What are risk factors that predispose a person to cardiac disease? (CAD, etc)
Elevated blood lipid levels
Smoking
HTN
DM
Obesity
Family History of premature cardiovascular disease (first degree relative with cardiovascular disease at 55 years old or younger)
Age - more than 45 years for men; more than 55 years for women
What are nonmodifable risk factors for cardiac disease?
Family history of coronary heart disease
Increasing age
Gender (men develop CAD at an earlier age than women)
Race (higher incidence of heart disease in African Americans)
What are modifiable risk factors for cardiac disease?
Hyperlipidemia
Cigarette smoking, tobacco use
HTN
DM
Lack of estrogen in women
OCP use
Obesity
Physical inactivity
How does increased cholesterol contribute to cardiac disease?
Total Cholesterol
LDL - bad; when there is an excess of LDL, the LDL adheres to vulnerable points in arterial endothelium, where macrophages ingest them, leading to the formation of foam cells and the beginning of plaque formation
LESS THAN 160mg/dL in a normal person
LESS THAN 100mg/dL in a person with CAD
HDL - good; promotes the use of total cholesterol by transporting LDL to the liver, where it is biodegraded and then excreted
MORE THAN 40mg/dL ; preferably 60mg/dL
Triglycerides
How to control cholesterol abnormalities to prevent cardiac disease?
Diet
Physical activity
Meds - STATINS
Soluble dietary fiber (fresh fruit, cereal grains, vegetables, and legumes)
How do STATINS work?
3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors
Blocks cholesterol synthesis, lowers LDL and triglyceride levels, and increase HDL levels
Watch for: LIVER and Rhadomyalosis (check tests for skeletal function)
What meds can you give for dyslipidemia?
STATINS
Nictonic Acids
Fibric Acids
Bile Acid Sequestrants
What is angina?
Chest pain caused by myocardial ischemia due to inadequate myocardial blood and oxygen supply
Usually caused by atherosclerosis
Can range from: mild indigestion feeling to agonizing pain
Feels like: tightness, heavy, choking, or strangling that has a viselike quality
May radiate to: neck, shoulders, jaw, and inner aspects of the upper arm (USUALLY ON THE LEFT SIDE)
OTHER SYMPTOMS ASSOCIATED WITH THE CHEST PAIN/ANGINA: weakness or numbness in the arms, wrists, and hands, SOB, pallor, diaphoresis, dizziness, lightheadedness, and N/V, anxiety (FEELING OF IMPENDING DOOM)
What factors can typically aggravate/precipitate angina?
Physical exertion
Exposure to cold
Eating a heavy meal
Stress / emotion-provoking situation
What are the different types angina?
Stable - relieved with rest, nitro
Unstable - unrelieved with rest and nitro, pain consists for more than 15 minutes
Refractory - incapicating excruciating pain
Variant - pain at rest with ST-segment elevation; thought to be caused by coronary vasospasm
Silent ischmemia - objective evidence of ischemia (ECG changes with a stress test) but is asymptomatic
What are the variations in angina pain?
Women - tends to present with fatigue
DM - tend to have dulled pain because of their peripheral neuropathy
How do you assess and diagnose angina, MI?
Signs and symptoms - is the chest pain relieved with rest or meds? or not?
Patient history (PMH of CAD, family history)
ECG - T-wave inversion and ST-segment elevation are classic signs of MI; ST-segment elevation in 2 contiguous leads is a key diagnostic indicator for MI; Abnormal Q-waves
CBC
Echocardiogram - used to evalute ventricular function; used to ASSIST in dx; can detect hypokinetic and akinetic wall motion and can determine EF
Cardiac biomarkers labs - CKMB, Troponin, and Myoglobin
How do you medically treat angina?
The objective is to decrease the oxygen demand of the myocardium and to increase the oxygen supply - through MEDS and CONTROL OF RISK FACTORS
First give - nitro - up to 3x - spaced 15 minutes apart
Second - give aspirin, rest
IF PAIN STILL CONTINUES AFTER 15 minutes - Call 911
What are the pharmacologic therapies for angina, MI?
Nitroglycerin
Beta-blockers
Calcium channel blockers
Anti-platelet
Anti-coagulant
In the ER, what is the medical treatment?
OXYGENATION - first
Nitro
Aspirin
Morphine
*Remember MONA
EKG
VS
How does morphine work in the treatment of angina?
What questions do you ask when you assess angina?
P - Where is the pain, can you point to it, what were you doing when the pain began?
Q - Could you please describe the pain, is like pain you've had before?
