My Notes On Ischemic Heart Diseases



My Notes On Ischemic Heart Diseases

My Notes On Ischemic Heart Diseases Peter  

5 years ago

~17.4 mins read
Ischemic Heart Disease

Coronary Ischemia is due to imbalance btw blood supply and Oxygen demand of the heart


General Clinical presentation of Ischemic Heart Disease

1. Asymptomatic

2. Angina pectoris

3. Myocardial Infacrction (NSTEMI or STEMI)

4. Sudden Cardiac Death


Types of Ischemic Heart Disease

1. Stable Angina

- Characterised by Stable Atherosclerotic plaques

2. Unstable Angina Pectoris

- Atherosclerotic plaque becomes unstable

3. Subendocardial Infarction

- Infarction of Inner 1/3 of myocardium

4. Myocardial infarction

- Transmural infarction due to thrombosis


Stable Angina (SA)

- Narrowing of the major coronary artery

- Due to fixed atherosclerotic lesions (Stable plaque)

- Symptoms occur when O2 demand exceeds available blood supply.


Major risk factors of SA

1. Diabetes Mellitus

- Worst risk factor

- due to increased adipose tissue

2. Hyperlipidemia/Dyslipidemia

- Increased risk of cholesterol deposition in vessels

- LDL Goal of < 100mg/dL for CAD pts




- Most common risk factor

- Hypertension puts pressure on arteries, causing hardening and narrowing of blood vessels

4. Cigarette smoking

5. Age

6. Family Hx of CAD

- in 1st degree relative (Men < 55, Women < 65)

Minor risk factors (Less clear significance)

1. Obesity

2. Sedentary lifestyle

3. Stress

4. Excess alcohol


Prognostic indicators of CAD

a. Poor prognosis If EF is < 50% (Diminishing LV function)

b. Poor Prognosis If the following Vessels are involved

- Left Main Coronary Artery (Covers approx 2/3 of heart)

- 2 or 3 vessel CAD


Features of SA

1. Chest pain

- Often described as Heaviness, Pressure, Squeezing and/or Tightness

- May rarely be sharp, stabbing.

- Gradual in onset

- Occurs when increase in Myocardial O2 demand (eg Emotions)

- Relieved with rest and/or Dilation of the Coronary vessels (Nitroglycerin)

- Lasts < 10 – 15 mins (average of 1-5mins)


When to suspect others causes of Angina



Pain change with Change in breathing

2. Presence of Chest wall tenderness

3. Pain change with Change in body position


Syndrome X

1. Metabolic Syndrome X

- Refers to factors inc fatsObesity/Insulin resist

2. Syndrome X = Exertion Angina + Normal Coronary artery


Coronary Artery Disease Diagnosis

1. Normal Physical Exam

2. Resting ECG

- ECG (Rest/Stress) is best initial for all forms of chest pain

3. Stress tests (ECG, ECHO, Nuclear isotope and Imaging)

- All patients with +ve stress test should undergo Catheterization

- Stress tests Confirms Angina Diagnosis

- Stress tests also evaluates response to therapy

- Identifies high risk pts (risk of Acute Coronary Syndrome)

4. Pharmacologic Stress test

- Takes place of exercise

5. Holter Monitor

- Ambulatory ECG

6. Catheterization


Resting ECG

1. Normal in Stable Angina

2. Q waves in prior MI

3. ST/T issues in USA during episode of pain


Stress Test

Based on Intermediate Pretest Probability

Age, Gender and Symptoms

Pts with positive stress test should undergo catheterization


Stress ECG

1. Highly Sensitive if Resting ECG = Normal

2. Perform before, during and after exertion.

3. 75% sensitive if patient exercises to 85% of MAX heart rate.

- Max hrt rate = 220 - Age

4. Stress ECG is positive if there is ST segment depression

5. HF, V. Arrhythmia and Hypotension are also positive signs


Stress Echocardiogram (more sensitive vs ECG)

1. Before and After Exertion (vs ECG  B4, during and after)

2. Stress Echocardiogram is based on Wall motion abnormalities (vs ECG’s ST segment depression)

- e.g Akinesia (localized lack of wall motion) or Dyskinesia (outward movement of a wall segment during systole)

- Wall motion abnormalities is due to exercise induced ischemia



Echocardiogram detects LV size and Function, Valve diseases and Coronary Artery Disease


Nuclear Isotope Imaging study

- IV administration of Thallium 201 or Technetium

- Stress Myocardial perfusion imaging

- If no blood flow in a myocardial area in the imaging = No blood flow in that myocardial area

