Ch 37: Care of Pts with Cardiac Problems

Question 0

Systolic heart failure

Answer 0

A.k.a. systolic ventricular dysfunction
It’s a subtype of left-sided heart failure

The heart does not contract forcefully enough during systole to eject adequate amounts of blood into circulation. Pre-load increases with decreased contractility and afterload increases. The ejection fraction drops from a normal of 50 to 70% to below 40%. Fluid backs up into the pulmonary system. If the ejection fraction is less than 30% they are a candidate for a cardioverter/defibrillator

Question 1

Left-sided heart failure

Answer 1

Left-sided heart failure/ventricular. Most heart failure begins with the left ventricle and progresses to the failure of both ventricles.

Causes include hypertensive, coronary artery, and valvular disease involving the mitral or aortic valve.

Decreased tissue perfusion from poor output, pulmonary congestion and increased pressure in the pulmonary vessels indicate left ventricular failure. It is also known as congestive heart failure. It can be acute or chronic, mild to severe, systolic or diastolic

Question 2

Diastolic heart failure

Answer 2

A.k.a. heart failure with preserved left ventricular function. This is a subtype of left sided heart failure.

The left ventricle cannot relax adequately during diastole and prevent the ventricle from feeling with enough blood to ensure adequate output. The ejection fraction is more than 40% but becomes less compliant overtime because more pressure is needed to move the same amount of volume. It is primarily seen in older adults and women who have chronic hypertension and undetected coronary artery disease.

Question 3

Right-sided heart failure

Answer 3

Right-sided ventricular failure can be caused by left ventricle failure, right ventricle MI, pulmonary hypertension. The right ventricle cannot empty completely. Increased volume and pressure develop in the venous system and peripheral edema results

Question 4

High output heart failure

Answer 4

Can occur when cardiac output remains normal or above normal. It is caused by increased metabolic needs or hyperkinetic conditions such as septicemia, fever, anemia, and hyperthyroidism.

Question 5

Classification and staging of heart failure

Answer 5

ACC/AHA

A. Class one patients at high risk for developing heart failure

B. Class one patients with cardiac structural abnormalities or remodeling who have not developed heart failure symptoms

C. Class two or three patients with current or prior symptoms of heart failure

D. Class four patients with refactory end stage heart failure

Question 6

Ventricular remodeling

Answer 6

1. Progressive myocyte/myocardial cell/contractile dysfunction over time. Results from activation of the Renin/angiotensin system caused by reduced blood flow to the kidneys, a common occurrence in low output states.
2. After a myocardial infarction, permanent changes in the size and shape of the left ventricle due to scar tissue. Such remodeling may decrease left ventricular function, cause heart failure, and increase morbidity and mortality

Question 7

Chemical responses when cardiac output is affected

Answer 7

And immunoresponse releases tumor necrosis factor in interleukins which contribute to ventricular remodeling. Natriuretic peptide and neurohormones promote vasodilation and diuresis. BNP is produced and released by the ventricles when there is fluid overload as a result of HF. BNP ^ age and women. ¥ obese.
Vasopressin/ADH is released because of decreased cerebral perfusion. This causes vasoconstriction and fluid retention which worsens heart failure. Endothelin is a vasoconstrictor that is released due to stretch to cells. This increases peripheral resistance and HTN. HF worsens.

Question 8

Myocardial hypertrophy

Answer 8

The walls of the heart thicken to provide more muscle mass for more forceful contractions and increasing cardiac output. There is not enough circulation to provide blood supply and it becomes oxygen deprived. All compensatory mechanisms contribute to an increase in the consumption of myocardial oxygen. When the demand for oxygen increases in the myocardial reserve has been exhausted, clinical manifestations of HF develop.

Question 9

Risk factors and causes of heart failure

Answer 9

Hypertension 75% of the time. Coronary artery disease. Cardiomyopathy. Substance abuse alcohol and drugs. Valvular disease. Congenital defects. Cardiac infections and inflammations. Dysrhythmias. Diabetes mellitus. Smoking. Family history. Hyperkinetic conditions such as hyperthyroidism.

