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141 Cards in this Set

  • Front
  • Back
myocardial supply-demand imbalance which can be chronic (_____), Sub Acute (_____) and Acute (___).
Stable Angina; Unstable Angina or Acute Coronary Syndromes; Acute Myocardial Infarction
Cause of angina
Imbalance Between Myocardial Blood supply and Metabolic Requirement
What is angina usually like?
Angina Pectoris is chest pain, described as a fullness or a tightness which is typically midsternal, but may begin in the upper abdomen or the neck or jaw with radiation to the left side or left arm. The symptom is usually not sharp, severe or stabbing, but rather a discomfort.
What is the typical associated symptom with angina?
Shortness of breath.

In some patients, particularly elderly, this may be the primary symptom.
_______ is the most common cause of Angina Pectoris.
Atherosclerotic coronary disease
5 general causes of myocardial ischemia (and thus angina)
1) Atherosclerotic coronary disease

2) Coronary vasospasm

3) Myocardial hypertrophy

4) Congenital abnormalities of coronary arteries

5) Angina pectoris with normal coronaries (rare)
The typical spasm presentation, known as Prinzemetal’s angina : characteristics
The typical spasm presentation, known as Prinzemetal’s angina is characterized by rest pain typically occurring in the early morning hours associated with ventricular dysrrhythmias including heart block and/or ventricular arrhythmias.
T/F Angina caused by coronary spasm usually by "normal" coronaries
Kinda both T and F. "normal" coronaries which usually have early endothelial damage.
Drug associated with coronary spasm
cocaine
In the case of Aortic Insufficiency, severe regurgitation causes retrograde aortic flow during (systole, diastole) essentially sucking flow from the coronaries during the normal maximal filling period.
diastole
Cause of angina in conditions of myocardial hypertrophy
Demand exceeds supply due to excess muscle mass.
How is a congenital coronary abnormality such as Left Main or LAD arising frmo R coronary artery a cause of ischemia?
It will usually course between the aorta and pulmonary artery. During exercise these vessels expand and occlude flow in the coronary arteries.

Associated with exercise-induced ischemia.
What is the first change to occur after coronary occlusion?
Diastolic change - a loss in compliance
In the case of transmural ischemic changes, there may be a total loss of systolic function resulting in what?
dyskinetic wall motion
What EKG changes are seen in early coronary ischemia?
See ST segment changes right before dyskinetic wall motion
When does angina occur after ischemia?
It's one of the last symptoms to occur before permanent changes. Before angina, there is decreased compliance, then ST changes, then dyskinetic wall motion.
In normal patients, what happens to systolic wall motion with exercise? In ischemic patients?
Normals - systolic wall motion globally increases with exercise

Ischemic - segmental changes occur in ischemia zones
Diastolic consequences of myocardial ischemia and what patients perceive
Reduced compliance increases left ventricular filling pressure and pulmonary pressure which patients perceive as shortness of breath.
Systolic consequences of myocardial ischemia and what patients perceive
Changes in systolic function produce fatigue secondary to low cardiac output.
T/F Angina symptoms mirror the extent of coronary disease
F
EKG changes that occur with myocardial ischemia.
flat ST segment depression
How are wall motion changes that occur with ischemia detected clinically?
Stress echo; Nuclear scans
What is the test to demonstrate reversible flow abnormalities?
Perfusion - use thallium sestimibi
What are stress tests useful for?
Diagnose ischemia and thus coronary disease.

Must induce stress either with drugs that increase myocardial work or with exercise. (also "coronary steal" methods).
what are the 3 major ischemic markers used after stress stimulation to determine if there's ischemia?
1) ECG changes

2) Changes in wall motion

3) Nuclear perfusion scans

2 and 3 tend to be better tests than 1.
What are physiologic factors that if found in a stress test are indicators of risk?
Poor exercise performance

Fall in blood pressure during non-peak exercise

Ischemic endpoints at low exercise.
What are EKG changes that if found in a stress test are indicators of risk?
>2 mm ST depression or ST elevation
What are perfusion scan results that if found in a stress test are indicators of risk?
large or multiple defects

Increase cardiac pool, increased lung uptake
What are LV function factors that if found in a stress test are indicators of risk?
Ejection fraction <35%

Acute decrease >5%

Multiple defects
most specific way to ID coronary obstructions
Coronary angiography
How is coronary angiography performed?
Inject coronary arteries with catheters inserted from the groin with radiopaque material to outline the coronary lumen.