- Rescue reversible areas with Percutaneous Coronary Intervention (PCI) or Coronary Artery Bypass Graft (CABG)

- Increases specificity and sensitivity of stress test

- Disadvantages

i. It is expensive

ii. Not helpful in diagnosing Left Bundle Branch Block

iii. Subjects patients to radiation imaging


Pharmacologic Stress Test

- Drugs takes the place of exercise

- ADD/ECG/Echo/Nuclear pefusion

- Adenosine IV - Dilation (Coronary artery steal)

- Dipyridamole – Dilation (Coronary artery steal)

- Dobutamine - O2 demand (Increases contractility)


Holter Monitor (PURAS)

- Ambulatory ECG

- Detects Silent Ischemia

- Continuous monitor (24 -72hrs)

- Evaluates (PURAS)

i.   Pacemaker and ICD function

ii.  Unexplained syncope/dizziness

iii. Rate variability

iv. Arrhythmias

v.  Silent ischemia


Cardiac Catheterizaton with Coronary angiography

- Coronary angiography is definitive for diagnosis Coronary Artery Disease

- Often performed with PCI and for patients considering CABG

- Contrast is injected into coronary vessels to visualize any stenotic lesions

- Defines location and extent of coronary disease

- If CAD is severe (Left Main Coronary Artery Disease or 3 - vessel Disease), refer for CABG



- Most Accurate cardiac diagnosis

- Invasive information is obtained

i. Hemodynamics

ii. Intracardiac presure

iii. CO

iv. O2 saturation

- For Coronary Angiography


Indications for Catheterization (PPAUSE)

1. Positive Stress test

2. PCI/Angiogram in Acute MI

3. Angina (Angina difficult to diagnose or Complications  MI or Angina + hard to Dx

4. Urgent diagnosis/MGT needed

5. Surgical Intervention or Revascularization considered

6. Evaluation (Valvular disease/determine surgical need)


Arteriography (Angiography)

Injects contrast into coronary artery

- Main Purpose is to diagnose CAD

- Most Accurate method to Diagnose presence and severity of CAD

- Precedes PCI and CAGB

- >70% Stenosis is significant


Treatment for Stable Angina

- Reduction of CAD Risk Factors (Modifiable)

1. Smoking

- reduces risk by 1/2 in 1yr

2. HTN

- Control is best for diabetes

3. Hyperlipidemia


- HMG-CoA inhibitors (Statins)

4. Diabetes Mellitus 2

- Cadiovascular disease equivalent

5. Obesity

- modifies other risks

6. Exercise

- helps Stress, Weight and other risks




- reduce saturated fat and cholesterol.

- Increase vegetables and fruits

- < 7% total calories, Xerol < 200mg/dy


Medical Therapy for Stable Angina

Treatment of all coronary artery disease aims at

-   Reducing Hypercholesterolemia, Hence lipid plaque deposition (Statins)

-   Reducing Myocardial Oxygen demand (B-blockers)

-   Reducing risk of Thrombosis around ruptured plaque (Aspirin)

-   Prevention of Symptoms (Nitrates)

1. Aspirin

- First lines for all Coronary Artery Disease

- Reduces risk of MI

- Prevents thrombosis

2. B-blockers

- Block sympathetic stimulation of the heart = Less contractility = reduced Oxygen demand

- Atenolol (Heartenolol) or Metoprolol are recommended

- reduces frequency of coronary event

3. Nitrates

- Side effects (SHOT) – Syncope, Headache, Orthostatic hypotension, Tolerance

- Causes generalized vasodilation (veNodilators)

- reduce preload myocardial O2 dmand

- take before exertion to prevent angina

- If chronic angina, route is Oral or Transdermal patch

- If ACS, route is Sublingual, Paste or IV

4. Calcium Channel blockers (Secondary treatment)

- Use when B-block/nitrates not fully effective.

