Ischemic Heart Disease (CM) Flashcards
The leading cause of death in the US
Ischemic Heart Disease
Definition of myocardial ischemia
Angina Decreased coronary artery perfusion leading to demand of oxygen>supply
Definition of myocardial injury
Occurs with ongoing ischemia, may either reverse to myocardial ischemia, or progress to myocardial infarction
Definition of myocardial infarction
Irreversible cell death leading to impairment of electrical activity and contraction
Cause of IHD
atherosclerotic obstruction of coronary arteries
Modifiable risk factors for IHD
smoking HTN hypercholesterolemia diabetes
Non-modifiable risk factors for IHD
age FHx (first degree relatives) gender–being a male (females not until post-menopausal)
3 basic presentations of IHD
Stable angina (typical or Prinzmetal’s) Unstable angina Acute MI
Stable Angina characteristics
episodic chest pain, lasting minutes (5-15) that is often provoked by exertion/stress Relieved by rest/NTG Reversible ischemia
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
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
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
Typical mechanism of unstable angina
Rupture of coronary artery plaque, leading to platelet aggregation and thrombosis
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
Cardiac enzyme findings of unstable angina
Possibly normal elevations
Prognosis of unstable angina
Can greatly improve chances of avoid MI and death by hospitalizing and treating agressively!!
Acute MI
Irreversible cell death
Acute MI EKG findings
ST elevation with evolving Q waves
Acute MI EKG cardiac enzymes
elevated
Acute Coronary Syndrome
encompasses the spectrum of presentations between unstable angina and acute MI
Components necessary to Dx IHD
History Physical exam EKG Cardiac Enzymes CXR Echo Radionuclide scan Coronary angiography
History
Single most important tool of chest pain evaluation
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
Associated symptoms of angina/MI CP
Anginal equivalents: SOB Diaphoresis Nausea Sometimes: dizziness, palpitations
Populations that present atypically CP silent or atypical
Women Elderly Diabetics
IHD presentation in women
Less likely to have CP, more likely to have: Pain in back, neck or jaw Diaphoresis Nausea
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
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
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)
Reciprocal changes in EKG
mirror image ST-T changes (usually ST depression) in leads distant to primary ST elevations
Classic EKG evolution in MI
Hyperacute T waves Giant R waves ST elevation Q waves
Hyperacute T waves
Tall, broad T waves that are transient and occur within minutes of interruption of blood flow
Giant R-waves
Form when R wave merges with elevating ST segment Last only minutes
ST elevation
classic sign of AMI-significant when >1mm may persist hour to days before returning; occasionally indefinitely
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
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
Myoglobin
Not specific because also in skeletal muscle Rises early: 1-2 hrs Normalize 1st day
CK-MB
Specific to cardiac muscle, not as widely used Earliest risk: 3-4 hrs Normalize 2nd day
Troponin
Sensitive and specific (most useful) Rise 3-6 hrs Normalize 7th day
Anterior leads
V1-V4
Inferior leads
II, III, aVF
Lateral leads
I, aVL, V5, V6
Artery obstructed in anterior MI
LAD
Artery obstructed in lateral MI
left circumflex
Artery obstructed in anterolateral MI
Main left coronary artery Widowmaker
Artery obstructed in inferior MI
90% right coronary 10% left circumflex
Artery obstructed in inferiolateral MI
Right coronary
Lateral MI
Anterior MI
Inferior MI
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
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)
LV pump failure cause
Large anterior or anterolateral infarctions cause death of tissue
Signs of LV pump failure
dyspnea
rales in lung bases
hypoxemia
hypotension
Cause of cardiogenic shock
massive anterior or anterolateral infarction that results in >50% loss of myocardium
Clinical signs of cardiogenic shock
hypotension, tachycardia
reduced urine output
confusion
cold extremities
Mortality >65%
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
Cardiac Rupture
Infarcted wall of heart ruptures, usually within 14 days of MI
Sudden hypotension, pericardial tamponade, cardiac arrest
95% mortality
Thromboembolism
Decreased motion of myocardium may lead to thrombus formation that may embolize
MC in large anterior MI
Dx: echo
Pericarditis
inflammation adjacent ot area of infarction with classic friction rub
Ventricular aneurysm
May lead to arrhythmias or thrombus/embolus
