Download Med surg Heart Disease , CAD, ACD/ MI Atherosclerosis

Med surg Heart Disease , CAD, ACD/ MI
Atherosclerosis
Abnormal accumulation of lipid deposits and fibrous tissue in arterial walls
Athroma: shell that covers lipids and occluded vessels
Patho: injury to the vascular endothelium causes an inflammatory response. The inflammation then causes the
release of normal antithrombic and vasodilating drugs to stop. Monocytes are sent out to eat the lipids “foam
cells” then transport the lipids to the arterial walls forming fatty streaks.
Vulnerable plaque: Thin athroma cap, the core may grow causing rupture thus attracting platelets and
may form a thrombus. Obstruction may occur , decreasing myocardial perfusion and causing MI or ACS. ( acute
coronary syndrome)
Stable plaque: thick athroma cap, lipids pool inside and can resist the stress of blood flow and vessel
movement.
Risk factors: damage or injury may result from smoking,HTN, hyperlipidemia
LDL: Known as bad cholesterol and most watched target is under 1oomg/dl, can advance CAD
HDL: Good cholesterol you want a target of above 40mg/dl transports LDL to the liver to be metabolized and
excreted by the kidney. .
Metabolic syndrome
metabolic abnormalities known as metabolic syndrome has emerged as a major risk factor for cardiovascular
disease . A diagnosis of this syndrome includes three of the following conditions:
• Insulin resistance (fasting plasma glucose more than 100 mg/dL or abnormal glucose tolerance test)
• Central obesity (waist circumference more than 35 inches in females, more than 40 inches in males)
• Dyslipidemia (triglycerides more than 150 mg/dL, HDL less than 50 mg/dL in females, less than 40 mg/dL in
males)
• Blood pressure persistently greater than 130/85 mm Hg
• Proinflammatory state (high levels of C-reactive protein [CRP])
• Prothrombotic state (high fibrinogen level)
CAD
MODIFIABLE RISK FACTORS FOR CAD: cholesterol abnormalities, tobacco use, hypertension, and
diabetes—have been cited as major risk factors for CAD and its complications. As a result, they receive
much attention in health promotion programs.
Nonmodifiable Risk Factors : Family history of CAD (first-degree relative with cardiovascular disease at 55
years of age or younger for men and at 65 years of age or younger for women)
Increasing age (more than 45 years for men; more than 55 years for women)
Gender (men develop CAD at an earlier age than women)
Race (higher incidence of heart disease in African Americans than in Caucasians)
Cigarette smoking contributes to the development and severity of CAD in at least three ways:
• Nicotinic acid in tobacco triggers the release of catecholamines, which raise the heart rate and blood
pressure ). Nicotinic acid can also cause the coronary arteries to constrict. These effects lead to an
increased risk of CAD and sudden cardiac death.
• Smoking can increase the oxidation of LDL, damaging the vascular endothelium ). This increases platelet
adhesion and leads to a higher probability of thrombus formation.
• Inhalation of smoke increases the blood carbon monoxide level and decreases the supply of oxygen to
the myocardium. Hemoglobin, the oxygencarrying component of blood, combines more readily with
carbon monoxide than with oxygen. Myocardial ischemia and reduced contractility can result.
Gerietrolgical manifestations of heart disease
- may not exhibit a typical pain profile because of the diminished pain transmission
- Most common s/sx is dyspnea.
- Sometimes there are no symptoms (“silent” CAD),
- Older patients should be encouraged to recognize their chest pain–like symptom (e.g., weakness) as an indication
that they should rest or take prescribed medications.
- Pharmacologic stress testing and cardiac catheterization may be used to diagnose CAD in older patients.
- Medications used to manage angina are administered cautiously in older adults because they are associated with
an increase risk of adverse reactions
- Invasive procedures (e.g., PCI) that were once considered too risky in older adults may be considered; when
these procedures are performed, many older adults benefit from symptom relief and longer survival. .
Angina
Angina is usually caused by atherosclerotic disease. Almost invariably, angina is associated with a
significant obstruction of at least one major coronary artery.
Ischemia of the heart muscle may produce pain or other symptoms, varying from mild indigestion to a
choking or heavy sensation in the upper chest. The severity ranges from discomfort to agonizing pain.