- coronary vasodilation

- Afterload reduction/reduce contractility

- may cause increase heart rate

5. ACE inhibitors/Diuretics

- use if CHF is present

- ACE inhibitor reduces mortality in MI patients



- preferred for high risk patients

- does not reduce incidence of MI (because it doesn’t reduce the incidence of cholesterol plaque rupture and thrombosis formation)

- Improves symptoms (Relieves obstruction)

- involves PCI or CABG


Management decisions for Stable Angina

- risk factors modification and aspirin for all Coronary Artery Disease Patients followed by specific treatments depending on severity

1. Mild disease

- Mild angina

- Single vessel disease

- Treatment Modalities

i. Nitrates

ii. B-blockers

iii. In addition to Nitrates and B-blockers, Calcium Channel Blockers for tough cases


2. Moderate disease

- Moderate angina

- Two - vessel disease

- Modalities

i. Treatment for Mild disease

ii. If the above doesn’t work, consider Revascularization


3. Severe disease

- decreased EF

- Severe angina

- 3-vessel disease or Left Main Coronary Artery disease

- Modality

i. Angiography and CABG


Acute Cornary Syndrome

- Clinical manifestation of atherosclerotic plaque rupture = coronary occlusion

- Generally refers to

i. USA


iii. STEMI


Unstable Angina (USA)

Plaque becomes unstable = Breaks off and incompletely blocks vessel

- Does not occur due to change in Oxygen demand Unchanged (Pain can occur at rest)

- Any Angina (Chronic or New) with worsening symptoms

- Increased Frequency, Duration and Intensity

- Any Angina at Rest


Only Cardiac Enzymes distinguish USA (Not elevated) from NSTEMI (Elevated)

- Both have similar presentation and lack ST elevation and Pathologic Q waves on ECG.

- NSTEMI has elevated

i. Troponin

ii. Creatinine Kinase-MB


Diagnosing USA

- Must exclude MI in all patients

- Initial test is ECG (To exclude MI)

- Stress testing - Exercise ECG, Echo or Nuclear imaging

- they have increased risk of adverse effect during stress testing.

- must be medically stabilized b4 stress testing

- Catheterization

i. Patients with high risk may undergo catherization initially


Treatment of Unstable Angina aims at


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Prevention of progression

B. Ameriolate symptoms

C. Treat risk factors


A. Preventive

- Stabilize plaque

- Prevent thrombosis formation

- Reduce Myocardial Oxygen consumption

- Reduce hypercholesterolemia


0. Admission with continuous cardiac monitor

1. Aspirin + Clopidogrel for 9-12 months

- Adjust Duration and therapy according to bleeding risk

- The combo reduces risk of MI vs aspirin alone

2. B-blockers (Reduces sympathetic stimulation of the heart)

- first line

- Decrease myocardial O2 demand

- For Diaphoresis

3. Nitrate

- Nitrates are 1st lines

- To vasodilate and increase blood flow

4. Morphine (for pain)

- Often mask symptoms of MI

5. Enoxaparin - LMWH vs Heparin

- EnoxHEARTparin

- to prevent clot/clot progress)


B. Ameliorate symptoms



Oxygen (For dyspnea)

2. Abciximab/Tirofiban - Glycoprotein IIb/IIIa inhibitors

(If undergoing PTCA or Stenting)

3. Replace deficient electrolytes

- K+

- Mg2+


C. Treat risk factors

1. Atorvastatin

- HEARTorvastatin

- Reduce LDL


Cardiac catherization

- 90% of improve in 1-2days

- Done only if Medical mgt fails after 48 hours

- If patient responds to Medical mgt, perform stress ECG to access need for catheterization.

- Other indications

i. Hemodynamic instability

ii. Ventricular arrhythmias

iii. New MR

iv. New Septal defect


Take home for USA (same for SA)

B-blocker (Metoprolol or Atenolol)

Risk factor reduction



Statins (Heartorvastatin)


Variant Prinzmetal Angina (PrinzNITal)

- PrinzNITal Angine

1. At Rest/classically at Night (Transient vasospasm)

- Can occur in normal or coronary arteries with fixed atherosclerotic lesions.

- ST Elevation during chest pain is hallmark

- Risk of Ventricular dysrhythmias (may be life threatening/fatal)

- Diagnosis (Angiography displays coronary vasospasm)

i. Angiography + IV Ergonovine/Acetylcholine (provoke Vasospasms)

- Treatment (Symptomatic)

Vasodilators CCB, NItrates

- Prevention

Reduce Smoking, drugs (Cocaine) and Lipids


Myocardial Infarction (MI)

