Med Surg 2 Exam 1 (CAD & Heart Failure)

Coronary Artery Disease (CAD)

blood vessel disorder in general category of artherosclerosis

-

Artherosclerosis

-begins as soft deposits of fat that harden w/ age

-referred to as “hardening of arteries”

-atheromas (fatty deposits) prefer coronary arteries

• called CAD when formed here

-also known as ASHD, CVHD, IHD, CHD

CAD Patho

-damage to endothelial lining can result from tobacco use, hyperlipidemia, HTN, toxins, diabetes, inflammation, and infection

-C reactive protein is nonspecific marker of inflammation that may also be increased in CAD

-high lipoprotein(a) and homocysteine levels may contribute to atherosclerorsis by

• damaging the inner lining of vessels

• promoting plaque build up

• changing the clotting mechanism to make clots more likely to occur

-Developmental stages of CAD

• fatty streak: streak of fat develops in smooth muscle cells and yellow tinge appears. Fatty streaks appear by age 20

• fibrous plaque: collagen covers fatty streak and forms a fibrous plaque w/ a grayish or whitish appearance → narrowing of the vessel lumen and reduced blood flow to distal tissue

• complicated lesion: continued inflammation can result in plaque instability, ulceration, and rupture. Platelets accumulate in large #s, leading to thrombus. Thrombus may adhere to wall of artery, leading to further narrowing or total occlusion of artery

Collateral circulation

arterial anastomoses (or connections) w/i coronary circulation

-increased w/ chronic ischemia

-may be inadequate w/ rapid onset of CAD

*think of highway = when highway is blocked and you get off on an exit, take some backroads and then get back on the highway. Going around the blockage.

CAD risk factors

Nonmodifiable risk factors:

-Age = CAD increases for men over age 45 and women over age 55

-Gender = women more likely than men to die from first MI, symptoms in women may be unrecognized as heart related

-Ethnicity

• whites have highest mortality from CAD. White males have highest incidence of CAD

• Black males have higher incidence of CAD compared to Hispanic and Asian males

• Hispanics have slightly lower rates of CAD than non-Hispanic whites or Blacks. Have lower death rates from CAD than non-Hispanic whites or Blacks

• Native Americans die from heart disease earlier than expected. Mortality rates for those under age 65 are twice as high of those for other Americans

-Family history

Major modifiable risk factors CAD

-High serum lipids:

• Cholesterol > 200 mg/dL

• Triglycerides > 150 mg/dL

• HDL < 40mg/dL (men) and < 50mg/dL (women)

• LDL > 130 mg/dL

• 10 year risk calculator is used for people age 40-79 who have not been diagnosed w/ CAD, MI, or Stroke to help guide treatment of high LDL levels

-Hypertension:

• the shearing stress of and elevated BP causes endothelial injury that increases the rate of atherosclerosis

• begin lifestyle changes for prehypertension

-Tobacco Use:

• increases catecholamine release (epinephrine and norepinephrine)

• ↑ LDL, ↓ HDL, ↑ toxic oxygen radicals

• ↑ carbon monoxide which reduces number of hemoglobin sites available for O2 transport

• non smokers exposed to second hand smoke increase risk for CAD by 25-30%

-Diabetes:

• incidence of CAD is 2-4 times greater in these individuals even with well-controlled glucose levels

• management should include lifestyle changes and drug therapy to achieve a A1C level < 7%

-Physical Inactivity:

• exercise training for those who are inactive reduces risk of CAD through more efficient lipid metabolism, increased HDL production, decreased risk of thrombus formation, and more efficient O2 extraction by muscles

• for people w/ CAD activity may reduce symptoms, improve functional capacity, and improve other risk factors = insulin resistance, glucose intolerance, obesity

-Obesity:

• people who tend to store fat in abdomen have higher incidence of CAD

Contributing Modifiable risk factors CAD

-Physiologic states:

• include depression, acute and chronic stress (poverty, serving as caregiver), anxiety, hostility and anger, and lack of social support

• stress induced mechanisms can cause increased lipid and glucose levels and changes in blood coagulation, which contribute to atherosclerosis

-Substance use:

• cocaine and methamphetamine can produce coronary artery spasm resulting in myocardial ischemia and chest pain

• pts often have sinus tachycardia, high BP, and chest pain

Reducing risk factors for CAD

-High serum lipid levels:

• reduce total fat intake

• reduce saturated fat intake

• take prescribed drugs for lipid reduction

• adjust total caloric intake to achieve and maintain ideal body weight

• engage in daily physical activity

• increase amount of complex carbs, fiber, and vegetable proteins in diet

• follow-up w/ HCP for regular lipid panel assessments

-Hypertension:

• monitor home-base BP and obtain regular checkups

• take prescribed drugs for BP control

• stop tobacco use. Avoid exposure to environmental tobacco (second hand smoke)

• control or reduce weight

• perform physical activity daily

-Diabetes:

• follow recommended diet

• control or reduce weight

• take prescribed meds for diabetes

• monitor glucose levels regularly and followup w/ HCP regularly

-Tobacco Use:

• begin a tobacco cessation program

• change daily routines associated w/ tobacco use to reduce desire to smoke

• substitute other activities for smoking

• ask caregivers to support efforts to stop smoking

• avoid exposure to secondhand smoke

-Physical Inactivity:

