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Clin Med Part 3 > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

Epidemiology of CAD (7)

A

16 million Americans have heart disease
Coronary Artery Disease (CAD) is the number 1 killer in the US and worldwide
1 out of 5 deaths are from CAD
Every 60 seconds someone dies from CAD in the US.
600,000 will die each year in the US
Death from CAD has decreased every year since 1968
Survival is much worse in the elderly
Approx 50% die before the hospital, presumed from VT arrest

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2
Q

Risk Factors for CAD

A 
Age > 65
Male Sex
Family History
Hypercholesterolemia
Smoker
Diabetes
Hypertension
Physical inactivity
Obesity
Poor diet
Alcohol, in excess
Metabolic Syndrome
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3
Q

Stable Angina

A

Stable angina is chest pain or discomfort that usually occurs with activity or stress. Angina is chest discomfort due to poor blood flow through the blood vessels in the heart.

Due to atherosclerotic heart disease
Vasospasm occurs at the site of a lesion
Can occur in normal vessels and in the setting of other heart disease

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4
Q

Symptoms of Stable Angina (5)

A

Usually occur during activity
Pts may want to be upright (lying down increases preload and myocardial work)
Tightness, squeezing, burning, pressing, choking, aching, bursting, “indigestion,” PRESSURE
Distribution of pain is pt dependent, BUT is usually in the same place in each pt unless there is some worsening occurring
Short duration (2-5 mins)
Nitroglycerin (NTG) usually resolves pain

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5
Q

3 Types of CAD

A

Stable Angina
NSTEMI
STEMI

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6
Q

Signs of Stable Angina (4)

A

HTN, hypotension in worsening disease
Cardiomyopathy (ischemic)
New Murmurs (MR from papillary muscle dysfunction)

Look for underlying diseases
DM
Thyroidtoxicosis
HTN
Myxedema
Cardiomyopathy
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7
Q

ECG for Stable Angina

A

ECG usually normal, may show chronic arrhythmias or old MIs, old BBB, LVH

Exercise ECG
Attempts to induce symptoms
Uses a treadmill to precipitate exercise
Uses the Bruce protocol to determine a + test or not
1 mm depression of the ST segment measured 80 milliseconds after the J point

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8
Q

Myocardial Stress Imaging for Stable Angina

A 
Give you med like dobutamine 
There is myocardial stress imaging
Scintigraphy (Nuclear)
Echocardiography
MRI
PET
CT
Angiography
Ambulatory ECG
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9
Q

Prevention of Stable Angina (6)

A 
Stop Smoking
Control HTN
Control DM
Control Dyslipidemia
Drug therapy
Diet
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10
Q

Treatment of Stable Angina

A

Sublingual nitroglycerin 0.4 mg q 3-5 mins
Onset in 1-2 mins
Nitrates
Vasodilate the arteries and veins
This reduces preload and afterload, reducing myocardial work

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11
Q

Treating the Underlying Cause for Stable Angina

A

Long acting nitrates (not good for acute angina)
Isosorbide
NO continuous use due to tolerance, so used 8 hours/day
Beta Blockers
Only med shown to prolong life
Inhibit myocardial O2 demand by dec HR and contractility
Calcium Channel blockers
No reduction of mortality (third line agent if can’t tolerate BB)
Ranolazine
New drug, decreases intracellular calcium by selective inhibition of sodium channels
Antiplatlet Therapy
Aspirin- if risk of benefit outweighs risk of bleeding
Plavix as an alt to ASA

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12
Q

Revascularization in Stable Angina

A 
Failed medical therapy
LMA stenosis
3 vessel disease with LV dysfunction
Unstable Angina
Post MI with angina
? 2 vessel disease with LV dysfunction, >90% stenosis in any vessel, + stress test
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13
Q

Prognosis of Stable Angina

A

Mortality rates depend on the number of diseased vessels, severity of stenosis, LV function, complex arrhythmias
Nearly half of all deaths are sudden
Duke Treadmill Score, based on the Bruce protocol can stratify the risk of annual mortality.

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14
Q

2 Types of Revascularization

A

Coronary artery bypass graft (CABG)

Percutaneous coronary intervention (PCI)

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15
Q

CABG

A

Very low mortality rate (1-3%) in healthy people
Mortality rate increases with worsening underlying disease
Can use the Left internal mammary artery (LIMA), Saphenous vein or radial artery
Venous grafts can occlude in 10-20% in first year, less as time goes on
Usually requires median sternotomy and cardiopulmonary bypass
Angina can reoccur in 25% of pts but often less severe

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16
Q

PCI

A

Can perform a balloon angioplasty or stenting
Two types of stents
Drug eluting (elute antiproliferative agents)
Bare metal
Risk are intimal dissection or rupture
Usually need anti-platelet therapy to prevent thrombosis, the length of time depends on the time of stent
6-9 months with BMS
12 months with DES

