ischemic heart disease Flashcards
- What questions would you ask him to be certain he had a “heart attack”?
- Describe the pain: should be the more severe than angina but with same general character (chest/ jaw/ back pain, cough, dizziness, increased heart rate, shortness of breath and sweating)
- How long did the pain last? (should be longer than 15 mins)
- Did you use vasodilators or stopped activity? (Pain should not be relieved)
- Did deep breathing aggravate it? No
- Did you have shortness of breath? Yes
What is the cause of coronary atherosclerosis?
not known. variety of risk factors: - male - older age - a family history of cardiovascular disease - hyperlipidemia - hypertension - cigarette smoking - physical inactivity - obesity - insulin resistance and diabetes mellitus - mental stress - depression
Increased levels of low-density lipoprotein (LDL) cholesterol pose the greatest risk for coronary atherosclerosis, whereas increased levels of high-density lipoprotein (HDL) cholesterol have been shown to reduce the risk.
A diet rich in total calories, saturated fats, cholesterol, sugars, and salts also enhances the risk.
Increased blood pressure appears to be one of the most significant risk factors for coronary atherosclerotic heart disease.
- cigarette smoking is the single most important modifiable risk factor for coronary heart disease. Persons who smoke 20 or more cigarettes daily have a two- to four-fold increase in coronary heart disease. Pipe and cigar smoking apparently convey little risk for development of heart disase.
Patients with diabetes mellitus have a greater incidence of coronary atherosclerotic heart disease and more extensive lesions.
Patients with diabetes have tow- to eight-fold higher rates of future cardiovascular events as compared with age-matched and ethinically matched nondiabetic patients.
METABOLIC SYNDROME - is the term used to describe a cluster of pathologic findings consisting of obesity, insulin resistance, low HDL cholesterol, elevated triglycerides, and hypertension, all of which are risk factors for atherosclerosis.
Other risk factors for the development of atherosclerosis have emerged and include elevated levels of C-reactive protein (inflammatory marker), fibrinogen (procoagulant), plasminogen activator inhibitor (thrombolytic), and homocysteine.
- NUMEROUS STUDIES HAVE REPORTED AN ASSOCIATION BETWENE PERIODONTAL DISEASE AND CARDIOVASCULAR DISEASE RAISING THE QUESTION OF WHETHER PERIODONTAL DISEASE IS A RISK FACTOR FOR CARDIOVASCULAR DISEASE. CAUSATION HAS NOT BEEN PROVED YET, ASSOCIATION HAS BEEN SEEN.
what is the pathophysiology of atherosclerosis?
- chronic endothelial injury - hyperlipidemia, hypertension, smoking, homocysteine, hemodynamic factors, toxins, viruses, immune reactions.
- endothelial dysfunction (e.g., increased permeability, leukocyte adhesion), monocyte adhesion and emigration (usually monocytes do not adhere to intact endothelium; however, triggers of atherosclerosis such as high saturated fat diet, smoking, hypertension, hyperglycemia, obesity, and insulin resistance initiate the experssion of adhesion molecules by the endothelial cells, thus promoting attachment, the monocytes become macrophages after their migration).
- Smooth muscle emigration from media to intima; macrophage activation.
- macrophages and smooth muscle cells engulf lipid (macrophages become foam cells when they engulf lipid)
- smooth muscle proliferation, collagen and other ECM deposition, extracellular lipid (foam cells are joined by T-lymphocytes, and together they produce a variety of inflammatory cytokines, which promote the migration and proliferation of smooth muscle cells and collagen to surround the foam cells, thereby forming a fibrous covering or cap. The arrival of the msooth muscle cells triggers a coalescence of the foam cells and small extracellular pools of lipid into a larger pool or lipid core. The T lymphocytes secrete cytokines that inhibit the further production of collagen, possibly leading to weakenig and thinning of the fibrous cap and rendering it susceptible to rupture. With rupture or disruption of the plaque surface, tissue factor comes into contact with blood, and a thrombus is subsequently formed).
If the plaque grows inwardly into the lumen the size of the lumen is progressively reduced (stenosis). Thus, blood flow may be chronically decreased, and when the demand for oxygen exceeds supply, the outcome is schemic pain. Ischemic symtpoms may be produced when occlusion reaches 75% of the cross-sectional area of the artery.
what causes most acute coronary syndromes (e.g. usntable angina, myocardial infarction)?
Caused by physical disruption or fracture of the atheromatous plaque, most commonly of a plaque that did not cause extreme stenosis. In plaque rupture, the fibrous cap tears, allowing arterial blood to enter the lipid core, where contact with tissue factor and collagen induces platelet adhesion and aggregation and activation of the coagulation cascade. This series of events results in thrombus formation and sudden expansion of the lesion. Blood flow through the affected artery may become compromised or completely blocked.
For lesions that do produce symptoms, flow-limiting intact plaques typically precipitate symptoms such as chest pain (angina) when oxygen need exceeds deman, such as during exercise.
HOWEVER
plaque rupture produces an acute or unstable clinical picture with signs and symptoms such as anginaat rest, MI, or sudden death.
what produces the pain experienced with MI and angina?
exact cause is unkonwn but it is lack of oxygen when it is needed
during what time period is mortality highest following a myocardial infarction?
