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S2B6: MEDI > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

What are the clinical stages of coronary artery disesase?

A

Endothelial dysfunction

positive remodeling

exertional angina

unstable angina

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2
Q

What is the relationship severity of pain & degree of oxygen supply?

A

weak relationship

there can be severe pain with minimal disruptionof oxygen supply or no pain in severe cases

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3
Q

What are the 4 types of angina?

A
  1. Stable angina
    • pain resolves at rest
  2. Unstable angina (ACS)
    • continues at rest
  3. Microvascular angina
    • no epicardial disease
  4. Prinzmetal’s angina
    • vasoconstrictive disease - arteries are constricting down causing a stenosis
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4
Q

What are the characteristics of stable angina?

What is another name for stable angina?

A
  • “Effort Angina” - think man showeling show after inactive fall
    • Discomfort is precipitated by activity
    • minimal or no symptoms at rest
    • symptoms disappear after rest/cessation of activity
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5
Q

What are the characteristics of unstable angina?

What is another name for unstable angina?

A
  • “Crescendo or Preinfarction angina”
    • acute coronary syndrom spectrum
    • may occur at rest or progressively less exertion
      • stable to unstable
    • severe & of acute onset or longer duration
    • Crescendo pain- pain increases over time
    • Nocturnal episodes
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6
Q

What are the characteristics of microvascular angina?

What is another name for microvascular angina?

What demographics are most affected by this disease?

A
  • Syndrome X
    • Angiographically normal epicardial arteries
    • “small vessel disease” with high resistance
    • diabetics, women more than men
    • unstable angina, objective evidence of ischemia (such as ischemic ST-T deviation), elevated biomarkers, Echo wall motion abnormalities during pain
    • Decreased coronary flow reserve
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7
Q

What are the characteristics of Prinzmetal’s angina?

What is another name for Prinzmetal’s angina?

What demographics are most affected by this disease?

A
  • Variant Angina
    • normal coronary vessels or minimal atherosclerosis
    • ST segment elevation (injury pattern) during pain
    • May have transient Q waves
    • Angiographic hallmark is coronary spasm with ST elevation during chest pain
      • history of migraines
    • Provocative testing
      • injecting directly into the coronary arteris & watching this occur & can reverse with nitrates
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8
Q

What are the causes of ischemia?

How is this related to the coronary vessels?

A
  • Either an increased oxygen demand or a decrease in oxygen supply
    • inadequate blood supply & decreased oxygen supply are directly related to obstructed or stenotic vessels
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9
Q

What are the 3 components of an typical anginal diagnosis?

What if you only have 2/3?

What if you only have 1/3?

A
  1. Substernal Chest pain
    • usually described as heaviness/pressure/squeezing
    • sometimes radiates jaw/LUE/back
  2. worse with exertion
  3. better with rest/nitroglycerin
  • 3/3 = typical angina
  • 2/3 = atypical angina
  • 1/3 = likely noncardiac
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10
Q

What are the classic symptom describtors & localization of angina?

A
  • Pressure, tightness, heaviness, squeezing, aching… “PAIN” may not even be described
    • Elephant on chest
    • Tight bnd around chest, like bra is too tight
  • Levine’s Sign (clenched fist)
  • retrosternal, eithe ror both sides of the chest, up to throat, down to epigastrium, medial sides of upper arms down to mid forearm
  • Women: frequently in jaw, lower teeth ears and sides of neck as well as interscapular (men, too)
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11
Q

What are the associated signs & symptoms with angina?

A
  • Dyspnea on exertion or at rest
  • Diaphoresis (women may describe “cold sweat”)
  • profound fatigue of sudden onset (may be the only symptom in some women)
  • palpitations with or without lightheadedness
  • nausea or “indigestion”
  • comiting
  • Tenesmus
  • Dizziness
  • Feeling of “Impending Doom”
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12
Q

You have a patient with suspected ischemic heart disease – what symptoms suggest this?

What do you do if they are intermediate or high risk?

What if they are stable?

A
  • Symptoms
    • Angina - ie. everytime I mow, my chest hurts, then I sit down & it gets better
    • or female specific symptoms
  • Intermediate/High Risk (Unstable Angina)
    • straight to unstable chart
  • Stable
    • comprehensive clinical assessment of risk including personal characteristics, coexisting cardiac & medical conditions, and health status
      • high risk lestion, prior sudden death or ventricular arrhythmia, prior stent in unprotected left main coronary artery
        • straight to guideline-directed medical therapy
      • for a patient where this is unknown, go down the algorithm
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13
Q

What procedures do you follow if you have a patient with stable angina who does not have a high-risk lesion, prior sudden death, ventricular arrhythmia or a prior stent in unprotected left main coronary artery?

A

Have they had a recent exercise or cardiac imaging study?

  • Yes
    • techincally adequate?
      • Yes -determine if they have any contraindications to stress testing
      • No- Test results indicated high-ris coronary lesion?
        • Yes- initiate guideline-directed medical therapy; consider coronary revascularization to improve survival
        • No- initiate guideline-directed medical therapy
  • No
    • Determine if they have any contraindications to stress testing
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14
Q

When working up a patient with stable angina & an unkown risk, what do you do after you determine if they have any contraindications to stress testing?