• develop and maintain at least 30min of moderate physical activity daily (min 5 days/ week)

• increase activities to fitness level

-Psychologic state:

• increase awareness of behaviors that are harmful to health

• change patterns that add to stress

• learn effective stress management strategies

Health promotion CAD (nursing care)

-identify high risk persons:

• health hx including family hx;

• presence of cardiovascular symptoms;

• environmental patterns s/a diet, activity;

• psychosocial hx;

• values and beliefs about health and illness

-manage high risk persons:

• encourage lifestyle changes (maintain ideal body weight, get adequate exercise, reduce intake of saturated fats, avoid tobacco and illicit drug use);

• clarify personal goals

• set realistic goals and choose which risk factors to change first

Physical Activity CAD (nursing care)

-FITT formula: 30 mins most days plus weight training 2 days a week

• everyone should aim for 150 min of moderate aerobic activity per week = brisk walking, biking, recreational swimming

• can also perform 75 minutes of vigorous aerobic activity each week = jogging, singles tennis, or swimming laps

-regular physical activity contributes to

• weight reduction

• reduction of > 10% in systolic BP

• in some men more than women, increase in HDL cholesterol

Nutritional Therapy CAD (nursing care)

-↓ saturated fats and cholesterol (red meat, egg yolks, whole milk)

-↑ complex carbs (whole grains, fruit, vegetables)

-fat intake should come mostly from unsaturated fats = walnuts, peanuts, almonds, avacado, canola oil, olive oil

-↑ intake of omega-3 fatty acids = eating fatty fish 2x a week s/a salmon, albacore tuna, and mackerel

Statins (HMG-CoA) Reductase Inhibitors

atorvastatin, simvastatin, lovastatin, rosuvastatin, pravastatin, fluvastatin, pitavastatin

-inhibit cholesterol synthesis, decrease LDL, increase HDL by inhibiting HMG CoA reductase (an enzyme that synthesizes cholesterol in the liver)

Adverse reactions:

-cataract development

-rash

-memory loss

-headache

-GI disturbances

-myopathy (muscle pain) which can progress to serious condition called rhabdomyolysis (muscle protein breaks down and its excretion causes kidney damage)

-hepatotoxicity

Interventions: Monitor pts for report of muscle pain. Measure CK levels if unexplained muscle pain occurs. Monitor baseline and periodic LFTs and report elevated levels.

Administration: available for oral use only. Take in the evening w/ or w/o food. Lovastatin absorbed better w/ food. Concurrent use w/ fibrate or other lipid lowering med can increase risk for myopathy or liver toxicity.

Education: Report unusual or unexplained muscle pain to provider immediately. Report abdominal pain, jaundice, unusual fatigue (indications of liver dysfunction). Comply w/ lab testing of liver function every 6-12 months, as prescribed. Avoid grapefruit juice.

*Simvastatin has increased risk for rhabdomyolysis when used w/ fibric acid derivatives, niacin, or erythromycin. Prothrombin times may increase in pts taking Warfarin. Dose should not exceed 40mg/day. Use w/ caution in pts on amiodarone bc it can increase the risk of myopathy

Niacin

-water soluble B vitamin effective in lowering triglyceride levels and mildly lowering LDL levels

-at high doses can increase HDL levels but does not correlate to reduced risk of CAD or MI

*Teach pt that flushing (especially of face and neck) may occur w/i 20 min after taking drug and last for 30-60 min. Premedicate w/ aspirin 30 min before to reduce flushing. Use pf extended-release niacin may decrease side effects.

Fibrates (Fibric acid derivatives)

gemfibrozil, fenofibrate, fenofibric acid

-increase HDL levels and indirectly lower LDL levels through their effects of HDL and triglycerides. Decreases production of triglycerides or VLDLs.

Adverse reactions:

-GI manifestations = nausea, abdominal pain, diarrhea

-Increased risk for gallstones, liver toxicity, and myopathy

Interventions: Monitor for and report GI manifestations, manifestations of gall bladder disease, and myopathy. Measure CK if muscle pain occurs. Monitor liver function tests and report impaired liver function to provider.

Administration: available for oral use only. Take twice a day 30 minutes before breakfast and evening meal. Monitor periodic LDL, HDL, triglyceride, and total cholesterol levels for expected improvement.

Education: Report to provider GI manifestations or unexplained muscle pain. Report new intolerance of fried foods, upper abdominal discomfort, and bloating (signs of gallbladder disease). Report abdominal pain, jaundice, or new onset of fatigue (signs of liver disorders). Comply w/ liver function testing.

*Gemfibrozil may increase the risk for bleeding in pts taking warfarin. Use cautiously in pts taking statins due to an increased risk of myopathy

Bile acid sequestriants

colesevelam, colestipol, cholestyramine

-increase conversion of cholesterol to bile acids in liver. Primary effect is a decrease in total cholesterol and LDL level

Adverse reactions:

-bleeding = due to binding w/ fat soluble vitamin K in the intestine

-pancreatitis

-bowel obstruction

-bradycardia

-MI

-hypertriglyceridemia

-hypoglycemia

-HTN

-dysphagia

-elevated liver enzymes

-N/V

-constipation

-dyspepsia

-headache

-fatigue

-flu-like manifestations

-rhinitis

-sore throat

-muscle pain

Interventions: Anticipate baseline lab tests s/a lipid panel and monitor periodic future levels. Monitor INR prior to starting med and periodically afterwards. Monitor blood glucose levels. Monitor therapeutic levels of meds w/ narrow therapeutic margins. Assess for and report GI manifestations, manifestations of pancreatitis and gall bladder disease.

