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NR202 Test 3 Altered Cardiac Function-Structural, infectious, and inflammatory d


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heart Failure-What happens when someone goes into HF
An impairment of the ventricle to eject blood- unable to pump enough blood at a rate sufficient to meet the metabolic demands of the body or can do so only with an elevated filling pressure. Although it can be acute onset, it more commonly results from chronic, progressive changes as pumping ability declines
Risk factors for HF
Coronary artery Disease and raised blood pressure are the most common
Smoking and diabetes are also risk factors
What happens to systolic and dyastolic blood pressures when a person is in Heart failure
Systolic-Difficulty emptying the left ventricle (impaired contractility or squeeze)
Diastolic-Unable to fill and relax the left ventricle sufficiently to accomodate an adequate amount of oxygenated blood returning from the lungs.
What happens to the left side of the heart when a person has HF
Cardiac output decreases
Increases pressures
impairing filling,
Blood accumulates in the pulmonary veins and lungs.
Manifestations of Left heart failure
-Crackles (rales) in bases
-dry hacking cough
-Decreased Urine output
-Activity intolerance
Right Heart Failure
Cor Pulmonale-Blood accumulates in the systemic venous system
Manifestations of Right heart failure
-Elevated central venous pressure
-Jugular vein distention
-Peripheral edema
-Liver enlargement
-abdominal distension
-hepatojugular reflex
BNP test
B type natriuretic peptide test
BNP is a nerohormone that the heart secretes in response to ventricular volume expansion and pressure overload
Differentiates HF from lung disease or pulmonary embolus in patients with dyspnea
Venous blood sample available in 20 minutes
Normal BNP levels are below 100 picograms/ml
Moderate HF 100-400 picograms/ml
Severe HF 400-800 or higher picograms/ml
symptoms of heart failure
Exercise intolerance,
history of MI,
chest pain,
gastrointestinal (liver problems),
paroxysmal nocturnal dyspnea, confusion,
and altered mental status
Symptoms of HF
Physical symptoms
Physical resting dyspnea,
Cyanosis and cachexia
Baseline height and weight
BP and P standing and sitting
Tachycardia above 120,
weak, thready pulse and pulsus alternans
Lowered left ventricular function
An elevation greater than 4 cm above the sternal angle with right-sided HF, point of apical impulse down and left of normal, S3 or regurgitation murmurs, lung sounds crackles and wheezing,
Liver enlargement
symmetrical edema
nursing diagnosis for HF
1. Decreased Cardiac Output
2. Fluid volume excess related to decreased cardiac output as manifested by chest x-ray pulmonary vascular congestion and cardiomegaly, echocardiography (valvular problems, lowered ejection fraction (<=40%), hypertrophy), transesophageal ECHO, dysrhythmias, serum osmolarity, NA, K, CL, liver function tests, raised CVP, weight gain, decreased urine output
Diuretics-K+ wasting hydrochlorothiazide HCTZ
Furosemide, Etharcrynic acid, Bumetanide, Demadex, Acetazolalmide (diamox)

K+ spairing- Spironolactone (aldactone) Triamterene (dyrenium)
ACE inhibitors
Angiotensin-Converting Enzyme (ACE) inhibitors-Decrease workload, decrease edema, and sodium retention
Enalopril, Lisinopril, Captopril
Beta Blockers
Decreases contractile force-negative inotrope
Digitalis Glycosides
positive inotrope
Negative chronotrope
Decreases preload and afterload
Decreases potassium
precipitates digitalis toxicity-Anorexia, nausea, vomiting, abdominal pain, weakness, vision changes (diplopia, blurred vision, yellow green halos seen around objects,) new onset dysrhythmias
Sympathomimetic agents
Sympathomimetic agents
Positive inotrope
Raises Cardiac Output
decreases afterload by vasodilation
Amrinone (Incor)
{Do not mix with D5W} and Milrinone (Primacor)
Vasodilators decrease afterload
Other sources
Human B type natriuretic peptide
Human B type natriuretic peptide: nesiritide (natrecor)-relaxes vascular smooth muscle, inhibits sodium and water retention, suppresses rennin secretion, reduces aldosterone secretion, reduces pulmonary capillary wedge pressure
Other sources
Aldosterone antagonist
Spironolactone (Aldactone)
Increases urine sodium excretion, decreases potassium secretion, weak diuretic
Other sources
Biventricular Pacer
has 3 leads
1. Rt ventricle
2. Rt atrium
3. Lt ventricle

pacer spikes for ventricles are seen as only one spike because they are timed exactly together. Greatly improves cardiac output with results apparent in 1-2 days. Should see improved urinary output immediately
