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123 Cards in this Set

  • Front
  • Back

Coronary Artery Disease

- Most common problem encountered in US adults

Ischemia

- Inadequate blood supply to the myocardium


- Myocardial contraction becomes abnormal immediately after the onset of ischemia

Order of Ischemia Occurrences

1. Ischemia


2. RWMA


3. EKG Changes


4. Pain

Coronary Angiogram

- Invasive procedure


- Visualizes coronary arteries directly


- Gold standard for assessing coronary artery anatomy

Role of Echo in CAD



- TTE and TEE should detect most, if not all mechanical complications of MI


- Use stress echo to predict myocardial viability and prognosis/detecting CAD


- Early detection of MI (before EKG changes)

Angiogram

- Patient is awake but lightly sedated


- Use catheter entered through the femoral or radial artery and threaded through to the coronary arteries


- Watch fluoroscope on screen and inject contrast dye to visualize arteries and look for blockages and determine whether intervention is needed

Atherosclerosis

Hardening of plaque forming in artery.

Angioplasty (PTCA)

- Procedure to open blocked arteries


- PTCA: Percutaneous Transluminal Coronary Angioplasty


- Use tiny balloon to push plaque into wall


- Sometimes put a stent in, a stent is a small metal coil or tube to prevent artery from narrowing

Atherectomy

- Use catheter with grinding device to find plaque into small bits which float away into bloodstream

CABG

- Coronary Artery Bypass Graft


- Performed when multiple arteries are blocked with diffuse disease (spread out over a lot of the heart)

Angina

- Chest pain due to myocardial ischemia that is not associated with clinical evidence of acute MI


- 3 Types: stable, unstable, and Prinzmetal's

Stable Angina

Occurs with exercise and is relieved by rest or medications.

Unstable Angina

May occur at rest or during sleep or may indicate a notable change in the nature of previously stale angina (pre-infarction angina).

Prinzmetal's Angina

- Occurs exclusively at rest and usually during the night


- Due to coronary spasm

Asymptomatic Ischemic Disease

- Diabetics are prone to this


- 2/3 of people with diabetes mellitus die of some form of heart or blood vessel disease

Medications Used in CAD

- Nitrates


- Beta Blockers


- Calcium Channel Blockers


- Digitalis Glycosides

Nitrates

- Names: Isordil, Isosorbide dinitrate, cardilate, nitrobid, Nitroglycerin


- Vasodilators


- Relax the smooth muscle in veins/arteries/arterioles


- Reduce RV and LV preload and afterload


- Decreases cardiac work


- Lowers myocardial oxygen requirement


- 1st drug of choice for treating acute angina

Beta Blockers

- Names: Inderal, corgard, lopressor, tenormin, atenolol


- Reduces HR at rest and during exercise


- Reduces contractility which effects myocardial demand


- Reduces systemic BP


- Blocks effects of epinephrine and adrenaline

Calcium Channel Blocker

- Names: Calan, cardizem, diltiazem, nifedipine, procardia, verapamil


- Potent arterial/coronary vasodilator


- Decreases myocardial contractility


- Decreases HR


- Increases coronary flow

Digitalis Glycosides

- Names: Digoxin, lanoxin


- Increases peripheral and coronary vascular resistance


- Increases the contractile state of the myocardium


- Increases HR


- Promotes elimination of fluid from tissues


- Used to treat some arrhythmias

ACE Inhibitors

- Angiotensin converting enzyme inhibitors


- Prevents constriction of blood vessels


- Decreases afterload


- Increases contractility

Antiarrythmics

- Lidocaine


- Bretylium


- Procainamide

Antihypertensives

Lopressor

Diuretics

- Fluid reduction


- Lasix


- Furosemide

Coronary arteries and their branches:

Right coronary artery--branches to posterior descending artery (70% of the time) and acute marginal artery




Left main coronary artery--branches to left anterior descending artery and left circumflex artery

When do the coronary arteries fill with blood?

Mostly during diastole.

Coronary Artery Dominance

- Where the posterior descending artery originates


- PDA supplies basal 1/3 of the septum


- RCA--70% (right dominant)


- LCA--10% (left dominant)


- RCA and LCX--20% (co-dominant

How much of the myocardium is supplied by each artery?

