Session 6

Differentiate the five physiologic causes of hypoxemia on clinical and laboratory grounds and identify
common causes of each.

1. Hypoventilation

• P(A-a) O2 is normal but PaCO2 is elevated (hypercapnia)

• Increase the fraction of inspired oxygen (FIO2) to alleviate hypoxemia • To
correct for hypercapnia, use mechanical ventilation CAUSES:

• Depression of CNS by drugs

• Neuromuscular weakness/dysfunction
• Inflammation, trauma or hemorrhage in the brainstem
• Airway obstruction (foreign body, kinked endotracheal tube, mucous plug)
• Abnormal spinal cord pathway

2. V/Q mismatch (ventilation-perfusion inequality)

• P(A-a)O2 is elevated and PaCO2 is normal

• MOST COMMON CAUSE OF HYPOXEMIA IN DISEASE STATES
CAUSES: lung diseases such as pneumonia, CHF, atelectasis (collapse of alveolar tissue) and asthma 3.

Shunt (R L)

• P(A-a)O2 is elevated and PaCO2 is normal

• KEY CLINICAL FEATURE: hypoxemia can NOT be corrected with administration of supplemental
oxygen

MECHANISM/CAUSES:

• Anatomic causes in patients with congenital anomalies

• Severe V/Q mismatch: Pneumonia, drowning, pulmonary edema
• Endotracheal tube slipping into a mainstem bronchus (endobronchial intubation)
• Lung collapse from significant atelectasis
4. Diffusion impairment

• P(A-a)O2 is normal at rest (may elevate during exercise) and PaCO2 is normal
• Is rare

CAUSES: interstitial lung disease

5. Low inspired oxygen (FiO2)

• P(A-a)O2 is normal but PaCO2 is decreased (hypocapnia) due to hyperventilation in response to

hypoxemia (chemoreceptors sense low arterial PO2 and initiate an increase in ventilation)
CAUSES:

• Decreased barometric pressure (ex. Breathing at high altitude)

• Accidental decrease in FIO2 (ex. Anesthesiologist didn’t supply enough oxygen, improper
installation of oxygen supply lines, etc.)
• Not due to disease, but environment
Note: this table from the supplementary reading might be helpful in distinguishing between causes of
hypoxemia:

Identify reasons for inaccurate or discordant paO2 or SpO2 readings.

Note: SpO2 is the peripheral capillary oxygen saturation (used as an estimate of the amount of oxygen in
the blood). It is the saturation of the arterial blood measurement (SaO2) determined by pulse oximetry.

Equipment malfunction can lead to inaccurate readings.

• Examples: probe falls off the patient, interference from cautery (burning a part of a body to
remove or close off part of it), patient motion, hypothermia leading to vasoconstriction of the
digit that the reading is being taken from.

Equipment malfunction can also cause a discrepancy between SpO2 and the actual oxygen saturation on
the blood gas through the following:
 • Equipment failure (faulty pulse oximeter or blood gas analyzer)
• Blood samples that are venous, not arterial
• Blood samples taken from sites affected by local hypoxemia (ischemic limb from BP cuff up or a
tourniquet on)

• Excessive oxygen consumption following blood sample collection (thrombocytosis or massive

leukocytosis)

Identify the expected effects of anemia, methemoglobinemia, and carbon monoxide poisoning on
CaO2, SpO2, paO2, and deoxygenated hemoglobin.

Quickly cram for exam answer:

CaO2 SpO2 paO2 Hemoglobin (Hb)

CO poisoning low normal normal Decreased O2

bound Hb

Anemia profoundly low normal normal Low amount of Hb

Methemoglobinemia low low normal Increased MetHb

In-depth answer:

CARBON MONOXIDE POISIONING

• Carboxyhemoglobin, absorbs at approximately the same wavelength as oxyhemoglobin, so

pulse oximetry readings are a summation of oxy- and carboxy- hemoglobin
• High carboxyhemoglobin levels in CO poisoning make for normal pulse oximetry readings and
thus mask life-threating arterial desaturation
• PaO2 is normal but poor total blood oxygen content (CaO2)
• Hemoglobin-bound O2 is reduced but since oxyhemoglobin and carboxyhemoglobin are the
same colour there is a normal SpO2 reading
• In a CO free environment, CO will release from hemoglobin and be expelled. This can be
accelerated by increasing the PaO2 with supplemental oxygen
• Low true oxygen saturation, red colour, 100% oxygen saturation on pulse oximetry (which is
false), and normal pO2 on arterial blood gas

ANEMIA

• Profoundly decreased CaO2

• Normal PaO2, normal SaO2/SpO2, adequate tissue perfusion
• No benefit to supplemental oxygen
• Small quantity of hemoglobin
Methemoglobinemia
 • SpO2 plateaus at about 86% with increasing levels of MetHb
• PaO2 will be normal
• Low true oxygen saturation, brown colour, low oxygen saturation on pulse oximetry, and
normal pO2 on arterial blood gas.