Nursing Diagnosis: Knowledge deficit
Pt teaching
1. Necessity of weighing daily-and understand the difference between fluid and dry weight.
2. understand the purpose and know the dosage of each medicine
3. Teach to stagger BP med if dizziness
4. Teach to take diuretic dose earlier in the evening if BID
5. Adjust diuretic dose by recording of their daily weight (extra dose if they gain 3 lbs) Consider K+
6. Beta blockers therapy might take several months to make them feel better
7. Low sodium diet--Avoid salting foods at the table, salt cured meats (bacon, ham, tuna fish, corned beef), cheeses, catsup, pickles, olives and potato chips. Canned vegetables much higher in Na+ than fresh or frozen. Teach to read labels.
8. Medication adherence-Involve family and friends, altering or skipping of doses, failure to refill prescriptions, seek financial assistance
Lifestyle changes when diagnosed with Heart Failure
1. Smoking cessation
2. Alcohol restriction
3. Stress management
4. Immunizations-Flu and pneumococcal
5. Advanced directives
6. Fluid intake restriction
7. Exercise
When do pts call primary care provider
1. Weight gain of more than 3 lbs. Lasting longer than 2 consecutive days
2. Increased swelling of the ankles, legs, or stomach
3. Increased SOA, especially when lying flat
4. Extreme fatigue
5. Very fast heartbeat (above 120 bpm)
6. Very slow heartbeat (below 50 bpm)
7. Irregular Heart rhythm such results from the heart skipping beats
8. Chest pain or discomfort when exercising that gets better with rest
9. Nausea or lack of appetite
10. Difficulty with speech, sudden weakness in the arms or legs, or lack of appetite
11. Fainting or loss of consciousness
Evaluation: Weight
Sodium levels
Weight: Total body weight = dry body weight (slow gains and losses = weigh weekly) + Fluid body weight (fast gains and losses = weigh daily)
1 lb = 454 cc
1 kg = 2.2 lbs = 1000 cc
Figure weight loss or weight gain by I and O balance
Figure weight loss or weight gain by weight to see if consistent. May lose 500 cc/day insensible losses. Is the I & O or weight accurate?
In heart failure: decreased sodium = decompensation tx with diuretics. Raised Sodium may mean dehydration but may also mean raised intake of sodium. Fluid Status determined by the osmolarity, specific gravity
Pulmonary Edema
Abnormal accumulation of fluid in the interstitial tissue and alveoli of the lung.
Pulmonary Edema
Cardiac causes include acute myocardial infarction, acute heart failure (rt sided heart failure) and valvular disease.
Non cardiac causes primary pulmonary disorders: acute respiratory distress syndrome, trauma, sepsis, drug overdose, or neurologic sequelae.
Pulmonary edema is a medical emergency
Lower fluid excess and raise gas exchange
What happens to ABGs when a pt has Pulmonary Edema
PCO2 lowers, and the PO2 lowers because of rapid respiration then PCO2 increases to acidosis. O2 Sat 80-100
Cardiogenic: Pulmonary Artery Wedge Pressure above 25 mm Hg
Diagnosis for Pulmonary Edema
1. Impaired Gas exchange related to alveolar and pulmonary interstitial edema
2. Fluid volume excess related to mechanisms to maintain cardiac output-Anxiety related to difficulty breathing
Tx of Pulmonary Edema
Oxygen to keep PO2 greater than 60, CPAP or ET with vent, HOB raised, Oximeter, I&O, Foley for accurate O,
Meds to treat Pulmonary Edema
Morphine Sulfate (Relieves anxiety and decreases pain, sedative
Vasodilator decreases afterload, loop diuretics (Furosemide is a venous dilator), Vasodilators nitroprusside or nitroglycerine decrease afterload,
Dopamine and Dobutamine, Aminophylline used cautiosuly to reduce bronchospasm and decrease wheezing.
