Ischemic heart disease Flashcards Preview

Coexisting 2016 > Ischemic heart disease > Flashcards

Flashcards in Ischemic heart disease Deck (68)
Loading flashcards...


Narrowing of the coronaries due to:

  1. Atherosclerosis
  2. Severe HTN or tachycardia
  3. Coronary artery vasospasm
  4. Severe hypotension
  5. Hypoxia
  6. Anemia
  7. Severe AI or AS
  8. Hypertrophied ventricle (bigger size, bigger O2 demand)


Clinical signs

  1. Angina
  2. Ischemia
  3. MI
  4. Arrhythmias
  5. Ventricular dysfunction
  6. Sudden death


Risk factors

  1. Increasing age
  2. Male gender
  3. HLD
  4. DM
  5. HTN
  6. Smoking
  7. Family history
  8. Obesity
  9. Vascular disease
  10. Menopause
  11. High-estrogen contraceptives
  12. Sedentary lifestyle
  13. Type-A personality


Main problem in ischemic heart disease

Imbalance between

myocardial O2 demand and myocardial oxygen supply


What is an atherosclerotic plaque composed of

  1. fatty acids
  2. cholesterol
  3. cellular waste products
  4. calcium deposits, other junk.
  5. Pro-inflammatory, pro-coagulant.


What are the chemical messengers involved in angina

Adenosine and bradykinin

  • these substances produce the chest pain typically associated with angina (thalamic/cortical stimulation).
  • They also slow AV conduction, decreasing contractility to hopefully improve oxygen demand/supply imbalance


Stable angina

No change in angina symptoms/precipitating factors over the past 60 or more days.

Frequency/duration of pain unchanged.


Unstable angina

  1. Crescendo
  2. Caused by less than normal activity, unpredictable
  3. New onset
  4. Lasts for prolonged periods
  5. Occurring more frequently or more severely
  6. Signals impending MI

Associated with acute plaque changes & usually partial thrombosis

Increasing medication need also indicates worsening even if symptoms are under control

Shouldn't be operating on these folks unless its an emergency. Probably gonna ruin your day.


Prinzmetal angina

At rest, usually not provoked by a specific action

Spasm of the coronary arteries

Can occur in completely normal vessel

Often associated with migraines, Raynauds, other vasospastic diseases


What is stunning

Brief ischemic period that can cause dysfunction for several hours. Not good.

Both contraction and relaxation of the heart muscle requires ATP, which becomes depleted in ischemia/hypoxia. If coronary flow is reestablished, ventricular function will slowly return to normal. The duration of reduced performance (myocardial stunning), depends on the duration of the preceding ischemia.



Impaired myocardial function from prolonged ischemia, but normal function is still restored following restoration of normal flow.

With hibernation restoration of normal coronary flow (e.g., by coronary bypass) will restore normal function in the affected region.



Provoked brief periods of ischemia that confer protection against future ischemia.

  • Short, repeating episodes of ischemia do not result in cumulative damage, but rather protect the heart from subsequent damage caused by a larger ischemic insult.

Shown to limit infarct size in later MI.

Pacing, exercise, opioids can evoke preconditioning

Inhaled anesthetics modulate this by blocking triggers (From what I read, this is good, but poorly understood. Interestingly COX-2 inhibitors completely abolish this protection. Who knew?)


Early management

Lifestyle modification

  1. diet
  2. execrcise
  3. smoking cessation

Treat any exacerbating factors:

  1. Fever
  2. Anemia
  3. Infection
  4. HTN
  5. HLD/Cholesterolemia

Pharmacological manipulation of O2 supply/demand


Drugs used in management

  1. BB
    • reduce contractility and HR
  2. Ca++ channel blockers
    • dilate coronaries, reduce contractility, reduce afterload
  3. ACE inhib
    • improve contractility and reduce afterload
  4. Nitrates
    • dilate coronaries and collaterals, decrease pre- and afterload (decrease in peripheral vasculat resistance and venodilation)
  5. Antiplatelets
    • reduce potential for thrombosis


Surgical interventions


  • balloons, stents, drug stents


  • off-pump, minimally invasive, robotics, all kinds of stuff

Transmyocardial revascularization- sounds impressive


Surgical delay post stent placement

Angioplasty, no stent- 4-6 weeks

Bare stent- 30-45 days

Drug stent- 1 year


Acute Coronary Syndrome

Occurs with plaque disruption leading to partial or complete occlusion of a coronary artery

Coag cascade is triggered--> local hypercoagulable state--> thrombus formation leading to greater occlusion


Characteristics of unstable plaques

  1. T-cell aggregation at the shoulder region with macrophage clusters
  2. Thin fibrous cap
  3. Lipid rich core
  4. Newly formed intra-wall capillaries
  5. Lymphocyte/mast cell infiltration into the adventitia


Worst kind of plaques

Plaque instability more significant than size of plaque


Events after plaque rupture

Platelet aggregation → thromboxane A released (vasoconstriction) → IIb/IIIa receptors on platelets activated → further aggregation, strengthening of thrombus → fibrin deposited → thrombus formation

  • Causes angina, infarction, sudden death
  • Microemboli can also be dislodged, clotting off smaller vessels elsewhere
  • Vasospasm also possible



  1. Necrosis caused by ischemia
  2. In the heart, begins to occur within 20-30 minutes of ischemia onset
  3. Typically starts in the subendocardium
  4. Full infarct size usually occurs in 3-6 hours
  5. Size depends on proximity of lesion, collateral circulation


Dx of MI

Need 2 out of 3:

  • Chest pain
  • Serial EKG changes indicative of MI
  • ST changes
  • Increase and decrease in serum cardiac enzymes

Cardiac MRI helpful to determine extent of infarct


Initial Acute MI treatment

Evaluate hemodynamics, what's your BP looking like

  1. Get a 12-lead
  2. O2, don't go crazy though
  3. Pain relief- morphine
  4. NTG
  5. ASA or plavix


Reperfusion therapy for ACS

Thrombolytic therapy - Must start within 30-60 minutes of arrival time.

  • streptokinase
  • TPA
  • reteplase
  • tenecteplase

Direct angioplasty - Perform within 90 minutes of arrival, 12 hours of symptom onset.

  • 5% fail and require surg.
  • CABG- high mortality if in the first 3-7 days post MI


Adjunctive therapy

  • Heparin
  • BB
  • ACE inhibitor - anterior MI, LV failure, EF


Unstable angina/Non-STEMI patho, Dx

Reduction in myocardial O2 supply

Change in angina symptoms

  • angina at rest
  • chronic angina that is becoming more frequent/severe, or
  • new onset EKG changes ST depression in two or more contiguous leads and/or
  • deep symmetrical T-wave inversion

Troponin levels


Tx for Non-STEMI

  1. Rest
  2. O2
  3. Analgesia
  4. BB
  5. NTG
  6. ASA/Plavix
  7. Heparin
  8. Possible revascularization


MI complications

  1. Arrhythmias
  2. LVF/CHF/pulmonary HTN
  3. Cardiogenic shock
  4. Thromboembolism/Stroke
  5. Papillary muscle dysfunction, valvular disease
  6. External infarct rupture
    • most common day 4-7
    • leads to acute tamponade, followed by death
  7. Ventricular aneurysm


Periop MI risk

Risk is less than 1% in the general population

Most occur in the 24-48 hours after surgery


Prognostic determinants in ischemic heart disease

  1. Extent of atherosclerosis
  2. EF
  3. Plaque stability