Explain the difference between CaO2, paO2, cyanosis, and SpO2.

• PaO2 reflects the O2 dissolved in the blood, it is the partial pressure of oxygen.

• SpO2 reflects the proportion of hemoglobin that is saturated with oxygen. It is the saturation of
the arterial blood (SaO2) as determined by pulse oximetry.
• CaO2 is a measure of the total blood oxygen content (the oxygen content of arterial blood) •
CaO2=O2 in HgB + dissolved O2
• Cyanosis:
o CENTRAL: bluish discolouration of skin, lips, tongue, mucous membranes. Is observed
when there is an increase in deoxygenated hemoglobin of >5g/dL (50g/L)
o PERIPHERAL: bluish discolouration limited to extremities. Peripheral without central
suggests poor perfusion such as in cold environments.

Explain the difference between hypoxemia, hypoxia, and asphyxia.

• Hypoxia: low oxygen in the body tissues

• Hypoxemia: low oxygen in the blood, determined by measuring the PaO2 in arterial blood
• Asphyxia: absence of O2 AND accumulation of CO2 in the tissues (hypoventilation) Calculate an
A-a gradient.

A-a gradient=PAO2-PaO2

Calculate a normal A-a gradient for a given age.

From Resp notes: When breathing room air, normal PA-aO2 is less than 12mmHg until age 25 and
increases by 1mmHg for every decade thereafter. At any age, PA-aO2 should be less than 18mmHg.

Ex. A 45-year-old should have an A-a gradient around 14mmHg

What happens to A-a gradient during shunt? What about during V/Q mismatch?

A-a gradient increases during shunt because “a” falls. In V/Q mismatch A-a gradient increases, but unlike
shunt it is treatable by increased FiO2 (fraction of inspired oxygen).

What are some advantages and disadvantages of pulse oximetry?

ADVANTAGES: rapid, non-invasive, provides continuous data

DISADVANTAGES: inability to detect hyperoxemia, inability to measure arterial oxygen tension, inability
to measure ventilation

When developing a differential for acute respiratory distress consider this:

Session 7
Narrow a differential diagnosis for acute focal loss of neurologic function based on history, physical
examination and knowledge of neuroanatomy.

When constructing a differential for acute focal loss of neurologic function, you want to focus on the
time of symptom onset, the course of symptoms over time, possible embolic sources, and concomitant
diseases. It is important to ask patients/relatives about whether the patient takes insulin or oral
hypoglycemic agents, has a history of epilepsy, drug overdose/abuse, or recent trauma. Various
symptoms allow us to rule in or rule out the causes of loss of neurologic function (see illness
scripts/descriptions below). Importantly, hypoxemia and hypoglycemia are not the most likely
conditions on the differential diagnosis of a patient with acute focal neurologic deficits, but we should
still check serum glucose and oxygen saturation. Ischemic stroke is the most common cause of acute
focal neurologic symptoms compared to transient ischemic attacks and intracranial hemorrhage.

Describe an illness script for ischemic stroke, hemorrhagic stroke, and transient ischemic attack.

HEMORRHAGIC STROKE

• Prevalence: Second most common cause of stroke

• Rate of occurrence is highest in Asians and Black Americans
• Risk factors that alter prevalence:
• Hypertension is the most important risk factor
• Older age, high alcohol intake, lower cholesterol, lower LDL cholesterol,
lower triglycerides
• Antithrombotic therapy with warfarin
• Drugs such as cocaine, amphetamines, phenylpropanolamine in appetite suppressants, cold
remedies, caffeine-containing medication
• Black ethnicity
• Positive predictors/presentation:

Onset during routine activity with symptoms increasing gradually over minutes
to hours
 Headache and vomiting are seen in ½ of all intracerebral hemorrhages, If large,
will have increased intracranial pressure and supressed consciousness
Headaches are most common with cerebellar or lobar hemorrhage

