NU 428 CAD & ACS
What are characteristics of atherosclerosis/CAD?
Focal deposit of cholesterol/lipids in vessels
Hardens w /age (progressive)
Fatty streak develops (15 y/o )
Fibrous plaque – beginning of endothelial changes (30 y/o )
Complicated lesion (last stage)
CAD is a plaque build up that results in obstructed blood flow to the heart muscle. This leads to hypoxia and infarction.
What are some characteristics of collateral circulation?
Develops in response to decrease blood flow to an area and over time it causes new vessels to grow and feed the area. (In body you can hear bruits when blood flow becomes hindered by narrowing arteries)
When occlusion of coronary vessel occurs slowly there is greater chance for collateral circ to develop.
Needs time to develop
Develops due to chronic ischemia
Not present in rapid onset CAD or coronary spasm
- Severe ischemia
Common in elderly
What are risk factors for CAD?
- Family History
- Tobacco Use
- Physical Inactivity
- Diabetes Mellitus Type 2
- Psychologic states
What are some health related goals for CAD patients? Why are these goals necessary?
HDL: M> /F>
HDL carry lipids to liver for metabolism, LDL contains more cholesterol (higher affinity for arterial walls)
HTN Goals: Under 120/80
preHTN (120-140/80-90) causes shearing stress on arterial walls, increases atherosclerotic development, narrows lumens, requires higher force.. Direct correlation w/Salt
No smoking or tobacco
Tobacco risk 2-6x higher than nonusers, decreases estrogen in premenopausal females. Risk proportional to number of cigarettes smoked (lower nicotine/filtered doesn’t reduce risk).
Nicotine releases catecholamine. Increases heart rate, causes vasoconstriction, HTN, and platelet aggregation. Decreases blood flow to your body.
Carbon monoxide affects O2 carrying capacity of Hgb.
Activity Goals: 30 min moderate 5+ times a week. Increases HDL, decreases platelet aggregation, encourages collateral circ. Development.
DM Goals: HgA1C <7%, decrease sat. fat & cholesterol (red meat, eggs, whole milk).. Increase complex carbs (grains, fruits, veg)
Type A/Depressed/Stressed correlates w/CAD.
What are some gender differences related to CAD?
- Highest incidence among white, middle aged males (gender equality >65 y/o)
- Men show symptoms 10 years earlier than women
- Greater than 75 y/o female incidence exceeds male
- Women tend to receive CABG later (higher surgical morbidity/mortality)
- African American women more frequent than white women
- Angina is most common initial event in women/ MI in men (but women more likely to delay tx)
- More MIs in men, more deaths in women (10x more deaths than breast cancer, leading COD >50)
- Mortality rate has fallen for men… not women!
- ASA/Statin/LHC more common in men when acutely ill, ASA men >45, women>65
- Premenopausal women have higher HDL/lower LDL than men.. LDL rises after menopause
- Women’s symptoms : fatigue, sleep disturbance, SOB, weakness, A typical pain: chest/arm/neck/shoulder/jaw/epigastric/back(often stress induced), GI sx : Nausea, anorexia, heartburn
- Estrogen not effective & increased risk of death from MI (if started 10+ yrs after menopause)
- Women and elderly may not exhibit chest pain, where men usually do.
What are some ethnic considerations relevant to CAD?
- Earlier age
- Females have higher incidence/mortality than white women
- Mortality (35-64 y/o double whites)
- Greater than 35 y/o have 2x CAD mortality rate
- Tobacco, HTN, obesity, highest rates of alcoholism and DM.
Hispanics lower rates of CAD & mortality
What should a nurse do initially for a patient who has sudden chest pain? What are the different types of electronic monitoring available?
Chest pain is not localized. It’s generalized pain over an area. If they come in with pain, hook them up to an EKG. Can be a 12 lead or 3 lead.
12 lead looks at all the areas of the heart from a bunch of different directions.
3 or 5 lead looks in one direction, doesn’t get as big a picture as a 12 lead.
Women and the elderly sometimes do not exhibit chest pain. Men have chest pain more typically.
What are the different types of angina and MIs a patient can experience?
Stable Angina (chronic stable chest pain syndromes) - With angina, the cells of the heart experience a little ischemia, enough to cause pain. Usually relieved with nitro and rest.