Administration: colesevelam available for oral use only and given once or twice daily at mealtimes w/ liquids. Available in tablets or powder that should be mixed w/ water or fruit juice. May be given at same time as statin. Meds that interact w/ colesevelam should be given 4hr prior.

Education: follow cholesterol lowering diet. Report any manifestations of potential adverse effects (abdominal pain, N/V,). Monitor and report dark tarry stools, hematuria, and ecchymosis. Monitor INR levels. Avoid taking other meds 4hr prior to administration. Be sure to mix powder form w/ 8 ounces of water or juice.

PCSK9 Inhibitors

alirocumab, evolocumab

-work in the liver to inactivate PCSK9 protein and lower LDL

Adverse reactions:

-vasculitis (inflammation of blood vessels which can cause headaches, fatigue, and fever)

-angioedema

-musculoskeletal pain

-injection site rxns = erythema, itching, swelling and pain at site, flu like manifestations

Interventions: Anticipate baseline laboratory tests s/a lipid panel and monitor periodic future levels. Assess and report any serious hypersensitivity reactions.

Administration: given by sub-q injection via prefilled syringe. Administered every 2 weeks or every 4 weeks at a higher dose. Rotate injection sites of the thigh, abdomen, upper arms. Prior to injection allow syringe to warm to room temp. for 30-40 mins. Give w/i 30 min after removed from refrigerator. Injection may take up to 20 seconds to give.

Education: Importance of rotating injection sites. Allow syringe to warm to room temp for 30-40 minutes. Give injection w/i 30 mins of fridge removal or throw away. Injection may take up to 20 seconds to give. If dose is missed self-administer w/i 7 days of missed dose, if it is past 7 days contact provider about what to do next.

Ezetimibe

cholesterol absorption inhibitor

-selectively inhibits the absorption of diet and biliary cholesterol across the intestinal wall

Adverse reactions:

-myopathy, rhabdomyolysis

-myoglobinuria

-angioedema

-pancreatitis

-cholecystitis

-thrombocytopenia

-Upper respiratory infection

-diarrhea

-arthralgia (joint pain)

-pain in extremities

-fatigue

-sinusitis

-influenza

-nasopharyngitis

-headaches

-back pain

-elevated liver enzyme levels

Interventions: Anticipate baseline lab tests s/a liver enzymes, CK, kidney function tests, and lipid panel. Tests will continue to be done throughout treatment. Assess manifestations of rhabdomyolysis (muscle pain, elevated CK levels) and manifestations of liver injury (fatigue, poor appetite, abdominal pain, dark urine, jaundice)

Administration: available for oral use only. Given once a day, anytime w/o regard to mealtimes. If also taking bile acid sequestrant take med 2hr before or more than 4 hr after bile acid sequestrant.

Education: Follow cholesterol lowering diet. Avoid drinking grapefruit juice. Avoid taking other lipid lowering drugs concurrently. Monitor fatigue, muscle aches and pain in extremities which could indicate myopathy. Report dark brown urine which could indicate rhabdomyolysis. Monitor for manifestations of liver injury or hepatotoxicity, pancreatitis, or cholecystitis (fatigue, poor appetite, abdominal pain, N/V, or jaundice). Report any type of allergic rxn to med. Report fever or malaise that could indicate infection.

Antiplatelet Therapy CAD (nursing care)

-it is recommended that low dose aspirin (81mg) to be used for primary prevention in adults age 40-59 years who are higher risk of CAD but do not have an increased risk of bleeding

-clopidogrel

Gerontologic Considerations CAD

-increased incidence and mortality associated w/ CAD in older adults

-strategies to reduce risk and treat CAD are effective

-treat HTN and increased lipids

-promote smoking cessation (may be resistant0

-Necessary to modify guidelines for physical activity

• longer warm-up

• longer periods of low level activity

• longer rest periods

• avoid extremes of temp.

• 30 minutes a day minimum

-Most likely to change lifestyle factors when hospitalized or symptomatic

Chronic stable angina

chronic and progressive

-chest pain that occures over a long period of time w/ same pattern of onset, duration, and intensity of symptoms

-O2 demand is greater than O2 supply → myocardial ischemia

• ischemia: blood flow reduced or blocked

-angina is the clinical manifetstation of myocardial ischemia

• occurs when arteries are blocked 70% or more; 50% or more for left main coronary artery

-few minutes in duration

-often provoked by physical exertion, stress, or emotional upset

-usually does not change w/ position or breathing

-pain at rest is unusual and may indicate unstable angina

-ST segment depression and/or T-wave inversion

Angina locations

-most angina is substernal

-may radiate to the jaw, neck, shoulders, and/or arms

-many people may describe feeling of indigestion or a burning sensation in the epigastric region

-sensation may be felt between the shoulder blades (intrascapular)

Silent ischemia

-ischemia that occurs in absence of any subjective symptoms

-associated w/ diabetic neuropathy

-confirmed by ECG changes

Prinzmetal’s angina

-rare form of angina that often occurs at rest w/o increased physical demand

-risk factors: hx of migriaine headaches, Raynaud’s phenomenon, and heavy smoking