1/3 MIs get HF
Structural changes such as valvular dysfunction, especially pulmonic and aortic stenosis.
Older adults: use of NSAIDS which cause fluid and sodium retention.
Thiazolidiniines for diabetes cause fluid and sodium retention

Africans 2x

Question 10

Manifestations of left sided heart failure

Answer 10

Early/first sign Cough that is irritating, nocturnal, and unproductive. As it becomes severe they may expectorate frothy, pink tinged sputum which is a sign of life-threatening pulmonary edema. Dyspnea

Manifestations due to decreased cardiac output include fatigue, weakness, oliguria during the day, nocturia at night, angina, confusion and restlessness, dizziness, tachycardia and palpitations, pallor, week peripheral pulses, cool extremities.

Manifestations due to pulmonary congestion include a hacking cough worse at night, dyspnea, crackles or wheezes, tachypnea, S3/S4 summation gallop

Question 11

Right-sided heart failure manifestation

Answer 11

Due to systemic congestion. Jugular neck vein distention, enlarged liver and spleen which can cause anorexia and nausea, dependent edema, distended abdomen and ascites, swollen hands and fingers, polyuria at night, weight gain, increased blood pressure from excess volume or decreased from failure.

Patients with heart failure may have thirst and drink excessive fluid because of sodium retention

Question 12

Proportional pulse pressure

Answer 12

Systolic-diastolic/systolic

If less than 25% it indicates severely compromised cardiac output.

Question 13

BNP

Answer 13

Is used for diagnosing heart failure, especially diastolic heart failure in patients with acute dyspnea. It differentiates between the dyspnea of heart failure and that associated with lung dysfunction. Patients with atrial dysrhythmias and renal disease may also have an elevated BNP

Question 14

Microalbuminuria

Answer 14

Is an early warning detector. It is an indicator of decreased compliance of the heart and occurs before BNP rises.

Question 15

Arterial blood gases

Answer 15

Respiratory alkalosis may occur because of hyperventilation.
Respiratory acidosis may occur because of carbon dioxide retention.
Metabolic acidosis may indicate accumulation of lactic acid.

Question 16

Diagnostic tests for heart failure

Answer 16

Echocardiography is considered the best tool in diagnosing heart failure. It can see cardiac valvular changes, pericardial effusion, chamber enlargement, ventricular hypertrophy. Also determine ejection fraction.

Radionuclide studies: thallium, technetium

ECG. Will show ventricular hypertrophy, dysrhythmias, myocardial ischemia, injury, or infarction but is NOT helpful in determining the presence or extent of heart failure

Pulmonary artery catheters.
RAP: normal of elevated with L/HF
elevated in R/HF
PAP and PAWP: are elevated in L/HF because of ^volume and ^pressure

Question 17

Nursing diagnoses for heart failure

Answer 17

Priority: impaired gas exchange, decreased cardiac output, activity intolerance. Additional: excess fluid volume, acute confusion, ineffective therapeutic regimen, anxiety, ineffective tissue perfusion, impaired physical mobility, potential for pneumonia depression and dysrhythmias

Question 18

ACE inhibitors. ARBs

Answer 18

ACE: Enalapril, fosinopril. Ramipril. 1st line
ARBs: valsartan, irbesartan, losartan

Side effects of Ace inhibitors include nagging dry cough. They suppress the renin angiotensin system, affecting arterial resistance, arterial dilation, and sodium and water retention which Decreases fluid overload. They work better on Euro-Americans then African-Americans. Monitor for hyperkalemia with people who have renal dysfunction

Start slowly, there may be a rapid drop in blood pressure. Monitor blood pressure for several hours after the initial dose.

Question 19

hBNPs

Answer 19

Nesiritide used for acute HF

Lowers pulmonary capillary wedge pressure and improves GFR. Give IV bolus over 60 seconds followed by a continuous infusion for up to 48 hours. Monitor blood pressure and pulse carefully because it can significantly decrease. Give thru separate infusion line because it is incompatible with heparin and most parent earl meds. Expect an increase in serum BNP

Question 20

Reduce preload

Answer 20

Ventricular fibers contract less forcefully when they are overstretched as in a failing heart. Decreased volume and pressure in the left ventricle, increasing muscle stretch and contraction. Use it when heart failure is accompanied by congestion with sodium and water overload.

