Cardio Alterations

Describe the nursing management of a patient that has just been defibrillated.

Asynchronous countershock depolarizes a critical mass of myocardium simultaneously to stop the re-entry circuit and allow the sinus node to regain control of the heart. --Maintain a patent airway. --Administer oxygen. --Assess vital signs and level of consciousness. --Administer antidysrhythmic drugs. --Monitor for dysrhythmias . --Assess for burns, emotional support, documentation.

Describe the function and use of sodium bicarb.

Sodium Bicarb: (NaHCO3): Give 1meq/kg IV bolus, repeat with 0.5meq/kg as needed Assess ABG's Given to tx metabolic acidosis

Describe the emergency care for acute cardiac tamponade.

**Cardiac tamponade is an emergency.** Report suspicious symptoms to physician immediately: --Jugular venous distension --Paradoxical pulse (systolic BP 10 mm Hg or more higher on expiration than on inspiration). --Decreased HR, dyspnea, and fatigue --Muffled heart sounds --Hypotension --The physician may initially order increased fluid administration to manage decreased cardiac output while waiting for ECG, x-ray, or **hemodynamic monitoring** results. --Doctor may perform pericardiocentesis to remove fluid and relieve the pressure on the heart. The nurse must monitor the pulmonary artery, wedge and right atrial pressures during the procedure (pressures should return to normal as the fluid id removed). A drain may be put in place once the procedure is completed and specimens may be sent to the lab. --Monitor for the reoccurrence of tamponade ( pericardiectomy may be needed)

List the features of arrhythmogenic right ventricular cardiomyopathy (dysplasia).

--Results from replacement of myocardial tissue with fibrous fatty tissue. --Most patients have left ventricular involvement. --Familial association affecting young adults. --Some have symptoms, some do not.

Describe the conduction system the heart.

--SA node-main regulator of HR 60-100 bpm --From the SA, the impulse travels to the AV node --Intrinsic rate of 40-60 bpm --From the AV node, the impulse travels to the Bundle of His, L&R bundle branches, and the Purkinje Fibers --Perkinje Fibers: intrinsic rate of 20-40bpm

List the manifestations of atrial septal defect.

---May be asymptomatic depending on size of lesion --Fatigue --DOE --Palpitations --Atrial dysrhythmias --Recurrent respiratory infections related to increased pulmonary blood flow --Systolic murmur from increased blood flow across the pulmonary valve; diastolic murmur with large shunting --Mitral valve regurgitation is possible --HF may develop during young adulthood; if not repaired --Risk for stroke --May go unrecognized because of sign and symptom subtlety --May cause atrial arrhthmias, secondary to right atrial overload --May interfere with conduction system --May cause pulmonary hypertension if defect is severe --May act as a life-saving safety valve if associated with a severe heart defect such as transposition of the great vessels --May result in complications, such as pulmonary thrombosis or embolism, bronchopulmonary infections, and pulmonary artery rupture --May close spontaneously within year after birth --Soft, pulmonic midsystolic murmur heard at second or third left intercostal space --In infants, dyspnea on exertion, fatigue, orthopnea --In older children with a large defect, frail, delicate appearance, left precordial bulge

What is the normal of pulmonary artery pressure during hemodynamic monitoring?

--15-26 mm Hg systolic --5-15 mm Hg diastolic Pulmonary Artery Catheter --Provides the most information indirectly to monitor LV function --Multi-lumen catheter, inserted through the right side of the heart --GOAL: to obtain information about left heart function --Systolic pressure: peak pressure attained as the RV ejects out stroke volume Normal range for PAS = 20-30 mmHg --Diastolic pressure: lowest pressure on waveform. Reflects the movement of blood from pulmonary artery out into lung capillaries Normal range for PAD = 5-10 mm Hg --Mean pressure: An average pressure exerted on the pulmonary vasculature Normal range for the PAP (mean) = 10-15 mm Hg

What is the normal of PAWP during hemodynamic monitoring?

--4-12 mm Hg --Elevated may indicate ventricular failure, hypervolemia, mitral regurgitation, or intracardiac shunt --Decreased may indicate hypovolemia or afterload reduction Pulmonary Capillary Wedge Pressure --Reflects the pressure ahead of the catheter, which is both the left atrial pressure (LAP) and the left ventricular end diastolic pressure (LVEDP) --PCWP is a reliable indicator of LV function Normal range = 5-12 mm Hg

Describe postoperative teaching for the client who has had a heart transplant.

--50% of patients survive 10 yrs after surgery --Many patients develop a form of CAD called coronary artery vasculopathy (CAV) the cause if thouth to involve a combination of immunologic and nonimmunologic processes that result in vascular endothelial injury and an inflammatory response. --Because heart is denervated patients do not usually experience angina. --Regularly scheduled exercise tolerance tests and angiography are required to identify CAV. Only a small percentage of patients w CAV benefit from revascularization procedures like balloon angioplasty or coronary artery bypass surgery. Stents maybe a better option. Retransplantation may be done in select patients. --To prevent CAV encourage patients to follow lifestyle changes similar to those with primary CAD. --The physician may prescribe a calcium channel blocker such as diltiazem (Cardizem)to prevent coronary spasm and closure. --Stress the importance of adhering to medication and dietary changes (including exercise program). --Transplanted heart has no nerve connections with the recipient's body (denervated heart) --Sympathetic and Vagus nerves do NOT affect the transplanted heart --Resting rate of transplanted heart 70-90 BPM --Atropine will NOT increase HR in these clients --Catecholamine release will gradually increase HR Health Teaching --Smoking cessation --Diet control --Complementary and alternative therapies --Physical activity --Sexual activity --Blood pressure, blood glucose control --Cardiac medications --Self-monitoring; seeking medical assistance if needed

List the features of hypertrophic cardiomyopathy.

--Asymmetric ventricular hypertrophy and disarray of the myocardial fibers. --Left ventricular hypertrophy leads to stiff left ventricle, which results in diastolic filling abnormalities. --Obstruction in the left ventricle outflow tract is most common. --Can be inherited by single-gene autosomal dominant trait. --Some patient have no symptoms, whereas others have DOE, syncope, dizziness, and palpitations. --Many athletes that die suddenly probably had hypertrophic cardiomyopathy.

Describe central venous pressure.

--CVP is clinically used as a guide to overall fluid balance. --CVP is the least sensitive indicator of LV pressure --CVP is affected primarily by changes in the right atrium and the system veins --CVP is used to: indicate blood volume, obtain blood samples, administer fluid or medications --Normal CVP 5 - 15 cm in water pressure A low CVP may be obtained when: --Inadequate venous return (dehydration, hemorrhage) --Excessive vasodilation (BP drops) CVP Complications --Pneumthorax --Infection --Fluid Overload Poor Infusion of Fluid A high CVP may be obtained when: --Increased preload --Fluid overload (IV or renal disease) --Increased afterload (resistance) COPD, Pulm. Edema, tricuspid and pulmonary valve stenosis

How does the body regulate flow?

--Change diameter of blood vessel --Capacitance blood vessels --Hearts ability to control heart rate --Strength of heart's contraction --Renin-angiotensin system

What are the causes of aortic valve stenosis?

--Congenital bicuspid or unicuspid aortic valves --Rheumatic disease (any stress can cause flare up of antibodies) --Atherosclerosis and degenerative calcification (older adults)

Describe how the calcium pump assists in cardiac muscle contraction.

--Dependent on the release of Ca+ ions from the sarcoplasmic reticulum --These ions diffuse into the myofibril sacromere (basic contractile unit of cardiac cells) --Ca+ promotes the cross-bridge of myosin and actin filaments --The sliding and crossing over of these protein filaments, causes the myofibril sacromeres to shorten or contract = myocardial contraction --As Ca+ is pumped back into the sarcoplasmic reticulum, the protein filaments disengage, and lengthen = cardiac relaxation

Describe anti-dysrhythmics drugs.

--Digoxin: increase vagal tone, slows AV nodal conduction, Tx Chronic AF, Does not convert to NSR --Atropine: Vagolytic drug, Used to Tx symptomatic "brady" rhythms --Adenosine: Endogenous nucleoside that slows AV nodal conduction, Tx of paroxysmal SVT --Magnesium Sulfate: Electrolyte administered to tx refractory VT or VF due to low magnesium level

Describe the drug therapy indicated for valvular diseases.

--Diuretics, beta blockers, digoxin, and oxygen for symptoms of HF --Nitrates are used cautiously for the patient with aortic valve stenosis because of the potential for syncope associated with a reduction in left ventricular volume (preload) --Calcium channel blockers are used to reduce the regurgitant flow from mitral or aortic stenosis --Drug therapy first focuses on controlling HR below 100 bpm and maintain cardiac output. Once this has been achieved drugs are used to maintain NSR using IV Cardizem or Cordarone. (monitor for normal rhythm and BP) --Synchronized counter shock (cardioversion) may be attempted in atrial fibrillation is rapid and uncontrolled by medications. Transesophageal echocardiography is done before cardioversion to make sure thrombi are not present. --Coumadin to prevent thrombus **Rest is often an important part of treatment**

What tests are done to diagnose and differentiate cardiomyopathies?

--Echocardiography --Radionuclide imaging --Angiocardiography during cardiac catheterization

How are valvular disease diagnosed?

--Echocardiography (noninvasive; visualize the structure and movement of the heart) --Transesophageal echocardiography or transthoracic echocardiography (invasive) --Exercise tolerance testing with echocardiography (assesses symptomatic response and assesses functional capacity) --Cardiac catheterization (assess the severity of the stenosis and its other effects on the heart --Chest x-ray 1. Mitral stenosis: left atrial enlargement, prominent pulmonary arteries, and an enlarged right ventricle. 2. Mitral regurgitation: increased cardiac shadow, indicating left ventricular and left atrial enlargement 3. Aortic stenosis: left ventricular enlargement and pulmonary congestion 4. Aortic regurgitation: left atrial and left ventricular dilation. If HF is present, pulmonary venous congestion may be present --ECG (atrial figuration)

List the features of dilated cardiomyopathy.

--Extensive damage to the myofibrils and interferes w myocardial metabolism. --Ventricular wall thickness is normal, but both ventricles are dilated (left is usually worse) and systolic function is impaired. --Caused by alcohol abuse, chemotherapy, infection, inflammation, and poor nutrition. --Decreased CO from inadequate pumping of the heart causes DOE, decreased exercise capacity, fatigue, and palpitation.

What are some complications associated with pacing?

--Failure to pace --Failure to capture --Failure to sense

Describe how to feed the child with HF.