-usually caused by hyperactivity of the smooth muscle of a major coronary artery resulting in strong contraction

• factors contributing to spasm: increased levels of alcohol & cocaine, exposure to medications that narrow blood vessels, or cold weather exposure

-may be relieved by moderate exercise, SL NTG, or it may disappear spontaneously

-treatment includes calcium channel blockers and nitrates

Microvascular angina

chest pain occurs in the absence of significant CAD or coronary spasm of a major coronary artery

-often angina is prolonged and brought on by physical exertion

-triggered by activities if daily living

-more common in women

-usually have positive stress test

-no obstructive coronary disease is present in major coronary arteries

-prevention and treatment follows CAD recommendations

Interprofessional Care Chronic stable angina

-goal is to decrease O2 demand and/or increase O2 supply

Acute Care:

1. position pt upright unless contraindicated and apply supplemental O2

2. assess vital signs

3. apply continuous ECG monitor

4. obtain a 12-lead ECG

5. provide prompt pain relief, first w/ SL or IV NTG, followed by and IV opioid analgesic if needed

6. obtain cardiac biomarkers

7. assess heart and breath sounds

8. obtain chest x-ray

-pt may have cool, clammy skin; BP and HR may be high; new systolic murmur may indicate ischemia mitral valve causing regurgitation

-Assess for other signs of pain s/a restlessness; ECG changes; high HR, RR, or BP; clutching of bed linens or chest; or other nonverbal cues

Patient Teaching:

-emphasize risk factor modification to slow the progression of CAD and ways to reduce modifiable risk factors

-teach pt and caregiver about diets low in salt and saturated fats

-give pt a regular individualized program of physical activity that conditions rather than stresses the heart

-help pt to avoid factors that precipitate angina

Short-acting nitrates

nitroglycerin (sublingual tablets or oral spray)

-first line therapy for acute angina episodes

-usually relieve pain in about 5 minutes and last about 30-40 minutes

Adverse reactions:

-headache

-hypotension

-tachycardia

-reflex tachycardia

-tolerance

Interventions: Monitor length and severity of headache and advise pt to take mild analgesic. Monitor baseline BP and pulse. Monitor for tachycardia, give beta blocker or calcium channel blocker if prescribed. Monitor response to med for tolerance, to prevent tolerance give on smallest needed amount.

Administration: when chest pain begins place 1 sublingual tablet under tongue to dissolve, if no pain relief in 5 minutes call 911. Take second tablet at that time and a third tablet 5 minutes later if there is still no relief. Dose of 1-2 sublingual sprays is equivalent to a sublingual tablet. TAKE NO MORE THAN 3 DOSES IN A 15 MINUTE PERIOD.

Education: Tell pt to sit down and place the NTG tablet under tongue and allow it to dissolve. If using spray the pt should direct the spray on the tongue. Can use prophylactically before starting an activity that is known to cause angina. Report dizziness or syncope to provider. Monitor HR and report tachycardia.

-Give sublingually or by spray. If no relief in 5 minutes, call EMS; if some relief, repeat every 5 mins for max 3 doses

Long-acting nitrates

isosorbide mononitrate, isosorbide dinitrate, nitroglycerin (transdermal patches or ointments)

-are longer acting than SL or translingual NTG

-can reduce frequency of angina attacks and treat Prinzmetal’s angina

Adverse reactions:

-headache

-orthostatic hypotension

Interventions: Caregivers should avoid touching ointment during application. Monitor baseline BP and take BP again when med reaches its peak effect. Use intermittent scheduling to avoid tolerance. Monitor client for hypotension and tachycardia during nitroglycerin IV infusion. Do not stop abruptly to avoid increased chest pain caused by vasospasm.

Administration: available in oral, ointment, and transdermal patch forms. Apply patches to hairless area on clients. Remove patches for 10-14 grs daily to prevent tolerance, apply patch in morning and remove it in the evening. Apply ointment to dry skin and cover w/ transparent dressing to keep intact. IV form of nitroglycerin infuses continuously from glass bottle w/ special tubing only.

Education: Report dizziness and syncope. Remove patch for part of each day. Move slowly from lying to sitting or standing position.

Nitrates

-Keep SL NTG tablets in dark, airtight container to maintain potency

-Tell pts to sit down before using short-acting nitrates

-SL NTG must be placed under tongue

-Spray translingual NTG onto or under the tongue

-Tell pt not to combine NTG w/ drugs used for erectile dysfunction as severe hypotension can occur

-Monitor for orthostatic hypotension after administration

-Headaches are common after taking any NTG preparation

-Caregivers should use gloves to apply and remove NTG ointment or transdermal patches to avoid contact w/ drug

-Never cardiovert or defibrillate over NTG ointment or a transdermal patch

-When using long-acting nitrates provide a 10-14hr nitrate free period

-Remind pt using long-acting nitrates that short acting nitrates can still be used when needed

Drug therapy Chronic stable angina

ACE inhibitors, ARBs, Beta Blockers, and Calcium Channel Blockers can also be used in the treatment of chronic stable angina

-refer to 1st knowt and pharm made easy for more info on these classes of drugs

-lipid lowering drugs may also be used in treatment (Statins, Bile acid sequestrants, etc.)