Allows ID of focal atherosclerotic lesions as well as LV function.
What is the usual treatment for unstable angina?
Coronary angiography

Early revascularization
What is the workup/treatment for stable angina?
Stress Test

If there's evidence of ischemia, consider the risk level:

Low risk: pharmacological tx. (medical mgmt)

high risk: Cath and revascularization as anatomy warrants
Medical therapy is principally directed at ______ while angioplasty and bypass surgery improve symptoms by improving myocardial blood flow.
reducing myocardial oxygen demand
Medical treatment of patients with vasospasm causing reduced blood supply
Nitrates and Calcium Channel Blockers
How do beta blockers reduce demand?
They lower the heart rate and decrease contractility
How do nitrates reduce ischemia?
They reduce preload and thus decrease myocardial wall stress
How do calcium channel blockers work to reduce demand?
They reduce afterload, against reducing myocardial wall stress
Coronary angioplasty: what is it used for?
percutaneous method of revascularization aimed at increasing coronary blood flow
What is restenosis and what is it a complication of?
A proliferative response to local injury that causes recurrent stenosis in 20% of patients.

It's a complication of angioplasty.
What has reduced restenosis rates from angioplasty?
The use of stents - small metal devices that improve the lumen.
What is coronary artery bypass grafting?
Direct bypass of coronary stenoses using arterial conduits and venous bypass grafts
What type of patient is coronary artery bypass surgery used in?
Those with extensive multivessel disease, left main disease and severe left ventricular dysfunction.
Patients who receive at least one (arterial, venous) graft have a much better prognosis in CABG.
arterial
What is an unstable atherosclerotic lesion characterized by?
Plaque rupture, thrombus formation, platelet adhesion, and often reduced flow.
Why does unstable angina occur at rest?
Because it's caused by a sudden decrease in flow from a plaque rupture
Percutaneous transluminal coronary angioplasty is aka
balloon angioplasty.

a technique used to dilate an area of arterial blockage with the help of a catheter that has an inflatable small sausage-shaped balloon at its tip
Acute treatment strategies of unstable angina are aimed at what?
Acute treatment strategies are aimed at stabilizing the plaque and reducing the probably of continued clot formation. Aspirin, heparin or Low Molecular Weight Heparin, Clopidogrel, IIB,IIIA antagonists all appear to improve outcome. Current practice also includes coronary angiography with frequent revascularization.
Most common etiology of acute MI
presence of intracoronary thrombus
To meet criteria for MI, there must be what?
necrosis
What is a Type I MI?
Supply/demand mismatch
<b>Due to decreased supply</b>.

Eg., thrombus
vasoconstriction
What is a Type II MI?
Supply/demand mismatch
<b>Due to increased demand</b>.

Eg., heart rate
blood pressure
afterload
Anatomic Classification of MI : Transmural vs Non-transmural
Transmural: involves >50% of ventricle wall, predominantly caused by total and persistent coronary occlusion

Non-transmural (subendocardial): generally involves more distal vessels supplying <50% of inner half of ventricular wall, along the LV cavity.
Classification by ECG of chronic MI
Q-wave vs Non-Q-wave
Classification by ECG of Acute MI
STEMI (ST elevation MI) vs. Non STEMI
What is a STEMI?
ST elevation MI.

Patient presents with ST elevation on the initial ECG, usually synonymous with complete vessel occlusion, leading to <b>transmural infarction with resultant Q waves.</b>
What is a NSTEMI?
Non ST elevation MI.

MI resulting without presence of ST elevation on EKG, considered synonymous with complete vessel occlusion, typically leading to transmural infarction with resultant Q waves.
The at-risk myocardium is larger in a STEMI or NSTEMI?
STEMI
How does the clot composition differ in a STEMI vs NSTEMI?
STEMI: thrombus-rich

NSTEMI: platelet rich
How does the coronary artery occlusion in STEMI vs. NSTEMI?
In a STEMI, it's usually persistently and completely occluded unless reperfusion treatment is given.

In NSTEMI: Significant stenosis with intermittent occlusion.
How are MI locations generally defined?
ECG zones: inferior, lateral, anterior, true posterior (though there can be overlap).
An anterior MI will show changes primarily in what leads and why?
Leads I, V2, V3, and V4. These are the ones closest to the front of the chest.
An anterolateral MI will show changes primarily in what leads and why?
Leads I, aVL, V5, V6

These are positioned closest to the L side of the chest
A diphragmatic/inferior MI will show changes primarily in what leads and why?
Leads II, III, aVF, V6
these are most inferior leads.
A true posterior MI will show changes primarily in what leads and why?
Leads V1
"Classic" presentation of acute MI
Severe, crushing sensation, lasting greater than 30-60 minutes, retrosternal or left precordial and frequently referred to neck, jaw, or arm.