Acute Coronary Syndrome - Acute coronary syndrome is not relieved by nitro or rest. Unstable angina is almost an MI.
- Unstable Angina - harder to treat, might happen at nighttime. There are different types. Can lead to an MI.
- Myocardial Infarctions
- NSTEMI - Non-ST elevation MI
- STEMI - ST elevation MI
Sudden Cardiac Death
What are the characteristics of angina?
Presentation of reversible myocardial ischemia d/t
Increased demand for oxygen
Decreased supply of oxygen
Consistent pattern, duration, intensity
Transient ST depression possible
Meds: Nitrates, Beta blockers, Ca Channel blockers, Na channel inhibitors
The pain typically subsides when the precipitating insult is removed (5-15 min). Rarely stabbing/sharp. Coronary artery at least 75% blocked for ischemia to occur.
Can usually be controlled with medication
SL NTG will relieve the pain of Stable Angina w/in 3 min, duration 30-60 min
You usually know when stable angina is going to happen (sexual activity, physical activity)
Usually have an inverted T wave with stable angina, maybe an ST depression. These two sightings on the EKG mean ischemia. There’s enough blood supply to keep the heart alive though.
What are some treatment reccommendations for stable angina?
Stop what you’re doing, sit down, take a nitro every 5 min for 3 doses (can have 3 within 15 min), take your blood pressure.
Taking nitro: Take 1, if pain isn’t relieved call 911, then take no more than 2 after.
Replace nitro q 6 months, keep it in a dark bottle (photosensitive). Will have a headache and should STING or BURN when placed under tongue if sublingual.
Long acting: Isordil, Imdur - can take daily PO for chronic angina.
Ca channel blockers if Beta blockers not tolerated.
Na channel inhibitors: Ranexa, prolonged QT, dizziness. Can’t take it if it causes a pro-longed QT wave (slows the heart rate).
How do the manifestations of ACS differ from stable angina?
ACS: unstable angina, NSTEMI, STEMI
Ischemia is prolonged and not immediately reversible
Deterioration of once stable plaque, rupture, thrombus occlusion at site (partial UA/NSTEMI, total STEMI)
Unstable: No relief with rest, maybe some relief w/ nitro.
STEMI: Usually 30% of pts will have ST elevation on an EKG. ST elevation is not a good thing. It just means that there is not much blood at all getting to the cells, might mean there’s necrosis.
NSTEMI: The rest of pts will not have ST elevation on EKG. Cannot diagnose w/ EKG.
What are some EKG changes to look for in ischemia patients? What do they mean?
Look for Q, ST, T wave changes. Look at slide 16 for Normal and examples of abnormal.
Changes on EKG mean a change in blood flow to the heart.
Ischemia – ST depression or T wave inversion (is reversible) will lead to infarction if blood flow is not restored. Sometimes, after an infarction, they keep the inverted T wave. Might even keep it for several years.
Injury – ST elevation (infarction is imminent) – could also have a pathologic Q wave.
Physiologic Q wave – less than ¼ height of R wave
Pathologic Q wave - greater than ¼ height of R wave
- Cell death –NECROSIS-- has occurred
- “Squatty-body” looking!
- Q waves usually appear within 8 to 12 hours of ST elevation if the artery is not reperfused; however, some patients do not develop Q waves until days after the MI
- If an artery is reperfused early, Q waves may disappear in subsequent ECGs.
Infarction – ST elevation +/- pathologic Q wave (sometimes shows up later than the initial injury).
ST elevation and T wave inversion looks like a Fireman's hat or a Tombstone.
What are the manifestations for unstable angina/NSTEMI?
New changing/worsening pattern and intensity
Occurs at rest
ST depression or T wave inversion
Unpredictable, no pattern, can occur during exertion or rest, constant increase in frequency and severity of symptoms. Shows less and less blood flow, not necessarily an infarction but getting there. Nitro may or may not relieve this pain. Nitro will not relieve pain if having an MI.
There may be an area of plaque that is in the process of rupturing, placing the patient at great risk of total occlusion of the coronary artery which will lead to an infarction of the myocardial tissue, or they may return to a more stable condition.
Require immediate hospitalization/monitoring
Biggest difference btwn stable and unstable is whether or not it is relieved with rest.
Sometimes happens at night. Massive chest pain that might wake them up. It’s VERY unstable angina. Prinzmetal angina. Very dangerous.