Morphine sulfate reduces anxiety, decreases preload and afterload, slows respirations, and reduces pain.

Diuretics are the first-line drug of choice in older adults with fluid overload and heart failure. They reduce circulating blood volume, decrease preload, reduces congestion

Question 21

Nutrition therapy for heart failure

Answer 21

Sodium <2-3G day
Fluids restricted if needed to 2L
Weigh daily

Question 22

Hypokalemia

Answer 22

Monitoring if on a diuretic. Signs include generalized weakness, depressed reflexes, irregular heartbeat, and nonspecific neurological symptoms. Aldactone diuretic helps retain potassium.

If creatinine is greater than 1.8, ask the doctor before giving supplemental potassium

Question 23

Nitrates

Answer 23

Are Venus vasodilators for heart failure with severe dyspnea. Return venous vasculature to a more normal capacity, decrease the volume of blood returning to the heart, and improve left ventricular function. They are usually for acute heart failure.

Monitor blood pressure closely. Headache at first that will go away with taller. To prevent tolerate one 12 hour free. Out of every 24 hours usually overnight.

Question 24

Nonsurgical management of heart failure

Answer 24

Continuous positive airway pressure which decreases afterload and preload.
Cardiac resynchronization therapy which uses a pacemaker and or defibrillator.
Investigated Gene therapy with injections of growth factor

Question 25

Surgical management

Answer 25

Heart transplant is the ultimate choice for end-stage heart failure. Ventricular assist devices use a mechanical pump to help the patients own heart work. People with end-stage kidney disease, severe lung disease, clotting disorders, infections, and those that don’t respond to antibiotics are not candidates.

Surgeries for ventricular remodeling include heart reduction surgery, partial left ventricularectomy, endoventricular circular patch, acorn cardiac support device, Myosplint

Question 26

Activity intolerance

Answer 26

If blood-pressure changes more than 20 mm or pulse increases more than 20 beats per minute, the activity is too stressful. The activity includes dyspnea, fatigue, or chest pain that is rated on a scale of 12 out of 20 is too much. Slowly increase Until the patient can walk 200-400 ft 3x day.

Question 27

Manifestations of pulmonary edema

Answer 27

Crackles, dyspnea at rest, disorientation or confusion, tachycardia, hypertension or hypotension, reduced urinary output, cough with frothy punk tinged sputum, premature ventricular contractions and other dysrhythmias, anxiety, restlessness, lethargy.

Question 28

Management of pulmonary edema

Answer 28

If the patient is not hypotensive, place in high Fowler’s with legs down to decrease venous return to the heart. Priority nursing action is to administer high flow oxygen therapy at 5 to 6 L per minute by facemask or 10 to 15 L per minute by non-rebreather mask. Apply a pulse ox and keep sats above 90%. Possible CPAP.

If systolic is above 100, give something will nitroglycerin to decrease afterload and Preload

Lasix or Bumex mix is given IV over 1 to 2 minutes to avoid ototoxicity. IV morphine sulfate maybe given to reduce venous return/preload, decrease anxiety, and reduce the work of breathing.

Question 29

Heart failure self management

MAWDS

Answer 29

Medications: take as prescribed, do not run out. Know the purpose and side effects. Avoid NSAIDs.

Activity: stay as active as possible but don’t overdo it. Know your limits. Be able to carry on conversation while exercising. Start with 200 to 400 feet per day and slowly increase. If chest pain or dyspnea occurs you have overdone it.

Weight: weigh each day at the same time on the same scale. Report a gain of more than 3 pounds in one week or 1 to 2 pounds in a day.

Diet: limit sodium 2-3 g. Limit fluid to 2 L.