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17
Q

PCI Indications

A

Indications
Stable angina
More effective than medical management for relief of angina
? Utility in MI or unstable angina, may not reduce risk of further ischemia

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18
Q

Risk with PCI

A 
Risk
Death < 0.5%
Emergency CABG < 1%
MI < 2%
Branch occlusion 5-10% (minor complications
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19
Q

Efficacy for PCI

A

Success in 95% of cases
More effective the medications up to 2 years post PCI
Restenosis in 20% in 6 months with bare metal stents
Angina in 10% in 6 months

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20
Q

PCI vs. CABG

A

PCI ok in 1 vessel disease
CABG better in severe multivessel disease
Mortality at 5 years is similar

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21
Q

PCI Benefit

A

Restenosis is a major limitation of the procedure

Risk at 6 months
Drug-eluting < 10 %
Bare metal 10-30%
No intervention 30-40%

PCI may not have any benefit over medical therapy in respect to mortality
Does improve symptomatology
Increased need to repeat procedures compared to CABG

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22
Q

Coronary Spasms

A

Coronaries can spasm (vasoconstriction) and cause similar effects of angina.
The blood vessels are without atherosclerosis

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23
Q

Causes of Coronary Spasms

A 
Cocaine
Prinzmetal (variant) angina
Cold
Vasocontrictive medications
Ergot
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24
Q

Prinzmetal angina is caused by

A

vasoconstriction
Most commonly the RCA
“Syndrome X”
Can see ST elevation
Women under 50 yo
Usually in the early AM, often awakens pts
Seen with conduction defects and arrhythmias

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25
Q

Treatment of Coronary Spasms

A 
ST elevations, should get a coronary angiogram.
Look for stenosis
Repair stenosis if indicated
Medications if indicated
Nitrates and CCB may help with Prinzmetal varient angina
Stop smoking and/or cocaine use
? Pure beta activity in cocaine use
Hotly debated in the literature
May want to use an alpha/beta medication
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26
Q

Unstable Angina

A

Chest pressure at rest or with minimal exertion lasting > 10mins, severe and of new onset, occurs with a crescendo pattern
NSTEMI is UA with signs of myocardial infarction

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27
Q

2 Types of NSTEMI

A

Unstable cardiac ischemia

Unstable Angina

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28
Q

Definition of Myocardial Infarction

A 
Elevated biomarkers (troponin)
Symptoms of cardiac ischemia
ECG findings of a new
New Q waves
Loss of myocardial tissue
New wall motion abnormality
29
Q

Causes of NSTEMI

A

Plaque rupture or erosion with superimposed nonocclusive thrombosis (most common)
Dynamic obstruction
Progressive mechanical obstruction
Increased myocardial oxygenation demand and decreased blood supply

30
Q

Symptoms of NSTEMI

A

Chest pain (pressure) is the most common symptom in the emergency department
Levine Sign Fist clenched over center of chest
May occur at rest or on exertion
May radiate
Very similar to symptoms of chronic angina
Signs of heart failure are usually associated with higher rate of mortality

31
Q

Lab tests for NSTEMI

A 
Markers of myonecrosis
Troponin I and T
CK and CK-MB
Myoglobin
Elevation of troponin and CK-MB maybe the only sign of myocardial ischemia
32
Q

ECG Finding with NSTEMI

A

ST segment maybe depressed or flat, T wave flattening or inversion present in 30-50%

33
Q

Treatment of NSTEMI

A 
Admit the patient
Treat symptoms= MONA
O2
Pain medications
Anxiolytics
34
Q

Anticoagulation and Antiplatlet Treatment for NSTEMI

A

Aspirin
Class 1A data
Clopidogrel (in ASA allergic pts)
Class 1C data
Low-molecular weight heparin (enoxaparin or Fondaparinux)
Unfractionated heparin
Glycoprotein IIa/IIIb antagonist (tirofiban, eptifibatide, abciximab)

35
Q

Nitroglycerin Treatment for NSTEMI

A

Nitroglycerin
Sublingal, buccal or transdermal
If pain persists may start IV

36
Q

BB and CCB Treatment of NSTEMI

A

Beta Blockers
Class IB in ACS and IA in MI

Calcium Channel Blockers
No favorable outcomes
Third line agents

37
Q

Statins and ACE-I Treatment of NSTEMI

A

Statins
PROVE-IT trial
Starting a statin immediately regardless of LDL levels improved outcomes (used atorvastatin 80 mg)

ACE-I
Class 1B3 for ACS and 1A for MI

38
Q

Revascularization of NSTEMI

A 
Class 1 Early (within 48 hours) invasive strategy for any of the following high-risk indicators
Recurrent angina/ischemia at rest or with low-level activity
Elevated troponin
ST-segment depression
Recurrent Ischemia with evidence of CHF
High-risk stress test result
EF < 40%
Hemodynamic instability
Sustained VT
PCI within 6 months
Prior CABG
39
Q