- Patients should receive thrombolytic drugs within the first 30 days following MI
- Rate of sudden death of a patient that has suffered an MI 4x higher than that in general population
what is angina? typical angina? and atypical angina? and acute coronary syndrome?
Angina: sensation of aching, heavy, squeezing pressure or tightness in the mid-chest region whereby an area of the heart is not getting enough oxygen –rich blood. Pain is brief: 5-15mins if the provoking stimulus is stopped or for a shorter time if nitroglycerin is used
Typical angina is the most common type and occurs when the heart is working harder than usual and subsides upon rest in 5 to 15 minutes or after taking nitroglycerin.
• Pain is typically precipitated by physical effort (walking, climbing stairs)
• May also occur with eating or stress
• Relieved by cessation of precipitating activity, rest, or with the use of nitroglycerin
• Intermediate cardiac risk
Atypical angina is characterized by a change in the pattern of pain. The pain occurs with less exertion or at rest, lasts longer, and is less responsive to medication. Atypical angina patient has a typical pattern of increasing severity, frequency, or duration of pain. Patients with atypical angina should be considered major cardiac risk.
Acute coronary syndrome: continuum of myocardial ischemia that ranges from unstable angina to non-ST segment MI. Used to describe a condition where blood supply to the heart is decreased.
what should you do if you felt he had ACS or unstable angina?
Dental care for patients with ACS or unstable angina must be postponed and the patient referred to his or her physician immediately for care. These patients are at increased risk for MI. However, if emergency dental care is necessary before the patient is stable, it should be attempted only with cardiac monitoring and sedation and consultation with the physician. Treatment should be performed as conservatively as possible, directed toward pain relief, infection control or control of bleeding.
if you plan to extract tooth #36, what considerations might you think of with someone with ischemic heart disease?
- Nitrous Sedation: the patient is apprehensive about dental treatment so this would keep him relaxed and thus, his blood pressure low, preventing a sudden onset of angina during treatment.
- A reduced concentration of epinephrine in the local anesthesia: 1:200 000 will keep the dose low and still provide adequate anesthesia.
- Limit epi to 0.04mg for any local anaesthetic given
- With an anxious patient pain management is really important → if you need to use epinephrine to get profound anesthesia then you should because it’s better than having an anxious patient who’s in pain.
- Post-operative you might want to recommend a post-operative regimen of 325 – 600 mg ? Tylenol every 6 hours and then a narcotic in between every 3 hours.
what should you do in a myocardial infarction situation?
Dx: Myocardial Infarction
Other Considerations: Question the patient about any his past heart history/episodes of angina.
Tx:
• Put patient in semi-supine position.
• Call for emergency care
• Administer 100 % Oxygen – increase O2 in blood at a rate of maybe 16L/min of flow.
• Nitroglycerin as a spray sublingual under the tongue for vasodilation and relief of “squeezing” sensation in chest. It is a venodilator not an arteriodilator. This relieves the stress on the heart. You can give 0.3mg spray every 5 minutes, after 3 doses it’s usually about the maximum. 100/60 OR 90/60 you might want to be weary of giving more because you could cause the blood pressure to go too low.
• Aspirin chew it, it will get there faster, don’t just keep it sublingual, it will burn, you need to chew it, 325 mg to thin the blood
• Morphine to reduce pain and anxiety (also has vasodilating effect and slows heart rate).
• Get patient to hospital for emergency care.
what are nitrates?
vasodilators, predominantly venodilators, and are a cornerstone of the pharmacological management of angina. MOA is unknown. However it is believed that their effec tmay be caused by a decrease in cardiac load, resulting in decreased oxygen demand. Nitroglycerin may be used acutely for the relief of anginal painand prophylactically to prevent angina.
what do beta blockers do?
they are effective in the treatmnet of many patients with angina, compete with catecholamines for B-adrenergic receptor sites, resutling in decreased heart rate and myocardial contracitlity and reducing myocardial oxygen demand. Non-selective beta blockers block the B1 and B2 receptors, whereas cardioselective beta blockers preferentially block the beta 1 receptors at normal therapeutic doses. Nonselective beta blockers may cause unwanted effects, such as increasing the tone of vascular smooth muscle and causing both vasoconstriction of peripheral vessels and contraction of bronchial smooth muscle. Thus, nonselective beta blockers are not prescribed for patients with a history of asthma. Injections of sympathomimetic drugs such as epinephrine or levonordefrin may result in elevation of blood pressure in patients taking nonselective beta blockers; therefore, caution is indicated in use of these agents.
what are calcium channel blockers?
these drugs decrease intracellular calcium, resulting in vasodilatation of coronary, peripheral, and pumonary vasculature, along with decreased myocardial contractility and herat rate.
What do statins do?
inhibit 3-hydroxy-3-methylgluatryl-coenzyme A reductase (HMG-CoA) in the liver, thereby leading to enhanced expression of the LDL receptors that capture blood cholesterol. They are therefore used to lower LDL cholesterol and increase HDL cholesterol and have been shown to decrease the risk for a major coronary event and the risk of death. Statins are also antiinflammatory.
What do angiotensin-converting enzyme inhibitors do?
indicated for use in patients with coronary heart disease who also have diabetes, left ventricular dysfunction, or hypertension. The benefit of these agents appears to be primarily due to their antihypertensive effects. This group of drugs cause relaxation of blood vessels, as well as a decreased blood volume.