R - Can you feel the pain anywhere else, did anything make the pain better? (like nitro or rest)
S - How would you rate the pain on a scale from 0-10?
T - How long ago did the pain start?
What is a myocardial infarction?
Occurs when myocardial tissue is abruptly or severely deprived of oxygen; ischemia can lead to necrosis of myocardial tissue if blood flow is not restored
Usually caused by an atherosclerotic plaque reducing blood flow in a coronary artery
Acute coronary syndrome - unstable angina --> MI - are the same process but at different points on the same continuum
The area of infarction develops over minutes to hours - as the cells are deprived of oxygen, ischemia develops, cellular injury occurs, and the lack of oxygen results in infarction (death of cells)
What are the causes of MI?
Rupture of an atherosclerotic plaque that may become a thrombis and occlude the coronary artery *most common*
Vasospasm (sudden constriction or narrowing) of a coronary artery
Increased demand for oxygen (from increased heart rate, thyrotoxicosis, or ingestion of cocaine)
What are the signs and symptoms of MI?
ANGINA (chest pain) that occurs suddenly and continues despite rest and nitroglycerin
SOB
Indigestion
Nausea
Anxiety
Cool, pale, moist skin
HR and RR - faster than normal
How do you assess and diagnose MI?
Signs and symptoms
ECG - Twave inversion, ST-segment elevation (in two continuous leads), and development of an abnormal Q wave
Serial cardiac biomarkers
Health history - history of risk factors, family history
Echocardiogram - evaluates ventricular function; can detect hypokinetic and akinetic wall motion and EF
What are the cardiac biomarkers related to MI?
Creatine Kinase of Heart Muscle - 72 hours
Troponin - must sensitive indicator of MI
Myoglobin
What is acute coronary syndrome?
The continuum of angina to MI; it is the essential the same process but on the same continuum
What are the clinical manifestations of MI? ...How can you tell that your patient may be experiencing an MI?
CHEST PAIN (angina) - that occur suddenly and continues despite rest and medications
USUALLY a current comorbidity of CAD
SOB
Indigestion
N/A
Cool, pale, moist skin
HR, RR - may be slightly elevated
What are the cardiac biomarker labs that are used to diagnose angina, MI?
Creatinine Kinase Heart Muscle - CKMB, a cardiac specific isoenzyme; increases when there is damage to the heart cells
Myoglobin - a heme protein that helps transport oxygen; increases when there is damage to cardiac and skeletal muscle (thus increased levels does not necessarily indicate MI); but negative results is helpful in excluding an MI dx
Troponin - a protein found in the myocardium; regulates the myocardial contractile process; an increase is detectable within a few hours of an acute MI; THE MOST HELPFUL INDICATOR FOR DXOF MI
What is the medical management purpose/goal for MI?
Minimize myocardial damage
Preserve myocardial function
Prevent complications (i.e heart failure)
After the patient comes in and you treat the angina, and they get diagnosed with acute MI. How do you medically treat it?
Thrombolytics - to dissolve and lyse the thrombus in the coronary artery (similar to what would be done for strokes); remember that the thrombolytic lyses the thrombus not the atherosclerotic plaque itself.
Analgesics - morphine sulfate - used to reduce pain and anxiety; but also reduces preload and afterload due to its vasodilating effects on the veins and the arteries respectively; MUST MONITOR BP and RR (BECAUSE BOTH CAN DANGEROUSLY DECREASE)
Ace-inhibitors - prevents the conversion of angiotensin I to II, then the BP decrease and the kidneys excrete sodium and fluid, decreasing oxygen demands on the heart. Do not give to a patient that is: hypotensive, hyponatremic, hypovolemic, or hyperkalemic
Emergenct PCI - an invasive procedure used to open the occluded artery; PCI treats the underlying atherosclerotic lesion
What are the medical treatment guidelines for acute MI?
Use rapid transit to the hospital
Obtain 12-lead EKG within 10 minutes
Obtain cardiac biomarker labs
Obtain other diagnostics to clarify dx
Supplemental oxygen
Nitroglycerin
Morphine
Aspirin 162-325mg
Beta-blocker
Angiotensin-converting enzyme inhibitor within 24 hours
Evaluate for indications for reperfusion therapy: PCTA (percutaneous coronary intervention), thrombolytic therapy
Continue therapy as indicated: heparin, plavix, ticlid, glycoprotein IIb/IIIa inhibitor
Bed rest for a minimum of 12 to 24 hours
What do you do after the acute MI phase, what do you do for cardiac rehabilitation?