--Feed the infant or child in a relaxed environment; frequent, small feedings may be less tiring ---Hold infant in upright position; may provide less stomach compression and improve respiratory effort --If child unable to consume appropriate amount during 30-minute feeding every 3 hours, consider nasogastric feeding --Monitor for increased tachypnea, diaphoresis, or feeding intolerance (vomiting) --Concentrating formula to 27 kcal/oz may increase caloric intake without increasing infant's work

How is Kawasaki disease diagnosed?

--Fever of 5 days in conjunction with at least five of the acute stage symptoms and no other known disease process to explain the signs and symptoms. --WBC elevated, ESR, and C-reactive protein levels are elevated during the acute stage --There is sterile pyuria. --ECG in acute phase may demonstrate first-degree heart block --Platelet levels dramatically rise during subacute phase --Aneurysms detected with ECHO

What is the top priority for the treatment of cardiac structural defects?

--Get oxygen to the system with intervention to increase oxygenation

Describe the function of the coronary arteries.

--Heart receives O2 and nutrients via the coronary arteries --2 main coronary arteries (p678 figure 36-3) 1. Left coronary artery LAD LCX --Right coronary artery --Mean arterial pressure must be > or = to 60mmHg to perfuse heart and other vital organs

How is Kawasaki disease treated?

--High doses of intravenous immune globin (IVIG) in combination with aspirin to lower the prevalence of coronary artery abnormalities given with in 10 days of fever onset. --Corticosteroids may be considered if the child is unresponsive to standard therapy

List clinical manifestations of infective endocarditis.

--High fever and shaking chills (May not be evident in older adults, causing them to be misdiagnosed) --Night sweats --Cough --Weight loss --General malaise --Weakness --Fatigue --Headache --Musculoskeletal complaints --**New regurgitant murmurs** (all patients develop murmur) --Symptoms of HF (right and left) --S3 or S4 --Low hemoglobin and hematocrit --Petechiae **examine mucous membranes, the palate, the conjunctivae, and the skin above the clavicles** --Splinter hemorrhages (black longitudinal lines or small red streaks) --Splenic infarction with sudden abdominal pain and radiating to the left shoulder **Note rebound tenderness during abdominal palpation** --Renal infarction **Note flank pain that radiates to the groin and is accompanied by hematuria or pyuria. --Mesenteric emboli **Note diffuse abdominal pain, often after eating and abdominal distension. --TIAs and stroke --Neurologic changes like confusion, reduced concentration, and aphasia/dysphagia --Pulmonary problems like pleuric chest pain, dyspnea, and cough are symptoms of pulmonary infarction related to embolization. --Skin abnormalities associated w septic emboli: Janeway lesions (lesions that are often hemorrhagic and present on the palms and soles), Osler nodes (red-purple lesions on the fingers or toes), splinter hemorrhages, and Roth spots (retinal hemorrhage). Skin lesions are referred to as the peripheral stigmata of endocarditis. ppt. Fever and Heart Murmur - the most common signs Other signs: Petechiae of skin and mouth, conjunctival mucosa, splinter hemorrhages in nail bed, headache, TIA's if emboli blocking cerebral blood flow

What preexisting heart conditions increase the risk of developing endocarditis?

--Implantation of artificial (prosthetic) heart valve --Previous history of endocarditis --Damaged heart valves (rheumatic fever) --Congenital heart defects --Valve defects

What are some causes of aortic regurgitation?

--Infective endocarditis --Congenital defects --Hypertension --Marfan syndrome

What information is important to collect during the assessment of a patient with a suspected valvular disease?

--Information about family history (genetic) --Attacks of rheumatic fever and infective endocarditis --History of IV drug abuse (may cause infective endocarditis) --Description of symptoms --Obtain vitals and auscultate lung and heart sounds

List the steps associated with advance cardiac life support.

--Initiate CPR (keep interruptions to CPR at a minimum) --When AED arrives, attach electrodes to chest and turn on the monitor --**If the patient is in VF or pulseless VT, the immediate priority is to defibrillate** CPR must continue at all times except during defibrillation. --An airway is placed to facilitate proper ventilation. A manual resuscitation bag is connected to an oxygen flow meter set to 10-15 L/min. Ensure proper technique of bagging (chin-lift) --Start two large bore IVs --Check carotid and femoral pulses (with or without chest compressions) every few mins along with BP and pupils --Additional measures include ET tube with oxygenation, emergency cardiac drugs, and occasionally external pacing --Chest compressions are continued as long as the patient remains pulseless or until the Dr. decides to terminate resuscitation attempts

List the clinical manifestations of coarctation of the aorta.

--Left-sided HF with low cardiac output, poor lower extremity peripheral perfusion, metabolic acidosis, shock --If PDA is present--right-to-left shunting with differential cyanosis (color and oxygenation differential between upper and lower extremities) --Asymptomatic children may show pulse and blood pressure differences between upper (systolic hypertension) and lower extremities; weakness, tingling, cramps, in lower extremities --Systolic murmur accompanied by ejection click (with bicuspid aortic valve) or thrill Acyanotic --Symptoms usually occur in either early infancy or adulthood (20 to 30 years of age) --Collateral circulation may develop around defect, minimizing pressure changes --If condition's severe, may lead to complications, such as congestive heart failure, endocarditis, cerebral hemorrhage, aneuryms, and premature arteriosclerosis secondary to hypertension --Elevated blood pressure and bounding pulses proximal to defect, hypotension, and weak or absent pulses distal to defect --Dizziness --Fainting --Headache --Epistaxis --Cold feet --Systolic ejection click heard at base and apex of heart. --Associated with systolic or continuous murmur between scapulae --Pulmonary hypertension --Aneurysm proximal to defect --Frequently associated with bicuspid aortic valve

What are the criteria for candidate selection for heart transplantation?

--Life expectancy less than 1 yr --Age generally less that 65 --NYHA class III or IV --Normal or only slightly increased pulmonary vascular resistance --Absence of active infection --Stable psychosocial status --No evidence of current drug or alcohol abuse

List the manifestations of pulmonary stenosis.

--Many asymptomatic; signs in symptomatic children include exercise intolerance, signs of right-sided HF --Systolic ejection murmur, possible palpable thrill --Cardiomegaly on radiograph --Cyanosis in severe cases --Usually acyanotic and asymptomatic unless defect's severe --Associated with a history of maternal rubella --Causes increased right ventricular pressure to overcome obstruction. This in turn elevates right atrial pressure leading to increased systemic venous blood pressure --May result in right ventricular failure --Low or normal pulmonary artery pressure --Dyspnea --Fatigue --Extremily coldness, peripheral cyanosis --Subjective complaints (such as tiring easily) that increase with age --Precordial pain possible --In valvular pulmonary stenosis systolic ejection murmur associated with a thrill (best heard at upper left sternal border). If defect's severe, murmur may radiate over precordium and back --If right ventricular end diastolic pressure increases, right ventricle hypertrophy occurs --To relieve respiratory distress, child may assume squatting position

What are some causes of mitral valve prolapse?

--Marfan syndrome --Congenital defects --Familial tendency

Describe nursing interventions for the child with Kawasaki disease.

--Monitor for HF, changes in VS, color, along with SOB, chest pain, and decreased activity (may indicate cardiac complications) --It is important to examine the child's eyes, mouth and skin for S/S of infection and the joints for redness, swelling, and tenderness --Assess parental anxiety and coping --Administer aspirin with milk or food and infuse IVIG as ordered. Monitor for adverse reaction to IVIG (facial flushing, tightness in the chest, chills, dizziness, N&V, diaphoresis, and hypotension). Check BP every 15 min for the first hr of the infusion. A precipitous fall in BP may occur 30-60 min after the infusion (often related to the rate of the infusion). Expect to lower infusion rate and administer Benadryl and acetaminophen as ordered to reduce side effects. Live-virus immunizations should be delayed for 11 mo after IVIG therapy. --Nursing care focuses on comfort measures and adequate hydration. Encourage fluid intake by offering ice pops of ice to numb affected mucosal membranes, giving liquids that are high in calories and low in acid through a straw. --Offer favorite foods that are soft and bland. --Apply salve to cracked lips. --Tepid sponge baths can reduce fever --Handle child only when necessary (if itching is severe notify provider) --Keep environment calm

Describe post-op interventions and teaching involved with typical cardiac surgery.

--Neurological Assessment --Assess skin color and temperature, capillary refill --Epicardial Pacing --Mediastinal and pleural chest tubes --Radial Arterial line --Indwelling catheter (Foley) --SaO2 monitor & ECG monitor --Swan Ganz catheter --NG tube, ET tube

List the cause of endocarditis.

--Nonbacterial growths because of rheumatic fever, systemic lupus erythematosus, and other collagen diseases --Bacterial (streptococcal and staphylococcal) or fungal (Candida, Aspergillus, Histoplasma) infections --Infections related to I.V. drug abuse --Congenital heart disease --Prosthetic valve surgery --Infective endocarditis usually seen in clients with valvular heart disease. --At great risk clients with rheumatic heart disease or MVP and those post prosthetic valve surgery

List the clinical manifestations of patent ductus arteriosus.

--Signs of heart failure, which are related to the size of the lesion and the amount of left-to-right sunting --Continuous murmur--machinery-like sound --Widened pulse pressure (increased difference between systolic and diastolic readings --Bounding pulses --Cardiac enlargement --Associated with history of: prematurity first trimester maternal rubella Coxsackie virus infection Birth at high altitude --Acyanotic usually asymptomatic --May be accompanied by coarction of aorta --May cause pulmonary congestion especially in premature infants --May lead to complications such as congestive heart failure, ductus arteriosus aneurysm (causing blood to dissect between duct walls), spontaneous aneurysm rupture, and recurrent respiratory infections --Continuous murmur with characteristic machine-like quality, loudest at second and third left intercostal spaces. --Murmur may obscure S2 heart sound and be only sign of disorder. --Dyspnea on exertion --Precordial asymmetry in infants overactive precordium --Widened pulse pressure --Full or bounding pulses --Pulmonary artery hypertension with right-to-left shunt and right atrial and ventricular hypertrophy

List the manifestations of tetralogy of fallot.