Valvular Heart Disease
Ca deposition,
rheumatic heart
post MI
congenital heart
Types of Valvular Heart Disease
Stenosis-when valve leaflets fuse together and are unable to open or close fully.
The opening narrows and becomes rigid. Scarring impedes the forward flow of blood decreasing cardiac output. Backflow of blood when valve not fully closed. Regurgitant valves (insufficient or incompetent do not close completely. Backflow of blood occurs through incompletely closed valves. Erosion of valve cusps by bacterial endocarditis, by scarring or tearing from myocardial infarction or cardiac dilation where the annulus or supporting ring is stretched so valve edges no longer close completely
Pathology of Valvular heart disease
Behind the diseased valve, volumes and pressures are increased (hypertrophy and heart failure.) Heart enlargement causes raised oxygen consumption-Ischemia and chest pain. Pulmonary edema-pulmonary hypertension-right ventricular failure. High pressure through an incompetent valve may damage endocardium resulting in infective endocarditis x 5 greater than those with functioning valves
Characteristics of Valvular Disease
Characteristics is a MURMUR. Symptoms are related to valve affected and effect of pressure changes related to affected blood flow.
Diagnosis: how Valvular Disease is diagnosed
Cardiac Cath
Chest x-ray for enlargement or calcification of leaflets, ECG, Echo, Transesophageal echo, MRI (new)
Treating Valvular Heart disease: meds
Vasodilators (ACE inhibitors)
Tx of atrial fibrillation (caused by atrial distension) antidysrhythmic and anticoagulant,
Antibiotics prophylactically prior to any dental work, invasive procedures, or surgery to minimize risk of bacteremia
Treating Valvular Heart
Percutaneous Balloon Valvuloplasty
Reconstructive surgery
Valve replacement (mechanical valves require life-time anticoagulation
Biologic tissue valves (pig, cow, or human) require no long term anticoagulation but frequent replacement because prone to deteriorate
Nursing Diagnosis for Valvular Heart Disease pts
1. Decreased Cardiac output related to backflow from regurgitant or stenotic valve
2. Activity intolerance
3. Risk for infection
4. Altered Protection related to anticoagulant therapy
primary abnormality of the heart muscle that affects its structural of functional characteristics (both systolic and diastolic). Idiopathic (cause unknown)
Cardiomyopathy: Dilated
Dilated-chambers are dilated-ventricular contraction is impaired-Extensive interstitial fibrosis or scarring. Progressively worse and die within 2 years.
Cardiomyopathy: hypertrophic
Decreased compliance of left ventricle and hypertrophy of the ventricular muscle mass, decreases filling small end-diastolic volumes and decreases cardiac output- 1/2 are genetically transmitted in an autosomal dominant pattern--most common cause of sudden cardiac death in young athletes. Sx: dyspnea, angina, syncope, fatigue, dizziness, palpitations, dysrhythmias
Cardiomyopathy: Restrictive
Restrictive-excessive stiffness and rigidity of the ventricles (decreased filling and decreased cardiac output) no transplantation
Diagnostic tests for Cardiomyopathy
Chest X-Ray
hemodynamic studies
Nuclear scans,
Cardiac cath
Endomyocardial biopsy
Nursing care: Caring for patients with Cardiomyopathy
Nursing assessment and care for clients with dilated and restrictive cardiomyopathy is similar to that of pts with HF. Teaching about the disease process and its management is vital. Some degree of activity restriction is often necessary; assist to conserve energy while encouraging self care. Support coping skills and adaptation to required lifestyle changes. Provide info and support for decision making about cardiac transplantation if an option
Discuss the toxic and vasodilator effects of alcohol, and encourage abstinence.