Women may not have chest pain! May complain of shortness of breath, anxiety, fatigue, GERD symptoms.
What are the characteristics of NSTEMI/STEMI?
Irreversible Cell death d/t sustained ischemia
80-90% d/t thrombus
Non ST Elevation Myocardial Infarction
- Transient thrombosis/incomplete occlusion
- NSTEMI is dangerous. People might even get sent home from the ER when the doctor doesn’t see an ST elevation on the EKG.
ST Elevation Myocardial Infarction
- Prolonged/complete coronary occlusion
- Q wave develops, reflects depolarization of dead cells (see slide 21)
Necrotic portion of the heart is dysfunctional (contractility of that portion of the myocardium stops). Cardiac cells can tolerate ischemia for about 20 minutes before cell death occurs. If infarction involves the entire width of the myocardial tissue, this is called a transmural infarction and will cause an elevated ST segment.
What is the sequence of MI evolution with thrombolysis treatment?
- Normal sinus complex. The ST segment is on the iso-electric line. At the onset of pain the ECG would be normal but the ST segment would soon start to change. The T wave might grow taller.
- Within an hour the ST segment would be noticeably elevated, indicating the onset on myocardial necrosis. (tissue death). This is the point at which we would be aiming to administer the thrombolytic (clot-busting) drug. You must do something when ST elevation appears!
- If thrombolysis is administered, we would be looking for specific changes on the ECG.
- A 50% reduction in ST segment elevation is a good indicator of success. We would expect to see these changes within 90 minutes of administering thrombolysis. You can also see the T wave invertion is much deeper. This is a good sign of reperfusion. (blood flow returning to the damaged area.)
- 24 hours later, the ST segment may have returned to the iso-electric line. In this picture you can see the ST segment is back on the iso-electric line but the T wave remains inverted. It may stay inverted for days, weeks or months.
- In some cases, after a few months the ECG looks relatively normal except for a deep Q wave. A deep Q wave is an indicator of myocardial tissue death and will remain on the ECG. A "pathological" Q wave is not "time-specific” and it is a little wider if an MI is occuring. It may be there from a previous heart attack and therefore is not part of the criteria for evaluating an Acute Myocardial Infarction.
What are the different types of MIs and the symptoms associated with each?
The size and location of the infarction determines the immediate and long-term effects. The higher the occlusion occurs in the coronary artery, the more muscle damage that occurs.
- proximal end of LAD and supplies most of LV. S/S: More likely to have SOB; decreased BP, tachycardia, chest pain, fatigue.
- Most serious, worse prognosis, means that the left coronary artery has been affected.
- Higher risk of LV dysfunction, high risk of recurrence, life threatening (10% die w/in 1st year), dysrhythmias most common
Inferior – RCA affected and supplies SA node in most people, means the right coronary artery has been affected. S/S: May have bradycardia, hiccups, SOB, fatigue, chest pain.
Posterior – Circumflex is affected
What are the general clinical manifestations of an MI? What should be done for those with any s/s?
Pain (+/- radiate up L jaw or down arm)
Pain: discomfort, heaviness, pressure, tightness, not relieved by rest, position change, nitrates
MI vs Angina: occurs in am, >20 min, more severe
Cool, pale, clammy skin
Nausea and vomiting (Especially w/ RCA)
Syncope or near syncope (more likely w/ LCA)
Fever (not immediate, but within the first 24 hours)
Women, the elderly, diabetics and African Americans may show atypical s/s - fatigue; SOB; indigestion and nausea; anxiety; insomnia; chest pressure, fullness or burning; mat have little to no symptoms
12 lead ECG should be done on anyone over 35 with vague s/s.
What are the steps in the healing process after an MI?
- Enzymes released. For inflammatory processes, we look at CKMB and troponin. Enzymes that tell us if inflammation is present.
- Weak, less compliant
- Hypertrophy/dilation: ”ventricular remodeling” (Remodeling isn’t a good thing, give ACE Inhibitor to help prevent this)
- HF, usually L sided
When scar forms, heart will not be as strong as before. Must start cardiac rehab to gradually work your way back to a certain activity level. Can’t just go right back to normal every day life immediately after the MI, risk rupturing the scar and causing further damage. Work up to exercise, no sex until the doctor tells you. Take it easy for the next 6 weeks.
What are some complications of an MI?