--Onset of severity of signs and symptoms are related to the extent of the obstructed pulmonary blood flow, which causes the right-to-left shunting; if lesions are mild, shunting is decreased and saturations are mildly low (pink tet) --**Tet Spells: sudden, marked increase in cyanosis followed by syncope and may result in hypoxic brain injury and death. Older children will often squat during a tet spell, which increases systemic vascular resistance and allows for temporary reversal of the shunt. Tet spells are treated with beta blockers, but acute episodes may be treated with morphine to reduce ventilator drive and a vasopressor (epinephrine) to increase blood pressure. Oxygen is also administered.** --Signs become worse in the neonate as the ductus arteriosus closes --Cyanosis, extreme fatigue, hypercyanotic episodes, chronic hypoxia --Harsh systolic murmur with a palpable thrill; boot-shaped heart radiography (related to poor development of the pulmonary artery) --Place patient in knee-chest position (legs are bent) --Child will not say, "I am short of breath" (they may say "I can't breathe"). They may squat down suddenly to caught their breath. --Cyanosis --Loud systolic ejection murmur heard along left sternal border. May diminish or obscure pulmonic S2 component --Finger and toe clubbing --Dyspnea --On palpation, possible cardiac thrill at left sternal border --In newborn intense cyanosis after patent ductus arteriosus closes; severe dyspnea on exertion; syncope; limpness; and occasional convulsions. If defect is untreated, it may be fatal --To compensate for respiratory distress, child may assume characteristic squatting position --Respiratory distress and fatigue during feeding --Growth retardation --Unoxygenated blood is shunted through VSD --Oxygenated and unoxygenated blood is mixed in left ventricle and pumped out aorta, causing cyanosis --Pulmonary stenosis restricts blood flow to lungs and increases right ventricular pressure --Defects may cause complications such as iron deficiency anemia, polycythemia, coagulation disorders, paradoxical embolism, cerebral infarction, and abscesses

Describe the treatment of pericarditis.

--Pain relief through analgesics (NSAIDS) and anti-inflammatory agents like colchicine and ibuproprofen. patients who do not obtain pain relief and who do not have bacterial pericarditis, may receive corticosteroid therapy. If pain is not relieved within 24-48 hrs, notify the primary car physician. --Antibiotics (if the causative agent is antibacterial) --Treatment of other systemic symptoms --Treatment of cardiac tamponade complication (pericardiocentesis) --Surgery may be required to remove part of the pericardium (pericardial window) --Chronic pericarditis caused by malignant disease may be treated with radiation or chemotherapy --Uremic pericarditis is treated with dialysis --Definitive treatment for chronic restrictive pericarditis is surgical excision of the pericardium --Monitor all patients for pericardial effusion which puts the patient at risk for cardiac tamponade. ppt. Hospitalization for diagnostic evaluation, observation for complications, and symptom relief Nonsteroidal anti-inflammatory drugs Corticosteroid therapy Comfortable position, usually sitting Pericardial drainage Chronic pericarditis: radiation or chemotherapy Uremic pericarditis: dialysis Pericardiectomy

What are S/S of aortic regurgitation?

--Palpitations may be noted with severe disease, especially when the patient lies on the left side --Nocturnal angina and diaphoresis --Bounding arterial pulse. --The pulse pressure is usually widened, with an elevated systolic pressure and diminished diastolic pressure --Signs & symptoms - none in most patients, eventually exertional dyspnea, fatigue, LV failure --High pitched blowing diastolic murmur (3rd - 4th intercostal space LSB) --Widen pulse pressure --Water Hammer pulse - pulse strikes the palpating finger with a quick, sharp stroke and suddenly collapses

Describe symptoms associated with pericarditis.

--Precordial pain (pain that radiates to the shoulder, neck, back, and arm and is intensified during deep inspiration, movement, coughing or even swallowing). Pain is worse in supine position and relieved when sitting up and leaning forward. It is important to ask questions to differentiate pain from that of acute MI. --Pericardial friction rub --Dyspnea --DOE --Weakness and fatigue --Persistent temperature elevation --Increased WBC and sedimentation rate --Increased anxiety level --Pulsus paradoxous (abnormally large decrease in systolic BP and pulse wave amplitude during inspiration) --Atrial fibrillation --Positional and pleuritic pain (worse with inspiration and cough) ppt. --Pain - characteristic symptom. Most commonly reported to exist over the precordium. Aggravated by breathing, turning in bed, twisting the body. --Pain is usually relieved by sitting up --Friction rub - classic sign --Dyspnea may occur --Fever, leukocytosis and friction rub are often the only signs/symptoms

What are some medications for preload problems?

--Preload: the amount of cardiac muscle fiber stretch before the next contraction. Pre-systolic fiber length (muscle stretch) is directly affected by the ventricular end diastolic volume. Examples: ventricular compliance & venous return. Morphine - dilates peripheral vessels which results in pooling/redistributing blood. Pooling reduces the volume returned to the heart and prevents blood from "backing up" into the lungs Furosemide - effective diuretic that diminishes total body blood volume by boosting UOP (as long as the heart works well enough to perfuse the functioning kidneys) Nitroglycerin - produces venous dilation, redistributing blood volume to the peripheral areas and pooling blood away from the heart. Also, lessens workload of the heart and reduces oxygen requirements. Dopamine - affects preload by causing vascular constriction or dilation through the sympathetic nervous systems. Dose specific. Low dose - 1 mcg/kg/min - 4 mcg/kg/min = renal vessel dilation. High dose - 5 mcg/kg/min = 10 mcg/kg/min = directly affects preload by causing venous constriction & increasing myocardial contractility.

List the S/S of mitral valve regurgitation.

--Progresses slowly --Symptoms begin to occur when the left ventricle fails in response to chronic blood volume overload resulting in decreased cardiac output --Anxiety --Atypical chest pains --Changes in respirations characteristic of left ventricular failure When right-sided HF develops symptoms may include: --Distended neck vein --Hepatomegaly --Pitting edema --High pitch systolic murmur at the apex, with radiation to the left axilla is heard on auscultation --Severe regurgitation exhibits third heart sound (S3) --Signs & Symptoms: dyspnea, fatigue, weakness, high pitched blowing systolic murmur best heard at apex --Results in LV failure --Angina is a frequent occurrence --Loud, rough systolic murmur, low pitched --Crescendo-decrescendo murmur --Thrill present --ECG & echocardiogram reveal LV hypertrophy

Describe the cardiac cycle.

--RA receives blood from the IVC and SVC --Blood passes from RA through the tricuspid valve to the RV --From the RV through the Pulmonic valve to the lungs via the --pulmonary artery --Oxygenation takes place in the lungs, then the blood returns via the pulmonary veins into the LA --From the LA through the Mitral valve into the LV --From the LV, through the aortic valve, into the aorta. --From the aorta to systemic circulation

List the features of restrictive cardiomyopathy.

--Rarest. --Stiff ventricles the restrict filling during systole. --Symptoms are similar to left or right HF or both. --Can be primarily caused by endocardial disease such as sarcoidosis or amyloidosis. --Poor prognosis.

Describe discharge instruction for the patient who has had valvular repair surgery.

--Stress the importance of rest --Explain the disease process and possibility of HF --Drug therapy --Prophylactic use of antibiotics --**Remind all doctors of valvular disease history and antibiotic therapy may be needed before all invasive procedures** --Prosthetic valve replacements require lifelong anticoagulant therapy. Avoid foods high in vitamin K (dark leafy greens), use electric razor; report excessive bruising or bleeding to doctor immediately --Report and redness, fever. or drainage associated with surgical site --Return to usual activity after 6 wks; avoid heavy lifting for 3-6 mo --Those with prosthetic valves may be required to avoid MRI --Need to have medic alert bracelet indicating past valvular surgery and anticoagulant therapy --Those who do not follow drug therapy are at increased risk of HF --Report any change in cardiovascular status (dyspnea, syncope, dizziness, edema, and palpitations) --May experience altered self image due to surgical scar and changes in lifestyle

What type of patients may need temporary pacing?

--Symptomatic, atropine-refractory bradydysrhythmias (particularly 2nd and 3rd degree heart block) --Left bundle branch block --Insertion of a pulmonary artery catheter (Have emergency equipment available in case patient goes into cardiac arrest)

List the S/S of rheumatic carditis.

--Tachycardia --Development of a new murmur or change in an existing murmur --Pericardial friction rub --Precordial pain --ECG changes (prolonged PR interval --Indications of HF --Evidence of a streptococcal infection ppt. --Tachycardia --Cardiomegaly --New or changed murmur --Pericardial friction rub --Precordial pain --Changes in electrocardiogram --Indications of heart failure --Existing streptococcal infection --Hypersensitivity to group A beta hemolytic streptococcal infection Often following throat/ear infections --Pharyngitis, Impetigo --Tonsillitis, Scarlet Fever, "strep throat" --Antibodies produce lesions in joints and heart valves --Most often affects children 6-15

Describe the postoperative care for the patient who has received a heart transplant.

--The nurse must be especially observant to identify occult bleeding into the pericardial sac with the potential for tamponade. The pericardium has been stretched considerably to accommodate the diseased, hypertrophied heart, predisposing it to have concealed postoperative bleeding. --The heart is denervated and is unresponsive to vagal stimulation. --Isoproterenol (Isuprel) may be titrated to support the HR and maintain cardiac output. --Atropine, digoxin, and carotid sinus pressure are not used bc they do not have their usual effects on the new heart. --Denervation may cause pronounced orthostatic hypotension so caution the patient to change positions slowly --Some patients may require a permanent pacemaker that is rate responsive to their activity level. the purpose id to increase CO and improve activity tolerance. --Combination immunosuppressants are used for life. Handwashing, aseptic technique, minimizing contact with infectious agents/people are important for the immunosuppressed client. --Ventilation provided for 3 to 6 hours postoperatively Monitor for: --Supraventricular dysrhythmias commonly occur --Sternal wound infections --Mediastinitis --Postpericardiotomy syndrome

Describe CABG surgery.

--The occluded coronary arteries are bypassed with the patient's own venous or arterial blood vessels or synthetic grafts. The internal mammary artery is the current graft of choice because it has a 90% potency rate at 12 yrs after the procedure. --CABG is indicated for patients who do not respond to medical treatment of CAD or when disease progression is evident. --On partial (L side) bypass, blood is not interrupted through the pulmonary circuit. --Monitoring for acute closure of the vessel, bleeding from the insertion site, reaction to dye, hypotension, hypokalemia, and dysrhythmias --Long-term nitrate, calcium channel blocker, and aspirin therapy --Beta blocker and ACE inhibitor if MI --Infusions of GPIIa/IIIb inhibitors Candidates for surgery: --Angina with greater than 50% occlusion of the left main coronary that cannot be stented --unstable angina with severe two-vessel disease, moderate three-vessel disease, or small-vessel disease in which stents could not be introduced --Ischemic HF --Acute MI with cardiogenic shock --Signs of ischemia or impending MI after angiography or PTCA --Vascular disease --Coronary vessels unsuitable for PTCA --Most patients are pain-free at 1 yr after surgery (pain may come back after 5 yrs) --May be done traditionally of MIS --Teach patient about drugs changes before surgery and administer necessary drugs before surgery. Teach patient how to splint the chest incision, cough, deep breathe, and perform arm and leg exercises. STRESS THAT: --The patient should report any pain to the nursing staff --Most of the pain will be in the site where the vessel was harvested --Analgesics will be given for pain --Coughing and deep breathing are essential to prevent pulmonary complications --Early ambulation is important to decrease the risk for venous thrombosis and embolism Tell the patient they may have a sternal incision, possibly a large leg incision, 1-3 chest tubes; indwelling catheter; pacemaker wires; and hemodynamic monitoring. They will be ventilated for several hrs after the procedure. The cabg and harvesting are often done simultaneously **CABG: NOT an open heart procedure**

List possible ports of entry for infecting organisms that can cause infective endocarditis.