A program that targets risk reduction by means of education, individual and group support, and physical inactivity
Goal: to extend life and improve the quality of life
How to accomplish goal: encouraging physical activity and physical conditioning, educating the patient and family, and providing counseling and behavioral interventions
Instruct patients to stop if: chest pain, SOB, dyspnea, weakness, fatigue, and palpitations
Patients who are able to walk 3-4 miles - can resume sexual activity
What are the different phases of cardiac rehabilitation?
Phase I
Phase II - occurs after patient is d/c. Lasts 4-6 weeks; but can last up to 6 months. Focuses on lifestyle modification for risk factor modification for risk factor reduction. When planning goals - YOU ALWAYS ASK WHAT THE PATIENT WANTS TO WORK ON FIRST.
Phase III - focuses on maintaining cardiovascular stability and long-term conditioning
What the nursing diagnosis for MI?
Ineffective cardiac perfusion related to reduced coronary blood flow from coronary thrombus and atherosclerotic plaque
Risk for imbalanced fluid volume
Risk for ineffective peripheral tissue perfusion related to decreased CO from left ventricular dysfunction
Death anxiety
Deficient knowledge about post-MI self-care
What is typical of a cardiac diet?
Low sodium - may reduce extracellular volume, thus reducing preload and afterload, and thus myocardial oxygen consumption
Low calorie - esp. in the obese patient, weight reduction may decrease cardiac workload and improve tidal volume
How to promote health after an MI?
Avoid any activity that causes CP, extreme dyspnea, or undue fatigue
Avoid extremes of hot or cold and walking against the wind
Losing weight - if indicated
Stop smoking and use of tobacco
Using personal strengths to support lifestyle changesDeveloping heart-healthy eating patterns and avoiding large meals and hurrying while eating
Modifying meals to align with the therapeutic lifestyle changes (TLC) or the dietary approaches to stopping HTN (dash) diet
Avoiding activities that tense the muscles: isometric exercises, weight-lifting, any activity that requires sudden bursts of energy
Alternating activity with rest periods
Contact physican: SOB, fainting, slow or rapid HR, swelling of feet and ankles
How does nitroglycerin work to treat angina?
A vasoactive agent
Reduces myocardial oxygen consumption, which decreases ischemia and relieves pain
PRIMARILY dilates the VEINS - causes venous pooling of blood throughout the body, which causes less return less blood return to the heart, and thus filling pressure (PRELOAD) is reduced
IN HIGHER DOSES dilates the arteries - causes a decrease in BP and thus decreases AFTERLOAD
Usually given sublingual - can tell it's working if you can feel tingling under the tongue
Don't exceed 3 doses - seperated by 4 minutes between each dose
How do beta-adrenergic blockers work to treat angina?
Blocks beta-adrenergic sympathetic stimulation to the heart
Decreases HR, decreases BP, Decreases contractility, slowed conduction of impulses through through the conduction system
Doses can be titrated to reach: 50-60bpm
SE/contraindications: hypotension, bradycardia, advanced atrioventricular block, and decompensated HF
Monitor: ECG, BP, and HR after administration
Never give to pulmonary obstructive disease: ASTHMA, COPD
Other SE: depression, fatigue, decreased libido, and MASKS SYMPTOMS OF HYPOGLYCEMIA
Do not stop taking abruptly
IF DM - monitor glucose
How do calcium channel blockers work to treat angina?
Decreases SA node automaticity
Decrease AV node conduction
Slows HR
Decreases the strength of heart contraction
Dilates smooth muscle wall of the coronary arterioles
Treats vasospasm
Caution: nifedipine
SE: hypotension, bradycardia, consptipation
How do the antiplatelet and anticoagulant medications work to treat angina?
they prevent platelet aggregation and subsequent thrombosis, which impedes blood flow
How does aspirin work to treat angina?
Anti-platelet
Prevents platelet activation
Give 160-325mg dose of aspirin with as angina asap (ER or physicians office)
Continue even if they are taking other NSAIDs
SE: GI upset/ulcer/bleeding (usually give with PPI: pepcid, zantac, prilosec)
How does plavis and ticlid work?
Similar to aspirin
Given if can't give aspirin
SE: same as aspirin, bleeding
How does heparin work to treat angina?
Anti-coagulant
Prevents the formation of new blood clots
SE: bleeding
Amount given based on aPTT (activated partial prothrombin time): 2-2.5x the normal aPTT value
Monifor for signs and symptoms of internal bleeding: low BP, increased HR, decreased serum Hg/Hct
Implement bleeding precautions
HIT (heparin-induced thrombocytopenia): decrease in platelet count - may result in thrombosis