- Necrosis of Myocardium

- due to Interruption of blood supply

- mostly due to Acute Coronary Thrombosis

- thrombus forms on top of a ruptured plaque

- associated with 30% mortality

- most pts have hx of arrhythmias, CAD disesase or risk factors,

- Suspect if sub-sternal pain > 30mins + Diaphoresis


Clinical Features

1. Asymptomatic

2. Severe chest pain + radiation to left (Jaw, Neck, Arm, Shoulder, Back)

3. Epigastric pain

4. No response to Nitroglycerin (Vessels are maximally obstructed)

5. Nausea + Vomiting (Due to intense pain)

6. Dyspnea

7. Syncope (Decreased cardiac output = Less Oxygen to brain)

8. Impending doom sense (Due to severe pain and decreased blood to brain)

9. Weakness/Fatigue (Decreased cardiac output = Less Oxygen to tissue)

10. Diaphoresis (Decreased cardiac output = Sympathetic stimulation)

11. V.


Fib (Due to abnormal contractility) = Death


MI may be asymptomatic (or have atypical presentation) in

1. Old

2. Diabetes

3. Women

4. Post-operation


Right Ventricular Infarction presentation

1. Inferior ECG changes

2. Hypotension

3. Elevated JVP

4. Hepatomegaly

5. Clear lungs


Contraindication in Right Ventricular Infarction

1. Nitrates (Reduce preload = Cardiovascular collapse)

2. Diuretics (Reduce preload = Cardiovascular collapse)


ECG of MI  - QST

1. Q wave (Deep)

- Specific 4 NeQrosis

- Seen in late stages

2. ST segment (Elevation or depression)

- Elevation = Most likely Transmural injury (represents infarction in 75% of time)

- Depression = Most likely Subendocardial injury (represents infarction in 25%)

3. T wave (Peaked or Inversion)

- Peaked = Occurs Early (Usually missed)

- Inversion is sensitive, but not specific (Might represent Hypokalemia)


Categories of Infarction

1. ST segment Elevation Infarction (STEMI)

- Transmural (Larger infarct)

2. Non- ST segment Elevation Infarction (NSTEMI)

- Subendocardial (Inner 1/3 or 11/2 of wall)

- It is a smaller infarct (distinguish from MI with Cardiac enzymes)


Diagnosis of Myocardial Infarction

Cardiac enzymes

- Gold standard for diagnosing of MI

- Troponins I and T, CK-MB (Less commonly used)


1. Troponins

- TRIopon10ns

- Most important

- Increases within 3-5hrs, Normal in 5-14 (avg 10) days

- Peaks in 1-2 days

- Greater sensitivity and specificity vs CK-MB

- Obtain serum levels 8hrly/24hrs

- Higher peak and prolonged elevation = poor prog/severe injury

- Troponin 1 is falsely elevated in Renal failure



TRI = 3 - 5 hours


10 = Normal in average of 10 days (5-14)


2. CK-MB (Creatinine Phosphokinase)


6 = Increased in average of 6 hrs (4-8)

Bi = Returns to normal in bi (2-3) days (48-72hrs)

- Peaks in 1 day

- Greater sensitivity and specificity if measured before returns to normal

- Detects re-infarction


Monitoring Patients with acute MI

BP and HR

- Gradual reduction

- HTN increases O2 demand

- Hypotension reduces coronary and tissue perfusion

- Nitrates and Morphine causes Hypotension


Rhythm strip (Continuous Cardiac Monitor)

- Watch for dysrhythmias

- Premature Ventricular Contractions (PVCs) can lower stroke volume and Coronary Artery filling time

- High frequency of PVCs may predict VFib or VT


Auscultate the heart

- 3rd and 4th heart sounds

- Friction rub


Auscultate lungs

- Crackles may = LV failure, Pulmonary edema


Hemodynamic monitoring with Pulmonary artery catheter if patient is unstable

Assesses need for IV fluids/Vasopressors




- Cardiac Index


Treatment for Acute MI

1. Admit to CCU

- IV access

- O2

- Analgesics (Nitrates n Morphine)


Medications for Acute MI

1. Aspirin

- Prevent reocclusion

- inhibits platelet aggregation

2. B-blocker - less contraction/HR/O2 demand, less arrhythmias, less remodelling

- Carvedilol (CHEARTvedilol reduces risk in Post MI LV dysfnx

- Acute and Maintenance therapy




- decrease demand by supplying O2 and relieving dyspnea

4. Enoxaparin -

- Prevent clot progression

- Part of acute treatment

- Decrease risk of another MI

5. Nitrates - less pain/less myocardial O2 demand by venodilation+coronary dilation

6. Morphine Sulphate

- relieve pain

- Also vasodilation

7. ACE inhibitor

- Decreases mortality

- Must initiate within hours of hospitalization

- Decreases preload and afterload

- Acute and Maintenace therapy

8. Atorvastatin (80mg)

- reduce further events

- stabilize plaques§

- Reduce LDL levels

- maintenance therapy



- Benefit highest if performed within 90mins of arrival

- consider in all pts

- Revascularization options

i. Thrombolysis

ii. PCI

iii. CABG

- PCI > Thrombolysis

- Enhanced survival

- Lower rates of MI recurrence or intracranial bleeds

- If delayed presentation, fibrinolysis alone may be better



- Additive to effects of Aspirin in MI pts

- Give to pts undergoing PCI/stent placement

- Aspirin + Clopidogrel x 30 days (if bare mental stent)