LAD- supplies 50% of the myocardium


RCA- supplies 25% of the myocardium


LCX- supplies 25% of the myocardium




PDA- supplies the basal 1/3 of the septum

Wall Motion Scoring

1- Normal


2- Hypokinetic


3- Akinetic


4- Dyskinetic


5- Aneurysmal

1- Normal Wall Motion

Systolic contraction and wall thickening increase more than 50%

2- Hypokinetic Wall Motion

Reduced systolic wall thickening (<40%)

3- Akinetic Wall Motion

Diastolic wall thickness is usually thin and systolic wall thickening of less than 10% (or no thickening)

4- Dyskinetic Wall Motion

Diastolic wall thickness is think and movement of the myocardium is outward in systole

5- Aneurysmal Wall Motion

Constantly deformed segment throughout cardiac cycle

WMSI (Wall Motion Score Index)

WMSI = sum of wall motion score / # of segments visualized




1 = Normal (any greater means infarct)

Stress Testing Purpose

- To induce ischemia by increasing oxygen demand.




- To increase cardiac workload to elicit signs of physiologic dysfunction in many types of cardiac disease




- GOAL: for patient to reach target heart rate

Types of Stress Testing

- Stress EKG


- Exercise Stress Echo (treadmill, supine bike, upright bike)


- Pharmacological (dobutamine)

Stress EKG

- Patient hooked to 12 lead EKG


- Take resting BP and EKG


- Exercised according to protocol


- END POINTS: target HR, EKG changes, abnormal BP change, symptoms




* not as sensitive as stress echo *

Treadmill Stress Echo Indications

- CAD (known or suspected)


- Chest pain, shortness of breath


- Before surgery/intervention (determine risk)


- Abnormal EKG


- Evaluate LV function


- Identity viable, hibernating, or stunned myocardium


- Evaluate hemodynamics in valvular/cardiomyopathy heart disease

Treadmill Stress Echo

- Combines baseline echo with peak/post exercise echo to detect and assess known or suspected CAD


- 12 lead EKG in addition to echo imaging

Contraindications for TSE

- Acute MI (within 2 days)


- Unstable angina


- Uncontrolled ventricular arrythmias


- Symptomatic AS (resting gradient >50 mmHg) **may cause them to pass out


- Acute pulmonary embolism


- Acute myocarditis/pericarditis


- Pregnancy

TSE Procedure

- Patient hooked to 12 lead EKG


- Take resting BP, EKG, and echo (evaluate valves, ventricular function, acquire before images)


- Exercised according to protocol (Bruce protocol)


- END POINTS: reaches target HR+, EKG changes, abnormal BP changes, symptoms, end of protocol reached


- Immediately POST exercise: attain images within 60 seconds ( A2C, A4C, PLAX, PSAX pap.)



Bruce Protocol

Target HR = 220 - age




- 3 minute stages


- % grade and mph change every 3 minutes


- Protocol starts at 10% grade and 1.7 mph

Advantages/Disadvantages TSE

Advantages:


- non-invasive


- high total workload




Disadvantages:


- imaging only done after exercise


- WMA's may resolve quickly and be missed

Dobutamine Stress Echo

- Use medication via IV infusion instead of physical exercise to raise HR and mimic effects of exercise


- Done on patients unable to exercise

Dobutamine Stress Echo Procedure

- Patient hooked to 12 lead EKG


- Take resting BP, EKG, and echo (evaluate valves, ventricular function, acquire before images)


- Saline IV started by RN prior to resting echo


- Infusion of dopamine begins (started at 5 mpg/kg/min and increased at 3 minute intervals (5, 10, 20, 30)


- Echo images acquired at low dose and peak dose as well as recovery


- Absolute end point: target HR reached

Supine Bike Stress Echo Protocol

- Begins at workload of 25 watts and a cadence of 60 rpm


- Increased by 25 watts every 2 minutes


- Images acquired throughout exercise

Supine Bike Stress Echo Advantages/Disadvantages

Advantages:


- Able to images throughout exercise, particularly at peak stress




Disadvantages:


- Some patients find bicycling in the supine position difficult, and inadequate levels of stress may be achieved


- May be hard to scan because they move as they bike

Normal at rest, Hyperkinetic when stressed

Interpreted as normal

Normal at rest, Hypokinetic/Akinetic when stressed

Interpreted as ischemic

Akinetic at rest, Akinetic when stressed

Interpreted as infarction

Hypokinetic at rest, Akinetic/dyskinetic when stressed

Interpreted as ischemic and or infarction

Hypokinetic/Akinetic at rest, Normal when stressed

Determines that the myocardium is still viable

Positive Stress Echo

- Normal wall motion at rest becomes hypokinetic, akinetic, or dyskinetic when stressed


- Wall motion after exercise fails to become hyperdynamic


- Increase in size of LV and or shape after exercise


- Decrease in EF

Negative Stress Echo

Normal

Positive SEKG with Negative SE

SEKG thought to be a false positive.