The client with hypertrophic cardiomyopathy is similar to myocardial ischemia: nitrates and other vasodilators are avoided though.
Inflammatory Cardiac Disorders
Rheumatic fever
Rheumatic Fever-systemic inflammatory disease, abnormal immune response to group A beta hemolytic strep--Peak incidence 5-15 years but can be any age--valve structures become red and swollen--fever and migratory joint pain are initial manifestations-nonpruritic skin rash, inability to concentrate, -chest discomfort, tachy or heart failure, pericardial friction rub, s3 or s4 or murmor of mitral or aortic regurgitation
Inflammatory Cardiac Disorders
Lab diagnosis:
CBC, ESR erythrocyte sedimentation rate, C-reactive protein evaluates the severity of active process, Antistreptolysin titer is a streptococcal antibody test,
Inflammatory Cardiac Disorders
Treatment of Rheumatic fever
Penicillin X 10 days (erythromycin or clindamycin if allergic)
Antibiotics for 5-10 years to prevent recurrences, joint pain and fever treated with salicylates
Notify MD of pericardial friction rub or a new murmur
Inflammatory Cardiac Disorders
Infective endocarditis-
Infective endocarditis-affects valves-infective in nature rather than inflammatory-port of entry for organisms into the blood stream--abrupt onset and is rapidly progressive severe disease (Staph aureus)
Inflammatory Cardiac Disorders
Infective endocarditis-Manifestations
raised temp above 101.5,
flu-like symptoms
joint pain
Murmurs (change or new)
Inflammatory Cardiac Disorders
Infective endocarditis-Treatment
tx with antibiotics, and preventative antibiotics
Tx-2-6 weeks of antibiotics IV peak and trough
Inflammatory Cardiac Disorders
Infective endocarditis-Diagnostic tests
Serologic immune testing
+rheumatoid factor
Blood cultures
Urine testing
Damage due to microemboli
Transesophageal echocardiography
Inflammatory Cardiac Disorders
Infective endocarditis-Nursing Diagnosis
Risk for Altered Body temp, ASA, tylenol
Risk for altered tissue perfusion related to emboli
Knowledge deficit
Inflammatory Cardiac Disorders
Inflammation of the pericardium-two layered sac with a thin layer of serous fluid 30-50 ml -protects and cushions the heart and great vessels--frequent complication of uremia--inflammation causes the pericardium to become rigid
Inflammatory Cardiac Disorders
1. Chest Pain with an abrupt onset rub (sharp and may radiate to the back or neck) is the most frequent. Pericardial pain is aggravated by respiratory movements (deep inspiration or coughing, changes in body position or swallowing). The client characteristically assumes an upright position and leans forward
2. Pericardial Friction rub-Heard most clearly in the left lower sternal border with the client sitting up or leaning forward-a leathery grating sound produced by the inflamed pericardial layers rubbing against the chest wall or pleura. The rub is usually heard on expiration and may be constant or disappear and reappear. heart sounds may be muffled
Fever, low-grade
Dyspnea, mild (splitting)
Inflammatory Cardiac Disorders
pericardial effusion
Pericardial effusion is an abnormal collection of fluid (pus, blood, or serum) between the pericardial layers that threatens normal cardiac function--causes compression of the heart, critically lowers Cardiac Output, raises intracardiac pressures, lowers diastolic filling pressures, lowers cardiac output.
Inflammatory Cardiac Disorders
pericardial effusion
paradoxical pulse
Hallmark of CARDIAC TAMPONADE is a paradoxical pulse-pulse markedly decreases in amplitude during inspiration. Palpation of the carotid or femoral artery, the pulse is either diminished or absent during inspiration in pulsus paradoxus. A drop in systolic blood pressure of more than 10 mm Hg during inspiration indicates pulsus paradoxus
Tx: Pericardiocentesis: Emergency procedure for cardiac tamponade
Inflammatory Cardiac Disorders
pericardial effusion: other symptoms of pericardial effusion
Distant muffled heart sounds another symptom
Beck's triad-Seen with pericardial effusion-
1. hypotension
2. distended neck veins
3. muffled heart sounds

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