Sodium Current inhibitor

Ranolazine

-used to treat angina in pts who have not had adequate response w/ other antianginal meds

-usually added only when angina is not well-controlled

-lowers cardiac oxygen demand and increases myocardial efficiency. Does not affect HR, BP, or vascular resistance

Adverse reactions:

-swelling of lips, tongue, or throat

-skin rash

-constipation

-nausea

-headache

-blurred vision, ringing in ears

-numbness and tingling of extremities

-syncope, dizziness, bradycardia

-palpitations, hypotension, orthostatic hypotension,

-SOB, peripheral edema, tremors, renal failure, pulmonary fibrosis

Interventions: Assess for and report adverse effects. Monitor electrolytes and heart rhythm for bradycardia, arrhythmias, and prolongation of the QT interval. Monitor kidney function tests, creatinine, BUN, and urine output. Monitor blood glucose levels of those taking metformin.

Administration: given orally twice a day w/ or w/o food. Extended release so should not be crushed, broken, or chewed by client. Avoid grapefruit juice.

Education: Avoid grapefruit and grapefruit juice. Avoid drinking alcohol. Report any manifestations of adverse effects. Move slowly from lying to sitting or standing position.

Cardiac Catheterization (stable angina and ACS interventions)

gold standard test for pts w/ increasing angina symptoms

-visualize blockages (diagnostic)

-open blockages (interventional)

• can be done by Percutaneous coronary intervention (PCI), Balloon angioplasty, or Stent

PCI:

-may be done at same time as cardiac catheterization

• a catheter w/ a deflated balloon tip is inserted int the blocked coronary artery. The deflated balloon us positioned inside the blockage and inflated. This is called a balloon angioplasty

• afterwards pt receives dual antiplatelet therapy (DAPT)

Stent:

• an expandable mesh-like structure designed to keep the vessel open by supporting the arterial wall. 2 types = bare metal (BMS) and drug-eluting (DES)

  • DES is coated w/ a drug that reduces the risk for overgrowth of the intimal lining within the stent

-Potential complications

• abrupt closure from coronary artery dissection or rupture

• vascular injury at the artery access site

• acute MI from acute stent thrombosis of from plaque dislodging and blocking vessel distal to original blockage

• stent embolization

• failure to cross blockage w/ balloon or stent

• coronary spasm

• dye allergy

• bleeding

• infection

• stroke

• need for emergency artery bypass graft

CABG

traditional surgery requires sternotomy (opening of chest cavity) and caridopulmonary bypass (CPB)

-CPB: blood is diverted from the pts heart to a machine. There it is oxygenated and returned

-uses arteries and veins for grafts

-The internal mammary artery (IMA) is most common artery used for bypass graft = tend to have longer patency rates

-Radial artery grafts

• thick muscular artery that is prone to spasm

• periop CCB and long-acting nitrates can control the spasms

• patency rates are not as good as IMA but better than saphenous veins

-Saphenous vein grafts

• more prone to develop diffuse intimal hyperplasia, future stenosis, and graft occlusion

MIDCAB (minimally invasive coronary artery bypass)

-for pts w/ disease of left anterior descending or right coronary artery

-does NOT involve sternotomy and CPB

-requires several small incisions btwn the ribs or a mini thoracotomy

Coronary Artery bypasses (Others types of CABG/ surgeries)

Off-pump coronary artery bypass:

-requires sternotomy but no CPB

-performed on a beating heart using chemical stabilizers

Totally Endoscopic coronary artery bypass (TECAB):

-uses robotic technology to perform CABG

-benefits include potentially less blood loss, less pain, less risk of sternal wound infection, and shorter recovery times

Transmyocardial Laser revascularization:

-used for pts w/ advanced CAD who are not candidates for conventional CABG surgery and who have persistent angina despite maximum medical therapy

-high energy laser creates channels in heart muscle to allow blood flow to ischemic areas

CABG post-op care

-ICU for first 24-36 hrs

-monitor pt for bleeding (chest tube drainage, incision site)

-moitor hemodynamics

-check fluid status

-replace blood and electrolytes as needed

-restore temp. if needed (warming blankets, bear-hugger)

-beta blockers should be started at least 24hrs before CABG surgery and restarted asap after surgery

-Pt w/ radial artery harvest should take CCB and/or long-acting nitrate after surgery to reduce incidence of arterial spasm at the arm or anastomosis site

-POCD (postop cognitive dysfunction) can manifest days to weeks after surgery = impairment of memory, concentration, language comprehension, and social integration

Alternative therapies (chronic stable angina)

-EECP (enhanced external counterpulsation)

• inflatable cuffs are placed around legs

• increase venous return

• augment DBP

• increases coronary perfusion, improves LV diastolic filling, and helps w/ collateral circulation

-Spinal cord stimulation

Acute Coronary Syndrome (ACS)

when chest pain from ischemia is prolonged and not immediately reversible

-deterioration of once stable plaque → rupture → platelet aggregation → thrombus

-results in either

• partial occlusion of artery: UA or NSTEMI

• total occlusion of coronary artery: STEMI

-pts w/ suspected ACS need immediate hospitalization

Unstable angina

chest pain that is new in onset, occurs at rest, or occurs w/ increasing frequency, duration, or less effort than the pts chronic stable angina pattern

-may occur during sleep

-usually lasts 10 min or more

-needs immediate treatment

-symptoms in women often under-recognized = SOB, nausea, fatigue, jaw pain, back pain

