarction
Signs of ischemia on EKG: - T wave inversion - ST segment depression Signs of active infarction on EKG: - ST segment elevation Signs of past infarction on EKG: - Presence of abnormal Q-wave - Abnormal Q-waves appear 1-3 days after infarction
48
Myocardial Infarction: Classifications - NSTEMI
Non-ST elevation Myocardial Infarction Characteristics: - No ST segment elevation - Positive cardiac enzymes - *Less damage to myocardium compared to STEMI* "Damage to myocardium, but less
49
Myocardial Infarction: Classifications - STEMI
ST Elevation Myocardial Infarction Characteristics: - Presence of ST segment elevation on EKG (necessary!) - Positive cardiac enzymes - 100% vessel occlusion - Damage is often irreversible
50
Acute Coronary Syndrome: Diagnostic Tests - Troponin What is it used for?
Protein found in myocardial cells Why is it used?: Levels of troponin rise within hours of myocardial ischemia - Levels may remain elevated for up to 2 weeks following ischemia Three subtypes: - Troponin I & T are specific for cardiac muscle - Troponin C less specific Think: Indicative of cardiac ischemia/infarction
51
Acute Coronary Syndrome: Diagnostics - CK-MB
Levels begin to rise very quickly secondary to ischemia - Levels peak within 24 hours of infarct = slow - Often to test reinfarction
52
Acute Coronary Syndrome: Diagnostics - Myoglobin
Not specific to cardiac muscle; also found in skeletal muscle Faster than troponin - Often used to rule OUT a heart attack; "If low, there's no skeletal muscle breakdown OR heart attack"
53
Acute Coronary Syndrome: Diagnostics - LDH
Normally LDH2 > LDH1 If LDH1 > LDH2, it indicates an ischemic event Limitations: Levels rise very late into ischemic event
54
In the context of acute coronary syndrome, what distinguishes NSTEMI from unstable angina?
NSTEMI is associated with positive cardiac biomarkers indicating myocardial injury. (But without St segment elevation on the ECG)
55
STEMI: Management
Goal: Minimize myocardial damage - Preserve myocardial function - Prevent complication Initial management: MONA - Morphine - Oxygen - Nitroglycerin - Aspirin 24 hours later: - Beta blockers
56
What is a Percutaneous Coronary Intervention (PCI)​ ?
Opens blocked artery and restores blood flow to the injured area of myocardium Purpose: - Procedure treats the underlying atherosclerotic lesion - "Door to balloon" time < 60 minutes - Utilizes Coronary Artery Stent
57
Percutaneous Coronary Intervention (PCI): Coronary Artery Stent
Used during PCI How does it work? - Stent is introduced into blood vessel -Balloon is deflated and withdrawn​ - Stent stays in place permanently, holding vessel open and improving blood flow​ - Endothelial tissue heals over stent​
58
Percutaneous Coronary Intervention (PCI): Complications
- Perforation - Emboli - Coronary artery dissection - Arrhythmia
59
Percutaneous Coronary Intervention (PCI): Post procedure Care
Similar to care after cardiac cath - Monitor EKG and vitals - IV Hep as prescribed - Pressure dressing on site - Distal pulse check
60
Thrombolytics: What is it? "Door to needle" time? Contraindicated? Risk?
"Clot busters"; works by dissolving the thrombus within the coronary artery to allow for reperfusion - Does not treat underlying atherosclerotic vessel - Preferred if PCI is not an option - "Door to needle" time is <30 minutes Contraindicated: - Patients with underlying bleeding disorder Risk: - systemic hemorrhage
61
PCI / Thrombolytics: Inpatient Care
Meds: - Aspirin - Beta blockers - ACE inhibitors - Monitor vital signs, urine output, sodium, potassium, creatinine
62
Thrombolytics Therapy: Indications
Chest pain >20 min ST elevation in 2 contiguous leads Less than 12 hours from onset of symptoms
63
Thrombolytics Therapy: Contraindications
- Active bleeding - History of bleeding disorder, hemorrhagic stroke, cerebral AVM, recent surgery or major trauma, uncontrolled HTN, pregnancy
64
Thrombolytic Therapy: Nursing consideration
- Minimize unnecessary trauma: IM injections, blood draws - Monitor signs of reperfusion - Monitor for s/s bleeding: decreased h/h, tachycardia, hypotension
65
Cardiac Rehabilitation: Goals? Phases?