Only occurs in a minority of patients.
What aspects of pain should be assessed in the interview?
Location, Onset, Character, Severity, Radiation, Alleviating/Exacerbating factors, Time course, H/o similar episodes, Associated sx
What are important associated symptoms of MI?
Nausea/vomiting, diaphoresis, shortness of breath.
"Atypical" presentation of MI
Stabbing, pleuritic, pin prick, sharp
"Typical" presentation of MI
Pressure, tightness, squeezing, indigestion, burning, similar to prior ACS events
Atypical presentations of MI are most common in what groups?
Elderly
Women
hypertension
How is the presentation for MI in the elderly different than for younger?
Over half won't have pain but will present with dyspnea, AMS, and other sx.
Traditional Coronary Artery Disease risk factors are just as important in dx'ing AMI as chest pain characteristics, ECG, and age.
F. They're less important for IDing patients with Acute Coronary Syndrome.
T/F Up to 20% of MIs may be clinically silent.
T
Peak incidence time for MIs
Close to wakening, 8am-12 noon.
Non-cardiac causes of chest pain
Pulmonary Embolism
<b>GI</b>
Costochondritis
Psychiatric
Panic disorder
Depression
Cryptogenic
T/F The ECG provides important information regarding infarct location
T
T/F The ECG is a very sensitive tool for picking up MIs.
False, it's less than 50%. Serial ECGs may be better.
Main marker used to dx MI
troponin
T/F elevations in troponin are always MI
F. There is a huge list of other things it could be.
PE findings in acute MI
Pallor
Rales
JVD
S3 or S4
New murmur
Cyanosis
Friction rub (pericarditis)
Muffled heart sounds
Fever
What are compensatory mechanisms after MI?
Increased sympatho-adrenal activity

Increased LV EDV (dilation)

Hyperfunction of non-infarcted segments
What are consequences of Increased sympatho-adrenal activity as a compensatory mech after MI?
increased systemic vascular resistance (SVR)

propensity toward arrhythmias

exacerbation of ischemia (incr O2 consumption)

inotropic effects (increased contractility)

chronotropic effects (increased heart rate)
What are consequences of Increased LV EDV as a compensatory mech after MI?
increased stroke volume
increased LV end diastolic pressure
increased wall tension
increased O2 consumption
What are consequences of hyperfunction of non-infarcted segments as a compensatory mech after MI?
May induce remote ischemia if there are flow-limiting stenoses of the coronaries subserving those areas.

May exacerbate ischemia via "steal" from collateral circulation.
Infarct expansion: defn
Fixed, permanent, regional thinning and dilation of the infarct zone.

<b>Not an increase in the mass of the infarct.</b>
infarct expansion: where is the original lesion located?
transmural, anterior and antero-lateral
How do ventricular loading conditions affect infarct expansion?
Anterior and antero-lateral lesions are more prone to expand.
What drugs may increase risk of infarct expansion?
NSAIDs, steroids
What drugs may decrease risk of infarct expansion?
ACE inhibitors
Complications of infarct expansion
Mural thrombus formation

Ventricular aneurysm formation
Infarct extension: defn
additional necrosis of myocardial tissue post-MI (2-10 days later).

There is an <b>increase in total mass of infarcted tissue!</b>
What is cardiogenic shock?
Most serious complication of MI. Pump failure.
What factors make cardiogenic shock more likely to occur post-MI?
1) >40% of myocardium is involved.

2) Atrial fibrillation

3) Supraventricular arrhythmias

4) Brady arrhythmias and heart-block

5) Administration of negative inotropic agents (beta blockers etc)

These all have to do with increased demand or decreased supply.
Which artery involvement is more associated wtih cardiogenic shock?
LAD.
T/F Arrythmias occur in over 90% of AMIs
T
Most common Arrythmia post MI
PVCs
Most AMI related deaths prior to arrival at hospital can be attributed to what?
Ventricular tachycardia/fibrillation (Arrythmia)
What type pf conduction changes are especially common with inferior/posterior AMIs?
atrial - ventricular cnoduction changes.
What is prognostic value of presence of AV conduction change with anterior MI?
Though less common than in inferior/posterior AMIs, they portend a poor prognosis.
What artery supplies the AV node, blockage of which may cause AV block?
Right coronary artery.
What is a "junctional" escape rhythm?
Junctional rhythm describes an abnormal heart rhythm resulting from impulses coming from a locus of tissue in the area of the atrioventricular node, the "junction" between atria and ventricles.
T/F junctional (AV) escape rhythms are especially dangerous and require pacemakers usually
F.
T/F Lower areas of block resulting in wide complex ventricular escape rhythms require pacemakers
T, if reperfusion is delayed. Not usually a permanent pacemaker.
delayed heartbeat originating not from the atrium but from an ectopic focus somewhere in the AV junction
Junctional escape beat
The ______ artery supplies the right bundle and superior segment of left bundle
LAD
What is the escape rhythm from an anterior (eg., LAD) infarction like?
Ventricular: slow, wide-complex, not reliable/stable, associated with hypotension.