MI (myocardial infarction)

occurs because of abrupt stoppage of blood flow through a coronary artery w/ a thrombus caused by platelet aggregation

-ST elevation and non-ST elevation

• STEMI = occlusive thrombus

• NSTEMI = non-occlusive thrombus

-STEMI is an emergency and artery must be opened w/i 90 minutes of presentation to restore blood and O2 to the heart muscle and limit the infarct size

• can be done either by PCI or thrombolytic therapy. PCI is first line of treatment if available

-NSTEMI does not need emergent catheterization but usually undergo catheterization in 12-72 hrs. Thrombolytic therapy is NOT a treatment option

Clinical manifestations of MI

Pain:

-severe chest pain not relieved by rest, position change, or nitrate administration

• heaviness, pressure, tightness, burning, constriction, crushing

• substernal or epigastric

• may radiate to neck, lower jaw, arms, back

-often occurs in early morning

-atypical in women: SOB, fatigue

-atypical in diabetes: asymptomatic bc of cardiac neuropathy

-atypical in elderly: change in mental status (confusion), SOB, pulmonary edema, dizziness, dysrhythmias

SNS Stimulation:

-ischemic heart cells release catecholamines (epinephrine, norepinephrine) → diaphoresis, increased HR and BP, and vasoconstriction of peripheral blood vessels

-pts skin may be ashen, clammy, cool to touch

Cardiovascular:

-initially ↑HR and BP, then ↓BP (secondary to ↓ in CO)

-crackles may persist for several hrs to days suggesting LV (left ventricular) dysfunction

-Jugular vein distention, hepatic engorgement, and peripheral edema mean RV (right ventricular) dysfunction

-abnormal heart sounds = S3 or S4 or new murmur suggest LV dysfunction

N/V:

-symptoms can result from reflex stimulation of the vomiting center by severe pain

Fever:

-may increase up to 100.4 degrees w/i 24-48 hrs

-may last 4-5 days

-systemic inflammatory process caused by heart cell death

MI healing process

-w/i 24hrs, leukocytes infliltrate the area of cell death

-proteolytic enzymes of neutrophils and macrophages begin to remove necrotic tissue by 4th day → thin wall

-necrotic zone identifiable by ECG changes

-collagen matrix laid down

-10 to 14 days after MI scar tissue is still weak

-heart muscle vulnerable to stress

-monitor pt carefully as activity level increases

-by 6 weeks after MI, scar tissue has replaced necrotic tissue

• area is said to be healed, but less compliant

-ventricular remodeling

• normal myocardium will hypertrophy and dilate in an attempt to compensate for infarcted muscle

Complications of MI

Dysrhythmias:

-most common complication = present in 80-90% of MI pts

-can be caused by ischemia, electrolyte imbalances, or SNS stimulation

-Ventricular tachycardia (VT) and ventricular fibrillation (VF) are most common cause of death in pts in the prehospitalization period

-bradycardias van develop when key areas of the conduction system are destroyed

Heart failure:

-occurs when pumping power of heart has diminished

-Left sided HF = occurs intially w/ subtle signs s/a dyspnea, restlessness, agitation, and slight tachycardia

• other signs include pulmonary congestion on X-ray, and S3 heart sound, crackles on auscultation of the lungs, paroxysmal nocturnal dyspnea, and orthopnea

-Right sided HF = jugular vein distention, hepatic congestion, lower extremity edema

Cardiogenic shock:

-occurs when O2 and nutrients supplied to tissues are inadequate bc of severe LV failure, papillary muscle rupture, ventricular septal rupture, LV free wall rupture, or right ventricular infarction

-has high death rate and requires aggressive management

Papillary muscle dysfunction or rupture:

-causes mitral valve regurgitation

-aggravates an already compromised LV → rapid clinical deterioration

Left ventricular aneurysm:

-myocardial wall becomes thinned and bulges out during contraction

-leads to HF, dysrhythmias, and angina

Ventricular septal wall rupture and left ventricular free wall rupture

-new, loud systolic murmur

-HF, and cardiogenic shock may occur

-pt must undergo emergency repair, either surgically or percutaneously

Pericarditis:

-inflammation of visceral and/or parietal pericardium

-mild to severe chest pain that increase w/ inspiration, coughing and is relived by sitting in forward position

-presence of pericardial friction rub\

-ECG changes

Dressler syndrome:

-pericarditis and fever that develops 1-8 weeks after MI

-chest pain, fever, malaise, pericardial friction rub, arthralgia

-high dose aspirin is treatment of choice

Diagnostics MI and UA

-detailed health history

-12 lead ECG

• one of the primary tools

• whenever possible we should compare a new ECG to a previous ECG. Changes in QRS complex, ST segment, and T wave caused by injury, ischemia, or infarction can develop slowly or quickly

• distinguishes btwn STEMI and NSTEMI

-Cardiac biomarkers

• the only way to tell if pt is having NSTEMI or UA is by drawing cardiac biomarkers (troponin, CK-MB, etc.)