Symptoms will differ with location of hemorrhage

Seizures 5-30% of the time, more common with superficial hemorrhage

• Negative predictors: Neurological symptoms abruptly begin and are maximal at
onset (note: this instead suggests brain embolism or subarachnoid hemorrhage)
• Confirmatory tests/Rule out tests: Use non-contrast head CT or MRI
• Prognosis/Diagnosis: Neurologic/medical emergency with elevated risk of
ongoing bleeding, progressive neurologic deterioration, permanent disability and
death

Note: underlying pathological conditions such as amyloid angiopathy, ruptured saccular aneurysm, and
vascular malformation are associated with intracerebral hemorrhages

TRANSIENT ISCHEMIC ATTACK

-A transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia,
without acute infarction

• Prevalence: Roughly half the rate of ischemic strokes

• Risk factors that alter prevalence: Hypertension, diabetes, smoking, cardiac disease, sickle cell
disease, birth control pill
• Positive predictors: Symptoms may be transient, lasting seconds to minutes, most TIAs last less
than one hour. Symptoms are focal suggesting they relate to a localized area of the brain.
Symptoms and signs fluctuate depending upon the adequacy of perfusion and underlying
vascular cause. Ex. Carotid artery occlusion can cause monocular blindness, weakness, aphasia.
Occlusive lesions to middle and anterior cerebral arteries causes loss of cerebral hemisphere
functions. Lesions to vertebral or basilar arteries cause brainstem and cerebellar symptoms.
Occlusion of posterior cerebral arteries cause visual and somatosensory symptoms.
• Negative predictors: Ischemic attack lasting longer than one hour, Vomiting, Headache at the
same time or directly after neurologic symptoms
• Confirmatory tests/Rule out tests: MRI or CT should be completed, Delayed imagining is
negative
• Prognosis: Symptoms and signs remain indefinitely if the brain becomes irreversibly damaged
and infarction occurs, Patients are at a 4-10% risk of ischemic stroke in following 2 days

ISCHEMIC STROKE

• Prevalence: Most common cause of stroke

 • Risk factors: Older age, Anemia, a fib, cancer, coronary artery disease, HYPERTENSION, Smoker
Birth control pill

• Positive predictors:

o Three most predictive examination finding for acute stroke are facial paresis, arm
drift/weakness, and abnormal speech
o Sudden loss of focal brain function
• Negative predictors: Normal examination, quick full recovery
• Confirmatory tests/Rule out tests: Urgent MRI or noncontrast CT should be completed-to
exclude hemorrhage, identify vascular lesion: Serum glucose, Oxygen saturation
• Treatment: Establishing time of symptom onset is main determinant for eligibility of intravenous
thrombolysis treatment

What are positive and negative Jacksonian symptoms?

Positive symptoms indicate active discharge from CNS neurons. Typical positive symptoms ca be visual
(ex. bright lines), auditory (ex. tinnitus), somatosensory (ex. burning, pain), or motor (ex. jerking
movements).

Negative symptoms indicate an absence or loss of function, such as loss of vision, hearing, feeling, or
ability to move a part of the body. Ex. incoordination of one limb

Differentiate stroke from other acute focal neurologic syndromes including migraine, seizures, brain
tumors, psychogenic illness, and hypoglycemia.

• SEIZURES: can be followed by paralysis or loss of other functions after the seizure. History and
physical exam may reveal presence of seizure disorder (minor twitching of a digit, tingling
sensation in a limb). Loss of consciousness is common in seizures, rare in TIAs. Seizures last
30seconds-3minutes.
• MIGRAINE AURA: an aura presents as a progressive neurologic deficit or disturbance with
subsequent complete recovery. Headaches occur with the aura, or after. Most migraine auras
resolve in 20-30minutes, but can persist for hours. Auras involve visual disturbances, sensory
symptoms, motor weakness, speech disturbances.
• HYPOGLYCEMIA: Uncommon, metabolic perturbation associated with focal neurologic deficits,
low serum glucose
• BRAIN TUMORS: Occasionally result in transient neurological symptoms, mechanical change
that results in pressure on structures adjacent to the tumor
• PSYCHOGENIC DISORDERS: can be confused with organic loss of function due to symptoms
(I’m guessing you could use a psych interview and neuroimaging to rule this in/out)
To differentiate TIAs from seizures and migraines:
Seizures and migraine auras begin with positive symptoms, while TIAs are characterized by negative
symptoms. Migraine auras progress slowly within one sense modality (ex. bright objects move slowly
across the visual field) and progress from one modality (ex. vision) to another (ex. somatosensation).
Differently seizures usually consist of positive phenomena in one modality which progress very quickly,
during seconds. In TIA, symptoms are negative and when more than one modality or function is
involved, they are all affected at about the same time.

