Cardiac Complications Flashcards
_________________ is the build up of ACS plaque inside coronary vessels.
Coronary Artery Disease
CAD risk factors include:
DM, age, heredity, male, dyslipidemia, obesity
_____________ and ________ are two populations who have issues with HTN and lipids.
African Americans and Hispanics
Estrogen is ________
Cardioprotective
_____ angina is the most common type and occurs with stress and activity. It is relieved by ____.
Stable, rest
Prinzmetal’s angina is caused by ________. In between spasms, tissue gets hypoxic.
vasospasm
alters calcium flow and reduces prostaglandins
Unstable angina occurs more frequently and lasts longer. It can occur with or without _____. Heralds an MI.
activity
Angina pectoris is decreased ___.
O2
Causes of angina:
Hypotension (can be exercise induced), cocaine, HF, pulmonic diseases.
Clinical manifestations of angina include:
Chest pain, Description of pain – very important
Dyspnea, pallor, tachycardia, anxiety, and fear
Atypical symptoms – indigestion
Precipitating factors
Relieving factors – what made it go away? Nitro, bed rest, O2
Sense of “doom”
Diagnostic tests:
EKG --> most important Troponin --> lab of choice. CHF can bump levels CK and CK-MB Stress test - Lexiscan and Dobutamine Echo or TEE Coronary angiogram (Cath Lab)
Serum Cholesterol and Triglyceride Values
Total Cholesterol Under 200
LDL Less than 100
Tricglycerides < 150
Meds for angina:
Nitrates (don’t give to patients who take Viagra)
Aspirin - antiplatelet
Beta-blockers –> work by decreasing workload of heart (decreases HR) Ex: Lopressor. Decreases O2 demands which limits ischemia. **c/a in COPD/asthma patients. Can send them into a bronchospasm.
Calcium Channel Blocker - for prinzmetals angina, bradycardia, conduction defects or certain types of HF
Primary goal for angina:
increase oxygen. Put PT on 02 and 2L/min. Or if home, lay down and take deep breaths.
Nursing interventions:
Perform 12 Lead for acute CP – truly diagnostic
Have SL Nitro available
Continuous cardiac monitoring
4-6L/min of oxygen per NC
Space activities
Reduce risk factors: physician follow up, Na restriction, diet change, cholesterol meds
MONA is what?
morphine, oxygen, nitrates, aspirin
Acute coronary syndrome is what?
collaborations of s/s of sudden myocardial ischemia
Causes:
unstable angina, STEMI, N-STEMI
Clinical Manifestations:
chest pain – most defining characteristic. Sub-sternal or epigastric. Can radiate to L arm, radiate to jaw and neck. Pain lasts 10-20 mins. Dyspnea, diaphoresis, pallor, tachycardia.
Diagnostic tests:
EKG & cardiac enzymes
Treatment Modalities:
If blocked, revascularize. Do percutaneous!
Meds: tPA –> 2-3 large bore IV’s to draw labs off of
Acute MI
Blood flow is completely blocked
Results in death of myocardial cells – goes through ischemia and then death
N-STEMI is a partial occlusion – minor elevation of cardiac enzymes
STEMI – abrupt disruption of blood flow – no way that the body can compensate
Elevated ST segments or Q wave on 12 lead. Once you’re “healed,” you will always keep your Q wave.
Damage usually occurs in 1 out of the 3 coronary arteries
Lethal arrythmias (v-fib and v-tach) and death can occur (more so than because of necrotic tissues.
Coronary Arteries:
Left Anterior Descending (widow maker) -> left ventricle pump failure
Right coronary artery -> supplies R atria and ventricle
Circumflex -> supplies the back of the heart
Left Main Coronary Artery -> divides into circumflex and LAD
Resulting Damage to Walls of the Heart – can be full or partial
Subendocardium – non Q wave MI – only takes 20 mins for damage to show
Epicardium
Transmural – Q wave MI – through all layers of cardiac muscle. ST elevation
Remodeling
Goal of all nursing interventions r/t MI
re-establish oxygen supply to area of MI
Door to ___ is 10 mins, to need IN artery is 90 mins.
EKG
Clinical Manifestations
Chest pain, nausea & vomiting, diaphoresis, tachycardia & tachypnea, hypotension or hypertension, dysrhythmias, signs of left heart failure, decreased LOC, fear and anxiety
Hiccupping – diaphormatic irritation,
cool/clammy, mottled skin
Nursing Interventions
12 Lead EKG Assess Chest Pain (CP) Vitals & cardiac monitoring IV access and labs Watch for dysrhythmias Monitor I & O – fluid balance and kidney fx (decreases GFR)
Tx for MI
Revascularization:
PTCI – cath lab, femoral approach. Can do angioplasty. Drug-eluding stents or bare metal stent.