--The oral cavity (especially if dental procedures have been performed . --Skin rashes, lesions, or abcesses --Infection ---Surgery or invasive procedures, including IV line placement

What causes mitral regurgitation?

--The primary cause is "degenerative" due to aging and infective endocarditis. --Papillary muscle dysfunction --Rupture resulting from ischemic heart disease or congenital abnormalities --Rheumatic heart disease is the number one reason in developing nations and is more common with women.

What is done if ACLS is successful?

--Therapeutic hypothermia helps protect brain function and is indicated for patients who had VF, VT pulseless activity, or asystole --Target temperature (89.6-93.2 F) is maintained for 24 hrs before rewarming ---Rewarming rate is 0.5-1 degree Celsius an hr

Describe the S/S of aortic stenosis.

--Thrill --Diastolic murmur (deadly) Late stage symptoms include: --Marked fatigue --Debilitation --Peripheral cyanosis --Narrow pulse pressure Left ventricle gets larger (check PMI further to the left). blood backs up into the left atrium and then the lungs (LSHF). 1st symptom is tachycardia. 2nd respirations/syncope. Electrical pathway is stretched causing dysrhythmias like VTach.

Describe the S/S of mitral valve stenosis.

--Usually asymptomatic --On palpation the pulse may be regular, rapid, or irregularly irregular --**Doctor must be notified of irregularly rhythm** (indicates the patient may decompensate) --**Rheumatic endocarditis - most common cause** --Valve opening - 3 fingers wide, stenotic width - pencil opening --Progressive fatigue (low C.O.), hemoptysis, dyspnea on exertion, repeated respiratory infections --Weak pulse, irregular (a-fib), low pitched diastolic murmur at apex --Atrial dysrhythmias (atrial stretching) --Client may become suddenly ill or slowly develop symptoms over many years. --**Question client about attacks of rheumatic fever, infective endocarditis, and possibility of IV drug abuse.** --Obtain chest x-ray, echocardiogram, and exercise tolerance test. Nursing Diagnoses --Decreased Cardiac Output related to altered stroke volume --Impaired Gas Exchange related to ventilation perfusion imbalance --Activity Intolerance related to inability of the heart to meet metabolic demands during activity --Acute Pain related to physiologic injury agent (hypoxia)

What are some pediatric considerations for the administration of digoxin?

--Usually given in the morning and evening (can be adjusted to fit the child's schedule) --Give 20-30 mins before eating. Give at the same time everyday so that it becomes a routine --Measure with a syringe --Give a few drops at a time and let the child swallow before giving more --If a dose is missed, administer and then resume schedule --If child vomits after dose, do not readminister. Resume with next dose. --If child vomits after two doses in a row call cardiology dept --Keep out of reach of children --If someone accidentally takes the digoxin, call poison control or take the person and the bottle to the ER --Obtain refills at least 1 week in advance

List possible causes of myocarditis.

--Viral infection, especially Coxsackie A and B strains, --Bacterial (seen in photo) --Parasitic, protozoal or spirochetal infection --Rheumatic fever --Toxins

What is the normal range of right atrial pressure during hemodynamic monitoring?

1-8 mm Hg **Increased pressure may occur with right ventricular failure** **Low pressure usually indicate hypokalemia**

Cardiomyopathy that involves A type of extensive damage to the myofibrils and interference with myocardial metabolism. There is normal ventricular wall thickness but dilation of both ventricles function.

Dilated cardiomyopathy.

Describe methods of diagnosing pericarditis.

1. Auscultation --Best heard in inspiration with the diaphragm of the stethoscope placed over the 2nd, 3rd, or 4th intercostal spaces at the sternal border. Can be heard better if the patient is leaning forward. Friction rubs are described as grating, scraping, squeaking, or scratching sounds. This rubbing sound results from an increase in fibrous exudate between the two irritated pericardial fibers. 2. ECG --Abnormal in 90% of patients with acute pericarditis. There are diffuse concave ST-segment elevation and PR-segment deviations opposite to P-wave polarity. T-waves progressively flatten and invert with generalized T-wave inversions present in all or most leads. The ECG is useful in visualizing effusion. ppt. Diagnosis confirmed by client history and physical exam, EKG, and Echocardiogram

Describe nonsurgical heart valve reparative procedures.

1. Balloon valvuloplasty, an invasive non surgical procedure: --Aortic: are older and have high risk for surgical intervention (effects rarely last more than 6 mo). The physician inserts the catheter through the femoral artery and advances it to the aortic valve, where it is inflated to enlarge the orifice; usually provides instant relief --Mitral: the physician passes a balloon catheter from the femoral vein, through the atrial septum, and to the mitral valve. The balloon is inflated to enlarge the mitral orifice **Complications - bleeding, emboli**

Describe the 4 classes of cardiac drugs.

1. Class I anti-dysrhythmics are membrane stabilizing agents, stabilizing phase 4, to decrease automaticity, has 3 sub-classes --Type IA drugs: slow conduction and prolong repolarization or QT interval Tx or prevent supraventricular and ventricular premature beats, and tachydysrhythmias Examples: Quinidine Sulfate and Procainamide hydrochloride (Pronestyl) --Type IB drugs: Shorten repolarization Tx or prevent PVCs, VT, VF Examples: Lidocaine and mexiletine hydrochloride (Mexitil) --Type IC drugs: Markedly slow conduction and widen QRS Tx or prevent recurrent life-threatening PVCs, VT, VF Examples: Flecainide acetate (Tambocor) and Propafenone hydrochloride (Rhythmol) 2. Class II anti-dysrhythmics control dysrhythmias associated with excessive beta-adrenergic stimulation with decreased HR and decreased conduction velocity Tx or prevent supraventricular and ventricular premature beats and tachydysrhythmias Examples: Beta-blockers like Propanolol (Lopressor), esmolol hydrochloride (Brevibloc) --Other class II drugs with anti-dysthrhythmic and noncardioselective beta-adrenergic blocking effects: Sotalol hydrochloride, for VT tx 3. Class III drugs: lengthen absolute refractory period and prolong repolarization and action potential duration of ischemic cells Used to prevent or tx PVCs, VT, VF Examples: amiodarone (Cordarone) and ibutilide (Covert) 4. Class IV drugs: impede the flow of Ca+ into the cell during depolarization, depressing SA and AV nodal automaticity, decreasing HR Used to tx and prevent SVT, A-Flutter, AF to decrease ventricular response Examples: Calcium Channel Blockers like verapamil hydrochloride (Calan, Isoptin) and diltiazem hcl (Cardizem)

Describe how infective endocarditis is diagnosed and treated treatment of infective endocarditis.

1. Diagnosis --Diagnose infecting agent. Both aerobic and anaerobic specimens are obtained for culture. Some slow growing organisms may take 3 wks to require a specialized medium to isolate. --Echocardiography --Transesophageal echocardiography allows visualization of cardiac structures difficult to see with transthoracic echocardiography. 2. Treatment --Antimicrobials (high dose) IV over 4-6 wks. Penicillins and cephalosporins. Patients may be able to complete IV therapy at home when they become afebrile, have negative blood cultures, and have no signs of HF or embolizations. Teach patients/family how to perform IV administration at home using aseptic technique (should be able to demonstrate before discharge). Supplies include prepared antibiotic, IV pump with tubing, alcohol wipes, IV access device, NS, flushes, saline lock/PICC line/central line. Teach to administer antibiotics as ordered. --Encourage proper oral hygiene (soft bristled toothbrush at least twice a day, rinse moth with water after brushing, no irrigation devices or floss.) --Teach to clean any open skin areas well and apply antibiotic treatment --Anticoagulants are contraindicated except to prevent thrombus formation on a prosthetic valve. --Activities are balanced with adequate rest --Aseptic technique --Monitor S/S of HF --Preventions is important and antibiotic prophylaxis is recommended for high risk patients prior to procedures. --Antibiotics are no longer indicated post stent of prophylaxis protection of endocarditis.

Describe the medical (nonsurgical) management options for the patient cardiomyopathy.

1. Dialted and Restrictive Cardiomyopathy: --Diuretics, Vasodilating agents, cardiac glycosides to increase cardiac output --Antidysrhythmic drugs --Implantable cardiac defibrillators --Beta blockers to block inappropriate sympathetic stimulation and tachycardia --Alcohol avoidance if alcohol related **Because patients are at risk for sudden death, teach them to report any palpitations, dizziness, or fainting, which may indicate a dysrhythmia** 2. Obstructive Hypertrophic Myopathy --Negative Inotropics agents such as beta-adrenergic blocking agents (carvedilol) and calcium channel antagonists (diltiazem). These drugs decrease the outflow obstruction that accompanies exercise. They also decrease HR, resulting in less angina, dyspnea, and syncope. **Vasodilators, diuretics, nitrates, and cardiac glycosides are contraindicated bc these drugs may worsen the obstruction. Strenuous exercise in prohibited bc it can lead to sudden death**

Describe the cardiac cycle.

1. Diastole --2/3 of the cardiac cycle --Relaxation and refilling of the atria and ventricles 2. Systole --Contraction --Emptying of the atria and ventricles

List the three types of endocarditis.

1. Native valve endocarditis (NVE); acute and chronic 2. Prosthetic valve endocarditis (PVE); early and late 3. Intravenous drug abuse (IVDA) endocarditis --Staphylococcus aureus most causative agent --Streptococcus and enterococcus organisms seen in subacute NVE

Describe noninvasive temporary pacing.

