Ischemic Heart Disease

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Ischemic Heart Disease

• Madeline Gervase RN,MSN,CCRN,FNP
• Clinical Nurse Specialist
• Somerset Medical Center

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What is ischemic Heart Disease?

• Angina
• Symptom experienced when coronary blood supply is
  insufficient to meet myocardial energy
  requirements.
• Myocardial Infarction
• Death of myocardial cells.

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Pathology of ischemic heart disease

• Angina
• Severe chronic coronary artery disease which is
  assumed to be fixed and therefore not amenable to
  pharmacological manipulation.
• Myocardial Infarction
• On a background of severe chronic coronary artery
  disease, an acute event such as thrombus
  formation or extension, or coronary artery spasm.
• Angina and Myocardial infarction represent two
  extremes of a continuous spectrum.

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Risk factors for ischemic heart disease

• Hypertension
• Hyperlipidemia
• Smoking
• Diabetes Mellitus
• Obesity
• Male sex

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Pharmacological Intervention in Ischemic Heart
Disease

• Aims
• Increase coronary blood flow (correct anaemia (Hb
  6) Norm 12g/dl)
• reduce myocardial energy requirements Nitrates,
  Beta-blockers, calcium channel blockers
• to stop or reverse coronary arterial occlusion in
  order to avoid or minimise myocardial cell death
  (aspirin, thrombolytic agents)

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Smooth muscle contraction
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NitratesMode of action

• Smooth muscle relaxation with widespread
  peripheral vasodilation activity.
• Reduces preload (venous return) by action on
  venules)
• Reduces afterload by peripheral arteriolar
  relaxation
• Also some action on coronary artery dilatation

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Pharmacokinetics

• Glyceryl trinitrate (GTN) 100 first pass
  metabolism therefore given sublingually.
  Half-life 2 minutes.
• Isosorbide mononitrate/dinitrate slow release
  preparations with longer half life

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Adverse effects

• Dose related
• Result from vasodilatation and subsequent
  hypotension headache, postural dizziness,
  flushing

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Clinical use

• Administered sublingually before carrying out an
  activity known to prevoke angina, or at onset of
  episode of angina
• Slow release preparations (isosorbide
  mononitrate/dinitrate) used as maintenance
  therapy to prevent angina
• Intravenous preparations used to control unstable
  angina/ threatened myocardial infarction

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Nitric Oxide
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Endothelium
Smooth Muscle
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Beta receptor blockadeMode of action

• Decreases myocardial oxygen consumption by
• Limiting the increased heart rate associated with
  exercise or anxiety (antagonise the effects of
  catecholamines on beta-receptors in the
  sino-atrial node).
• Limiting the increased force of contraction
  associated with exercise or anxiety (antagonise
  beta1-receptors in the myocardium which have a
  positive inotropic effect).
• Improving myocardial perfusion by effect on rate.
  The slower the rate, the longer diastole is
  relative to systole. Since coronary artery
  filling only occurs in diastole, the length of
  the cardiac cycle in which coronary filling may
  occur is increased by decreasing the rate.

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Pharmacokinetics

• Variable, depends on preparation, hepatic
  metabolism and renal elimination and lipid
  solubility.
• Generally beta-blockers have a short half-life
  (lt4hrs) but long acting preparations are
  available.

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Adverse effects

• Result of beta-blockade
• Tiredness, weakness
• Bradycardia and heart block
• Bronchospasm
• Congestive cardiac failure negatively inotropic
• Cold hands, worsening claudication
• Impotence in males mechanism not known

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Clinical considerations

• Selective b1-receptor antagonists used however
  still contraindicated in asthmatics (bronchospasm)

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Beta Blockers
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Calcium antagonists

• Mode of action
• Inhibition of slow calcium-channel component of
  action potential results in
• decreases contractility in myocardial cells
• decreased tone in vascular smooth muscle cells
  including coronary arteries
• verapamil and dilitizem have additional effect on
  sinus node to reduce rate
• Nifedipine reduces

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Pharmacokinetics

• well absorbed following oral administration
• cleared by liver metabolism, extensive first pass
  metabolism

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Adverse effects

• Verapamil and Diltizem should not be given with a
  beta-blocker because both reduce heart rate and
  are negatively inotropic.

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Calcium channel blockers
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Potassium channel activators
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Thrombolysis

• Aspirin Streptokinase
• GUSTO and SAVE
• Aspirin Streptokinase has better effect than
  either aspirin alone or streptokinase alone, and
  adding heparin just increases bleeding risks.

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Non-Pharmacological Intervention

• Angiography, angioplasty, coronary artery disease
• Comparison of asp thrombolysis with immediate
  angioplasty
• Similar outcome, but angioplasty is more
  expensive, more difficult out of hours, and
  impossible in most UK hospitals, which are
  district generals with no facilities for
  angioplasty!

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