CABG – seen less and less. Usually take the saphenous vein from leg. Flip it upside down (because of valves)
Types of Cardiomyopathies
Dilated, hypertrophic, & restrictive
Cardiomyopathy definition:
enlarged, thickened, or rigid. Regular heart muscle is replaced with scar tissue (which is not functional). As the heart gets weaker due to nonfunctional cardiac muscle, it decreases the ability to pump the blood and maintain normal sinus rhythm. Most people get HF.
Etiology
usually uknown, recurrent MI, small genetic component, high mortality rate
Dilated cardiomyopathy definition
when heart chambers (atria and ventricles) are dilated…stretched thin. Chest X-ray shows enlarged heart – takes up most of chest. Usually starts in L ventricle and spreads to R ventricle.
Incidence
in pts with heart failure. The thinner the muscle wall gets, the less pumping that occurs. The L ventricle wall is typically thicker. Most dilated pts are between the ages of 20-60. Men ^.
Diagnosis
symptoms of HF. Echo, chest xray, stress test, murmur – valve – either rupture of cordi tendi or stretched valve.
Clinical Manifestations
SOB on exertion Weakness S3, S4, & AV murmur Dysrhythmias – because of overload (same as arrhythmias) Activity intolerance R and L heart failure signs
Treatment
Heart failure management Beta blockers, anti-arrhythmic, ACE’s – decrease afterload (reduces work of heart), & ARBS Diureticss Anticoagulants Inotropes – contractility Pacing therapies Pacemaker/AICD – implantable defib/Bi-V Revascularization therapies
Hypertrophic Cardiomyopathy definition and incidence
thickening of muscle fiber, characterized by decreased compliance. Impairs ventricular filling, which decreases cardiac output
mostly genetic. Affects 600,000-1.5 million patients.
Diagnosis
H&P, murmur, chest x-ray, Echo – can measure thickness of left ventricle
Clinical Manifestations
Asymptomatic – for years! Sudden death, SOB, angina, syncope – decreased cardiac output, Ventricular arrhythmias, Fatigue, palpitations, S3 – marker for fluid overload
Treatment
• Medications Beta blockers Calcium channel blockers Anti-arrhythmics • Non-surgical/surgical procedures Ablations AICD Septal myectomy
Restrictive cardiomyopathy defintion
rigid, wont expand with filling. Pumping or systolic can be normal, filling or diastolic is abnormal. Least common type.
Diagnosis
Diagnosis – H&P, EKG, chest x-ray, TEE
Clinical Manifestations
S3 & S4 Dyspnea on exertion Increased jugular venous pressures - JVD Exercise intolerance Lungs crackly
Treatment
• Lifestyle changes Diet, sodium restriction Exercise! • Medications ACE inhibitors Digoxin Beta blockers (cautiously) Anticoagulants Anti-dysrhythmics
Cardiogenic Pulmonary Edema
Definition-severe form of heart failure. Due to severe cardiac decompensation. Usually caused by MI, acute HF, or valvular disease. Contractility of ventricle is decreased. Ejection is decreased, lots of pressure in lungs. Large volume of fluid. Impaired gas exchange.
Can be due to cardiac or lungs
MEDICAL EMERGENCY!
Clinical Manifestations
- Respiratory: tachypnea, labored respirations, dyspnea, pink frothy sputum, crackles and wheezes
- Cardiac-tachycardia, hypotensive, cyanotic, hypoxic, cool, clammy skin
- Neuro: restless, anxious, impending doom – life-threatening medical emergency
Interventions
Sit upright legs dangle
ABG’s – RESPIRATORY ACIDOSIS
Manage pain
tripod
Oxygen applied & sats continuously monitored (CPAP or BI-PAP or vent)
Morphine sulfate – alleviates air hunger
Chest X-ray
Meds – lasixs, 3-D’s digoxin, dobutamine, & dopamine. Sometimes aminophylline. Narcan 0.4mg-2mg initial doses, up to 10mg
I&O
Suction or coughing secretions – pink frothy sputum.
Rheumatic Heart Disease is caused by
occurrence of abnormal immune response to group A strep
Rheumatic fever
Carditis
Risk factors: crowded living conditions, poor hygiene, poor access to medical care
Clinical Manifestations
Diagnosis
Treatment
Clinical Manifestations: chest pain, heart murmur, rash, migratory polyarthritis
• Diagnosis – H&P, labs: ESR, CBC, elevated WBC, C reactive protein – inflammatory marker, positive throat culture for strep
• Treatment
Medications – antibiotic of choice is PCN, clindamycin or arythromycin
-manage joint pain, etc.