Seizures occur sporadically over the years, but sometimes appear in flurries. TIAs cluster during a finite
period of time and can occur as frequent “shotgun”-like attacks. Attacks that are scattered over many
years are almost always either faints, migraines, or seizures; TIAs almost never continue over this
time span.

Headache is common after migraine aura and following a seizure. Headache can occur during a TIA, but
rarely at the same time or directly after neurologic symptoms.

Vomiting is common after migraine, but extremely rare after/during TIA and seizures.

Seizures occur at any age, while TIAs are not common in young individuals without risk of vascular
disease

Define stupor.

A partial or nearly complete unconsciousness, a lowered level of consciousness.

Document clinical reasoning using a SOAP note.

S=subjective=what the patient reports and what the family reports

O=objective=what the physician observes directly; physical exam and patient’s demeanor, tone,
organization. Observations made by other health professionals is also objective.

A=assessment=the most important part of the SOAP note. Where the writer communicates his/her
understanding of the problem in a few words.

P=plan=record of all tests ordered, procedures performed, prescriptions written, and a summary of
what was discussed with the patient.

Session 8
What is the purpose of diagnostic studies?

Diagnostic studies aim to measure the accuracy of a diagnostic test by comparing the results of the
diagnostic test being studied to the results of a “gold-standard” test that is assumed to be 100%
accurate. The accuracy of a dichotomous variable (ex. alive or dead) is measured with sensitivity and
specificity.

Quantify the value of a diagnostic imaging study using sensitivity and specificity.
Sensitivity and specificity are useful measurements to quantifiably compare different diagnostic tests
because their value is independent of the prevalence/pretest probability of the disease in the
study/your patient. A highly specific test will have no false positives. A highly sensitive test will not miss
anyone with the disease (there would be no false negatives).

Be able to calculate and interpret sensitivity, specificity, positive predictive value, and negative
predictive value for a test.

*Note the background readings go through an example of how to do these calculations.

Recall from pop health:

Sensitivity: proportion of people with the target disorder who have a positive test
Specificity: proportion of people without the target disorder who have a negative test
Positive predictive value: probability that a patient with a positive test result truly has the disease
Negative predictive value: probability that a patient with a negative test result truly doesn’t have the
disease
Use sensitivity, specificity and pretest probability to calculate a post-test probability.

*NOTE that the values of PPV and NPV are dependent on the prevalence/pretest probability of the
disease. This is a serious limitation in interpreting and using PPV and NPV-they will be completely
different numbers if the pretest probability or disease prevalence are different.

Sensitivity= (True positives/total with disease) x100

Specificity= (True negatives/total without the disease) x100
PPV= (True positives/total testing positive)
NPV= (True negatives/total testing negative)

Use sensitivity, specificity and pretest probability to calculate a post-test probability.

To calculate a post test probability, you need to create likelihood ratios. Likelihood ratio values are
independent of the prevalence/pretest probability of a disease. Once you have likelihood ratios you can
use a nomogram to determine the post test probability.

LR+=Sensitivity/ (1-specificity)

LR-=(1-sensitivity)/specificity

Evaluate a diagnostic study for bias based on the criteria from JAMAevidence

When evaluating a diagnostic study for bias, JAMAevidence suggests you ponder the following
questions:

Did participating patients constitute a representative sample of those presenting with a diagnostic
dilemma? o Ex. enrolling target-positive patients (those with the underlying condition of interest) and
target-negative patients (those without the condition) from separate populations results in
overestimates of the diagnostic test’s power
Did investigators compare the test to an appropriate, independent reference standard? o Investigators
should apply an appropriate reference, criterion, or gold standard to every patient who
undergoes the test under investigation

Were those interpreting the test and reference standard blind to the other result? o Ex. once a
clinician sees a pulmonary nodule on CT, they may see the previously undetected lesion
on the chest radiograph
Did all patients receive the same reference standard irrespective of the test results? o Partial

verification bias: only a sample of the patients receive the reference standard o Differential
verification bias: using different reference tests for positive and negative results
Analyze the balance between risk and benefit of a therapeutic or diagnostic intervention.