- Aspirin + Clopidogrel x 12months (if drug eluting stent)


Cardiac Rehabilitation

- Post MI

- Physician supervised

- Regimen of Exercise and Risk factor reduction

- Reduces symptoms and prolongs survival


MI Complications

-   CHF

-   Arrhythmias

-   Re-infarction

-   Mechanical complications

-   Acute Pericarditis

-   Dresslers syndrome (Autoimmune phenomenon)

1. CHF

- Most common cause of in-hospital mortality

- If Mild = ACE inhibitor/Diuretic

- If Severe = Invasive hemodynamic monitoring


2. Arrhythmias

If Pre Ventricular Contractions (PVCs)

- Observe

If A.Fib

- Anticoagulation, Rate control, Rhythm control, cardioversion.

If sustained VT

- Antiarrhythmic if Pt is stable (IV amiodarone)

- Electrical cardioversion if pt is unstable

If Ventricular Fibrillation

- Fatal

- Common cause of death few days post MI

- Requires immediate treatment

- Immediate Unsynchronized defibrillation and CPR

If Accelerated Idioventricular rhythm

- No tx needed



If Sinus tachycardia

- Treat underlying cause

- May worsen ischemia

- causes include

i. Pain

ii. Anxiety

iii. Fever

iv. Pericarditis (Post-MI)

v. Medications (e.g CCB)

If Sinus bradycardia

- seen in early stages of MI (often in right/inferior MI)

- may be protective

- Observation, No management required

- if severe bradycardia = Atropine (Anti-mus)

If Asystole

- High mortality rate

- First mgt is Electrical defibrillation (done for Ventricular fibrillation, its difficult to differentiate it from Asystole)

- If Asystole is clear causes, Mgt is transcutaneous pacing

If AV block

- refers to Ishemia affecting conduction tracts

- 1st and 2nd degree (Type 1) heart blocks don't require therapy

- 2nd degree (Type 2) and 3rd degree require treatment

-- Prognosis is usually poor

-- Management is Emergent temporary pace maker

-- Prognosis is better in inferior MI (Use IV atropine, Temp pacemaker if conduction is not restored)


3. Recurrent infarction

- Either Extension or reinfarction of new arrea

- Dx is difficult

- re-elevation of CK-MB after about 2days may be used for dx.

- if repeat ST segment elevation within first 24 hours.

- Tx with

-- Repeat thrombolysis or

-- Urgent catheterization and PCI

-- Continue standrd acute mi therapy (BAAS)


Mechanical Complications of MI

Free wall ruupture

- Often fatal (90%)

- Occurs in < 2weeks (often 1-4 days)

- leads to

i. Hemopericardium

ii. Tamponade (Twoponade occurs in < 2 weeks)

- Treatment

i. Stabilizaion

ii. immediate pericardiocentensis



Surgical repair


Rupture of Interventricular septum

- Post-MI VSD

- Better prognosis vs free wall rupture

- InTENventricular septum rupture occurs within 10 days after MI

- Survival correlates with size of defect


Papillary muscle rupture

- Presents with a new murmur (MR)

- Obtain echocardiogram immediately

- Requires Emergent Mitral valve replacement

- Reduce afterload with

i. Nitroprusside or

ii. Intra-aortic balloon pump (IABP)


Ventricular Pseudo-aneurysm

- Pericardium contains myocardial rupture

- Risk of progression to complete free wall rupture

- Diagnosis is bedside echocardiogram

- It is a Surgical emergency


Ventricular Aneurysm

- Rarely ruptures

- Associated with ventricular tachy-arrhythmias

- Surgery may be appropriate


Acute Pericarditis

- Decreased. incidence since revascularization techniques

- Management is Aspirin


i. NSAIDS (May hinder scar formation)

ii. Steroids (May hinder scar formation)


Dressler syndrome

- Post MI autoimmune syndrome

- occurs weeks/months post MI

- Syndrome of

i. Fever

ii. Malaise

iii. Pericarditis

iv. Leukocytosis (cause of fever)

v. Pleuritis

- Management is Aspirin > Ibuprofen.


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