Carditis
Occurs in 50% of rheumatic fever
Affects all three layers of heart
Clinical manifestations: Chest Pain, Tachycardia,
Pericardial friction rub- can hear it at L, lower sternal border on expiration**
Endocardial affects valve structure – murmur and additional scarring
HF symptoms
Treatment: Medications
Endocarditis affects:
valves!
Definition-Inflammation of the endocardium
Diagnosis – TEE
damaged endothelium via valve damage, surgery, previous endocarditis, entry for pathogen. IV drug abuse… Central line. Foley catheter. Dental procedures.
Clinical Manifestations
Fever >101.5 Flu like symptoms and cough SOB and joint pain Heart murmurs heard in 90% Anorexia & abdominal pain Splenomegaly -if spleen is removed, immunizations need to be up to date!
Interventions
Medications – ABX (amoxicillin)
Anti-inflammatory
Anti-pyretics
Teaching – dentist, abx prior to procedure
Surgery
Valve replacements (regurgitation – back flow)
Removal of large vegetations
Myocarditis can occur to an _________ response.
immunologic
Definition-Inflammation of the heart muscle.
Causes – due to a virus – coxsackie B (rules out ABX)
Incidence and risk factors – radiation, toxins, or drugs ***
Diagnosis – CBC, WBC, C reactive protein
Clinical manifestations – (depends on amount of tissue damage) HF symptoms
Asymptomatic for a while
Fever, fatigue, general malaise
SOB, palpitations, arthralgias
Sore throat, muffled S1, S3 murmur
if caught early, may not have a lot of symptoms
Treatment
Medications
Antibiotics
Antiviral
Corticosteroids - swelling
ACE inhibitors, anti-arrhythmics, and anti-coagulants – no blood clots and make the blood less viscous
Bedrest (for a couple weeks) and activity restrictions
Dietary modifications – low salt diet “heart healthy”
Tx goal is for cause of inflammation – keep in mind myocardial O2 demand
Pericarditis is the inflammation of the
pericardium! Usually viral.
High risk: end-stage renal disease pts, cancer pts
Diagnosis
CBC
Cardiac enzymes-elevated but not as high as MI
EKG- ST segment elevation
Echo
Chest x-ray
CT and/or MRI
Hemodynamic monitoring – arterially monitor BP, decreasing window btwn systolic and diastolic. Why? Still have resistance r/t inflammation
Clinical Manifestations
Abrupt chest pain – usually the 1st sign Pericardial friction rub Low grade fever Dyspnea Reflex Tachycardia
Treatments
• Medications Aspirin Acetaminophen NSAIDS – anti-inflammatory Corticosteroids Incentive spirometer Oxygen Positioning Pericardiocentesis – aspirate the fluid Surgery – pericardectomy (large section of the pericardium is removed, done in severe cases, keep going into cardiac tamponade)
Complications
Pericardial effusion
Cardiac tamponade – increase in pressure inside the heart (heart is trying to compensate for not filling, using more pressure to try to fill. Decreased diastolic filling – no room drop in BP!) Pulsus paradoxus – pulses diminish during expiration.
Chronic Constrictive pericarditis – scar tissue develops between pericardial layers
Valvular Heart Disease
• Aortic Valve Disease
Aortic Stenosis
Aortic Regurgitation
• Mitral Valve Disease Mitral Stenosis Mitral Regurgitation Mitral Valve Prolapse Tricuspid Stenosis
Diagnosis & Tx
Echo, Chest X-ray, EKG, cardiac cath, and exercise testing
Medications – diuretics, ACE inhibitors, vasodilators, anticoagulants
Teaching
Percutaneous balloon valvotomy
Surgery- Valve replacement
Abdominal Aortic Aneurysms
(AAA) more common in men, aging, and smoking
Clinical Manifestations
depends on where the AAA is. If it is thoracic (above the diaphragm – pretty uncommon. 10% are aortic) Neck pain, jaw pain, back pain. Non-descript. AAA is usually below the renal arteries. Urine output is decreased. Usually called the silent killer
Diagnosis and Treatment
CT/MRI Arteriogram TEE – can sometimes see the dissection Ultrasound – out pouching Medications Beta blockers – decrease HR Anti-hypertensives HTN will kill these patients, keep systolic under 120. Surgery Open Endovascular stent grafts (EVSG) S3 --> heart failure (murmur after the lub-dub diastolic murmur) kentuc-ky S4 --> stiff ventricle (happens before S1, S2 systolic murmur) Tennessee – takes more effort