To treat patients properly we need to consider what level of post test probability to place the treatment
threshold at and the testing threshold. We don’t want to miss cases, by requiring a high post test
probability, but we also don’t want to treat people for something they don’t actually have. For example,
a treatment for ischemic strokes is thrombolytic therapy. Diagnosis of ischemic stokes is based on
history and physical exam alone so that patients with seizures, migraines, or psychogenic illness do not
get this potentially dangerous treatment. The onset of symptoms, serum glucose levels, and head CT
should be consistent with a diagnosis of ischemic stroke to start thrombolytic therapy.

Session 9
Understand the factors that influence the exact location of the treatment threshold in a patient.

The ideal level for the treatment threshold is where the likely benefits are at least equal to the likely
harms. The level of the pretest probability influences the treatment threshold. The pretest probability
may need to be increased to raise a treatment threshold. If there is controversy over the effectiveness
of a treatment then the exact treatment threshold will also be controversial.

Describe the importance of the following in understanding a randomized controlled trial: A control
group, randomization, allocation concealment, blinding, double blinding, triple blinding, intention to
treat analysis, per protocol analysis, placebo effect, and placebo response.

CONTROL GROUP-group not exposed to the intervention. Is important because variables other than the
one you are studying (confounding variables) could impact the outcome you are trying to measure.
Without a control group, we can’t determine how much of the observed benefit was due to the
intervention, or due to confounders that we didn’t measure.

RANDOMIZATION-ensures that possible confounding variables are balanced between the treatment
and control groups.

ALLOCATION CONCEALMENT (randomization concealment)-important so that the groups do not differ. If

the researcher who is recruiting patients for the study can predict which group a patient will be assigned
then that recruiter may be influenced about whether to recruit the patient. Ex. If the recruiter believes
 the treatment is beneficial and is worried that a patient is very sick, they may only be willing to enroll
the patient if it is known that the patient will receive the therapy.

BLINDING-when the patient is unaware of whether they are receiving the intervention or the control.
Important because patients may report their subjective outcomes differently depending on whether
they were exposed to the intervention or not.

DOUBLE BLINDING-when the caregivers are also unaware of whether their patient received an
intervention or the control. Important so that caregivers do not treat patients differently.

TRIPLE BLINDING-when a third party involved in measuring a potentially subjective outcome (ex.
physician reading a CT scan) is also blinded.

PLACEBO EFFECT-purported therapeutic effect of the placebo. This includes both actual therapeutic
effects of believing that one is receiving an active therapy, and changes in the reporting of subjective
outcomes (whether conscious or subconscious).

PLACEBO RESPONSE-describes everything that happens to the control group when they receive a
placebo; this includes the placebo effect plus the natural history of the disease.

INTENTION TO TREAT ANALYSIS-when patients are analyzed by the groups they were randomized to,
regardless of if they crossed over (ex. control patient at risk of dying, given treatment) or were lost to
follow-up. This is important because in clinical trials there may be a variety of reasons why patients do
not receive the treatment to which they have been assigned.

PER-PROTOCOL ANALYSIS-when patients who crossover or are lost to follow-up are simply excluded
from the analysis.

Note: intention to treat does a better job of preserving the benefits of randomization than per protocol,
and is usually preferred as it decreased the risk of bias. The effect size that you calculate for a study will
typically be larger when a per-protocol analysis is used.

Evaluate a randomized controlled trial for bias.

When evaluating a randomized controlled trial for bias consider the following:

Were the patients in the treatment and control groups similar with respect to known prognostic factors?

o The smaller the sample size, the more likely the trial will have prognostic imbalance

Was prognostic balance maintained as the study progressed? To what extent was the study blinded?

o Blinding is the optimal strategy for maintaining prognostic balance

Were the groups prognostically balanced at the study’s completion?

o Was follow-up completed for all patients? o Was the trial stopped too early?

o Were the patients analyzed in the groups to which they were randomized? (intention to
treat analysis)
Apply the results of a therapeutic trial to clinical reasoning in a specific patient.

This is what we did in the actual tutorial (compared a patient with stroke symptoms to study
participants). When applying results from a trial to a patient you need to consider the differences and
similarities between the patient and the trial participants.

Session 10
Define the specified terms in the background notes. These include: atherosclerosis, plaque rupture,
ischemia, infarction, coronary artery disease, ischemic heart disease, angina, stable angina, unstable
angina, myocardial infarction, acute coronary syndrome, STEMI, NSTEMI, crescendo angina, rest
angina, new-onset angina, troponin, cardiac arrest, and congestive heart failure!