1. Noninvasive Temporary Pacing --Application of two large external electrodes. --Used as an emergency measure to provide demand ventricular pacing in a profoundly bradycardic or asystolic patient until invasive pacing can be used or the patient's heart returns to normal. --May be used prophylactically for bradydysrhythmias Depending on facility, nurses on telemetry unit may perform procedure: --Explain procedure to patient. --Wash skin with soap and water --Apply electrodes on the chest according to package instructions (one placed on upper chest to the right of the sternum, and one placed over the heart apex--may have to displace female breast) --Turn the pacer on to the ordered rate and establish the stimulus threshold --Palpate right radial or carotid pulse and assess BP using right arm to check perfusion --Vital signs are not taken bc they may not be accurate --Observe for discomfort from muscle stimulation, skin irritation, and diaphoresis from the patch electrodes. --Be sure the electrodes have good contact w the skin and is in the correct position --Give analgesics or sedatives as ordered for comfort

Describe the treatment of rhematic carditis

1. Prevention with antibiotic therapy when the following symptoms are present: --Moderate to high fever --Abrupt onset of sore throat --Reddened throat with exudate --Enlarged and tender lymph nodes 2. Antibiotic therapy with penicillin or erythromycin for at least 10 days **reoccurrence can occur w streptococcal infection**

Describe surgical management of valvular heart disease.

1. Reparative procedures --Direct (open) commissurotomy: accomplished during bypass surgery, thee surgeon visualizes the valve, removes thrombi from the atria, incises the fussed commissures (leaflets), and debrides calcium from the leaflets, widening the orifice --Mitral valve annuloplasty (reconstruction) the surgeon sutures the leaflets to an annuloplasty ring or takes tucks in the patient's annulus to make it smaller. Leaflet repair is often done at the same time. Elongated leaflets may be shortened, and shortened leaflets may be repaired by lengthening the chordae that bin them in place. Perforated leaflets may be patched with synthetic grafts 2. Heart valve replacement --Prosthetic (synthetic): aortic valves can only be replaced with synthetic due to high pressure --Biologic: can be xenograft (made from pig or cow), autograft, or from cadaver; not as durable as synthetic graft and may need to be replaced every 7-10 yrs (calcium breaks down graft) Valve replacement is performed by open heart surgery Patients taking anticoagulants should stop treatment 72 hrs before surgery Preoperative dental examination; periodontal disease and dental caries must be resolved before surgery --Check pulses before and after repair. --**Complications**- related to sudden changes in intracardiac blood pressures. Surgery abruptly "corrects" the way blood flows through heart. Patients with valve replacements are more likely to have significant reductions in cardiac output after surgery, especially those with aortic stenosis or left ventricular failure from mitral valve disease. Carefully monitor cardiac output and assess for HF. **Reports S/S of postoperative HF to the physician immediately**

What are some interventions that affect afterload?

Afterload: The pressure or resistance to blood flow out of the ventricle. Principle resistance to blood flow out of ventricles is arterial blood pressure. Examples: blood volume, blood viscosity, peripheral vascular resistance, aortic impedance --Nitroprusside - dilates both arterial and venous vessels, diminishing both systemic vascular resistance and venous return --ACE inhibitors - block the conversion of Angiotensin I to --Angiotensin II. Thereby reducing SVR or afterload . Also, results in less plasma aldosterone with accompnaying reduction in sodium and water reabsorption in the kidneys = decreased preload --Intra Aortic Balloon Pump

Describe the function and use of Amiodarone hydrochloride (Cordarone).

Amiodarone hydrochloride (Cordarone): Given for PVCs, VT, and VF 300mg IVP for cardiac arrest 150mg IVP over 10 min, followed by 360mg IVP over next 6 hrs, followed by 540mg over next 18 hrs; after 1sr 24hrs, continue maintenance infusion of 720mg/24hrs or 0.5mg/min Monitor rhythm Be cautious with administration of other anti-dysthrhythmics Be cautious with pulmonry, hepatic, and/or thyroid dz Continuous cardiac monitoring for initial bolus dosing—high risk

Describe the pathophysiology of Kawasaki disease

An infections or possibly toxic trigger initiates an immune system response that affects medium-sized arteries, especially the coronary arteries. A generalized immune response becomes more specific, with increasing numbers of T lymphocytes and B lymphocytes infiltrating the smooth muscle cells of the vascular walls. The infiltration causes edema and inflammation, which progressively weaken vascular walls, leading to aneurysms. As the disease progresses, fibrous connective tissue forms at the inflammatory sites, eventually thickening and scarring the vascular walls. These vascular changes, along with increased platelets that occur as a part of the disease process, can cause thrombus formation, myocardial infarction, and death in some children.

Describe S/S of myocarditis.

Assessment - possible cardiac enlargement, faint heart sounds, gallop rhythm, systolic murmur. Pulsus alternans (regular alternation of weak & strong beats), fever & tachycardia are frequently seen, Heart failure may develop Diagnosis confirmed by endomyocardial biopsy

The aortic valve leaflets do not close properly during diastole and the annulus (the valve ring that attaches to the leaflets) may be dilated, loose, or deformed. This allows flow of blood from the aorta back into the left ventricle during diastole. The left ventricle, in compensation, dilates to accommodate the greater blood volume and eventually hypertrophies.

Aortic regurgitation (insufficiency)

Narrowing of the aortic valve orifice and obstruction of left ventricular outflow during systole. This increased rejection to ejection or afterload results in ventricular hypertrophy. Cardiac output becomes fixed and cannot increase to meet the demands of the body during exertion. Eventually, the left ventricle fails, blood backs up in the left atrium, and the pulmonary system becomes congested. Right-sided HF can occur late in the disease process.

Aortic stenosis

Describe the pathophysiology of rheumatic carditis.

Aschott bodies form on the myocardium and are replaced by scar tissue. A diffuse cellular infiltrate also develops and may be responsible for the resulting HF. The pericardium becomes thickened and covered with exudate, and a serosanguineous pleural effusion may develop. The most serious damage occurs to the endocardium, with damage to the valve leaflets. Hemorrhagic and fibrous lesions form along the inflamed surface of the valves, resulting in stenosis or regurgitation of the mitral and aortic valves.

Describe the cause of Kawasaki disease.

Cause: Unknown but may be immune-mediated vasculitis triggered by an acute infection or by bacterial toxin; may have a genetic component; may have a seasonal component (usually diagnosed in late winter and early spring); most often seen in children younger than 5 and less frequently in children older than 8 Result: Vasculitis, Aneurysms, Platelet aggregation, Thrombi

Describe the pathophysiology of aortic stenosis.

Blood has difficulty flowing through the aortic valve, causing increased pressure and hypertrophy in the left ventricle, decreased cardiac output, decreased blood supply to the coronary arteries. --3-6% of cardiac defects --Narrowing of the entrance to the aorta; may be supravalvular, subvalvular, or at the valve level (most common); thickened, rigid, with some fusion of the leaflets; the valve may be bicuspid

Describe the function and use of Calcium Chloride.

Calcium Chloride Given for cardiac arrest associated with hyperkalemia, hypocalcemia, or calcium channel blocker toxicity Monitor for cerebrovascular spasm

A subacute or chronic disease of cardiac muscle; classified into four categories based on abnormalities in structure and function: dilated, hypertrophic, restrictive, and anthropogenic.

Cardiomyopathy. --May have wide QRS and large U wave --Decreased contractibility

Synchronized countershock that may be used for emergent hemodynamically unstable ventricular or supraventricular tachydysrhythmias or electively for stable tachydysrhythmias resistant to medical therapies.

Cardioversion.

Describe the therapeutic management for atrial septic defect.

Conservative because spontaneous closure can occur --Diuretics and digoxin for signs of HF --Antidysrhythmics for atrial dysrhythmias --Interventional cardiac catheterization Occluder devices placed if criteria related to size of lesion, significance of shunting, and availability of septal tissue to anchor the device are met; usually done between 2-5 yrs of age. **Daily low-dose aspirin for 6 mo following procedure** --Surgical placement of sutures or prosthetic patch through open heart procedure using cardiopulmonary bypass. Surgical complications include dysthymias and postpericardiotomy syndrome (Inflammation with pericardial effusion)

Describe invasive temporary pacing.

Consists of an external battery-operated pulse generator and pacing electrodes, or lead wires. These wires attach to the generator on one end and are in contact with the heart on the other end. Electrical impulses, or stimuli, are emitted from the negative terminal on the generator, flow through a lead wire, and stimulate the cardiac cells to depolorize. --Patients do not usually feel invasive pacemaker stimuli. However, they occasionally feel an uncomfortable sensation from the stimuli if strong electrical currents are delivered by the pacemaker. This discomfort may be alleviated by decreasing the generator current if possible Complications: --Infection or hematoma at the pacemaker wire insertion site --Ectopic complexes (usually PVCs) caused by irritability from the pacing wire in the ventricle, use of high current, or undersensing with pacemaker competition. --Loss of capture, noted by the presence of a pacing stimulus or spike but no QRS complex --Undersensing or pacemaker competition, noted when pacing stimuli occur at a fixed rate in the presence of an adequate intrinsic rhythm --Oversensing, noted when the pacemaker fails to fire in the presence of an inadequate intrinsic rhythm --Electromagnetic interference, noted by altered generator variables --Stimulation of the chest wall or diaphragm, noted by rhythmic contraction of the chest wall muscles or hiccups with the use of high current or from lead wire perforation, which could cause cardiac tamponade.

Describe the pathophysiology of a ventricular septal defect.

Decrease in pulmonary vascular resistance compared to systemic vascular resistance in the weeks after birth results in left-to-right shunting through the VSD. Increased pulmonary blood flow, pulmonary hypertension, and progressive pulmonary vascular disease can occur over time. --15-20% of cardiac defects --Abnormal opening between the ventricles. Three types according to location: (1) conoventricular, (2) atrioventricular (AV) canal (About 1 in 9 children with Down's syndrome have this cardiac defect), (3) muscular, depending on the size, complete absence of the septum results in a common ventricle. --Most common type of cardiac defect; may be accompanied by other defects

Describe the pathophysiology of an atrial septal defect.

Decreased right ventricular compliance (ease of ventricular filing during diastole) compared to left ventricular compliance leads to left-to-right shunting across the abnormal septal opening; right atrium is enlarged and pulmonary blood flow is increased. --5-10% of cardiac lesions --Seen more often in girls --Abnormal opening between the atria --Three types predominate: 1. Ostium secondum--located in the middle of the septum and is the most commonly seen 2. Ostium primum--lesion is low in the septum, associated with endocardial tissue formation defect, associated with cleft mitral valve 3. Sinus venosus--located high in the septum near superior vena cava

Describe the function and use of dobutamine hydrochloride (Dobutrex).

Dobutamine hydrochloride (Dobutrex): Beta-adrenergic stimulating agent Given to tx low CO 2-20mcg/kg/min IV infusion Assess BP

Describe the function and use of dopamine hydrochloride (Intropin).