The pain may be accompanied by severe apprehension and a feeling of impending death
Stable angina: predictable and consistent pain that occurs on exertion and is relieved by rest and/or
nitroglycerin
• Unstable angina (also called preinfarction angina or crescendo angina): symptoms increase in frequency
and severity; may not be relieved with rest or nitroglycerin
• Intractable or refractory angina: severe incapacitating chest pain
• Variant angina (also called Prinzmetal’s angina): pain at rest with reversible ST-segment elevation;
thought to be caused by coronary artery vasospasm
• Silent ischemia: objective evidence of ischemia (such as electrocardiographic changes with a stress
test), but patient reports no pain
Several factors are associated with typical anginal pain:
• Physical exertion, which precipitates an attack by increasing myocardial oxygen demand
• Exposure to cold, which causes vasoconstriction and elevated blood pressure
• Eating a heavy meal, which increases the blood flow to the mesenteric area for digestion, thereby
reducing the blood supply available to the heart muscle
• Stress or any emotion-provoking situation, causing the release of catecholamines, which increases blood
pressure, heart rate, and myocardial workload
Nitroglycerin
- standard treatment for angina pectoris.
-Nitroglycerin is a potent vasodilator that improves blood flow to the heart muscle and relieves pain
-. Nitroglycerin dilates primarily the veins and, to a lesser extent, the arteries.
- Take patients blood pressure prior to administration , if too low hold the med and contact the physician
-pt may become hypotensive and pass out
-given sublingual and can be given 3x 5 mins apart, if no relief on third dose call the HCP
Heparin
Unfractionated IV heparin prevents the formation of new blood clots (i.e., it is an anticoagulant).
-reduces the occurrence of MI.- If the patient’s signs and symptoms indicate a significant risk for a cardiac event, the patient is hospitalized and may
be given an IV bolus of heparin and started on a continuous infusion.
- The amount of heparin administered is based on the results of the activated partial thromboplastin time (aPTT).
Heparin therapy is usually considered therapeutic when the aPTT is 2 to 2.5 times the normal aPTT value.
-A subcutaneous injection of low-molecular-weight heparin (LMWH; enoxaparin [Lovenox] or dalteparin [Fragmin])
may be used instead of IV unfractionated heparin).- LMWH provides effective and stable anticoagulation, potentially reducing the risk of rebound ischemic events.
-LMWH increase the risk of bleeding, the patient is monitored for signs and symptoms of external and internal
bleeding, such as low blood pressure, increased heart rate, and decreased serum hemoglobin and hematocrit. The
patient receiving heparin is placed on bleeding precautions, which include:
• Applying pressure to the site of any needle puncture for a longer time than usual
• Avoiding intramuscular (IM) injections
• Avoiding tissue injury and bruising from trauma or use of constrictive devices (e.g., continuous use of an automatic
blood pressure cuff)
A decrease in platelet count or evidence of thrombosis may indicate heparin-induced thrombocytopenia (HIT), an
antibody-mediated reaction to heparin that may result in thrombosis). Patients who have received heparin within the
past 3 months and those who have been receiving unfractionated heparin for 5 to 15 days are at high risk for HIT
Acute coronary syndrome
emergent situation characterized by an acute onset of myocardial ischemia that results in myocardial death (i.e.,
MI) if definitive interventions do not occur promptly. (Although the terms coronary occlusion, heart attack, and
myocardial infarction are used synonymously, the preferred term is myocardial infarction.) The spectrum of ACS
includes unstable angina, NSTEMI, and ST-segment elevation myocardial infarction (STEMI).
Assessment
Cardiovascular
• Chest pain or discomfort not relieved by rest or nitroglycerin; palpitations. Heart sounds may include S3, S4, and new onset of
a murmur.
• Increased jugular venous distention may be seen if the myocardial infarction (MI) has caused heart failure.
• Blood pressure may be elevated because of sympathetic stimulation or decreased because of decreased contractility,
impending cardiogenic shock, or medications.
• Irregular pulse may indicate atrial fibrillation.
• In addition to ST-segment and T-wave changes, the electrocardiogram may show tachycardia, bradycardia, or other
dysrhythmias.