LV Volume Changes during Stress

Normal Response:


- A decrease in both ESV and EDV




Abnormal Response:


- Failure of the ESV to decrease


- Increase in both ESV and EDV usually indicates severe and extensive multi-vessel disease

False Negative Stress Echo

- Inadequate response to stress by not reaching target HR


- Mild CAD or single vessel disease present


- Collaterals have formed

False Positive Stress Echo

- Hypertrophic Cardiomyopathy


- Hypertension

Ischemia

Ischemia:


- Myocardium will appear hypokinetic/akinetic


- WMA will return to baseline between ischemic events


- Reversible WMA



Hibernating Myocardium

Hibernating Myocardium:


- Reversible WMA


- Due to chronic disease in blood supply


- Viable myocardium

Stunned Myocardium

Stunned Myocardium:


- Occurs after reperfusion therapy


- Reversible WMA


- Viable myocardium

Other Modalities to Assess Ischemia

- Doppler SE


- Intravascular US


- Contrast agents to assess perfusion


- CT angiography


- Cardiac MRI


- Nuclear medicine stress test


- PET imaging


- Angiography (gold standard)

Sensitivity

% of sick people correctly identified as having the disease




100%--predicting all sick people as being sick

Specificity

% of healthy people correctly identified as not having the disease




100%--not predicting any healthy people as having the disease

Which leads are related to which parts of the heart?

Inferior: II, III, aVF


Septal: V1, V2


Anterior: V3, V4


Lateral: I, aVL, V5, V6


RV Infarct: V4R

P Wave

Atrial systole/depolarization

PR Interval

Onset of atrial depolarization to onset of QRS (ventricular depolarization)

QRS Complex

Ventricular systole/depolarization

ST Segment

Represents period when ventricles are depolarized.

T Wave

Ventricular repolarization

How many electrodes in a 12 lead EKG?

10 (6 on chest, 4 on limbs)

Chest Leads

V1-V6

Bipolar Leads

Limb leads (I, II, III)

Unipolar Leads

Augmented limb leads (aVR, aVL, aVF)




Precordial leads (V1, V6)

ST Depression

- Any lead but aVR


- Ischemia


- Subendocardial infarct


- During exercise, its a positive stress test

ST Elevation

- Any lead but aVR


- Also called STEMI


- Acute MI


- Could also be pericarditis/tamponade/cardiac contusion

Q Waves (Significant vs. Insignificant)

Significant: 1 mm wide (one small square), and/or at least 1/3 the height of the QRS



Insignificant: Does not meet above criteria




- any lead but aVR

Flattened T Waves

- in leads V2-V6




Ischemia

Inverted T Waves

- in leads V2-V6




Ischemia

Atherosclerosis

- Disease of the intima (inner layer of artery)


- Gets thick with fatty deposits, calcium, and fibrous tissue (lumen gets smaller)


- Has to be 75% narrowed for symptoms on exertion


- Has to be 90% narrowed for symptoms at rest


- How well myocardium works is better prognosis than how badly occluded arteries are.

Arteriosclerosis

- Characterized by hardening, loss of elasticity, and thickening of arterial walls


- Results in decreased blood supply

Ischemia

- Inadequate perfusion


- Reversible


- See hypokinetic or akinetic RWMA

Most deaths from infarcts occur with:

Anteroseptal infarcts

Most hospitalizations from infarcts occur with:

Inferoseptal infarcts

Infarction

- Dead myocardium


- Irreversible


- See akinetic or dyskinetic RWMA

Acute MI

- Akinetic wall motion with normal wall thickness


- Opposing walls may be hyperkinetic


- ST segment elevation usually seen on EKG

Old MI

- Akinetic wall motion with thinned echogenic myocardium


- Significant Q waves may be present on EKG

Transmural MI

- Injury > 50 % of myocardium thickness

Subendocardial MI/Non Q wave MI

- Injury < 50 % of myocardial thickness

Silent MI

- Asymptomatic


- Up to 1/3 of MI's are silent


- Often seen with diabetic patients

Stunned Myocardium

- Associated with reperfusion therapy


- WMA may last up to 72 hrs after therapy

Hibernating Myocardium

- Prolonged ischemia


- Reversible


- Bi-phasic response to dopamine

Echo Assessment to Rule Out MI

- Use all windows to assess wall motion


- Must see endocardium!!!


- Assess diastolic function


- Be aware of imaging pitfalls

Diagnosing MI

Two of the following:


- Symptoms


- EKG changes


- Cardiac enzymes

Cardiac Enzymes

Proteins from the heart muscle cells that are released into the bloodstream when heart muscle is damaged.