Symptoms: note any new or worsening symptoms and notify the doctor. A decrease in exercise tolerance lasting 2 to 3 days. Cold symptoms more than 3 to 5 days. Nocturia, Dyspnea or angina at rest or worsening angina. Increased swelling in the feet, ankles, or teams.

Question 30

Mitral stenosis

Answer 30

Usually from rheumatic carditis which can cause valve thickening by fibrosis and calcification. Other causes include a tumor, calcium accumulation, and thrombus formation. Normal blood flow from the left atrium to the left ventricle is restricted. Therefore you get an increased left atrial pressure, the left atrium dilates, pulmonary artery pressure increases, and the right ventricle hypertrophy’s. Pulmonary congestion, right-sided heart failure and later preload and cardiac output is decreased.

Features include fatigue, dyspnea, orthopnea, hemoptysis, hepatomegaly, Neck vein distention, pitting edema, atrial fibrillation, rumbling apical diastolic murmur

Question 31

Mitral regurgitation

Answer 31

Key features include fatigue, dyspnea, orthopnea, palpitations, atrial fibrillation, neck vein distention, pitting edema, high-pitched holosystolic murmur.

Fibrotic and calcific changes occur and prevent the mitral valve from closing completely during systole. This allows back flow of blood into the left atrium when the left ventricle contracts. During diastole, that regurgitant output flows back into the left ventricle, increasing the volume that has to be pumped out next time, leading to left ventricle hypertrophy. Rheumatic heart disease is a major cause. More common in women if rheumatic. If congenital it is more common in men. It can eventually lead to right-sided heart failure.

Question 32

Mitral valve prolapse

Answer 32

Key features include atypical chest pain, dizziness, syncope, palpitations, atrial tachycardia, ventricular tachycardia, systolic click. It occurs because the valvular leaflets enlarge and prolapse into the left atrium during systole. It can progress to mitral regurgitation.

Question 33

Aortic stenosis

Answer 33

Key features include dyspnea on exertion, angina, syncope on exertion, fatigue, orthopnea, paroxysmal nocturnal dyspnea, harsh systolic crescendo decrescendo murmur

Most common valve dysfunction from where in tear. The aortic valve narrows and obstructs left ventricular outflow during systole. This results in ventricular hypertrophy. Cardiac output becomes fixed and cannot increase to meet demands during excursion. Left ventricle fails then the left atrium backs up, pulmonary congestion, and eventually right sided heart failure can occur late in the disease. If the surface area of the valve becomes 1 cm or less common surgery is urgently needed

Question 34

Aortic regurgitation/insufficiency

Answer 34

Aortic valve leaflets do not close properly during diastole and allows flow of blood from the aorta back into the left ventricle during diastole. The left ventricle in compensation dilates and eventually hypertrophy’s.

Key features include palpitations, dyspnea, orthopnea, paroxysmal nocturnal dyspnea, fatigue, angina, sinus tachycardia, a blowing decrescendo diastolic murmur. There is a bounding arterial pulse and a widened pulse pressure.

Question 35

Testing for valvular disease

Answer 35

Echocardiography is the choice test. It defines cardiac structure, movement of the valve leaflets, size and function of the cardiac chambers.
TEE is the gold standard.
Possible exercise tolerance testing and stress echocardiography

Question 36

Nonsurgical management of valvular disease

Answer 36

Diuretics, beta blockers, did jocks send, oxygen. Nitrates are given cautiously to patients with aortic stenosis because of the potential for syncope and a reduction of left ventricular preload. Basal dilator’s such as calcium channel blockers may be used to prevent regurgitation

** Prophylactic antibiotic therapy is required for all patients with valvular disease before any invasive procedure. Procedures include bronchoscopy, endoscopy, sigmoidoscopy, colonoscopy, genitourinary instrumentation, surgery, and any dental procedures.

Monitor for atrial fibrillation and notified the doctor. Possible use of IV diltiazem or Amiodarone. Cardioversion may be attempted. Anticoagulation therapy if they have atrial fibrillation. Rest is important because activity will cause an increase in metabolic demands which can lead to heart failure.