ATHEROSCLEROSIS: gradual process of artery obstruction by atherosclerotic plaques (over months to

years)

PLAQUE RUPTURE: a sudden event when the atherosclerotic plaque is disturbed resulting in sudden
severe obstruction of an artery (over minutes to hours).

ISCHEMIA: when tissue is deprived of oxygen, often due to a lack of blood flow, causing cellular
dysfunction.

INFARCTION: tissue death due to prolonged ischemia.

CORONARY ARTERY DISEASE (CAD): atherosclerosis of the coronary arteries.

ISCHEMIC HEART DISEASE (IHD): ischemia or infarction of myocardium due to atherosclerosis of the
coronary arteries.

ANGINA: pain caused by temporary cardiac ischemia without infarction.

STABLE ANGINA: a condition usually due to atherosclerosis and does not greatly increase the short-term
risk of infarction. It consists of angina that occurs only with exercise or other increases in cardiac
demand.

MYOCARDIAL INFARCTION: infarction of cardiac muscle due to prolonged ischemia. The muscle is
replaced with scar tissue and the heart loses some function. Usually caused by plaque rupture.

ACUTE CORONARY SYNDROME (ACS): includes all categories of myocardial ischemia that result in tissue
death or imminent danger of tissue death. This includes STEMI, NSTEMI, and unstable angina.

ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION (STEMI): a diagnosis based on the clinical

presentation and specific ECG findings (ST elevation). In general, STEMIs are larger MIs and have more
tissue loss than NSTEMIs.

NON-ST-SEGMENT ELEVATION MYOCARDIAL INFARCTION (NSTEMI): any myocardial infarction that

doesn’t meet the EKG characteristics of a STEMI
UNSTABLE ANGINA: Unlike MI, ischemia never lasts long enough to cause cell death. It is associated with
high short-term risk of infarction, and/or is not temporally stable. Subtypes include crescendo, rest, and
new-onset anginas.

CRESCENDO ANGINA: Unstable angina, symptoms occur with increasing frequency and with less and less
exertion over a short period of time.

REST ANGINA: Unstable angina, symptoms occur when the patient is at rest.

NEW-ONSET ANGINA: Unstable angina, new symptoms of anginal with minimal physical exertion

TROPONIN: gold-standard blood test to detect cardiac muscle cell death. If negative 3 hours after the
onset of pain, it can be considered negative, and rules out MI as the cause of symptoms. It remains
positive for more than a week after an MI.

CARDIAC ARREST: sudden failure of blood circulation, often due to an irregular heart rhythm. MI results
in irritability to cardiac tissue, that triggers the irregular rhythm and can result in cardiac arrest.

CONGESTIVE HEART FAILURE (CHF): state of cardiac output is insufficient to meet the needs of the body.
This can occur during an MI or after multiple myocardial infarctions, and is characterised by cardiogenic
shock and/or pulmonary edema.

Use the HEART score to identify a patient’s risk of Major Adverse Cardiac Events (MACE). (This
includes memorizing the HEART score and its resultant risks).

The HEART score predicts MACE within 6 weeks of presentation. It is to be used in patients 21 years old
or older presenting with symptoms suggestive of ACS. The HEART score is calculated as followed:
History Slightly suspicious=0
Moderately suspicious=+1 Highly suspicious=+2

EKG* Normal=0
Non-specific repolarization disturbance=+1 Significant ST
depression=+2

Age <45=0
45-64=+1
65+=+2

Risk factors** No known risk factors=0

1-2 risk factors=+1
3 or more risk factors or history of atherosclerotic disease=+2

Initial troponin Equal or less than normal limit=0

1-2x normal limit=+1
>2x normal limit=+2
*EKG: 1 point=no ST depression but LBBB, LVH, repolarization changes (ex. digoxin). 2 points=ST
depression/elevation not due to LBBB, LVH, or digoxin
**Risk factors=HTN, hypercholesterolemia, DM, obesity (BMI >30 kg/m2), smoking (current, or cessation
within last 3 months), positive family history (parent or siblings with CVD before age 65); atherosclerotic
disease: prior MI, PCI/CABG, CVA/TIA, or peripheral arterial disease
Score Risk of MACE

Low score (0-3 points) 0.9-1.7%

Moderate score (4-6 points) 12-16.6%

High score (7-10 points) 50-65%

Use illness scripts to differentiate stable angina, acute coronary syndrome, muscular chest pain, and
gastroesophageal reflux.