Troponin

- Cardiac enzyme


- Early marker of cardiac cell damage


- Elevates 3-6 hrs after MI


- Peaks 10-24 hrs after MI


- Falls > 7 days

Creatine Kinase

- Cardiac enzyme


- Later marker of cardiac cell damage


- Elevates in 3-12 hrs after MI


- Peaks in 12-24 hrs after MI


- Falls in 1-3 days

What cardiac enzyme is useful in patients who present late?

Lactic Dehydrogenase (LDH)

What enzyme is released when body tissue is damaged and isn't specific to the heart?

Aspartate Transaminase (AST)

Different Methods to Diagnose MI

- Perfusion study (good specificity)


- Echo (portable, better sensitivity)


- Coronary Angiogram (both diagnosis/intervention)


- Cardiac Short Stay Units: non diagnostic but suspicious for ruling out MI (monitor things before doing anything invasive)

Infarction Stages

Week 1: Inflammation stage (increase WBC's)


Week 2: Clean up stage


Week 3-4: Healing phase (scar formation)

Ischemic Heart Disease

- Impaired systolic function due to numerous MI's over time


- Definite areas of akinesia or thinned myocardium


- MR in absence of MV abnormalities


- Elevated PA pressures

Chronic Valve Disease

- Mitral regurgitation due to anatomic abnormalities of the mitral valve


- LV enlargement due to systolic dysfunction


- High PA pressures

Dilated Cardiomyopathy

- Often idiopathic


- More global WMA's than specific RWMA


- Usually both RV and LV are dilated


- MR in absence of MV abnormalities


- Moderate to severe TR


- Elevated PA pressures

Warning signs of MI

- Chest discomfort


- Upper body discomfort


- Shortness of breath


- Nausea


- Lightheadedness


- Anxiety

What percentage of patients with coronary atherosclerosis who suffer an acute cardiac arrest will die within one hour?

50%

Of the patients that survive and have a diagnosis of acute MI, what percentage will have an uncomplicated hospital course?

50%, the other 50% will experience one or more complications

Complications of MI

- LV remodeling


- True aneurysm


- Pseudoaneurysm


- Cardiac rupture


- LV thrombus


- Dressler's syndrome


- Cardiogenic shock


- RV infarct

LV Remodeling

- Volume does not get bigger but infarcted region begins to stretch and thin


- Outward bulging of the infarcted wall during systole


- Not a good prognosis

True Aneurysm

- Lined by myocardium


- Wall motion is dyskinetic & fixed


- Area of bulging result in wall thinning and or infarct expansion


- Apical aneurysms are most common


- Usually don't rupture once healed


- 50% are filled with thrombi


- Only found in transmural infarctions

Pseudoaneurysm

- Chronic, contained ventricular rupture


- Wall is made of pericardium


- Narrow neck from LV into pseudo aneurysm


- Only found in transmural infarctions


- Surgical repair necessary due to high chance of spontaneous rupture

Cardiac Rupture

- Catastrophic and often fatal complication of acute MI


- Tends to occur in first week


- Infarcted wall is maximally soft and weak


- Types: free wall, ventricular septal, papillary muscle

Free Wall Rupture

- Blood enters pericardium causing pericardial tamponade


- Life threatening unless sealed by thrombus


- Rapidly fatal in 85% of cases


- Only found in transmural infarctions

Ventricular Septal Rupture

- Acute VSD: shunt between LV and RV


- New, loud, harsh systolic murmur


- Bad prognosis: makes up 10% of rupture cases


- 50% mortality



MV Papillary Muscle Rupture Types

Partial: rocking or flapping of papillary muscle




Complete: flail MV with an attached mass in LA



MV Papillary Muscle Rupture

- 80% posteromedial pap. muscle


- 20% anterolateral pap. muscle


- New systolic murmur


- Better prognosis: makes up 5% of rupture cases

Conditions for thrombus formation:

- Area of dilation


- Area of WMA


- Presence of spontaneous echo contrast ("smoke" in the LV)

Types of LV Thrombus

Pedunculated thrombus:


- protrudes into LV cavity




Mural thrombus:


- adheres to endocardium

Dressler's Syndrome

- Post-infarction syndrome occurs weeks to months after MI


- Characterized by: recurrent low grade fever, pleropericardial chest pain, pericardial friction rub, pleural effusions, pericardial effusion

Cardiogenic Shock

- Cannot maintain CO


- May lead to death


- Complication of large MI (>40% loss of LV mass)

RV Infarct

- Associated with LV inferior wall infarct


- Assess for WMA or chamber enlargement


- Observe for right heart failure

Pericardial Effusion

Fluid in pericardial space