CAD 1

Question 1

classical angina

Answer 1

*angina = chest pain
*visceral pressure - tightness/discomfort that is vaguely substernal (difficult to localize)
*classically radiates up to the neck & jaw & down the left arm
*often associated with a sense of unease, dyspnea, diaphoresis, and/or nausea

Question 2

typically, angina is NOT:

Answer 2

*pleuritic
*positional
*reproducible with arm movement
*focal

Question 3

drivers of the symptoms of classical angina

Answer 3

*visceral ischemia → activation of the sympathetic nervous system → anxiety, diaphoresis, nausea
*dyspnea: possibly from mild pulmonary edema in s/o higher LA pressure
*tightness/pain: dermatomal pain distribution

Question 4

dermatomal pain distribution of angina

Answer 4

*the heart itself does not have pain sensation
*when ischemia is present, afferent nerve fibers head from the heart to the spinal column and synapse in part with sensory nerves leaving the spinal column at the same nerve root to apply sensation of different dermatomes
*results in the dermatomal pain distribution associated with angina of radiation to the neck, jaw, and left arm

Question 5

angina is a result of supply-demand mismatch

Answer 5

*when myocardial demand out-strips coronary supply, symptoms can occur
*BUT coronary supply and myocardial demand can vary

Question 6

factors that affect coronary supply

Answer 6

1. amount of time spent in diastole
2. thickness of myocardium
3. coronary stenoses

Question 7

factors that affect coronary supply: amount of time in diastole

Answer 7

*coronary arteries fill during diastole
*faster heart rate → less time in diastole → less blood in coronaries

Question 8

factors that affect coronary supply: myocardial thickness

Answer 8

*thicker myocardium → increased perfusion pressure needed to get to the subendocardium → more difficult to get blood into coronaries

Question 9

factors that affect coronary supply: coronary stenoses

Answer 9

*fixed, stable atherosclerotic plaque in the coronary artery
*mechanical obstruction which limits coronary blood flow
*when demand exceeds supply, patient develops symptoms
*note - blood flow is coronary arteries is not typically limited until a stenosis is > 70% (because coronary arteries have high coronary flow reserve → you can dilate to accommodate stenosis that happens over the decades)

Question 10

factors that affect myocardial oxygen demand

Answer 10

1. contractility
2. heart rate
3. wall stress

Question 11

factors that affect myocardial oxygen demand: contractility

Answer 11

*increased contractility = heart squeezes harder = more work → need more O2
*contractility increases with a rise in sympathetic tone:
-exertional symptoms: climbing stairs/hills, running
-stress/anxiety: getting upset/arguing

Question 12

factors that affect myocardial oxygen demand: heart rate

Answer 12

*increased HR = heart beats faster = more work → need more O2
*HR increases with a rise in sympathetic tone:
-exertional symptoms: climbing stairs/hills, running
-stress/anxiety: getting upset/arguing

Question 13

factors that affect myocardial oxygen demand: wall stress

Answer 13

*increased wall stress → need more O2
*increased wall stress → high LVEDP, high preload → volume overload & stiff LV

Question 14

3 principal clinical causes of angina

Answer 14

1. stable angina (often caused by progression of atherosclerosis
2. acute coronary syndromes (including unstable angina and MI; ACUTE, SEVERE CORONARY OBSTRUCTION)
3. Prinzmetal’s Angina (coronary vasospasm)

Question 15

stable angina

Answer 15

*often progression of atherosclerosis
*angina occurring with a CONSISTENT STIMULUS or CONSISTENT AMOUNT OF EXERTION
*present without significant changes for at least 2 months
*i.e. precipitated by walking 5 blocks 6 month ago; still precipitated by walking 5 blocks now

Question 16

unstable angina

Answer 16

*acute, severe coronary obstruction (ex. MI, ACS)
*3 principal presentations:
1. angina occurring at rest and prolonged, usually > 20 min
2. new-onset angina within the past 2 months
3. previously diagnosed angina that has become distinctly more frequent, longer in duration, or lower in threshold of activity