A
  • Contraindications
    • Yes- Guideline-directed medical therapy OR CCTA
    • No- Determine if the patient is able to exercise
      • Yes - Determine if the patient has had previous coronary revascularization
      • No- Pharm stress MPI or Echo; Pharm CMR or CTA or Pharm Stress echo
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15
Q

When working up a patient with stable angina & an unkown risk, what do you do after you determine if they have had previous coronary revascularization?

A
  • Previous Coronary Revascularization
    • Yes- MPI or echo with exercise
    • No- Resting ECG interpretable?
      • Yes-
        • intermediate likelihood IHD: Standard ECG
        • low likelihood IHD: Standard exercise ECG
        • intermediate to high liklihood IHD: MPI or Echo w/ exercise or pharm CMR
      • No- MPI or Echo w/o exercise
  • If test results indicate high-risk coronary lesions?
    • Yes- guideline-directed medical therapy; consider coronary revascularization to improve survival
    • No- guideline-directed medical therapy
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16
Q

Draw this if you don’t yet feel comfortable

A
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17
Q

What are the goals of treatment for angina?

A
  • Aims:
    • relief of symptoms
    • slowing progressin of the disease
    • reduction of future events like myocardial infarction
18
Q

What are the “arms” associated with guideline-directed medical therapy witj ongoing patient education for a patient with stable ischemic heart disease?

Which is the foundational arm?

A
  • Foundational arm
    • aspirin- 75 - 162 mg daily
  • Lifestyle modification
    • diet, weight loss, physical activity
    • smoking cessation
  • moderate to high dose statin
    • if hypertension, treat hypertension
    • appropriate glycemic control if diabetic
  • if any anginal symptoms present
19
Q

How do you treat continued anginal symptoms for a patient with stable ischemic heart disease?

A
  • Sublingual NTG
    • beta-blocker (decrease O2 demand) if no contraindication
      • add/substitute CCB and/or long-acting nitrate if no contraindications
        • add/substitute ranolazine (last resort)
          • consider revascularization to improve symptoms
20
Q

Draw this diagram if you do not yet feel comfortable with it

A
21
Q

What class of drugs do you use to treat the following situations in ischemic heart disease? Why do you choose them?

acute attacks?

prophylaxis?

A
  • Acute attacks
    • organic nitrates
      • vasodilation - improve flow - improve oxygen supply
        • ​decreases preoad b/c venous return is decreased from the dilation - decreases oxygen demand
  • Prophylaxis
    • organic nitrates
    • beta blockers
      • decrease heart rate & contractility - decrease oxygen demand
    • calcium channel blockers
      • vasodilation - improve flow - improve oxygen supply
      • decrease heart rate & contractility - decrease oxygen demand
    • ranolazine
      • decreases cardiac contractility- decrease oxygen demand
    • K+ channel opener- Nicorandil
      • (?)
22
Q

How can antithrombic & statins improve ischemic heart disease?

A

Improve flow so they improve the oxygen supply to the heart, lessening the mismatch between supply & demand of oxygen that leads to ischemis

23
Q

Nitrates are contraindicated in what type of MI?

Why?

What if you accidentally do this? What do you do?

A

Nitrates are contraindicated in an inferior MI (affecting the right ventricle) because if you drop their preload then the amount of blood in the RV will drop, which can kill the patient

  • Response
    • have to bolus them with fluids if you didn’t lose their heart rate (code)
24
Q

Describe the mechanism of action of organic nitrates

Uses?

A
  • Pro drug that release NO
    • NO increases intracellular levels of cGMP
    • this leads ot dephosphorylation of myosin light chain & a decrease in cytosolic calcium
      • causes relaxation of smooth muscle & hence vasodilation but also relaxation of bronchi & GI tract
  • NO-mediated guanyl cyclase activation inhibits platelet aggregation (obviously beneficial in setting of MI)
  • Uses
    • angina pectoris, CHF, MI
25
Q

What is EDRF?

A

endothelium derive relaxing factor = NO

26
Q

What are the cardiovascular specific effects of nitrates?

A
  • Vasodilation - low concnetrations prefferentially dilate veins
    • dilation of meningial vessels can cause headache
    • can cause dilation of arterioles of face & neck and cause flushing
    • Coronary blood flow may increase transiently & then decrease due to decreased BP
      • increased collateral flow to ischemic areas
      • normalize blood flow to subendocardial regions of heart - redistribution of blood
      • dilate stenoses & reduce vascular resistanc ein ischemic areas
  • Venodilation – decreased venous return to heart
    • Decreased chamber size & end-diastolic pressure of ventricles
    • Cardiac output slightly reduced
  • systemic vascular resistance changes minimally
  • systemic BP may fall slightly
    • higher dose may cause more significant fall due to venous pooling & decrased arteriolar resistance
    • HR- unchanged/ incrase slightly (reflex tachycardia) - tend to restore blood pressure
27
Q

How can you reduce the headache associatd with nitrates?