Question 37

Surgeries for valvular disease

Answer 37

Direct/open Commissurotomy the surgeon removes thrombi from the atria, incises the fused commissioners, debrides calcium from the leaflets.
Mitral valve annuloplasty/reconstruction

Valve replacement can be done with a prosthetic/synthetic or biologic tissue valves. With prosthetic valves all patients must receive anticoagulation. Xenograft is from another species. They are not as durable as prosthetic valves and need to be replaced every 7 to 10 years. Pulmonary autografts are donated from cadavers. A mechanical valve is used to replace the aortic valve.

Preop: open heart surgery similar to CABG. Teach about pain, incision care, and breathing. Stop taking oral anticoagulants 72 hours before. Have all dental work done.

Post op: similar to CABG. Monitor respiratory status closely because of previous pulmonary hypertension and stiff lungs. Be alert for bleeding if aortic valve replacement. There is usually a significant reduction in cardiac output and it needs to be monitored closely. Pulmonary artery wedge pressure greater than 18 may be required to maintain an acceptable cardiac output. They will require lifetime prophylactic anticoagulation therapy to prevent thrombus formation. Normal activity after six weeks but no heavy physical labor with the upper extremity for 3 to 6 months. No dental work for six months afterwards. Avoid MRIs. Wear a medical alert bracelet.

Question 38

Invective/bacterial endocarditis

Answer 38

Most commonly from Streptococcus or Staphylococcus. Primarily in patients who abuses IVdrugs, have had valve replacements, systemic infection, or structural cardiac defects. The valves can become obstructed and stenotic and embolism can occur. Manifestations of fever, anorexia and weight loss, cardiac murmur, development of heart failure, systemic embolization, petechiae, splinter hemorrhage on the nails, Osler nodes On palms of hands and soles of the feet, Janeway’s lesion is a flat reddened maculas on hands and feet, positive blood cultures. Onset is usually within 2 weeks. Either right or left to sided heart failure can occur. Embolization is the major complication and occurs from fragments of vegetation that break loose and travel through circulation. With the left side it involves the spleen, kidneys, G.I. tract, brain, and extremities. With the right side it involves the pulmonary circulation.

Blood cultures and monitored for 3 to 4 weeks. Echocardiography and TEE

Antimicrobials are given IV and can last 4 to 6 weeks. Penicillins or cephalosporins are used. Anticoagulants do not help prevent embolization from vegetations. Get adequate rest and use good hygiene. No flossing. Monitor temp daily for 6 weeks.

Surgical interventions include removing the infected valve, repairing or removing congenital shunts, repairing injured valves, draining abscesses in the heart or else where.

Question 39

Pericarditis

Answer 39

Inflammation or infection of the pericardium, the fact that encloses the heart. Acute viral follows a respiratory infection. Dressler’s syndrome occurs 1 to 12 weeks after an MI. It is characterized by pericarditis, fever, and pleural effusions. Post pericardiotomy syndrome occurs after cardiac surgery. Chronic constrictive pericarditis. Occurs when inflammation causes a fibrous thickening of the pericardium. This can be caused by TB, radiation, trauma, renal failure, or metastatic cancer. Chronic usually results in cardiac failure.

Manifestations include sub sternal precordial pain that radiates to the left side of the neck, shoulder, or back. It is grating and oppressive and aggravated by breathing usually on inspiration, coughing and swallowing. It is worse in supine position. Pericardial friction rub could be heard.

If chronic they will have signs of right-sided heart failure, and elevated systemic venous pressure with jugular vein distention, hepatic engorgement, dependent edema. If acute they may have an elevated white blood cell count and fever. ECG normally shows and ST/T spiking. Atrial fibrillation is common.

Treatment usually consists of NSAID. Relief in 48 hours With no relief and no bacterial pericarditis, corticosteroid therapy. Relieve pain by sitting upright and leaning forward. Avoid anticoagulants which can worsen it. Monitor for paradoxical blood pressure.