What are some characteristics of dysrhythmias after an MI?
Most common (80%), and most common pre-hospital cause of death
R/O hypoxia and electrolyte disturbances
Heart blocks common after inferior wall MI
Most severe after anterior wall MI
Ventricular fibrillation (sudden cardiac death/SCD) is most serious form, frequent COD w /in 4h. No cardiac output, going to die if not treated.
Electrical dysfunction that commonly causes mortality in the first 72 h includes tachycardia (from any focus) rapid enough to reduce cardiac output and lower BP.
Bradycardia could occur after inferior (R sided) MI.
What are some characteristics of heart failure as a complication of MI?
Large MI’s and those with mechanical complications, HTN, or LV dysfunction are more likely to develop heart failure.
Severity associated with
- Location of occlusion
- Time of treatment
Cardiogenic shock: Decrease in cardiac output, have decreased perfusion of tissues, caused by lack of pumping ability not lack of volume.
- O2 & nutrients supplied to tissues are inadequate d/t severe LV dysfunction.
- IABP, dysrhythmics , vasodilators
Manifestations depend on infarct size and degree of reduction in cardiac output. Dyspnea, crackles at the lung bases, hypoxemia, agitation, are common.
HF occurs more so after an anterior MI, usually a larger one.
What are some characteristics of ventricular aneurysm as a complication of an MI?
Ventricular aneurysms are common, especially with a large transmural infarct (usually anterior).
Aneurysms may develop in a few days, weeks, or months. They are unlikely to rupture but may lead to recurrent ventricular arrhythmias, low cardiac output, and thrombosis with systemic embolism.
It’s weakness in the ventricle that could rupture into the pericardial sac, basically stops the heart from expanding.
Thinning and bulging of ventricular wall
Occur most frequently with large STEMIs
May develop thrombosis
- Embolic stroke
What are some characteristics of acute pericarditis as a complication of an MI?
Inflammation of pericardial sac
Occurs in 1/3 of STEMIS (2-3d after MI)
Cardiac compression>> decreased ventricular filling/emptying
Complication: Effusion +/- Tamponade
Chest pain aggravated by chest wall movements
Pain relieved with sitting up and leaning forward
Diffuse ECG changes
S/S: chest pain that’s aggravated by cough, deep breath or upper body movement, high temperature from infection.
Hallmark sign is friction rub (with pulse not resp.) Two major complications are pericardial effusion and cardiac tamponade.
Aspirin or another NSAID usually relieves symptoms. Could also treat with steroids.
Dressler's Syndrome: rare form of pericarditis with effusion that shows 3-4 weeks after MI. Will have pain, fever, and increased WBC's. Treat with steroids.
What are some methods of diagnosis of MI?
12-lead Electrocardiogram (ECG)
- Rate, Rhythm, ST’s, Q’s (serial ECGs)
- STEMI vs. NSTEMI vs. UA
Serum cardiac markers
- Troponin – most specific, more sensitive of cell death than CKMB. Good for diagnosis of late MI elevates for NSTEMI or STEMI.
- CreatineKinase (CK): CKMB, cardiac specific, elevated during tissue necrosis.
- Myoglobin - usually gone within 24 hours.
Other: Cath , Angiography, Stress Tests, Echo
What are the goals of treatment for the patient presenting with MI s/s? What steps should a nurse anticipate taking in the emergent treatment of a possible MI patient?
Goals: - relieving pain, adequate oxygenation, preventing platelet aggregation, restoring coronary blood flow & salvaging the functional myocardium
M - morphine sulfate 2 to 4 mg IV repeated at 5 to 15 min. intervals – Given for pain/anxiety, but it also dilates veins to decrease the pre-load on the heart which decreases the overall workload.
O - oxygen 2-4L/min for hypoxemia
N - nitroglycerin 0.4 mg SL every 5 min for 3 doses; then IV NTG – Decreases pre-load, increases oxygenation to the heart by opening the coronary arteries
A - aspirin 324 mg chewed for rapid absorption – Decreases platelet aggregation
Be (Beta blocker within 24 hours of admission)
ACE inhibitor or ARB for left systolic dysfunction remodeling.
Polite (Percutaneous coronary intervention) within 90 minutes of arrival. Door to balloon in 90 minutes. After a certain period of time, plaque becomes hard and unmovable.