Dopamine hydrochloride (Intropin): sympathomimetic catecholamine Given for shock, low CO, and hypotension 2.5-5 mcg/kg/min IV infusion, titrate to desired response 1-2mcg/kg/min for renal perfusion 2-10mcg/kg/min for beta-adrenergic effects 10-20mcg/kg/min for alpha-adrenergic effects Assess for increased BP Monitor HR Monitor IV site for infiltration which leads to necrosis Assess UOP, skin color, numbness in extremities Be aware of dangers of severe vasocontriction

Describe the pathophysiology of patent ductus arteriosus.

Due to a drop in pulmonary vascular resistance and failure of the ductus arteriosus to close, increased systemic pressure movvs saturated blood from the aorta into the pulmonary arteries (left-to-right shunt), the lungs, and the left side of the heart causing both increased left-sided cardiac workload and increased pulmonary blood flow.

Describe the pathophysiology of tetralogy of fallot.

Equal right-to-left ventricular pressures related to the pulmonary artery obstruction and size of the VSD; desaturated blood enters the systemic system by shunting right to left across the VSD, or into the overriding aorta. --5-10% on congenital cardiac defects; most frequently seen cyanotic lesion --Constellation of lesion results from malalignment of the ventricular septum during fetal development--(1) ventricular septal defect, (2) right ventricular outflow tract obstruction (e.g., pulmonary stenosis), (3)overriding of the aorta (arises partially out of the right ventricle), (4) right ventricular hypertrophy

Occurs when microorganisms circulating in the bloodstream attach onto an endocardial surface. It is caused by various microbes, and frequently involves the heart valves.

Endocarditis. ppt Inflammation of cardiac endothelium usually from bacterial infection of normal or damaged heart valves Vegetative growths develop on inflammed areas produce emboli to lungs, brain, spleen, kidneys

Describe the function and use of epinephrine.

Epinephrine (Adrenaline): **First line agent in all cardiac arrests** Alpha-adrenergic effects: increase vasomotor tone in heart and brain Beta-adrenergic effects: stimulated heart and increases myocardial contractility and increases CO 1mg IV bolus, followed by 20ml NS flush q 3-5min Can give endotracheal route: increase dose 2-2.5 times IV dose Monitor rhythm continuously

Describe intra-op interventions and teaching involved with typical cardiac surgery.

Extra Corporeal Circulation --Cannulas placed in upper and lower circ. (Vena Cavas) to drain blood to pump --Blood is oxygenated and returned to arterial system via aortic cannula --Heat exchanges control body temp by cooling body during surgery (decrease metabolic demands and decrease 02 demands) - Rewarm when surgery is over --Filters aid in decrease clots and embolization --Heparin (3 mgm/kg IV) renders blood incoaguable bto prevent clotting along circuit --Discontinuing of bypass: --Perfusion is gradually decreased and perfusion warming begun --As blood is rewarmed heart begins to beat spontaneously (occasional electric shock required) --When RAP and LAP are adequate extra corporeal circulation is withdrawn --Blood coagulation is restored with protamine sulfate 3 mg/kg IV Complications: 1. Metabolic --Acidosis --Hypo/Hyperglycemia --Hypokalemia --Hypocalcemia 2. Hemotologic --Hemolysis --Coagulation Abnormalities --DIC --Thrombocytopenia --Hypotension 3. Pulmonary --Atelectasis --Pulmonary edema 4. Renal --Hemoglobinuria --Aortic renal failure 5. Neurological --Cerebral ischemia

Describe the surgical management options for the patient cardiomyopathy.

HCM: --Ventriculomyomectomy (ventricular septal myectomy)-a portion of the hypertrophied ventricular septum is removed to create a wider flow tract. --Percutaneous alcohol septal ablation: absolute alcohol is injected into the target septal branch of the left anterior descending coronary artery to produce a small septal infarction. Arrythmogenic: --Radiofrequency ablation or placement of an implantable defibrillator. DCM and RCM: --Heart transplant

An invasive system used in critical care areas to provide quantitative information about vascular capacity, blood volume, pump effectiveness, and tissue perfusion. It directly measures pressures in the heart and great vessels.

Hemodynamic Monitoring. **Requires informed consent** --Chest x-ray used to confirm placement --Values are checked every 1-4 hrs --Patency of the catheter is maintained with a slow continuous flush of normal saline, usually infused at 3-4 mL/hr under pressure to prevent the backup of blood and occlusion of the catheter --Because the atrial vasculature is a high pressure system, frequent assessment of the arterial site and infusion system is essential. **Note any bleeding or loose connections and correct the situation immediately.** --Monitor distal pulses for compromise --Change dressing per facility policy Complications --Pulmonary infarction or rupture (if remains in wedge) --Air embolism if balloon ruptures and several attempts are made to reinflate it --Ventricular dysrhythmias occur during insertion or if the catheter slips back into the right ventricle and irritates the myocardium --Thrombus and embolus can occur at insertions site --Infection --Bleeding if system is disconnected --Pressure = Flow X Resistance --Blood Pressure = Cardiac Output (flow) X Peripheral (Systemic) Vascular Resistance Cardiac Output: The volume of blood that circulates through the body per minute. Reflects flow. Normal range 4-6 liters/min (at rest) Peripheral SVR: The opposition to blood flow exerted by the blood vessels. Is affected by blood viscosity, vascular tone and friction imposed by the inner lining of the blood vessels Normal range 800-1400 dynes/sec/cm-5 --LUMEN SIZE will directly affect SVR Lumen size narrows-- resistance increases Lumen size widens-- decreases resistance --In critical care, vasoactive drugs (Nipride or Nitroglycerin) are administered to alter the lumen size of peripheral vessels. Predominantly the arterioles. --CO = HR X SV --Normal range for Stroke Volume 60-70ml Frank Starling Principle --Ventricular contraction is stronger as fiber muscle stretch (preload) increases. Clinical significance: A decrease in preload (EDV) for a client often results in a decreased force of contraction. Arterial Lines --Provides continuous BP recordings --Allows for obtaining arterial blood for ABG's Mean Arterial Pressure --MAP is the average perfusion pressure created by the arterial BP during the cardiac cycle --Normal range - 70-100 mm HG CARDIAC INDEX --Used because this parameter takes into account the body size --Considered to be a more precise measurement of cardiac output --CI = CO (L/min)Body surface area Normal CI: 2.5 to 4.0 l/min/m3 Clinical states of decreased CI --2.0 - 2.2 l/min/m3 - onset cardiac failure --1.5 - 2.0 l/min/m3 - cardiogenic shock --< 1.5 l/min/m3 - irreversible stage of shock Left Ventricular End Diastolic Pressure --Most important cardiac pressure because it is a major determinant of systemic perfusion --The pressure in the LV just before systole is LVEDP - it reflects the compliance of the LV --Compliance means the ability of the LV to accept blood from the LA during diastole

List S/S of HF in children.

Infants Tachypnea Dyspnea Tachycardia Restlessness Anxiety Sweating with feeding Hepatomegaly Pulmonary rales Poor wt. Gain Periorb. Edema Children 2 yo & older Dyspnea Tachypnea Tachycardia Anxiety Decrease exercise tolerance Hepotomegaly Periph. Edema Venous distention Gallop Heart rhythm (S4) Treatment Digoxin Diuretics (lasix or aldactone) Drugs to decrease afterload (Procardia, hydralazine, captopril) O2 & Rest Sedation (morphine or barbiturates) Daily weights Palliative or corrective surgery

Describe the pathophysiology of endocarditis.

Infections legions, referred to as vegetation, form on the heart valves. these legions have irregular edges, creating a cauliflower-like appearance. The mitral valve is the most common valve to be affected. The vegetative process can grow into the chordae tendineae, papillary muscles, and conduction system. Therefore the patient may have dysrhythmias or acute HF. Patients with IVDA endocarditis usually do not have underlying structural disease. With a cardiac defect, blood may flow rapidly from a high-pressure area to a low-pressure zone, eroding a section of endocardium, forming vegetative lesions. During bacteremia, bacteria become trapped in the low-pressure "sink hole" and are deposited in the vegetation. Additional platelets and fibrin are deposited, which causes the vegetative lesion to grow. The endocardium and valve are destroyed. Valvular insufficiency may result when the lesion interferes with normal alignment of the valve. If vegetation becomes so large that blood flow through the valve is obstructed, the valve appears stenotic and then is very likely to embolize. **Arterial embolization is major complication. Fragments of vegetation break loose and travel randomly thorough the circulation. When the left heart is involved, vegetation fragments are carried to the spleen, kidneys, GI tract, brain, and extremities. When the right side of the heart is involved, emboli enter the pulmonary circulation.**

A microbial infection (e.g., virus, bacteria, fungi) involving the endocardium; previously called "bacterial endocarditis" The most common infective organism is Streptococcus viridians and or Staphylococcus aureus.

Infective endocarditis.

An invasive intervention that is used to improve myocardial perfusion during an acute MI, reduce preload and afterload, and facilitate left ventricular ejection. May be used when patients do not respond to drug therapy with improved tissue perfusion, decreased workload of the heart, and increased cardiac contractibility.

Intra-aortic balloon pump Intra Aortic Balloon Pump (IABP) indicated for: --Cardiogenic Shock after AMI --LV failure in post-op cardiac surgery --Severe unstable angina --Post infarction VSD or Mitral Regurgitation --Bridge to transplantation Inflation increases: --Aortic diastolic pressure --Aortic root pressure --Coronary perfusion pressure --Oxygen supply Deflation decreases: --Aortic End-Diastolic Pressure --Impedance to Ejection --Afterload --Oxygen Demand Indications for Weaning - IABP --Hemodynamic Stability: CI >2L/min PCWP < 20 mmHg SBP > 100 --Minimal requirements for vasopressor support --Evidence of adequate cardiac function --Evidence of good coronary perfusion

Describe the function and use of Isoproterenol (Isuprel).

Isoproterenol (Isuprel): Given to heart transplant pts to increase HR 2-10mck/kg/min IV infusion, titrate Assess HR, should increase Increases myocardial O2 demand, assess for CP Monitor for ventricular dysrhythmias: increases ventricular irritability, especially with hypokalemia or digoxin receiving pts

How does digoxin effect the body?

It helps the heart pump blood more effectively, thereby improving the circulation of the blood, and promoting the normal elimination of excess fluid.

An acute, febrile, exanthematous illness of children.

Kawasaki Disease. Also known as Mucocutaneous lymph node syndrome.

Describe the therapeutic management of ventricular septal defect.