It can cause pericardial effusion and cardiac tamponade

Question 40

Acute cardiac tamponade

Answer 40

Manifestations include jugular venous distention with clear lung sounds, paradoxical pulse (When systolic blood pressure is 10 mm higher on expiration), Decreased cardiac output, muffled heart sounds, circulatory collapse. It only takes 20 to 50 mL of fluid. It is an emergency. Hemodynamic monitoring will show all pressures being elevated. It is treated with a pericardiocentesis

Question 41

Pericardiocentesis

Answer 41

Removes fluid and relieves pressure on the heart. Use echocardiographic or fluroscopic and hemodynamic monitoring. And 8 inch needle is inserted into the pericardial space. A drain maybe temporarily placed. Monitor PAWP and RAP.

After monitor for reoccurrence. Provide adequate fluid volumes to increase cardiac output and prepare for an emergency sternotomy if tamponade occurs. A portion of the pericardium can be removed to allow adequate ventricular filling and contraction. The surgeon can create a pericardial window To allow fluid to drain into the plural space.

Question 42

Rheumatic carditis

Answer 42

AKA rheumatic endocarditis, is a sensitivity response that develops after an URI with group A beta-hemolytic streptococci. The inflammation impairs contractile function of the myocardium, thickens pericardium, and valvular damage
Formation of Aschoff bodies (small nodules in the myocardium that are replaced by scar tissue). Stenosis or regurgitation of the mitral and aortic valves is seen
Manifestations: tachycardia, cardiomegaly, new or changed murmur, pericardial friction rub, precordial pain, ECG changes prolonged PR interval, indications of HF, previous strep infection
Primary prevention is extremely important. Streptococcal pharyngitis presents with high fever, abrupt onset of sore throat, reddened throat with exudate, enlarged lymph nodes. Treat with pcn or erythromycin.
Always complete the full coarse of antibiotics. Once you get rheumatic carditits, you may need prophylaxis rest of life

Question 43

Cardiomyopathy types

Answer 43

Sub acute or chronic disease of the muscle. There are four different types.
1. Dilated cardiomyopathy/DCM is a structural abnormality. Ventricular wall thickness is normal, both ventricles are dilated, systolic function is impaired, decreased cardiac output, dyspnea on excursion, Decreased exercise capacity, fatigue, palpitations. Can be caused by alcohol abuse, chemotherapy, infection, inflammation, and poor nutrition. Most common

2. Hypertrophic cardiomyopathy/HCM are asymmetric ventricular hypertrophy and disarray of myocardial fibers. Obstruction in left ventricular outflow. usually an autosomal dominant trait. Some die without symptoms such as athletes.
3. Restrictive cardiomyopathy is the rarest, stiff ventricles that restrict filling during diastole, symptoms are similar to left or right heart failure. Caused by sarcoidosis or amyloidosis. Prognosis is poor.
4. Arrhythmogenic right ventricular cardiomyopathy/dysplasia. Myocardial tissue is replaced with fibrous and fatty tissue. It is familial and affects young adults.

Therapy is initially the same as for heart failure.

Question 44

Heart transplant

Answer 44

Preop criteria is the only thing discussed for preop: life expectancy under a year, less than 65, NYHA class III or IV heart disease, normal or only slightly increased pulmonary vascular resistance, absence of active infection, stable pyshcosocial status, no drug or alcohol abuse

Postop: Similar to post cardiac surgery. Identify occult bleeding into the pericardial sac with the potential for tamponade. HR is usually between 90-110 and responds slowly to exercise, stress, or position changes. Isoproterenol may be titrated to maintain CO. Atropine, digitalis, and carotid sinus pressure are NOT used. Orthostatic hypotension precautions. Possible permanent pacemaker. Immunosuppressant’s required for rest of life. Infection is a major cause of death, be sure to follow aseptic techniques. Regular scheduled exercise tolerance tests and angiography are performed because the heart is denervated and the pt will not feel angina.

Signs of rejection: SOB, fatigue, fluid gain, abdominal bloating, new bradycardia, hypotension, Afib or Aflutter, decreased activity tolerance, decreased ejection fraction is a late sign