January 7, 2016 - Clinical Presentations of IHD Flashcards Preview

COURSE 3 > January 7, 2016 - Clinical Presentations of IHD > Flashcards

Flashcards in January 7, 2016 - Clinical Presentations of IHD Deck (22):

Chest Pain

Caused by a wide variety of disease processes involving a number of systems such as cardiac, pulmonary, MSK, GI, vascular etc.

Results in millions of ER visits each year, and can be difficult to sort out.

You need to rule out the causes of chest pain which can kill a patient.


DDx for Chest Pain

Life Threatening: MI/Cardiac ischemia, aortic dissection, tension pneumothorax, esophageal rupture, pulmonary embolus, perforating ulcer

Non-Life Threatening: Pericarditis, myocarditis, vasospastic angina, dysrythmia (Afib, SVT) with hypoperfusion

Non-Cardiac: GERD, MSK-related, pleurisy/pneumonia, biliary/pancreatic, neuropathic, anxiety



Angina is pain, discomfort, or pressure localized in the chest caused by an insufficient supply of blood (ischemia) to the heart muscle.

Not everyone gets chest pain.

Can also get "Angina Equivelants" which are symptoms such as dyspnea, SOB, diaphoresis, extreme fatigue, or pain at a site other than the chest. When this occurs in a patient at high cardiac risk, it is considered an angina equivelant.

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Distinguishing Cardiac from Non-Cardiac Pain

Character/sensation: anything goes

Location and radiation: anything from epigastrium to the teeth

Mode of onset/pattern: usually occurs with activity, stress, post-prandially, or in ice weather

Excaberating/alleviating factors: usually with rest

Severity: anything goes


More likely to be cardiac if pain gets worse and better with...

Gets worse with...


Cold weather

Eating a large meal



Gets better with...




Typical Angina

Begins gradually and increases over minutes.

Worsened by activity, stress, cold, and/or eating.

Not affected by movement, position, or respiration.

Relieved within 5-10 minutes of rest or NTG.


♦ The more typical the angina, the more likely it is to be due to myocardial ischemia and the more likely the patient has coronary artery disease.


Atypical Angina

Lasts for seconds or hours.

Not worsened by activity, cold or eating.

Not relieved by rest or NTG.

Plueritic, focal, or reproduced by movement or palpation.


Stable vs Unstable Angina

Stable angina has a predictable pattern, no rest pain, and no change in frequency, severity or duration.

Unstable angina is the new onset of angina, an increase in the frequency, severity or duration of angina, or angina at rest.


CCS Classification of Angina

Class I - ordinary phyiscal activity does not cause angina. Angina with strenous, rapid or prolonged exertion.

Class II - slight limitation of ordinary activity. Angina with walking more than two blocks on level or climbing more than one flight of stairs.

Class III - marked limitation of ordinary physical activity. Angina with walking one or two blocks.

Class IV - inability to carry out any physical activity without discomfort; angina may be present at rest.


Pathophysiology of Angina

Angina results from myocardial ischemia. 

This is a result of imbalance between myocardial oxygen requirements and myocardial oxygen supply.


Coronary Vasospasm

Accounts for ~2% of angina - also known as Prinzmetal's Angina.

Almost always occurs at rest and not usually associated with physical exertion. Triggers can include exposure to cold, emotional stress, smoking, cocaine use, and medications that cause the coronary arteries to narrow (ventolin, epi, etc.)

Usually quickly relieved with NTG. Can be made worse by beta blockers.

If prolonged, untreated coronary vasospasm can result in myocardial infraction, ventricular dysrhythmias, heart failure or death.

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Acute Coronary Syndromes

1. Unstable angina

2. Non ST-elevation myocardial infarction (NSTEMI)

3. ST-elevation myocardial infraction (STEMI)


Making the Diagnosis of ACS

1. History (including pain history)

2. ECG

3. Cardiac markers



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Why is ECG Different in UA/NSTEMI vs STEMI

Due to the nature of the cardial injury.

In UA/NSTEMI there is subendocardial injury which causes the current to go towards the damage if the artery is not completely closed, resulting in an ST depression.

In a STEMI there is transmural (epicardial) injury where the current will flow towards the positve node and show ST elevation.

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Cardiac Necrosis Biomarkers

Most specific markers are cTnT and cTnI

More specific markers are CK-MB and CK isoforms


Troponin takes about 4 hours to rise and will stay elevated for up to 10 days. CK is more short lived and can be useful in determining if the patient had a second MI.

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Plaques and MI

90% of acute MIs are caused by thrombus formation from rupture of unstable plaques.

Plaques rupture, and when they do fibrin is exposed to clotting factors in the blood which causes a thrombus to form and may block the artery.


Clinical Features of UA

Angina is new in onset or more frequent, more severe, or more easily provoked than before.

Symptoms can be progressive over the course of days or weeks (crescendo angina) or can occur acutely. Angina will usually settle with rest and/or medical management.


Clinical Features of NSTEMI

Angina will typically begin at rest and last for more than 20 minutes. Patients may have had episodic angina in the preceding weeks. Associated symptoms are often present. Symptoms usually settle with medical management, especially NTG.


Clinical Features of STEMI

Generally the sickest of ACS patients. Angina usually persists despite rest and medical management. Patients usually have associated symptoms and look unwell. Angina persists until the occluded artery is opened or until the infract has completed (dead muscle is painless).



An inflammation of the pericardium. 

Chest pain is often present. The causes of pericarditis can include infections of the pericardium by viruses and bacteria, uremic pericarditis, post-infarct pericarditis, or Dressler's syndrome (weeks to months after a heart attack).

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