• biomarkers will be high in NSTEMI pt but normal in UA pt

-Pharmacologic stress test

• for pts w/ abnormal but nondiagnostic ECG and negative biomarkers

Emergency management of chest pain

-If unresponsive, assess ABCs (airway, breathing, circulation)

-If responsive, monitor ABCs

-Position pt upright unless contraindicated

-Give O2 by nasal cannula or nonrebreather mask

-Obtain baseline vital signs

-Auscultate heart and breath sounds

-Obtain 12 lead ECG

-Insert 2 IV catheters

-Assess pain using COLDSPA

-Medicate for pain as ordered (nitroglycerin, morphine)

-Start continuous ECG monitoring and identify unusual rhythm

-Obtain baseline blood work (cardiac biomarkers, CBC, basic metabolic panel, coagulation studies)

-Obtain portable chest x-ray

-Assess for contraindications for antiplatelet, anticoagulation, or thrombolytic therapy or PCI as appropriate

-Give aspirin for heart-related chest pain unless contraindicated

-Give a high-dose statin

-Give antidysrhythmic drug for life-threatening dysrhythmias

-Perform ongoing monitoring

• monitor ABCs, vital signs, LOC, heart and breath sounds, heart rhythm, O2 sat

• assess and record response to drugs

• provide reassurance and emotional support

• explain all interventions and procedures

• anticipate need for intubation if respiratory distress is present

• prepare for CPR and defibrillation if cardiac arrest is evident

• anticipate need for transcutaneous pacing for symptomatic bradycardia or heart block

Interprofessional Care ACS

1. Obtain vital signs, 12 lead ECG, and start continuous ECG monitoring

2. Position pt in an upright position unless contraindicated

3. Start O2 via nasal cannula to keep O2 sat at least 93%

4. Obtain IV access for drug admin

5. Give SL NTG and 162 to 325mg of chewable aspirin if not given before arrival to ED

6. Give morphine for pain unrelieved by NTG

7. Give high dose statin

8. Obtain baseline labs including Cardiac biomarkers

-Drug therapy for ACS may include:

• Nitroglycerin = initial treatment used to reduce angina pain and improve coronary blood flow

• Morphine = if chest pain unrelieved by NTG; monitor for bradypnea or hypotension

• Beta blockers = reduce O2 demand, HR, BP, and contractility; reduce risk for reinfarction and HF

• ACE inhibitors = started w/i first 24hrs and taken indefinitely

• Antidysrhythmic drugs

• Lipid lowering drugs = taken indefinitely

• Aldosterone Antagonists = can decrease mortality after STEMI regardless of LV function

• Stool Softeners = prevent straining and the resultant vagal stimulation from valsava maneuver

-Nutrition Therapy:

• initially NPO then progress to low salt, low saturated fat, low cholesterol diet (Cardiac diet, Mediterranean Diet, etc.)

*Remember that ACS can be

• Unstable Angina / NSTEMI (differentiated by levels of cardiac biomarkers)

• STEMI

and each will need different interventions/ management

Interprofessional care for UA or NSTEMI (ACS)

-Dual antiplatelet therapy and heparin

• Nitroglycerin

• Antiplatelet therapy (aspirin, clopidogrel, glycoprotein llb/llla inhibitors)

• Anticoagulation therapy (heparin, direct thrombin inhibitors)

-Cardiac catheterization w/ PCI once stable

• coronary angiography (shooting dye via radial artery or saphenous vein into coronary arteries to visualize blockages/ narrowing)

• PCI

• CABG surgery

-DAPT should be continued for 1 year, Aspirin should never be stopped

Reperfusion Therapy STEMI (ACS)

Interprofessional care of STEMI = Reperfusion therapy = emergent PCI or Thrombolytic therapy

-Emergent PCI is first line treatment for pts w/ confirmed STEMI

• goal is to open blocked artery w/i 90 minutes of arrival to agency that has interventional cardiac catheterization to limit infarction size

• during procedure, BMS or DES is inserted into blocked coronary artery

• some pts may need emergent CABG surgery if: there is dissection or rupture of coronary artery; abrupt closure; acute stent thrombosis; failure to cross blockage w/ balloon or stent

• Advantages of PCI: faster reperfusion to limit infarction size; performed w/ IV sedation and local anesthesia; pt is ambulatory shortly after procedure; length of stay is about 3-4 days; pt can return to work several weeks sooner

• After PCI DAPT (dual antiplatelet therapy) should continue for 1 year. Aspirin should be continued forever

Thrombolytic Therapy STEMI (ACS)

Thrombolytic therapy is only used for pts w/ STEMI in agencies that do not have cardiac catheterization resources

-given IV w/i 30 minutes of arrival to ED

-must meet criteria:

• chest pain less than 12hrs w/ 12 lead ECG findings consistent w/ STEMI

• no absolute contraindications = active internal bleeding; hx of intracranial hemorrhage; intracranial or intraspinal surgery w/i 2 months; known structural or vascular abnormality (arteriovenous malformation); known intracranial cancer; recent ischemic stroke (w/i 3 months); severe uncontrolled HTN; significant closed-head r facial trauma w/i past 3 months; suspected aortic dissection; for streptikinase, prior treatment w/i past 6 months

-Draw blood and start 2-3 IV sites

-Complete invasive procedures prior to beginning

-Administer according to protocol (IV bolus or via infusion over 3hrs)

-Monitor closely for signs of bleeding, if signs occur stop the drug and notify the provider