Respiratory
Shortness of breath, dyspnea, tachypnea, and crackles if MI has caused pulmonary congestion. Pulmonary edema may be
present.
Gastrointestinal
Nausea, indigestion, and vomiting
Genitourinary
Decreased urinary output may indicate cardiogenic shock.
Skin
Cool, clammy, diaphoretic, and pale appearance due to sympathetic stimulation may indicate cardiogenic shock.
Neurologic
Anxiety, restlessness, and lightheadedness may indicate increased sympathetic stimulation or a decrease in
contractility and cerebral oxygenation. The same symptoms may also herald cardiogenic shock.
Psychological
Fear with feeling of impending doom, or denial that anything is wrong.
Pathophysiology
-unstable angina: there is reduced blood flow in a coronary artery, often due to rupture of an
atherosclerotic plaque. A clot begins to form on top of the coronary lesion, but the artery is not
completely occlude causing pain ( dull achy, elephant sitting on your chest)
- MI, plaque rupture and subsequent thrombus formation result in complete occlusion of the artery,
leading to ischemia and necrosis of the myocardium supplied by that artery.
S/sx: chest pain, shortness of breath, indigestion, nausea, and anxiety. They may have cool, pale, and
moist skin. Their heart rate and respiratory rate may be faster than normal. the 12-lead ECG and
laboratory test( serial cardiac biomarkers) are performed to clarify whether the patient has unstable
angina, NSTEMI, or STEMI. Unstable angina: The patient has clinical manifestations of coronary ischemia,
but ECG and cardiac biomarkers show no evidence of acute MI.
• STEMI: The patient has ECG evidence of acute MI with characteristic changes in two contiguous leads on
a 12-lead ECG. In this type of MI, there is significant damage to the myocardium.
• NSTEMI: The patient has elevated cardiac biomarkers (e.g., troponin) but no definite ECG evidence of
acute MI. In this type of MI, there may be less damage to the myocardium.
Coronary artery bypass graft (CABG)
surgical procedure in which a blood vessel is grafted to an occluded coronary artery so that blood can
flow beyond the occlusion; it is also called a bypass graft.
CABG may result in complications such as hemorrhage, dysrhythmias, and MI
The major indications for CABG are:
• Alleviation of angina that cannot be controlled with medication or PCI
• Treatment for left main coronary artery stenosis or multivessel CAD
• Prevention of and treatment for MI, dysrhythmias, or heart failure
• Treatment for complications from an unsuccessful PCI
CABG procedures are performed with the patient under general anesthesia. In the traditional CABG
procedure, the surgeon performs a median sternotomy and connects the patient to the cardiopulmonary
bypass (CPB) machine. Next, a blood vessel from another part of the patient’s body (e.g., saphenous vein,
left internal mammary artery) is grafted distal to the coronary artery lesion, bypassing the obstruction.
Nursing interventions for CAGB
Assessment
• Knowledge and understanding of the surgical procedure, postoperative course, and recovery
• Fears and concerns regarding the surgery and future health status
• Coping mechanisms helpful to the patient
• Support systems available during and following hospitalization
Reducing Fear and Anxiety
For patients with extreme anxiety or fear and for whom emotional support and education are not
successful, medication may be helpful. The anxiolytic agents most commonly used before cardiac surgery
are lorazepam (Ativan) and diazepam (Valium).
Monitoring for potential complications
Angina may occur because of increased stress and anxiety related to the forthcoming surgery. The patient
who develops angina usually responds to typical therapy for angina, most commonly nitroglycerin. Some
patients require oxygen and IV nitroglycerin infusions. Physiologically unstable patients may require
preoperative management in a critical care unit.
-Hypovolemia (most common cause of decreased cardiac output after cardiac surgery)
-Persistent bleeding
-Cardiac tamponade
-Fluid overload
-Cardiac failure
-Electrolyte imbalance
Providing Patient Education
Prior to surgery, patients and their families are given specific instructions. This includes information on
how the patient should take or stop specific medications, including anticoagulant agents, antihypertensive
medications, and medications that control diabetes. The patient is instructed to shower with an antiseptic
solution.