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111 Cards in this Set

  • Front
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Stable Angina Pectoris

8 Risk factors
* Diabetes mellitus (DM)
* Hyperlipidemia—elevated LDL
* Hypertension (HTN)
* Cigarette smoking
* Age (men >45 years; women >55 years)
* Family history of premature coronary artery disease (CAD) or myocardial infarction (MI) in first-degree relative: men <45 years; women <55 years
* Low levels of high-density lipoprotein (HDL)
* Elevated homocysteine levels
Prognostic indicators of CAD
* Left ventricular function (ejection fraction [EF])
o Normal >50%
o If <50%, associated with increased mortality
* Vessel(s) involved (severity/extent of ischemia)
o Left main coronary artery–poor prognosis because it covers approximately two thirds of the heart.
o Two- or three-vessel CAD–worse prognosis.
Coronary artery disease (CAD) can have the following clinical presentations:
* Asymptomatic
* Stable angina pectoris
* Unstable angina pectoris (USA)
* Myocardial infarction (MI)
* Sudden cardiac death
Stable Angina Pectoris

Clinical features (ie HPI)
*Chest pain or substernal pressure sensation
o Lasts less than 10 to 15 minutes (usually 1 to 5 minutes)
o Frightening chest discomfort, usually described as heaviness, pressure, squeezing; rarely described as frank pain
*Brought on by exertion or emotion
* Relieved with rest or nitroglycerin
Stable Angina Pectoris

Stress ECG (exercise testing) is used in the following situations:
* To confirm diagnosis of angina
* To evaluate response of therapy in patients with documented CAD
* To identify patients with CAD who may have a high risk of acute coronary events
Diagnosis (of CAD)
WRT

Resting ECG
* Usually
* Q waves
* ST segment or T wave abnormalities
* Usually normal in patients with stable angina
* Q waves are consistent with a prior myocardial infarction.
* If ST segment or T wave abnormalities are present during an episode of chest pain, then treat as for unstable angina.
Diagnosis (of CAD)

next step in patients with normal resting ECG
determine whether the patient is capable of performing treadmill exercise. If so, proceed to an exercise stress test.
Stress ECG

sensitivity
75% sensitive if patients are able to exercise sufficiently to increase heart rate to 85% of maximum predicted value for age.
Stress ECG

positive findings
-Exercise-induced ischemia results in subendocardial ischemia, producing
-ST segment depression.
-Other positive findings include
-onset of heart failure
-ventricular arrhythmia
-hypotension.
Patients with a positive stress test result should
undergo cardiac catheterization.

both for EKG or Echo
Stress echo

procedure and what it looks for
Performed before and immediately after exercise. Exercise-induced ischemia is evidenced by wall motion abnormalities (e.g., akinesis or dyskinesis) not present at rest.
Advantages of stress echo
over stress ECG. It is more sensitive in detecting ischemia, can assess LV size and function, and can diagnose valvular disease.
Stress Thallium

importance of them. What do you need to determine
It is important to determine whether the ischemia is reversible, i.e., whether areas of hypoperfusion are perfused over time as blood flow eventually equalizes
PTCA
aka
percutaneous transluminal coronary angioplasty
CABG
aka
coronary artery bypass graft
Stress Thallium

why is it important to determine whether ischemia is reversible,
Areas of reversible ischemia may be rescued with percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass graft (CABG). Irreversible ischemia, however, indicates infarcted tissue that cannot be salvaged.
Stress Thallium

pros and cons
Perfusion imaging increases the sensitivity and specificity of exercise stress tests, but is also more expensive.
pharmacologic stress test.

agents used
IV adenosine, dipyramidole, or dobutamine
pharmacologic stress test.

mechanism of agents
#IV adenosine and dipyramidole cause generalized coronary vasodilation. Because diseased coronary arteries are already maximally dilated at rest to increase blood flow, they receive relatively less blood flow when the entire coronary system is pharmacologically vasodilated.