-Assess for signs of reperfusion

• return of ST segment to baseline is best sign

-Give IV heparin to prevent reocclusion of artery

-DAPT should continue for 1 year, Aspirin should continue forever

Absolute contraindications for thrombolytic therapy

-active internal bleeding; hx of intracranial hemorrhage; intracranial or intraspinal surgery w/i 2 months; known structural or vascular abnormality (arteriovenous malformation); known intracranial cancer; recent ischemic stroke (w/i 3 months); severe uncontrolled HTN; significant closed-head r facial trauma w/i past 3 months; suspected aortic dissection; for streptikinase, prior treatment w/i past 6 months

Nursing management ACS (Acute)

nursing care focuses on thr priority problems of pain and impaired cardiac function

-immediate goals for pt are: pain relief, quick and appropriate treatment, preservation of heart muscle

Acute Care:

-monitor vital signs and pulse ox frequently

-start on continuous ECG monitoring, obtain serial ECGs and draw serial cardiac biomarkers

-maintain bedrest according to agency policy

-for pts w/ STEMI reperfusion therapy begins immediately

Pain:

-provide NTG, morphine, and supplemental O2 as needed to eliminate or reduce chest pain

-provide info about importance of continued therapy to limit myocardial damage

Monitoring:

-continuous ECG monitoring

-heart and breath sounds

-perform physical assessment to detect changes from baseline findings

-assess for s/sx of early HF (dyspnea, tachycardia, crackles, distended neck veins, S3 heart sound)

-monitor I&O

Rest and Comfort:

-balance rest and activity = no evidence for prolonged bed rest for the pt w/ uncomplicated MI

-plan nursing and other interventions to ensure adequate rest periods free from interruption

-gradually increase pts heart workload through more demanding physical tasks

Anxiety Reduction:

-identify source and alleviate

-provide pt teaching

Emotional and Behavioral reactions:

-assess support structure of pt and caregiver

-consider open visitation

Nursing management ACS (Ambulatory)

Ambulatory Care:

Patient Teaching:

-carefully assess pts literacy and learning needs to help set realistic goals

-answer questions in simple, brief terms. Often need repetition

• s/sx of angina and MI

• when and how to seek help

• anatomy and physiology of heart and coronary arteries

• cause and effect of CAD

• identification of and plan to decrease risk factors

• reasons for test and treatments, activity limitations and rest, diet, and drugs

• appropriate expectations about recovery

• resumption of work, physical activity

• measures to promote recovery and health

• importance of the gradual, progressive resumption of activity

Physical activity:

-METs scale

-monitor HR, should return to resting rate w/i few minutes of inactivity

-low level stress test before discharge

-isometric vs isotonic activities

Cardiac Rehab:

-restoration of a person to an optimal state of function in 6 areas

• physiologic

• psychologic

• mental

• spiritual

• economic

• vocational

Resumption of Sexual Activity:

-teach when discussing other physical activity

-erectile dysfunction drugs contraindicated w/ nitrates

-prophylactic nitrates before sexual activity

-when to avoid sex (anal intercourse)

-typically okay to resume sexual activity 7-10 days post MI or when pt can climb 2 flights of stairs

Phases of Rehab (ACS)

Phase 1: Hospital

-occurs when pt is still hospitalized

-activity level depends on severity of angina or MI

-pt may first sit up in bed or chair, perform ROM exercises and self-care, and progress to walking in hallway and limited stair climbing

-attention focuses on management of chest pain, anxiety, dysrhythmias, and complications

Phase 2: Early Recovery

-begins after pt is discharged

-usually lasts from 2-12 weeks and is held in an outpatient facility but may be done in the home

-activity level is gradually increased under supervision of cardiac rehab team and w/ ECG monitoring

-team may suggest that physical activity (walking program) be started at home

-info about risk factor reduction is provided at this time

Phase 3: Late Recovery

-long term maintenance program

-individual physical activity programs are designed and implemented at home, a local gym, or rehab center

-pt and caregiver restructure lifestyles and roles

-therapeutic lifestyle changes should become lifelong habits

-medical supervision recommended

Sudden cardiac death (SCD)

an abrupt, unexpected death resulting from a variety of cardiac causes

-abrupt disruption in cardiac function → loss of CO and cerebral blood flow

-most commonly caused by

• ventricular dysrhythmias

• structural heart disease

• conduction disturbances

Manifestations:

-no warning signs or symptoms if no MI

-some people have symptoms w/i 1 hr of SCD event

• angina, palpitations, dizziness, lightheadedness, chest pain, dyspnea

Interprofessional/ Nursing Care:

-serial analysis of cardiac biomarkers and ECGs to rule out ACS

-cardiac catheterization to identify significant CAD

-PCI or CABG surgery if needed

-assessment of dysrhythmias, electrophysiology study (EPS)

-for pts w/ syncope suspected to be caused by ventricular dysrhythmias

• outpatient cardiac monitor (Holter monitor) can be used for 48hrs

• Mobile Cardiac Outpatient Telemetry (MOCT) may be worn up to 30 days

• Implantable cardiac loop recorder may be worn up to 3 years

-most common approach to preventing recurrence and improving survival is use of ICD (implantable-cardioverter defibrillator)

• drug therapy w/ antiarrhythmic may be used w/ ICD to decrease episode of ventricular dysrhythmias if pt is receiving multiple ICD shocks due to dysrhythmias

-provide teaching about rapid CPR and defibrillation w/ an automatic external defibrillator (AED)

-Psychosocial adaptations

• brush w/ death

• time bomb mentality

• driving restrictions

• role reversal

• change in occupation