Friend (Fibrinolytic within 30 of arrival, T-PA, must meet criteria to receive.
What are some diagnostics and methods of treatment available through heart catheterization after an MI? Characteristics of each?
Emergent PCI is first line treatment for patients with confirmed MI
Diagnostic Procedures (Non-Interventional):
- Involves the insertion of a catheter into the heart by way of a major vein to get to the right side, but more commonly by way of an artery (femoral) to get to the left heart and coronary arteries (and collaterals):
- Measures heart chamber pressures, oxygen saturation levels, examines structure/motion (LV function)
- Perform angiography: injecting dye into the coronary arteries to evaluate patency and look for stenosis.
Percutaneous Coronary Intervention:
- Angioplasty - A balloon is inflated into the stenosed coronary artery to press the plaque into the artery wall to allow for better blood flow and perfusion of the myocardium.
- Stent Placement (most common) - These are drug deluding “wire mesh” tunnels that are placed within the stenosed coronary artery.
Emergency PCI may not be required as long as the patient is stable, but needs to be scheduled soon. Use ASA, Heparin, and a glycoprotein inhibitor (Integrilin or ReoPro; to prevent platelet aggregation and clot formation). PCI may be done later or if angina worsens.
STEMI: PCI within 90 minutes (this is the ideal and preferred course of action)
Atherectomy – a rotational blade is used to shave off areas of plaque
Laser Angioplasty – a laser is used to vaporize the area
Ticagerlor (Brilinda) + 81 mg aspirin.
What arrhythmia may occur as the heart is suddenly re-infused with solid blood flow after a stent opens up the artery?
The pt could have ventricular tachycardia. Haven’t had enough blood flow to the myocardium. After blood flow is restored, the heart is re-invigorated by the restored oxygenation. Can go into an arrhythmia. Have crash cart available.
What option is available for those who are not candidates for surgery or angioplasty?
Laser guided into LV during diastole creates 15-40 one-mm channels through the myocardium. Promotes growth of new small blood vessels (called angiogenesis)
What are the advantages of PCI? Complications?
Shortened recovery time
- Ambulatory <24h
- Length of Stay (LOS)
Dissection of an artery
- Cardiac tamponade - Muffled heart sounds, low BP, JJVD, pulses paradoxus.
Abrupt closure within 24 hours
Restenosis within 30 days
Retroperineal (signs of shock, flank pain)
Hyperplasia over stents
Hematoma at the insertion site
Long-term - Risk of restenosis is about 30% in first 3 – 6 months and is more common in diabetic patients. or those with hyperlipedemia. Intimal Hyperplasia - cells grow through stent and causes stenosis. Newer drug lined stents are helping this problem.
What are the 3 major symptoms of Beck's Triad?
1.Hypotension: Fall in arterial blood pressure -- pericardial fluid accumulation to a degree that it impairs ventricular stretch, thus reducing stroke volume and cardiac output, two major determinants of systolic blood pressure
2. Increased CVP: Rising central venous pressure (nl 2-6) is evidenced by distended jugular veins while in a non-supine position. Caused by reduced diastolic filling of the right ventricle, due to the outside pressure being exerted on it by the expanding pericardial sac. This results of a backup of fluid into the veins draining into the heart, most notably, the jugular veins. Increased pressure in the R atrium. In severe hypovolemia , the neck veins may not be distended
3. Muffled heart sounds: Suppressed, quiet heart sounds occur due to the muffling effects of the sounds passing through the fluid surrounding the heart.
What are the preop and postop considerations for heart catheterization?
- Allergies (iodine sensitivity or renal impairment) Mucomyst
- NPO if MD orders
- Marking pedal pulses – why? Need to know what to compare post-op pulses to after they get back from the procedure. Make sure there’s not problem with arteries after procedure.
- ASSESS for CP, PULSES and BLEEDING at the site of incision!
- Assess circulation to the foot and lower leg used for the procedure: Pulses, color, sensation, temperature every 15min for an hour, every 30 min for the next hour, then every hour.
- Assess for recurrent angina
- Continuous ECG monitoring
- Bedrest with limb straight for 6 – 8 hrs.
- IV antiplatelets for 12 – 24 hrs. and orally for several months, IV NTG
- Monitor uop and renal function
- PT and INR and PTT
What are the characteristics of fibrinolytics and their use?