Goals: - Limit effects and progression of atherosclerosis Phase 1: - Inpatient, lot of education - When to call 911 - Med education Phase 2: - After discharge - Attends sessions 3x/week, lasting 1-6 months - Supervised EKG monitored exercise Phase 3: - Long term outpatient program - Self-directed, no EKG supervision
66
ACS: Interventions
Relieve s/s ischemia: - Administration of oxygen to maintain O2 sat - Administer meds as ordered - HOB elevated: improves tidal volume, decreases preload - Pain relief decreases workload of heart - Encourage patient to rest in bed Improve respiratory function: - Incentive spirometer - Cough and deep breathe - Frequent repositioning of patient Promote tissue perfusion:
67
Coronary Artery Bypass Graft (CABG): What is it? Function Indications
Open heart surgery; patient's own artery or vein is grafted and placed into the heart Grafted vessel bypasses the blocked artery and brings blood from ascending aorta Indications: - Alleviation of angina not controlled by meds or PCI - Treatment of multi vessel CAD or left main coronary artery stenosis - Vessel(s) must be at least 50-70% occluded
68
CABG: Cardiopulmonary Bypass System
"Hard to work on a moving target, aka the heart. Need something to replace the heart pumping blood and the lungs oxygenating blood." - Heart is completely stopped - Body is cooled to hypothermia to slow metabolic needs - Venous blood bypasses the heart during the procedure and removed from body at the vena cava - Blood is oxygenated, cooled and returned to the body - Blood is rewarmed at the end of the procedure
69
CABG: Alternative CABG Techniques
Off-Pump CABG: - Standard sternotomy incision - Slows heart using beta blockers, avoids use of CPB pump - Stabilizes heart using a device to hold it still Pros: Reduced short term morbidity Cons: Long term outcomes may be inferior to standard CABG Minimally Invasive Direct CABG: - Smaller incision using thoracotomy approach - Uses robotic system to place grafts - Indicated for one vessel or LAD disease - May or may not use CPB
70
CABG: Pre-Op Nursing Care
- NPO - Antiseptic shower with chlorhexidine - Tests: H&P, labs, coags, type and screen
71
CABG: Post-op Care
Patient teaching: - Post-op sternal precautions: no bending or heavy lifting, no raising arms - Cough and deep breathe, incentive spirometer, early and frequent ambulation - Warming blanket (cold d/t CPB) - Manage confusion - Monitor for impaired gas exchange:: ABG, cyanosis, O2 Sat - Critical care for >24 hours - Monitor for potential complications
72
How does ezetimibe (Zetia) work to treat hyperlipidemia?
Zetia helps lower cholesterol by blocking its absorption in the small intestine
73
A patient has chronic stable angina, when should they be taking their isosorbide mononitrate?
Everyday, even if the patient feels fine - Isosorbide mononitrate is a nitrate used for the long-term prevention of angina by dilating blood vessels and reducing the heart’s workload. It is taken daily to prevent chest pain, even when no symptoms are present. It is not meant for acute relief of chest pain (A), as short-acting nitrates like nitroglycerin are used in those situations
74
A patient with a history of unstable angina presents to the emergency department with chest. Which of the following electrocardiogram (EKG) findings is most commonly associated with unstable angina during an episode of chest pain?
T-wave inversion or ST-segment depression
75
A patient with a history of hypertension and heart failure is prescribed a beta-blocker. What can the patient expect to experience?
"This medication may cause me to feel more tired or fatigued.“ - Beta-blockers work by blocking the effects of adrenaline on the beta-adrenergic receptors, which leads to a decrease in heart rate and blood pressure. Patients may experience fatigue as a side effect due to the reduced heart rate and cardiac output.
76
Which of the following processes is most directly responsible for the development of ACS?
Rupture of an atherosclerotic plaque with subsequent thrombus formation
77
Which of the following best describes the pathophysiological difference between NSTEMI and STEMI?
NSTEMI is caused by partial coronary artery occlusion, while STEMI involves complete occlusion. - The primary pathophysiological difference between NSTEMI and STEMI is the degree of coronary artery occlusion. In NSTEMI, the artery is partially occluded, resulting in subendocardial ischemia. In contrast, STEMI involves a complete occlusion, leading to transmural (full-thickness) ischemia.
78
A nurse is caring for a 58-year-old male who presents to the emergency department with chest pain. The healthcare provider is trying to differentiate between unstable angina and myocardial infarction (MI). Which of the following clinical findings would best help the nurse differentiate between unstable angina and a myocardial infarction?
Elevated cardiac biomarkers are present only in myocardial infarction.
79
A patient arrives at the emergency department with severe chest pain that began 30 minutes ago. The healthcare provider suspects a STEMI and orders an electrocardiogram (ECG). Which of the following best describes the timing of ST-segment elevation in a STEMI?
ST-segment elevation only appears once troponin levels peak and resolves as soon as troponin levels start to decline.
80
Why would Cholesterol absorption inhibitors (ezetimibe) be used over bile acid sequestrants (Cholestyramine & colestipol)?
Cholesterol absorption inhibitors are tolerated better than bile acid sequestrants
81
Compare and descirbe the following for diagnosing an MI: Troponin CK MB Myoglobin LDH
Troponin: - Very specific to heart - Slow; 12-48 hours to peak CK-MB: - Less specific, can be elevated in muscle damage - Peaks 24 hours post-MI Myoglobin: - Not specific, can rule out MI if negative - Peaks 2-4 hours post injury LDH: - Normally LDH2 > LDH1 - LDH1 > LDH2 = ischemia - Late, slow into ischemic event
82
What is the ideal "door to balloon/PCI" time?
Less than 60 minutes