Medical Management --Conservative--30-40% close spontaneously --Diuretics, digoxin, and medications for afterload reduction (ACE inhibitors) --Management of associated HF Interventional Cardiac Catheterization --May be done as a hybrid procedure--using a surgical approach to visualize and directly access the ventricle and catheterization to place the device Surgical Management --Suture or patch closure using open heart surgery with cardiopulmonary bypass. Consideration of pulmonary artery banding to reduce pulmonary blood flow for children with multiple defects and severe HF. Complication include residual VSDs, pulmonary hypertension, heart block that requires temporary or permanent pacemaker, abdominal rhythm (junctional ectopic tachycardia) that decreases cardiac output, and postpericardiotomy syndrome

Describe the medical management of coarctation of the aorta.

Medical Management --Diuretics and digoxin to improve cardiac output; PGE1 infusion to open the ductus arteriosus and improve perfusion to the body Internal Cardiac Catheterization --Balloon dilation with placement of stent for reoccurrences; **balloon angioplasty for the initial procedure can increase the incidence of reoccurrences** Surgical Management --Performed shortly after diagnosis in most cases --Several surgical procedures available--end-to-end anastomosis, use of prosthetic patch, left subclavian artery patch (results in postoperative absence of left palpable pulse) --Surgery is usually planned by age 2 --Girls must have the defect repaired before childbearing age --After surgery, abdominal vessels receive more blood - abdominal pain or generalized abdominal discomfort may occur --Some children continue to have elevated upper body hypertension after the repair

Describe the therapeutic management of patent ductus arteriosus.

Medical Management --Interventions to address HF --Administration of indomethacin (Indocin), a PG inhibitor, that constricts the ductus **monitor respiratory status, renal function, and growth** Interventional Cardiac Catheterization --A coil is placed to occlude the ductus. Tissue grows around the coil (endothelializes) forming permanent occlusion Surgical Management --Ligation of the ductus via left thoracotomy, usually within the first year of life

Describe the therapeutic management of pulmonary stenosis.

Medical management --Cardiac observation and antibiotic prophylaxis for children who are asymptomatic --Additional intervention related to increasing pulmonary pressure gradient across the pulmonary valve Interventional Cardiac Catheterization --Balloon valvuloplasty with dilation of the valve to decrease the pressure; pulmonary regurgitation may be a complication; may have to be redone later Surgical Management --Surgical valvulotomy for unsuccessful valvuloplasty or if stenosis is supravalvular --Placement of a shunt from aorta to pulmonary artery (systemic to pulmonary artery shunt) for critical pulmonary stenosis with small right ventricle or for children who must remain on PGE1 after interventional cardiac catheterization

Describe the therapeutic management of tetralogy of fallot.

Medical management --PGE1 infusion to maintain patency of the ductus arteriosus and blood flow to the lungs; management of hypercyanotic episodes; treatment of iron deficiency anemia. Surgical management --Primary repair of defects during infancy is the procedure of choice; surgery occurs after 4 mo of age and is timed according to the degree of cyanosis and other symptoms --Surgery requires cardiopulmonary bypass --For infants who are poor canidates for early primary repair, palliative shunt procedures increase pulmonary blood flow; modified Blalock-Taussig procedure (creation of a systemic-to-pulmonary-artery shunt using a Gore-Tex tube) is used most frequently --Surgical complications: rhythm disturbances, residual VSD, low cardiac output, residual right ventricular outflow obstruction, pulmonary valve regurgitation, residual right-sided HF; mortality is low --Surgery is done at 1 -2 years --Hypoxic episodes are managed by placing infant in knee chest position and administering morphine. --Temporary surgical repair - Blalock Taussig procedure; first performed in 1944 at John Hopkins

Describe the therapeutic management of aortic stenosis.

Medical management --Mild/moderate: regular follow-up. especially for athletes; restriction from competitive athletics depending on the degree of stenosis and severity of signs and symptoms Interventional Cardiac Catheterization --Aortic balloon valvuloplasty decreases stenosis and improves cardiac output; may be performed to delay surgical intervention; aortic insufficiency, thrombosis, infection of artery damage may occur Surgical management --Surgical valvulotomy --Aortic valve replacement for stenosis: (1) mechanical valve replacement requires warfarin treatment; valve does not grow with child; (2) use of child's pulmonary valve to replace the aortic valve; pulmonary valve hemografy to replace the pulmonary valve; new aortic valve grows with the child; homograft will need later replacement

List the manifestations of aortic stenosis.

Mild/moderate --Asymptomatic; exercise intolerance, ECG abnormalities with exercise, cardiomegaly, systolic ejection murmur with thrill or click; sudden death with strenuous exercise is a possibility --Narrowing of aortic valve or left ventricular outflow obstruction. --More common in males. --Acyanotic unless defect is severe --Usually asymptomatic in infants and children In infants --atypical systolic murmur and possible intractable congestive heart failure --Systolic ejection click followed by systolic ejection murmur and a thrill felt at the second right intercostal space or suprasternal notch --Irritability --Tachycardia --Dyspnea and fatigue on exertion --Angina pectoris --Syncope --Pale skin --Narrow pulse pressure --Weak peripheral pulses --Possible abdominal pain --Diaphoresis --Epistaxis --Severe obstruction causes increased left ventricle pressure to maintain aortic pressure. This condition may lead to left ventricle hypertrophy Severe --Severe HF; decreased cardiac output with decreased peripheral perfusion (critical aortic stenosis); if uncorrected, chest pain, dizziness, and syncope

Inability of the mitral valve to close completely during systole, which allows the back flow of blood into the left atrium when the left ventricle contracts; usually due to fibrosis and calcification caused by rheumatic disease. Also called mitral valve insufficiency.

Mitral regurgitation.

Occurs when the valvular leaflets enlarge and prolapse into the left atrium during systole. This abnormality is usually benign but may progress to pronounced mitral regurgitation.

Mitral valve prolapse.

Thickening of the mitral valve due to fibrosis and calcification and usually caused by rheumatic fever. The valve leaflets fuse and become stiff, the chordae tendineae contract, and the valve opening narrows, preventing normal blood flow from the left atrium to the left ventricle. As a result, the left atrial pressure rises, the left atrium dilates, pulmonary pressure increases, and the right ventricle hypertrophies. Pulmonary congestion and right-sided HF occur first. Later the left ventricle receives insufficient blood volume, preload is decreased, and cardiac output falls.

Mitral valve stenosis.

A focal or diffuse inflammation of myocardium.

Myocarditis. --Myocarditis can cause heart dilatation, thrombi on the heart wall (mural thrombi) and degeneration of the muscle fibers themselves. It is theorized that dilated cardiomyopathy is a latent manifestation of myocarditis.

Describe the pathophysiology of coarctation of the aorta.

Narrowing of the aortic structure obstructs the left ventricle output, increasing afterload to the left ventricle; blood supply is decreased in the abdominal organs and the lower periphery, left ventricular pressure increases, aortic pressure is high proximal to the constriction and low distal; pulmonary edema can occur. If coarctation is mild, collateral blood supply can develop to channel blood past the constriction --8-10% of cardiac defects --Aorta is constricted near the ductus arteriosus insertion location; associated with bicuspid aortic valve that can later be stenotic.

Describe the function and use of Norepinepherine (Levaphed).

Norepinepherine (Levaphed) Potent vasoconstrictor 0.5-1mck/kg/min IV infusion, titrate to desired effect, up to 8-30mcg/kg/min Assess BP, should increase Assess HR, might cause reflex bradycardia Administer through a CVL Assess UOP, skin color, and extremity changes Assess for CP because of the increase myocardial O2 demand after administration

Describe the pathophysiology of pulmonary stenosis.

Obstruction causes resistance to blood flow at the right ventricular outflow track; increased pressure in the right ventricle leads to right ventricular hypertrophy. Critically severe pulmonary artery obstruction elevates right ventricular pressure severely, causing blood to regurgitate into the right atrium; rising right atrial pressure forces the foramen ovale open, allowing blood to flow from the right to the left side of the heart --10% of cardiac defects --Narrowing at the entrance to the pulmonary artery at the valve, below the valve, or above the valve --The valve itself may be normal (tricuspid), bicuspid, or dysplastic

What should the nurse do when a pediatric BP is high when taken on the arm?

Obtain reading from the leg.

Describe the pathophysiology of infective endocarditis.

Occurs primarily in patients that abuse IV drugs, have had valve replacements, have experienced systemic infection, or have structural cardiac defects. With a cardiac defect, blood may flow rapidly from a high pressure area to a low pressure zone, eroding a section of the endocardium. Platelets and fibrin adhere to the denuded endocardium, forming a vegetative lesion. During bacteremia, bacteria become trapped in the low pressure "sink hole" and are deposited into the vegetation. Additional fibrin and platelets are deposited, which causes the vegetation to grow. The endocardium and the valve are destroyed. Valvular insufficiency may occur when the lesion interferes with normal alignment of the valve. If vegetation becomes so large that blood flow through the valve is obstructed, the valve appears very stenotic and is very likely to embolize.

Acute or chronic inflammation of the pericardium.

Pericarditis. Pericarditis (causes) --Viral, bacterial, or fungal infection --Rheumatic fever --Postcardiac injury --Uremia --Toxins Often called bread and butter pericarditis due to its appearance.

Describe pre-op interventions and teaching involved with typical cardiac surgery.

Pre Operative Care -Client will have undergone extensive testing prior to decision for surgery: CXR Cardiac Cath Coronary Angiography Echo cardiography Phono cardiography Nuclear cardiac studies ECG Stress tests Blood serum analysis --Important for nurses to be aware of past cardiopulmonary or circulatory conditions or disorders that increase risk of post-op complications: MI Bacterial endocarditis Pulmonary embolus Blood clotting abnormalities History of smoking --Important for nurses to know pt's current home medical regimen. These may have to be changed in hospital pre-op Pt. Needs to understand this is not an indictment against his/her current care. --Physiologic Prep of Pt. Admitted to hosp 1-2 days before procedure CXR, ECG, Full lab screening ABG's and pulmonary function studies Baseline U.S Apical & radial pulses Bilateral blood pressures Status of all pulses Neuro status Ht, Wt. Nutritional status Elimination patterns Psychologic status Psychologic Preparation Address patient's fears very seriously Patient may reject too much information as defense mechanism --Explain pre-op and post-op procedures. Family may be requested to identify one spokesperson who will be told where to meet the surgeon after surgery. This person may be the one allowed to call ICU for Information. Friends and family may tour and receive orientation to ICU. --Teaching Plan Nursing Diagnosis Knowledge deficit related to the surgical procedure and invasive lines Expected Patient Outcomes Describes the anatomy of the heart and valve repair Describes events pertaining to the surgery Describes purpose of lines Describes events related to breathing tube Describes drainage tubes Expresses less concern about postoperative pain

What may be some S/S that may bring a patient with a possible dilated cardiomyopathy to seek medical treatment?