Question 17

Prinzmetal’s Angina (vasospastic angina)

Answer 17

*occurs as a result of vasospastic disease
*usually idiopathic, occasionally caused by cold stimulus or COCAINE

Question 18

management for vasospastic angina

Answer 18

*beta blockers & calcium channel blockers relieve and prevent idiopathic vasospasm
*benzos (such as diazepam) can calm the patient and relieve the anginal pain associated with cocaine
*AVOID beta-selective beta blockers (such as metoprolol), as this can lead to unopposed alpha-adrenergic tone and exacerbate cocaine-associated vasospasm

Question 19

management for stable angina: decreasing demand

Answer 19

1. beta blockers → decrease HR/limit contractility
2. long-acting nitrates → decrease preload/LV wall stress
3. ranolazine → sodium channel blocker
4. calcium channel blockers → limit vasospasm (increase oxygen supply), lower BP

Question 20

management for stable angina: prevention of progression

Answer 20

1. HMG-CoA reductase inhibitors (STATINS) or PCSK-9 inhibitors
2. aspirin → prevent acute coronary syndromes occurring from stable atherosclerosis

Question 21

management for stable angina: increase coronary supply

Answer 21

*coronary stent to open up the coronary artery
*only used in stable angina if other managements (meds) fail

Question 22

atypical symptoms of angina

Answer 22

angina symptoms CAN BE:
*localized instead of diffuse
*sharp, stabbing instead of pressure-like
*non-radiating
*absence of chest pain; isolated nausea, dyspnea, abdominal pain

atypical symptoms are more common in: WOMEN, diabetics, post-transplant, elderly

Question 23

goal of assessing chest pain with the clinical history

Answer 23

*classical features of angina:
a) substernal chest pain (described as pressure/tightness)
b) provoked by physical exertion or emotional distress
c) relieved by rest or nitroglycerin

*goal is to classify the pain as either:
1. typical angina (all 3 features are present)
2. atypical angina (2 features present)
3. non-cardiac chest pain (1 or fewer features)

Question 24

pre-test probability & risk factors for cardiac chest pain/CAD

Answer 24

*SMOKING
*diabetes, HLD, HTN
*older age
*male sex
*sedentary lifestyle, obesity
*chronic inflammatory states (HIV, autoimmune conditions, etc)

Question 25

objective data consistent with cardiac chest pain/CAD

Answer 25

*ECG changes
*echo changes
*perfusion changes
*cardiac catheterization

Question 26

ischemic cascade

Answer 26

*groundwork for understanding timeline of objective changes that are consistent with cardiac chest pain/CAD

1st: perfusion abnormality (no sx)
2nd: regional diastolic function (no sx)
3rd: regional systolic function (no sx)
4th: ischemic EKG changes (no sx)
5th: ANGINA

overall: symptoms usually do not precede echo or EKG changes

Question 27

ischemic EKG changes associated with cardiac chest pain (esp. MI)

Answer 27

*EKG can be normal
*T wave inversions can suggest ischemia
*ST depressions can suggest ischemia
*ST elevations suggest transmural ischemia and usually coronary occlusion

Question 28

echo changes associated with ischemia/cardiac chest pain

Answer 28

*echo used to assess regional diastolic & systolic function
*stress echocardiogram imaging: echo images of the heart at rest compared to after stress (ex. running)

Question 29

perfusion abnormalities associated with ischemia/cardiac chest pain

Answer 29

*nuclear stress test: give a radioisotope that the myocardium picks up, assess the heart at rest and following stress/exercise
*imbalance of radiotracer uptake leads to differential photon emission from the LV
*the “hottest” areas on rest and stress images are normalized against each other to standardize images
*“perfusion defects” result if flow to the myocardium is imbalanced