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Flashcards in Ischemic Heart Disease (CM) Deck (61):
1

The leading cause of death in the US

Ischemic Heart Disease

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Definition of myocardial ischemia

Angina Decreased coronary artery perfusion leading to demand of oxygen>supply

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Definition of myocardial injury

Occurs with ongoing ischemia, may either reverse to myocardial ischemia, or progress to myocardial infarction

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Definition of myocardial infarction

Irreversible cell death leading to impairment of electrical activity and contraction

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Cause of IHD

atherosclerotic obstruction of coronary arteries

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Modifiable risk factors for IHD

smoking HTN hypercholesterolemia diabetes

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Non-modifiable risk factors for IHD

age FHx (first degree relatives) gender--being a male (females not until post-menopausal)

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3 basic presentations of IHD

Stable angina (typical or Prinzmetal's) Unstable angina Acute MI

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Stable Angina characteristics

episodic chest pain, lasting minutes (5-15) that is often provoked by exertion/stress Relieved by rest/NTG Reversible ischemia

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EKG and cardiac enzymes--stable angina

EKG findings: ST depressions +/- T wave inversion or flattening that return to normal after attack Cardiac enzymes: normal b/c no cell death

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Prinzmetal's Angina

"Variant angina" Occurs at rest, usually at the same time of day ST elevation during attack, returns to baseline after Caused by coronary artery spasm (1/3 have normal coronary arteries) Usually relieved by NTG, give CCB prophylactically

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Unstable Angina

"crescendo angina or accelerated angina" a change in prior angina pattern 1. new onset of exertional angina 2. increased severity, frequency or duration of pain 3. more NTG to relieve pain 4. pain now comes at rest

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Typical mechanism of unstable angina

Rupture of coronary artery plaque, leading to platelet aggregation and thrombosis

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EKG findings of unstable angina

Similar to stable angina ST depression +/- T wave inversion/flattening that may persist for several hours before returning to normal May progress to MI

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Cardiac enzyme findings of unstable angina

Possibly normal elevations

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Prognosis of unstable angina

Can greatly improve chances of avoid MI and death by hospitalizing and treating agressively!!

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Acute MI

Irreversible cell death

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Acute MI EKG findings

ST elevation with evolving Q waves

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Acute MI EKG cardiac enzymes

elevated

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Acute Coronary Syndrome

encompasses the spectrum of presentations between unstable angina and acute MI

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Components necessary to Dx IHD

History Physical exam EKG Cardiac Enzymes CXR Echo Radionuclide scan Coronary angiography

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History

Single most important tool of chest pain evaluation

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Typical CP in Angina/MI

Location: substernal or left sided Radiation: to neck, jaw, left or both arms Quality: heaviness, pressure, tightness, squeezing Not positional or pleuritic Often brought on by physical exertion/stress Relieved by rest/NTG

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Associated symptoms of angina/MI CP

Anginal equivalents: SOB Diaphoresis Nausea Sometimes: dizziness, palpitations

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Populations that present atypically CP silent or atypical

Women Elderly Diabetics

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IHD presentation in women

Less likely to have CP, more likely to have: Pain in back, neck or jaw Diaphoresis Nausea

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Physical exam findings of MI

Can often be deceptively normal OR: Anxious, pale and diaphoretic May have inc'd HR and BP by inc'd sympathetic stimulation May have dec'd HR in inferior MI May have dec'd BP because myocardial damage New murmur may suggest papillary muscle rupture, ventricular septal rupture, or mitral regurgitation May see signs of congestive heart failure

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Does a normal EKG rule out MI?

NO! Only 50% of MI's initially have class ST elevation Use in conjunction with H&P and serial cardiac enzymes to r/o

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EKG changes in AMI

ST elevation Variable T wave changes Followed hours later by permanent Q waves Possible new bundle branch block Reciprocal changes (help r/o pericarditis)

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Reciprocal changes in EKG

mirror image ST-T changes (usually ST depression) in leads distant to primary ST elevations

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Classic EKG evolution in MI

Hyperacute T waves Giant R waves ST elevation Q waves

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Hyperacute T waves

Tall, broad T waves that are transient and occur within minutes of interruption of blood flow

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Giant R-waves

Form when R wave merges with elevating ST segment Last only minutes

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ST elevation

classic sign of AMI-significant when >1mm may persist hour to days before returning; occasionally indefinitely

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Q waves

Significant when wider than one box, 1/3 the height of the QRS Develop 8-12 hrs after MI Can be normal in inferior leads in young men

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Cardiac enzymes in MI

Rate of rise and peak is proportional to severity Normal serial enzymes r/o possibility of MI, but not underlying IHD

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Myoglobin

Not specific because also in skeletal muscle Rises early: 1-2 hrs Normalize 1st day

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CK-MB

Specific to cardiac muscle, not as widely used Earliest risk: 3-4 hrs Normalize 2nd day

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Troponin

Sensitive and specific (most useful) Rise 3-6 hrs Normalize 7th day

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Anterior leads

V1-V4

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Inferior leads

II, III, aVF

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Lateral leads

I, aVL, V5, V6

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Artery obstructed in anterior MI

LAD

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Artery obstructed in lateral MI

left circumflex

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Artery obstructed in anterolateral MI

Main left coronary artery Widowmaker

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Artery obstructed in inferior MI

90% right coronary 10% left circumflex

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Artery obstructed in inferiolateral MI

Right coronary

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Q image thumb

Lateral MI 

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Q image thumb

Anterior MI 

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Q image thumb

Inferior MI 

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Complications of Acute MI 

  • Dysrhythmia 
  • LV pump failure/cardiogenic shock 
  • Papillary muscle insufficnecy 
  • Ventricular septal rupture
  • cardiac rupture 
  • thromboembolism 
  • pericarditis 
  • ventricular aneurysm 
  • right ventricular infarction 

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Major cause of out of hospital mortality in context of MI 

Dysrhythmia 

  • Occurs in >90% of AMI
  • Any arrhythmia possible 
  • Sinus brady/tach
  • PVC's (Very common)
  • AV block 
  • V. tach/V.fib (most lethal)

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LV pump failure cause 

Large anterior or anterolateral infarctions cause death of tissue 

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Signs of LV pump failure 

dyspnea 

rales in lung bases

hypoxemia 

hypotension 

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Cause of cardiogenic shock

massive anterior or anterolateral infarction that results in >50% loss of myocardium

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Clinical signs of cardiogenic shock

hypotension, tachycardia 

reduced urine output 

confusion 

cold extremities 

Mortality >65%

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Papillary muscle insufficiency 

muscle becomes ischemic/infarcted and may rupture

leads to mitral regurgitation (apical systolic murmur)

Most commonly seen with inferior MI 

Dx with echocardiogram

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Cardiac Rupture

Infarcted wall of heart ruptures, usually within 14 days of MI 

Sudden hypotension, pericardial tamponade, cardiac arrest

95% mortality 

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Thromboembolism 

Decreased motion of myocardium may lead to thrombus formation that may embolize 

MC in large anterior MI 

Dx: echo 

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Pericarditis 

inflammation adjacent ot area of infarction with classic friction rub 

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Ventricular aneurysm 

May lead to arrhythmias or thrombus/embolus