Fibrin specific agents (less mortality than non-fibrin)
- Alteplase ( t -PA)
Non-fibrin specific agents
If you don't have a cath lab, use fibrinolytics!
Stop, Dissolve, Reperfuse
Availability & rapid administration (IV)
80% - 90% of MI’s are caused by a thrombosis.
Stop infarct (mortality reduced by 25% if given w/in 1hr of symptom onset)
4 – 6 hrs. for full thickness myocardium death.
Most effective if given soon after thrombus formed (after a few hrs. clot hardens/more resistant)
AHA goal of less than 30 min. for fibrinolytics, initiate in ED if no lab.
Dissolve thrombus (breakup firbrin meshwork)
Reperfuse (GOAL: restore circulation, salvage muscle/prevent more loss)
Cath still necessary to correct the problem, most often an area of stenosis.
What are the eligibility criteria for fibrinolytic therapy?
Not selective to coronary thrombus, will dissolve preformed clot anywhere in the body.
- CP typical of MI <6h, unrelieved by nitro
- MI on ECG, ST elevation in at least 2 leads.
- No absolute contraindications
Contraindications (Absolute vs. Relative)
- Absolute: bleeding, Intra/Extra cerebral events (aneurysm, CVA/ trauma within 3 months, arteriovenous malformation, hx of bleeding), aortic dissection.
- Relative: peptic ulcer disease, anticoagulants, CVA, surgery within 3 weeks, bleeding in the last 2-4 weeks, serious chronic illness, uncontrolled HTN, CPR greater than 10 min.
What are some principles for the RN with fibrinolytic therapy?
Start 2-3 IVs
Try not to remove or start more after fibrolytic started bc of bleeding!
Monitor ECG, VS, assessment.
What are some expected and adverse outcomes of fibrinolytic therapy?
- Reperfusion ~ 1h after thrombolytics started, chest pain resolution
- Serial CK’s and serial ECGs should be obtained.
- Dysrhythmias common as blood reaches ischemic myocardium (May have VT for brief moments)
- Minor bleeding expected and not a reason to stop infusion, apply pressure or ice.
- Major – should call MD and stop infusion: low BP, high HR, bloody NG/Foley drainage, significant oozing, change in LOC (cerebral hemorrhage)
What are the principles of the coronary artery bypass graft surgery?
Major coronary artery is blocked (stenosed), a good vessel is used to “bypass” the area of stenosis to transport blood from a large artery, like the aorta, to the myocardium that has been supplied by the blocked coronary artery.
Saphenous – taken from the leg and is easy to get to and is large enough multiple grafts can be obtained. Tends to restenose.
Internal Mammary Artery –Most common, better rate of patency/long-term prognosis, if left attached to the subclavian artery. Difficult to obtain (poor choice for emergency) and it tends to cause a lot of postop pain.
Radial, gastroepiploic, inferior epigastric artery.
How to perform:
- The heart stopped (aorta cross-clamped, heart cooled by cold cardioplegia solution (K+) to stop contractions).
- Blood is diverted to the cardio-pulmonary bypass machine, preferably for no more than 3 hrs while surgeon operates.
- When grafting is complete, the heart is restarted (the solution is flushed out of the heart and it resumes beating.
- The pt. is then weaned from the bypass machine
- Mediastinal chest tubes are placed in pericardium to drain excess blood and fluids
- Epicardial pacing wires are placed on the heart.
Palliative: Improved outcomes, QOL, survival (women higher mortality.. Later treatment)
What preoperative management is required for CABGs?
- Baseline V/S, peripheral pulses, cardiovascular and pulmonary assessment, labs, and x-rays.
- Consent signed
- Betadine shower
- Clip hair on pts
-preop IV antibiotics (within 1 hr) and continued for at least 24 hrs.
What should a nurse teach the client before a CABG?
Will allow family to visit, but limited amounts
TC/DB – very important, provide chest splint
May require blood
Probably sit up on day 2 and walk on day 3 (Or day 2, sooner the better)
CCU very loud and bright, will try to let rest, but expect lots of interruptions.
What are some alternatives to CABG surgery?
Off pump coronary artery bypass (OPCAB)
- Full/partial sternotomy
- Beating heart
- High risk: Low EF, lung disease, RF, CVA risk
- dramatic reduction in the number of strokes during surgery
- pump>> microemboli: the aorta is clamped and a large tube inserted into it. After many years of plaque growth inside the aorta, manipulation of it loosens the plaque, thereby causing the microemboli to develop.