MOST SERIOUS.

Requires pacemaker insertion, at least temporarily.
Most common result of left ventricular free wall rupture
hemopericardium resulting in tamponade and death
What happens when there's a ventricular septum rupture?
Left --> Right shunt with elevation of right sided pressures that causes <b>pulmonary edema</b>. Size of the defect varies depending on the size of the infarct, and will determine the magnitude of the shunt.
After what type of AMIs are ventricular septum and LV free wall ruptures most common?
Anterior
After what type of AMIs are papillary muscle (those that attach to the AV valves and close them via the chordae tendinear) ruptures most common?
Inferior MI
Which papillary muscle is more likely to rupture - postero-medial or anterolateral?
posteromedial
What is the timing of ruptures post MI?:
There's bimodal timing.

The first is <24 hours. The second is in 3-5 days.
What is papillary muscle dysfunction post MI from?
Not a mechanical disruption (so not a rupture) but rather a loss or diminution of contractile ability.
Where are ventricular aneurysms most likely to occur?
Apically (LV)
T/F Isolated RV infarction is common
F.
What coronary artery must be occluded for RV infarction to occur?
Right Coronary ARtery
Sx of RV infarct
Profound hypotension with poor CO as a result of not enough blood getting to the LV.
tx of RV infarct
volume infusion to elevate the Right sided pressure and enhance LV filling pressure and volume
Pericarditis implies the occurrence of what type of MI?
Transmural
Remains one of the most accurate predictors of subsequent morbidity and mortality
LV function
Variables that are the most important for predicting 30 day mortality in STEMI and non STEMI patients
Age
Blood pressure
Killip classification
Systolic function (ejection fraction)
Heart rate
Infarction location
Prior infarction
Renal function
What is the Killip classificaiton?
Amount of remaining LV function
Killip Class I
No evidence of LV failure
Killip Class II
S3 gallop or basal rales
Killip Class III
pulmonary edema
Killip Class IV
cardiogenic shock
Pharmacologic revascularization as tx for AMI: what categories of drugs?
fibrinolytics
anti-platelet
anti-coagulant/thrombotic
Mechanical revascularization
as tx for AMI: what techniques?
primary percutaneous coronary interventions (PCI):
Can be done with a variety of tools—balloon, stents, atherectomy, rotoblader, laser, thrombectomy
rescue PCI
Thrombolytics: defn
Drugs that can "dissolve" or lyse clots (aka fibrinolytics)
What is t-PA?
Tissue plasminogen activator. Human protein normally produced by endothelial cells.
What is r-PA and TNK-t-PA
Thrombolytic agents made by recombinant technology with post-transcriptional engineering and chemical restructuring, respectively.
Mortality reduction from r-PA, t-PA and TNK-t-PA is proportional to what?
The time that they're administered after the onset of symptoms. Usually given within 30 minutes of arrival to ED.
T/F Fibrinolytics dissolve the clot and also help correct underlying arterial injury
F. Dissolve clot ONLY.
Aspirin and heparin are used to help reduce propensity for clot to reform. Aspirin works through an anti _____ effect while heparin works through and anti ____ effect
platelet; thrombin
T/F Thrombolytics are given to dissolve the clot, and then aspirin and heparin are given to prevent the clot from reforming
T
There is no proven benefit frmo the use of fibrinolytics for ischemia in the absence of _____
STEMI (ST elevation used as a surrogate for vessel occlusion)
2 Indications for Fibrinolytics therapy (IMPORTANT)
1) ST-segment elevation >1mm in two or more limb leads or in adjacent precordial leads (signs of a true posterior MI)

2) Symptoms consistent with MI unresponsive to initial nitroglycerin and not lasting >6 to 12 hours
Absolute contraindications for fibrinolytics
Active bleeding

Prior Intracranial bleeding

Intracranial neoplasm

Recent stroke except acute ischemic stroke (within 3-4.5 hours)

Hypertension not responsive to tx
What is a major complication of fibrinolytics therapy?
Intracranial hemorrhage
What is primary coronary intervention (PCI)?
The preferred treatment for STEMI. Mechanical revascularization