#Dobutamine increases myocardial oxygen demand by increasing heart rate, blood pressure, and cardiac contractility.
Holter monitoring

what and why
(ambulatory ECG) can be useful in detecting silent ischemia (i.e., ECG changes not accompanied by symptoms).
definitive test for CAD
Cardiac catheterization with coronary angiography
Cardiac catheterization with coronary angiography

what does it mean and what to do if If coronary artery disease is severe
If coronary artery disease is severe (e.g., left main or three-vessel disease), refer patient for surgical revascularization (CABG).
Two Conditions Termed Syndrome X
Syndrome X
describe Syndrome X
* Exertional angina with normal coronary arteriogram: chest pain after exertion without coronary stenoses at cardiac catheterization.
* Exercise testing and nuclear imaging show evidence of myocardial ischemia.
* Prognosis is excellent.
describe Metabolic Syndrome X
Any combination of hypercholesterolemia, hypertriglyceridemia, impaired glucose tolerance, diabetes, hyperuricemia, HTN
indications for cardiac catheterization
* positive stress test
* angina in any of the following situations: when noninvasive tests are nondiagnostic, despite medical therapy, soon after MI, or is a diagnostic dilemma.
*If patient is severely symptomatic and urgent diagnosis and management are necessary
* For evaluation of valvular disease, and to determine the need for surgical intervention
A stress test is generally considered positive if the patient develops any of the following during exercise
S-T segment depression,
chest pain,
hypotension,
significant arrhythmias.
CAD Treatment
WRT risk factors
* Smoking cessation
* HTN—vigorous BP control reduces the risk of CHD, especially in diabetic patients.
* Hyperlipidemia—reduction in serum cholesterol reduces CHD risk.
*DM—
* Obesity—weight loss modifies other risk factors
* Exercise
* Diet: Reduce intake of saturated fat (<7% total calories) and cholesterol (<200 mg/day).
* Hyperhomocystinemia–value of treating yet to be established.
CAD Treatment

role of aspirin
* Indicated in all patients with CAD
* Decreases morbidity—reduces risk of MI
CAD Treatment

role of beta blockers
Reduce HR, BP, and contractility, thereby decreasing cardiac work (i.e., β-blockers lower myocardial oxygen consumption)
CAD Treatment

role of Nitrates
-mech
-how they help
-wrt exercise
-wrt prognosis
-wrt administration
cause generalized vasodilation

* Relieve angina; reduce preload, therefore the load and oxygen demand.
* May prevent angina when taken before exertion
* Effect on prognosis is unknown; main benefit is symptomatic relief
* Can be administered orally, sublingually, transdermally, or intravenously
CAD Treatment

role of Calcium channel blockers
-mech
-when
Cause coronary vasodilation and afterload reduction

Now considered a secondary treatment when β-blockers and/or nitrates are not fully effective.
CAD Treatment

role of ACEI's
If CHF is also present, treatment with ACE inhibitors and/or diuretics may be indicated as well.
CAD Treatment

role of Revascularization
May be preferred for high-risk patients, although there is some controversy whether revascularization is superior to medical management for a patient with stable angina and stenosis >70%.
CAD Treatment

what is Revascularization
Two methods—PTCA and CABG
CAD Treatment

problems with Revascularization
* controversy whether revascularization is superior to medical management for a patient with stable angina and stenosis >70%.

*does not reduce incidence of MI, but does result in significant improvement in symptoms.
CAD Treatment

definition and treatment for
all patients
Risk factor modification and aspirin are indicated in all patients
CAD Treatment

definition and treatment for
Mild disease
#Mild disease (normal EF, mild angina, single-vessel disease)

* Nitrates (for symptoms and as prophylaxis) and a β-blocker are appropriate.
* Consider calcium channel blockers if symptoms continue despite nitrates and β-blockers.
CAD Treatment

definition and treatment for
Moderate disease
#Moderate disease (normal EF, moderate angina, two-vessel disease)

* If the above regimen does not control symptoms, consider coronary angiography to assess suitability for revascularization (either PTCA or CABG).
CAD Treatment

definition and treatment for
Severe disease
#Severe disease (decreased EF, severe angina, and three-vessel/left main or left anterior descending disease)

* Coronary angiography and consider for CABG
Percutaneous Transluminal Coronary Angioplasty (PTCA)

*who needs
*best for
*problem and %'s
*wrt stents
* Should be considered in patients with one- or two-vessel disease
* Best if used for proximal lesions
* Restenosis is a significant problem (up to 40% within first 6 months); however, if there is no evidence of restenosis at 6 months, it usually does not occur.
* Stents significantly reduce the rate of restenosis.
Coronary Artery Bypass Grafting (CABG)

*who needs
Indicated in patients with
*left main disease,
* three-vessel disease with reduced left ventricular function,
*two-vessel disease with proximal LAD stenosis,
*or severe ischemia for palliation of symptoms
Treatment of choice in patients with high-risk CAD
Coronary Artery Bypass Grafting (CABG)
Side effects of nitrates
* Headache
* Orthostatic hypotension
* Tolerance
* Syncope
Unstable Angina Pectoris