- After being on a blood bypass, lots of people have problems with clots and some people have mental symptoms. Confusion, memory problems, cognitive issues.
Minimally Invasive Direct Coronary Artery Bypass (MIDCAB)
- Reduced cost, LOS, mortality
- 1-2 Bypasses in 1-2 arteries on anterior surface
- High risk patients
- Don’t stop the heart. Beating-heart surgery reduces risk (such as stroke and postoperative bleeding) associated with cardiopulmonary bypass.
- Smaller thorocotomy approach, more painful.
- Slows heart w/Beta blocker or stops w/adenosine.
What are some complications of CABG?
Low Cardiac Output Syndrome –
- Most common early complication. May be caused by the bypass machine, especially if on for > 3 hrs. More common in elderly. May also be caused by hypovolemia. Or could just be poor LVF.
- Cardiac Output can be maximized by making adjustments in HR, preload, afterload, and contractility.
- HR – adjust meds &/or pacing wires may improve CO.
- Decreased Preload –commonly the result of hypovolemia d/t fluid and blood loss (will need volume replacement). However, decreased preload may also be due to peripheral vasodilatation (will need vasopressors).
- Increased Afterload –sometimes the result of the peripheral vasoconstrictive effects of hypothermia, postop HTN common. Can cause bleeding and increase LV workload. Vasodilator therapy with Nipride or NTG is common to decrease afterload and therefore CO.
- Contractility – If corrections to maintain HR, preload and afterload do not work, may have to try pos. inotropic drugs (which will increase O2 demand)
Cardiac Tamponade –
- Bleeding into pericardial sac compressing the heart. Keep mediastinal tubes open!!! (explain what they are)
- Beck’s Triad: rising CVP with JVD, narrow pulse pressure, muffled heart sounds. (narrow PP: sys. down as CO falls, diastolic up as systemic vasculature compensates)
- Pulsus Paradoxus – Difference in the first BP sound during expiration and normal respiration., If > 10 mm Hg, is positive.
Arrhythmias –electrolyte imbalances (hypokalemia most common), hypothermia, pH, ischemia, or catheter placement. Keep K on high side of normal (4.5 to 5.0) and Mag > 2.0 Atrial arrhythmias are common in first 36 hrs. (a fib) may treat with beta-blockers or calcium channel blockers if tachy.
Pulmonary Complication – PE common on 3rd postop day, especially w/SVG use. Encourage leg exercise/early ambulation to try to prevent.
What are the main post-op goals and objectives for CABG?
Goal: identify complication to provide for early intervention.
- Maintain adequate CO and tissue perfusion
- Through adjustments to preload, afterload, and contractility
- Recognize/ and Intervene Promptly to Prevent complications
- freq. V/S
- freq. Assessments: cardio/resp, cap. Refill, peri pulses, UOP, med. Tube drainage, incisions, lab results
- wean from vent. ASAP
- wean from meds. ASAP
- remove invasive lines ASAP
- Assist to begin rehabilitation
- OOB ASAP (day 1 –2 post op; up to chair then ambulate)
- Promote ADL
- Returning to the pre-surgical level of functioning is the goal: work, school. ADL’s, etc.
- Changes in lifestyle to promote recovery and health.
- READ Ambulatory/Home Care
- Educate abt the s/s of decreased perfusion.
What are the principles of inpatient nursing care after CABG?
Pain – morphine and NTG IV infusions
Managing Emotional Responses to Cardiac Disease
Anxiety – maintain calm, restful environment; may limit visitors; sedatives may be ordered PRN
Depression – common problem, getting out of bed early and back into normal activities
Nutrition – poor appetite, tasty food small amounts.
1500 to 1800 kcal/day with Na reduction to 2 to 3 g, low fat/cholesterol
Na reduction is not required after the first 2 or 3 days if there is no evidence of heart failure.
Monitoring lab values (especially K+ and Mag due to low levels leading to arrhythmias)
ECG – continuous cardiac monitoring for arrhythmia detection and serial ECG to look for ST changes
Monitoring O2 sats – use O2 @ 2L per NC to keep over 93%
Managing physical activity (should not stay in bed after 12 - 24 hrs. unless hemodynamically unstable) Prolonged bed rest results in rapid physical deconditioning and increased risk of DVT; also intensifies feelings of depression and helplessness.