MUSCULAR CHEST PAIN

• Prevalence: 1/3 of chest pain presenting to Emergency

• Positive predictors: Localized chest pain. Pain occurring after unusual exertion or trauma,
especially if it started during the exertion or trauma. Reproducibility of pain with specific
movements
• Negative predictors: Visceral symptoms such as nausea or diaphoresis
• Reference standard, tests to confirm or rule out: None
GASTRO ESOPHAGEAL REFLUX DISEASE (GERD)

• Prevalence: 1/3 of chest pain presenting to Emergency

• Positive predictors: Burning character to the pain. Pain may be epigastric, retrosternal, or may
radiate to one or both arms. Associated symptoms include a sour foul taste in the mouth at
times. Pain may be worsened after eating.
• Reference standard: pH testing by esophageal probe (generally not practical)
• Confirmatory test: none
• Test to rule out: none

ACUTE CORONARY SYNDROME

• Prevalence: 13% of chest pain presenting to Emergency

• Positive predictors: STRONG PREDICTOR=chest pain radiating to both arms o Weak predictors:
left arm pain, right shoulder pain, third heart sound on auscultation, hypotension, pulmonary
crackles on auscultation, diaphoresis, nausea or vomiting, history of MI o ECG findings are
better positive predictors: any ST-segment elevation, new ST-segment elevation, new/any
conduction defect, new/any Q wave, ST-depression, T-wave peaking or inversion
o Chest pain is severe and has at least one of 3 features: 1. occurs at rest, lasting
>10minutes 2. Relatively recent onset (within prior 2 weeks) 3. Occurs with a crescendo
pattern (getting more severe, prolonged, frequent)
 o Pain is described with adjectives like squeezing, crushing, and pressure, sometimes
present with dyspnea and syncope.

• Negative predictors: pleuritic chest pain, sharp/stabbing chest pain, positional chest pain, chest
pain reported by palpation
• Confirmatory test: Positive troponin test, ECG with ST segment changes
• Tests to rule out: Negative troponin three hours after the onset of pain
• Reference standard: detection of a rise and/or fall of cardiac biomarker value (preferably
cardiac troponin) with at least one value above the 99th percentile upper reference limit, and at
least on of the following:
o Symptoms of ischemia, development of pathologic Q waves, new significant ST-segment
T-wave changes o Identification of intracoronary thrombus by angiography o Imaging
evidence of new loss of viable myocardium or a new regional wall motion abnormality
OR pathologic findings of acute MI on autopsy
• Treatment: ASA, thrombolytics, PCI
STABLE ANGINA

• Prevalence: 4% of chest pain presenting to Emergency (most patients whose pain resolves in 15
minutes do not go to Emergency)
• Positive/negative predictors: Many positive and negative predictors are the same as those for
ACS. Pain lasting longer than 15 minutes is strongly predictive against stable angina.
• Test to rule in/out: MI can be ruled out with a 3-hour troponin. Stable angina is diagnosed either
clinically, or more commonly with some sort of provocative testing (ex. exercise stress test)
• Prognosis is better for stable angina compared to ACS
• Treatment: mortality is low, and treatment has a modest effect on mortality compared to ACS o
ASA, statins, supervised exercise, quitting smoking, treating hypertension all have a substantial
effect on reducing mortality in the longer run (i.e. over several years). The precise amount of
risk reduction varies but will be in the 25-75% range for the relative risk reduction.

What are atherosclerotic risk factors that are traditionally considered to make ACS more likely?

Smoking, diabetes, hypertension, hyperlipidemia, obesity, physical inactivity, cocaine use, and family
history. Family history is a continuous variable-the more relatives, more closely related, and younger age
of onset make family history more of a risk factor. These factors have poor diagnostic utility for
predicting ACS as a cause of chest pain in ER patients.

How do we decide if a predictor is strong or weak?

Positive predictors with an LR+ >5 are at least moderately predictive. An LR+ of 2-5 is weakly predictive.

Negative predictors with an LR- <0.2 is considered moderately predictive. An LR- of 0.2-0.5 is weakly
predictive.
Make an illness script on their own.

DONE!

Use the SOAP documentation format to communicate and document clinical reasoning.

ALSO DONE! (see tutorial 7 notes above)