Pathophysiology
oxygen demand is unchanged. Supply is decreased secondary to reduced resting coronary flow. This is in contrast to stable angina, which is due to increased demand.
The following patients may be said to have Unstable Angina Pectoris
* Patients with chronic angina with increasing frequency, duration, or intensity of chest pain
* Patients with new-onset angina that is severe and worsening
* Patients with angina at rest
Acute coronary syndrome

*cause
*who it applies to
* The clinical manifestations of atherosclerotic plaque rupture and coronary occlusion
* Term generally refers to unstable angina or acute MI
Unstable Angina Pectoris

wrt stress test
These patients should be stabilized with medical management before stress testing or should undergo cardiac catheterization initially.
Unstable Angina Pectoris vs NSTEMI
often considered together because it is very difficult to distinguish the two based on patient presentation. If cardiac enzymes are elevated, then the patient has non-ST segment elevation MI.
The ESSENCE trial showed
in Unstable Angina Pectoris and NSTEMI MI, risk of death, MI, or recurrent angina was lower in the enoxaparin group than in the heparin group and The need for revascularization was also lower in the enoxaparin group.
what 2 things have not been proven to be beneficial in unstable angina.
Thrombolytic therapy and calcium channel blockers
Unstable Angina Pectoris

intial Tx before medical managment
Hospital admission on a floor with continuous cardiac monitoring. Establish IV access and give supplemental oxygen. Provide pain control with nitrates (below) and morphine.
Unstable Angina Pectoris

medical management
# Aspirin
# β-Blockers – first-line therapy if there are no contraindications
# Low-molecular-weight heparin (LMWH) (IV) or unfractionated heparin
#Nitrates are first-line therapy.
#Glycoprotein IIb/IIIa inhibitors (abciximab, tirofiban)
Role and Tx guidlines for Low-molecular-weight heparin (LMWH) (IV) or unfractionated heparin in Unstable Angina Pectoris
# Should be continued for at least 2 days
# Keep PTT at 2 to 2.5 times normal if using unfractionated heparin; PTT not followed with LMWH
# Enoxaparin is the drug of choice based on clinical trials (see Quick Hit on ESSENCE trial)
name and uses of Glycoprotein IIb/IIIa inhibitors in unstable angina
Glycoprotein IIb/IIIa inhibitors (abciximab, tirofiban) can be helpful adjuncts in USA, especially if patient is undergoing PTCA or stenting.
unstable angina

After the acute treatment what to do
Continue aspirin (or other antiplatelet therapy), β-blockers, and nitrates

Reduce risk factors
TIMI

aka
Thrombolysis in Myocardial Infarction (TIMI) Risk Score
TIMI score

points given for
#One point given for each of the following:
* Age ≥65 years
* More than three risk factors for CAD
* Known CAD (stenosis ≥50%)
* At least two episodes of severe angina in past 24 hours
* Aspirin use in past 7 days
* Elevated serum cardiac enzymes
* ST changes ≥0.5 mm
TIMI score

what it tells you
all-cause mortalityat 14 days is based on number of points above:
* 0–1 point: 5%
* 2 points: 8%
* 3 points: 13%
* 4 points: 20%
* 5 points: 26%
* 6–7 points: 41%
The CARE trial
patients with prior history of MI were randomized to treatment with statins or placebo. The statin group had a reduced risk of death (by 24%), a reduced risk of stroke (by 31%), and a reduction in need for CABG or coronary angioplasty (by 27%).
Variant (Prinzmetal's) Angina

mech
transient coronary vasospasm that usually is accompanied by a fixed atherosclerotic lesion (75% of cases), but can also occur in normal coronary arteries.
Variant (Prinzmetal's) Angina

hallmark
Hallmark is transient S-T segment elevation (not depression) on ECG during chest pain, which represents transmural ischemia.
Variant (Prinzmetal's) Angina

test
Coronary angiography is definitive test—displays coronary vasospasm when the patient is given IV ergonovine (to provoke chest pain)
Variant (Prinzmetal's) Angina

Tx
Vasodilators—calcium channel blockers and nitrates
Myocardial Infarction (MI)

Most cases are due to
acute coronary thrombosis:
Myocardial Infarction (MI)

mortality rate
30% mortality rate; half of deaths are pre-hospital.
Myocardial Infarction (MI)