TIMI Risk Score (Thombosis in Myocardial Infarction)

A 
Age > 65
3 or more cardiac risk factors
Prior coronary stenosis > 50%
ST segment deviation
2 anginal events in prior 24 hours
ASA in past 7 days (given for some cardiac event)
Elevated cardiac markers
Get 1 point for each and with each one increases the risk of mortality at 14 days
40
Q

NSTEMI Treatment Summary

A 
ABCs
Morphine
ASA
Plavix if ASA allergey
Some data for Prasagruel
NTG
Anticoagulation
LMWH vs Heparin
Bivalrudin and Glycoprotein IIa/IIB inhbitors for PCI lab only
BB
ACE
Statin
Cardiology Consultation
\+/- Revascularization
41
Q

STEMI

A

Most caused by an occlusive lesion in one of the coronaries at the site of an atherosclerotic lesion
Some can be caused by vasospams, cocaine, emboli, hypotension, increased metabolic demand, vasculitis, aortic root and coronary dissection

42
Q

3 Phases of a STEMI

A

Acute from onset to 7 days
Healing 7 to 28 days
Healed > 29 days

43
Q

Symptoms of a STEMI

A

Worsening angina, chest pressure, discomfort, crushing pain
Pain usually at rest and, commonly in the AM
NTG has little effect
Fever, diaphoresis, malaise, anxiety
Syncope, pre-syncopal, dyspnea, orthopnea, cough, n/v
1/3 of STEMIs are painless
Elderly, women, DM
Sudden Death
50% don’t make it to the hospital

44
Q

Signs of a STEMI

A 
Bradycardia common with inferior MI
Tachycardia
Decreased CO
Arrythmia
HTN
Hypotension
Respiratory failure, may indicate CHF
Fever
45
Q

Killip Classification and STEMIs

A

Standard way of classifing HF in pts with AMI
Class I = absence of rales and S3
Class II = Rales that do not clear with coughing over 1/3 or less OR presence of an S3
Class III = Rales that do not clear with coughing over more than 1/3 of the lung fields
Class IV = Cardiogenic shock (rales, hypotension and/or hypoperfusion)

46
Q

Cardiac/PV Exam in STEMI

A 
May have no signs
JVD may reflect R sided failure
S3 (less common) and/or S4
MR murmur
Pericardial rub (with transmural MI)
Edema +/-
Cyanosis
47
Q

Lab Findings in STEMI

A 
CK-MB
Troponin I and T
More sensitive than CK-MB
Each test maybe + in 4-6 hours after onset of the MI
Abnormal for 8-12 hours
Trops may hang around for 5-7 days
CK-MB normalize within 24 hours
More helpful for looking for reinfarction
48
Q

ECG Findings with STEMI

A 
ECG changes evolve as time progress
Peaked T waves (hyperacute)
ST segment elevation
Q wave development
T wave inversion
Can occur over hours or days
A new LBBB in a pt with symptoms of an MI is considered a STEMI
49
Q

Imagining in STEMI

A

CXR may show pulmonary edema
ECHO may show new WMA, new valve disorders (MR from pap dysfunction), VSD
MRI
Nuclear Scans

50
Q

Hemodynamic Monitoring in STEMIs

A 
Same as you would with any other critically ill patients
Central lines
Arterial lines
Telemetry
\+/- Pulmonary artery monitors
51
Q

Anticoagulation in STEMI

A

All patients should receive 162 to 325 mg of Aspirin at once
Chewing increases absorption rate
Reduces mortality by 27% (14.2% to10.4%)
ASA allergies should receive clopidogrel a 300 mg loading dose then 75 mg daily
Clopidogrel and ASA has shown benefit
CLARITY Trial
Clopidogrel with thrombotic therapy improved coronary patency on cath 3.5 days after thrombolysis, no increase in bleeding

52
Q

Anticoagulation in STEMI–> COMMIT/CCS-2 trial

A

Clopidogrel reduced death, MI and CVA, with no increase in bleeding
ASA and clopidogrel for min 14 days out to 1 year post STEMI
“Double dosing” of clopidogrel may decrease restenosis post stent (600 mg x 1 then 150 mg daily)

53
Q

Reperfusion Therapy in STEMI

A

Reperfuse within 12 hours of onset of symptoms
PCI Therapy
Superior to thrombolysis (with tpa)
Need expertise, and lots of processes in place
“Door to balloon” time is <90 mins
Glycoprotein IIa/IIIb antagonist (specifically abciximab) or bivalrudin with stenting is generally standard of care
HORIZONS trial
Bivalrudin vs heparin and abciximab resulted in similar rates of thrombotic events but 40% less bleeding

54
Q

So what if I cant get a PCI in < 90 mins?