A

coffee or anything with caffeine

28
Q

Why are nitrates considered the cornerstone of treatment for ischemic heart disease as compared to beta blockers?

A

nitrates directly effect the stenosis & lack of blood supply

whereas beta-blockers are primarily decreasing oxygen demand

29
Q

How do nitrates decrease myocardial O2 consmption?

A
  • Peripheral pooling of blood - reduced preload
  • arteriolar dilation- reduced afterload
  • decrease in end diastolic volume & LV filling pressure
    • in platelets increase cGMP- inhibits aggreagation
    • strongest factor for nitrate effect is peripheral pooling
    • epicardial coronary dilation occurs with IC NTG
30
Q

What procedure mimics the effects of nitrates?

A

Venous phlebotomy mimics effects of nitrates

31
Q

How are nitrates administered?

Why does tolerance happen & how is it avoided?

A
  • Administration
    • orally ineffective b/c first pass metabolism
      • for prophylaxis, require long-acting high doses (20mg +)
    • sublingually to avoid first pass metabolism (4mg)
    • cutaneous - ointment 2.5 -5 cm of skin
      • onset is a little slower w/ peak 1-2 hrs
      • interrupt for 8hr/day to prevent tolerance
  • Tolerance - decreased capacity of vascular smooth muscle to convert nitrates to NO
    • repeated doses lead to tolerance
    • dose spaceing is necessary
32
Q

What are the adverse effects of nitrates?

drug-drug interactions?

A
  • Headache - may be severe
    • may disappear after continued use OR decrease dose
  • transient episodes of dizziness, weakness, pallor etc - symptoms of postural hypotension
  • rash (allergic or vasodilatory)
  • PDE5 inhibitor (sildenafil) and nitrates given simultaneously can produce severe hypotension
33
Q

Describe the mechanism of action for Ca2+ - antagonists

A
  • decrease calcium influx
    • negaitve inotropic & chronotropic effect (most marked in phenyalkylamine group)
    • peripheral vasodilation (most marked in dihydropyridine group)
  • Uses:
    • variant angina (spasm), exertional angina, unstable angina, hypertension & antiarrhythimc
34
Q

Beta-blockers are contraindicated in what type of angina?

They are most used for what type of angina?

What are the 2 most commonly prescribed beta-blockers?

A
  • Contraindicated: vasospastic angina
  • Best: Exertional angina
  • Most commonly prescribed
    • Carvetilol (vasodilator)
    • Metroprolol (cardioselective)
35
Q

Describe the mechanism of action of Ranolazine

A
  • Use
    • chronic, resistant angina
    • patients unable to use usual drugs
  • MOA
    • inhibits cardiac late Na+ current
    • Effects the Na+ dependent Ca2+ channels and prevents Ca2+ overload that causes cardiac ischemia
    • decreases cardiac contractility
    • no change in HR, BP
    • Prolongs QT interval but has never been associated with Prolonged QT arrhythmias
36
Q

Describe the progression of drug therapies for patients with angina

A
  1. Aspirin (always the foundation)
  2. Beta-blockers
    • cardio-protective, decrease oxygen deman & prolonged action
  3. Long acting nitrates
    • increase oxygen supply via epicaridal coronary dilation & decrease oxygen consumption by preload reduction
  4. Calcium channel blockers
    • dilate epicardial & microvascular vessels
  5. Late Sodium chanel blocker (Ranolazine)
    • especially good for microvascular vessel dilation
  6. Statins
    • endothelial stabilization
37
Q

How can you tell if your anti-anginal therapy is effective?

A
  • decreased frequency of episodes
  • shorter duration of episodes
  • harder to trigger episodes
    • exertional
    • emotional
    • post prandial (after eating)
    • cold exposure
    • sex
  • Less anginal equivalent symptoms
    • dyspnea on exertion
    • exertional palpitations
38
Q

How much angina is too much?

What is considered stable?

A
  • Want to decrease angina as much as possible b/c
    • Cumulative effects of recurrent ischemia with ultimat destruction of myocardium
  • ATP stores can be decreased even after a few minutes of ischemia
  • ATP stores may not rebound to normal for several days
  • “hitting the heart when it’s already down”
  • More than one episode per week is NOT STABLE YET
39
Q

How different is the effectiveness of medical therapy vs revascularization surgery (PCI)?

A

extremely close

which is why we focus on medical therapy until it is failing

40
Q

Signs & symptoms to look for best treat angina?

A
  • ask about more than “chest pain” as a symptom
  • examine & document your exams carefully from visit to visit
  • watch for changes like S4, paradoxical splitting of S2, lung congestion, change in quality of pulse
  • quantify functional status via activities of normal daily living (lawn mowing, vacuuming, making the bed) and don’t forget erectile dysfunction
  • Do nto accept “I feel OK” as evidence of good angina control

S2B6: MEDI (15 decks)

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