Managing elimination - Maintaining normal bowel function with stool softeners to prevent straining is important. Urinary retention is common among elderly patients, especially after several days of bed rest or if atropine was given. A catheter may be required but can usually be removed when the patient can stand or sit to void.
Assessing for s/s of HF (talk about more in acute HF lecture)
Assessing heart sounds:
murmurs = possible valve involvement
muffled = possible cardiac tamponade
friction rub = pericarditis
What are the principles of pharmacological management post-op CABG?
Antiplatelet (Inhibits platelet aggregation) Therapy
- ASA - ASAP with suspected ACS
- Plavix - Alternative to ASA
- Effient - Alternative to plavix
- Heparin IV or a LMW heparin (Lovenox) subcutaneous
- Sublingual, translingual, IV (for ACS), transdermal/po (longacting) for anginal prophylaxis.
- peripheral vasodilatation
- decreases preload and afterload (decreases stress and O2 demand placed on heart)
- Central vasodilation
- coronary arteries (as well as collateral arteries) improves blood flow to the myocardium.
- Side Effects: HA (due to cerebral vasodilation and orthostatic hypotension), watch w/other vasodilators esp for ED w/in past 24h
- Goal: achieve pain relief while maintaining BP (perfusion pressure of 60 mm Hg.)
- Decrease morbidity/mortality related to CAD and MI’s & reduce infarct size.
- Decrease contractility, HR, BP (afterload), all of which reduces myocardial O2 demand.
- ASAP po or IV.
- Contraindicated in heart blocks, bradycardia, low BP, and asthma. Monitor HR and BP closely.
- recommended following anterior MI’s or MI’s that result in LV dysfunction (EF less than 40%)
Calcium Channel Blockers
- If already on adequate dosed Bblockers/can’t tolerate BB
Morphine – IV for pain (esp unrelieved by NTG) and anxiety control
- Decreases BP, HR, preload and afterload.
- Watch for hypotension, especially if on NTG (may need IVF)
- Resp. depression.
Antidysrhythmics – to control dysrhythmias
Antilipemics – to lower lipid levels
What are some principles of patient teaching post-CABG?
- Use terms appropriate to pt. level of understanding
- not “MI,” say “heart attack.”
- Models of the heart and videos are good
- Smoking cessation
- Diet - Don’t eat canned foods! Cut the fat off the meat, buy lean burgers or turkey.
- Taking meds.
Sexual activity: 4-6 wks post MI, if can climb flight of stairs OK, sex is OK.
Referral to Cardiac Rehab: The heart muscle needs to regenerate and repair before they to too much activity. R sided MI and L sided MI will have different rehabs.
What are the management principles for sudden cardiac death?
Majority of MI deaths occur during the first 1 hr, usually from V. fibrillation.
If you have someone who is revived from Sudden Cardiac Death:
- Full workup to r/o MI: ECG, cardiac enzymes, cath,
- Monitoring for repeat dysrhythmia: Holter, EP study (pacing pads, antidysrhytmics)
- Implantable cardioverter: Shocks them if it feels v. fib coming on. They need to sit down bc they might pass out.
- To calm fears: Go to rehab, go to support groups, talk to the doctor, talk to a counselor.
- Lots of damage to the heart. Need a lot of teaching post-event.
What are the quality control measures for acute myocardial infarction?
- ASA within 24 hrs. (also Plavix for at least 2 wks. Both are antiplatelets and prevent plt aggregation)
- Beta-blocker within 24 hrs. (decreases mortality by 30%)
- Percutaneous Coronary Intervention (PCI) within 90 min. can restore perfusion in 90 – 95% of pts. and reduce mortality rates)
- Fibrinolytic therapy within 30 min. (if PCI not available within 90 min)
- Smoking cessation counseling
- Prescribe ACE inhibitor or ARB at discharge
- Prescribe Beta-blocker at discharge
- Prescribe ASA at discharge
These are all measures that have been proven to decrease mortality and morbidity following AMI. Hospitals must agree to not only be in compliance with these practices, but to prove they are in compliance through reporting how they are doing to M/M. This information is also made public. It is thought that complete transparency will improve compliance and therefore patient outcomes.