A

No benefit of fibrinolytics and glycoprotein IIa/IIIB antagonists
Either fibrinolytic and rescue PCI ASAP for reperfusion failure or PCI alone

55
Q

Thrombolytic therapy– Reperfusion in STEMI

A 
Reduces mortality (by 50%) if given within 3 hours
Major bleeding can occur (0.5-5%)
Contraindications previous hemorrhagic CVA, CVA in past year, intracranial neoplasm, recent head trauma, active bleeding, HTN, recent major surgery
56
Q

Types of fibrinolytics– Reperfusion in STEMI

A

Alteplase (tpa)
Reteplase
Tenectplase
Streptokinase (less commonly used in the US)
Post Fibrinolytic Therapy
ASA and heparin (at least 48 hours post), then lovenox (EXTRACT /OASIS-6 trials)/fondaparinux (OASIS-5 trial) x 8 days

57
Q

Assessment of Effect for Reperfusion in STEMI

A 
Improved Pain
Resolution of ST changes
At least 50% by 90 mins
10-20% of vessels with re-occlude and re-infarction
Recurrence of pain and ST changes
58
Q

Treatment Summary for STEMI’s

A 
ASA
Plavix if going to cath lab
Anticoagulation
Heparin vs LMWH
Fibrinolytic vs PCI
Bivalrudin and glycoprotein IIa/IIB inhibitors for PCI lab
BB
ACE
Statin
Morphine and NTG for analagesia
No NTG in R sided MI (drops preload as it increased venous capacity by vasodilation)
59
Q

CCB and Anti- thrombotic therapy for STEMI’s

A

CCB
Not indicated, no trials support its use

Long term anti-thrombotic therapy
ASA daily
WARIS-II trial warafarin post MI showed decreased mortality, MI, and CVA (not done in the US)
CURE trial clopidogrel 75 mg/d for 3-12 months for NSTEMI and 1 year for STEMI reduced mortality, MI and CVA

60
Q

Aldosterone Antagonist Treatment for STEMI’s

A

RALES trial shows spironolactone reduces mortality in pts with advance HF
EPHESUS trial showed 15% reduction in mortality with eplerenone with either HF or infarction

61
Q

ARB Treatment for STEMI’s

A

VALIANT trial showed valsartan is equivilant to captopril in reducing mortality
Used in pts with ACE-I intolerance

62
Q

ACE-I and Nitrate Treatment for STEMI’s

A

Nitrates
No improvement in outcomes (ISIS-4 and GISSI-3 trials)

ACE-I
(SAVE, AIRE, SMILE, TRACE, GISSI-III and ISIS-4 trials) show short and long term improvement in survival
Esp good in pts with EF of < 40%
Start early in pts wit no contraindications

63
Q

Beta Blocker Treatment for STEMI’s

A

Short term benefit started in first 24 hours (with no contraindications)
No difference of IV over PO (COMMIT/CCS-2 trial)
Prevents reinfarction, increased risk of shock in pts with HF (so no BB in HF)
CAPRICORN trial showed carvedilol after acute phase showed benefit

64
Q

Analgesia Treatment for STEMI’s

A

NTG (SL, buccal, TD, IV)
Opiods (Morphine)
NSAIDS (other than ASA) can increase mortality

65
Q

Post MI Angiography in STEMI

A

If reinfarciton noted, need rescue PCI
Stress testing
Poor stress testing should get a PCI

66
Q

Complications of STEMI

A 
Postinfarction ischemia
Arrhythmias
Myocardial Dysfunction
RV infarction
Mechanical Defects
Myocardial Rupture
LV Aneurysm
Pericarditis (Dressler Syndrome)
Mural Thrombus
67
Q

Postinfarction Management

A

After 24 hours, treatment is based on prevention of reinfarction
Risk stratification (TIMI)
ACE if EF < 40%
Stress testing

68
Q

Secondary Prevention for STEMI

A

Hyperlipidemia treatment (Statin started before discharge)
Smoking Cessation
BP control
Cardiac Rehab
Exercise
Beta Blockers
Carvedilol 25mg IBD
ASA
Plavix x 1 year (? Praugrel, increased bleeding)
? Warfarin x 3 months (not compared to ASA and plavix)
Antiarrhythmics
? ICD placement (postinfarct LV dysfunction, HF) DINAMIT trial showed no benefit in the 40 days post infarct

69
Q

Demand Ischemia

A

Hypoperfusion to the myocardial tissue in the setting of increased physiologic requirements (oxygen) can result in a troponin leak
Can see it in septic shock
NOT an atherosclerotic lesion
Need to restore perfusion

Clin Med Part 3 (1 decks)

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