Most patients with MI have history of
angina, risk factors for CAD, or history or arrhythmias.
The combination of ???? strongly suggests acute MI.
The combination of substernal chest pain persisting for longer than 30 minutes and diaphoresis strongly suggests acute MI.
Myocardial Infarction (MI)

Clinical features
# Chest pain
* Dyspnea
* Diaphoresis
* Weakness, fatigue
* Nausea and vomiting
* Sense of impending doom
* Syncope
# Sudden cardiac death

!! Can be asymptomatic in up to one third of patients
Myocardial Infarction (MI)

painless infarcts or atypical presentations are more likely in
postoperative patients, the elderly, diabetic patients, and women.
Myocardial Infarction (MI)

5 ECG findings
* Peaked T waves: occur very early and may be missed
* S-T segment elevation indicates transmural injury and can be diagnostic of an acute infarct.
* Q waves: evidence for necrosis (specific) – Q waves are usually seen late; typically not seen acutely.
* T wave inversion is sensitive but not specific.
* S-T segment depression: subendocardial injury
Myocardial Infarction (MI)

WRT CK-MB
*timing
*accuracy
*when to measure
* Increases within 4 to 8 hours and returns to normal in 48 to 72 hours; reaches a peak in 24 hours
* When measured within 24 to 36 hours of onset of chest pain, has greater than 95% sensitivity and specificity
* Levels of total CK and CK-MB should be measured on admission and every 8 hours thereafter for 24 hours.
Myocardial Infarction (MI)

WRT Troponins
*which ones
*timing
*accuracy
*when to measure
*problems
* (Troponin I and T) – most important enzyme test to order

* Increase within 3 to 5 hours and return to normal in 5 to 14 days; reach a peak in 24 to 48 hours
* Greater sensitivity and specificity than CK-MB for myocardial injury
* Obtain serum levels of either troponin T or troponin I on admission, and again every 8 hours for 24 hours.
* Troponin I can be falsely elevated in patients with renal failure.
Contraindications to Thrombolytic Therapy
* Uncontrolled HTN (>180/110): first control HTN
* Trauma: recent head trauma or traumatic CPR
* Active peptic ulcer disease
* Previous stroke
* Recent invasive procedure or surgery
* Dissecting aortic aneurysm
MI and indications to Thrombolytic Therapy
S-T segment elevation in two contiguous ECG leads in patients with pain onset within 6 hours who have been refractory to nitroglycerin
MI and PTCA
* the first-line treatment for MI.

* PAMI trial showed that PTCA reduces mortality more than t-PA.
first-line treatment for MI.
Percutaneous Transluminal Coronary Angioplasty (PTCA)
describe how Cardiac enzymes are drawn
Cardiac enzymes are drawn serially—once on admission and every 8 hours until three samples are obtained.
In MI ????? the only agents shown to reduce mortality.
aspirin,
β-blockers,
ACE inhibitors
The CAPRICORN trial
showed that the β-blocker carvedilol reduces risk of death in patients with post-MI LV dysfunction.
aspirin and MI Tx

mech
benefit
* Antiplatelet agent reduces coronary reocclusion by inhibiting platelet aggregation on top of the thrombus
* Has been shown to reduce mortality and should be part of maintenance therapy long-term
β-Blockers and MI Tx

mech
benefit
* Block stimulation of HR and contractility therby Reduce afterload
* Have been shown to reduce mortality and should be part of maintenance therapy
ACE inhibitors and MI Tx

when/who
benefit
* Initiate within hours of hospitalization if there are no contraindications

* Have been shown to reduce mortality and should be part of maintenance therapy long-term
Statins and MI Tx

benefit
mech
when
* Reduce risk of further coronary events
* Stabilize plaques and lower cholesterol
* Should be part of maintenance therapy
Oxygen and MI Tx

benefit
May limit ischemic myocardial injury
Nitrates and MI Tx

mech
benifits
* Dilate coronary arteries (increase supply) and Venodilation (decrease preload and thus demand)
* Reduce chest pain, although not as effective as narcotics
Morphine sulfate and MI Tx

mech
benifits
* Analgesia
* Causes venodilation, which decreases preload and thus oxygen requirements
Heparin and MI Tx

mech
benifits
what type
* Initiate in all patients with MI; prevents progression of thrombus; however, has not been shown to decrease mortality
* LMWH, specifically enoxaparin, is preferred over unfractionated heparin.
Revascularization and MI Tx

timing/type
who
# Benefit highest when performed early; time is more important than type of reperfusion chosen
# Should be considered in all patients
Rehabilitation and MI Tx

what is it
why
* Cardiac rehabilitation is a physician-supervised regimen of exercise and risk factor reduction after MI.
* Shown to reduce symptoms and prolong survival
ECG Findings Based on Location of Infarct

Anterior Infarct
S-T segment elevation in V1-V4 (acute/active)
Q waves in leads V1-V4 (late change)
ECG Findings Based on Location of Infarct

Posterior Infarct
Large R wave in V1 and V2
S-T segment depression in V1 and V2
Upright and prominent T waves in V1 and V2
ECG Findings Based on Location of Infarct

Lateral Infarct
Q waves in leads I and aVL (late change)
ECG Findings Based on Location of Infarct

Inferior Infarct
Q waves in leads II, III, aVF (late change)
The HOPE trial
showed that the ACE inhibitor ramipril reduces mortality, MI, stroke, and renal disease in a broad range of patients with high-risk cardiovascular disease.
The following 7 things are indicated in patients with MI:
* Oxygen
* Nitroglycerin
* β-blocker
* Aspirin
* Morphine
* ACE inhibitor
* IV Heparin
The GUSTO trial
showed that t-PA plus IV heparin give the greatest mortality benefit compared with other thrombolytic regimens (streptokinase and IV/SC heparin) in patients with acute MI.
6 general Complications of acute MI
1 Pump failure (CHF)
2 Arrhythmias
3 Recurrent infarction (extension of existing infarction or reinfarction of a new area)
4 Mechanical complications (ruptures, etc)
5 Acute pericarditis
6 Dressler's syndrome
Complications of acute MI

Most common cause of in-hospital mortality
Pump failure (CHF)
Complications of acute MI

treatment of Asystole
transcutaneous pacing
Complications of acute MI

Second-degree (type II) and third-degree block:
prognosis is dire in the setting of an anterior MI—emergent placement of a temporary pacemaker is indicated (with later placement of a permanent pacemaker). In inferior MI, prognosis is better, and IV atropine may be used initially. If conduction is not restored, a temporary pacemaker is appropriate.
Complications of acute MI

when to suspect recurrent infarction
**re-elevation of CK-MB after 36 to 48 hours may be due to recurrent infarction.

**repeat S-T segment elevation on ECG within the first 24 hours after infarction,
Complications of acute MI

Treatment of recurrent infarction
Repeat thrombolysis or urgent cardiac catheterization and PTCA. Continue standard medical therapy for MI.
Complications of acute MI

Free wall rupture
* Mortality
* leads to

* Tx
# 90% mortality rate
# Usually leads to hemopericardium and cardiac tamponade
# hemodynamic stabilization, immediate pericardiocentesis, and surgical repair
Complications of acute MI

timing of ruptures
Free wall rupture
* occurs during the first 2 weeks after MI (90% within 2 weeks, most commonly 1 to 4 days after MI)

Rupture of interventricular septum

* Occurs within 10 days after MI
Complications of acute MI

which is worse Free wall rupture or Rupture of interventricular septum
Both are emergencies but Free wall rupture is worse
Complications of acute MI

Tx for Papillary muscle rupture
Emergent surgery is needed (mitral valve replacement is usually necessary), as well as afterload reduction with sodium nitroprusside or intra-aortic balloon pump (IABP).
Complications of acute MI

pseudoaneurysm
Incomplete free wall rupture (myocardial rupture is contained by pericardium)

Surgical emergency because ventricular pseudoaneurysms tend to become a free-wall rupture
Complications of acute MI

Ventricular aneurysm
* Rarely rupture (in contrast to pseudoaneurysms)
* Associated with a high incidence of ventricular tachyarrhythmias
* Medical management may be protective.
* Surgery to remove aneurysm may be appropriate in selected patients.
Complications of acute MI

Tx for Acute pericarditis
* Treatment consists of aspirin.
* NSAIDs and corticosteroids are contraindicated (may hinder myocardial scar formation).
Dressler's syndrome

aka
What is it
Tx
* ("postmyocardial infarction syndrome")
* Immunologically based syndrome consisting of fever, malaise, pericarditis, leukocytosis, and pleuritis, occurring weeks to months after an MI
* Aspirin is the most effective therapy.