Pronounced symptoms of left ventricular failure (Left=Lung): --Progressive DOE --Orthopnea --Palpitations --Activity intolerance --S3 gallop Right-sided HF develops late in the disease process (poor prognosis) --System congestion --Jugular distension --Enlarged liver and spleen --Anorexia and nausea --Dependent edema (legs and sacrum) --Distended abdomen --Swollen hands and fingers --Polyuria at night --Weight gain --Increased BP (from excess volume) or decreased BP (from failure) Atrial fibrillation may develop (associated with embolism)

A form of car diomyopathy that restricts the filling of the ventricles; a type of lung disease that prevents good expansion and recoil of the gas exchange unit.

Restrictive cardiomyopathy.

Inflammatory lesions in the heart due to a sensitivity response that develops after a respiratory tract infection with group A beta-hemolytic streptococci. Inflammation results in impaired contractile function of the myocardium, thickening of the pericardium, and valvular damage,

Rheumatic Carditis. ppt. --Directly from rheumatic fever caused by group A streptococcal infection --Polyarthritis is seen due to the involvement of bony joints --The heart damage and the joint lesions of rheumatic are not infectious in origin. They represent a sensitivity reaction occurring in response to hemolytic streptococci. Leucocytes accumulate in the affected tissues and form nodules which become replace by scars. --Inflammation in all layers of the heart --Impaired contractile function of the myocardium, thickening of the pericardium, and valvular damage --The contractile power of the myocardium is temporarily weakened --Permanent and often crippling side effects results --Vegetations are the starting point for a process that gradually thickens the leaflets --This prevents valve leaflets from closing completely --Valvular regurgitation results --Mitral valve most often affected

Describe the S/S, medical management, and teaching associated with mitral valve prolapse.

S/S --Exercise intolerance --Atypical chest pain described as a sharp pain localized to the left-side of the chest --Blackouts, dizziness, and palpitations may be associated with atrial or ventricular dysrhythmias --Usually produces no symptoms; first sign may be the auscultation of **"systolic click"** --If symptoms are present: fatigue, SOB, light headedness, dizziness, syncope, palpitations, chest pain, anxiety Medical Management --Control symptoms --Eliminate caffeine & alcohol from diet --Stop smoking --Antiarrhythmic meds --Nitrates or Calcium Channel Blockers for chest pain --Surgery as needed Teaching --Teach to read product labels for food products and over the counter meds --Explain that alcohol, ephedrine, and epinephrine may produce dysrhythmia --Educate regarding prophylactic antibiotics

List the manifestations of a ventricular septal defect.

S/S related to the size of the defect--some children asymptomatic --Loud, harsh systemic murmur, varies in intensity and duration depending on degree of shunting and size of defect --Palpable thrill --Diastolic murmur and gallop rhythm may be present --HF may occur with moderate to large defects --Overactive precordium, especially after feeding --Within 6 weeks after birth, harsh systolic murmur heard best in third and fourth left intercostal spaces; associated with palpable thrill. Murmur may be only sign of disorder Increased right ventricular and pulmonary artery pressure If condition's severe, poor growth development; labored breathing; and frequent feeding pattern (hungry infant wakes, feeds vigorously, becomes dyspneic, slows and stops feeding, sleeps a short time, wakes and repeats cycle) --If opening's large, may result in cardiac complications, such as congestive heart failure and bacterial endocarditis --Large VSD may eventually cause pulmonary vascular disease and pulmonary artery hypertension

Describe the S/S of Kawasaki disease.

Stage I, Acute Phase (10 days): --High Fever (unresponsive to meds) --Lethargy or irritability --Cervical lymph node enlargement --Tachycardia --Red, swollen hands & feet --Conjunctivitis (bilateral and non-purulent) --Strawberry tongue --Red, cracked lips --Rash --Cervical lymph node enlargement --Internal node enlargement with abdominal pain, anorexia, & diarrhea --Joint swelling --Elevated WBC & ESR Stage II, Subacute Phase (11-25 days): (most dangerous due to possible thrombus) --Fever and most symptoms resolve --Formation or aneurysm rupture --Skin desquamates, palms & soles --arthritis and arthralgia --HF --Aneurysms may form (coronary arteries) --Severe platelet count elevation --High risk of thrombosis and MI Stage III, Convalescent Phase (begins about day 25) --Begins when symptoms have disappeared --Lasts until ESR returns to normal --Beau's lines may appear on nails

Describe surgical management of infective endocarditis.

Surgery is indicated when antibiotic therapy is ineffective in sterilizing a valve, refractory HF develops, secondary to defective valve, if large valvular vegetations are present, or if multiple embolic events occur. --Valve replacement surgery may be indicated in severe cases --Repairing or removing congenital shunts --Repairing injured valves and chordae tendineae --Draining abcess in heart

List S/S of Congenital Heart DefectsChildren

Symptoms Dyspnea Decreased exercise tolerance Growth failure Recurrent respiratory infections Squatting after exertion Fainting or dizzy spells Chest pain Signs Cardiac murmur Abnormal or extra heart sounds Cyanosis and clubbing of nails Enlarged liver Blood pressure higher in arms than in legs (coartation) Precordial bulge Arrhythmias

List S/S of Congenital Heart DefectsInfants

Symptoms Dyspnea Feeding difficulties Excessive perspiring Failure to gain weight Recurrent respiratory infections Chronic cough Hypoxic spells Signs Cardiac murmur Cyanosis Tachycardia Tachypnea Weak or absent femoral pulses Bradycardia or arrhythmia Enlarged liver

List the S/S of rheumatic fever.

Symptoms of the original infection subside in a few days with or without an antimicrobial therapy. Children appear well again. After 1-3 weeks, if no treatment with appropriate antibiotic for the original infection , the onset of rheumatic fever symptoms can occur. Major Symptoms --Carditis (most serious), systolic murmur and prolonged PR & QT intervals are present due to inflammation --Chorea (sudden involuntary movement of limbs --Erythema Marginatum (macular rash on trunk) --Polyarthritis --Subcutaneous Nodules Minor Symptoms --Fever --Arthralgia (joint tenderness) --Elevated sed rate --C - reactive protein --Damaged valves can become further damaged with repeated infections --Streptococcal prophylaxis is lifelong if there is actual valve involvement --Intramuscular penicillin, administered monthly, is the drug of choice --Alternatives include oral penicillin twice daily or oral sulfadiazine once a day

What may be some S/S that may bring a patient with a possible hypertrophic cardiomyopathy to seek medical treatment?

Symptoms result from the hypertrophied septum causing a reduced stroke volume and cardiac output: --DOE --Angina (atypical in that it occurs at rest, is prolonged, has no relation to exertion, and is not relieved by nitrates) --Syncope --Ventricular dysrhythmias (Sudden death may be the first manifestation of the disease). Apical pulse my be displaced to the left upon assessment.

A non surgical intervention that provides a timed electrical stimulus to the heart when the impulse initiation or conduction system of the heart is defective.

Temporary pacing. --When a pacing stimulus is delivered to the heart, a spike is seen on the ECG strip. Successful P wave followed by QRS is referred to as "capture" --Most pacing is done synchronous `

Describe the pathophysiology of pericarditis.

The pericardium has an inner and outer layer with a small amount of lubrication fluid between the layers. When the pericardium becomes inflamed, the amount of fluid between the two layers increases (pericardial effusion), This squeezes the heart and restricts its action and may result in cardiac tamponade (**Cardiac Tamponade=BAD**). Chronic inflammation can lead to scarring. The pericardium may thicken and calcify. --Can be complication of acute MI, cardiac surgery, kidney injury (uremic pericarditis), or infection. --Chronic constrictive pericarditis occurs when chronic pericardial inflammation causes a fibrous thickening of the pericardium. Caused by tuberculosis, radiation therapy, trauma, renal failure, or metatastic cancer. May have symptoms of right-sided HF, elevated systemic venous pressure, with jugular distension, hepatic engorgement, and dependent edema. --Can cause left-sided diastolic HF --Mild inflammation of viseral and parietal pericardium. May occur as primary illness or in the course of another illness. --Leads to accumulation of fluid in pericardial sac this produces decreased C. O. and possible cardiac tamponade.

Describe the operative procedures associated with heart transplantation.

The surgeon transplants a heart from a donor with a comparable body weight and ABO compatibility into a recipient less than 6hrs after procurement using one of two methods: 1. Bicaval technique: the intact right atrium of the donor heart is preserved by anastomoses at the patient's (recipient's) superior and inferior vena cavae. 2. Orthotopic technique: (more traditional) cuffs of the patient's right and left atria are attached to the donor's atria. Anastomoses are made between the recipient's and donors atria, aorta, and pulmonary arteries. **Because the remaining remnant of the recipient's atria contains the SA node, two unrelated P waves are visible on ECG**

Pulmonary veins return to the RA or SVC instead of to the LA. Systemic blood flow must be shunted across a patent foramen ovale or a patent ductus arteriosus.

Total Anomalous Pulmonary Venous Return --Child must be maintained on a continuous IV infusion containing PGE1

Aorta leaves right ventricle; pulmonary artery leaves left ventricle. Usually associated with ventricular septal defect (VSD), atrial septal defect (ASD), and/or patent ductus arteriosus (PDA).

Transposition of great vessels --More common in males --Associated with history of maternal diabetes --Causes unoxygenated blood to flow through right atrium and ventricle and out aorta to systemic circulation. --Oxygenated blood flows from lungs to left atrium and ventricle and out pulmonary artery to lungs --May cause premature contractions and escape beats --May be fatal unless VSD, ASD, or PDA develops as safety valve for two independent circulations Signs and Symptoms --Cyanosis. (In infants with large PDA or VSD, cyanosis is minimal.) --High birth weight possible --Signs of congestive heart failure such as severe dyspnea, within 12 to 24 hours after birth --Poor sucking reflex --Systolic murmur, if VSD is present --Hepatomegaly --Metabolic acidosis from hypoxia. (Hypothermia intensifies signs of acidosis.) Treatment of Transpositon --IV infusion of PGE1 --Septal pull through operation to crease an artificial ASD --Surgical correction involves an arterial switch procedure

Tricuspid valve is completely closed. Blood may cross through a patent foramen ovale into the left atrium, bypassing the lungs and the step of oxygenation. Blood reaches the lungs by being shunted back through a patent ductus arteriosus.

Tricuspid Atresia --Infant develops severe cyanosis --Maintain on IV infusion of PGE1 --If patent ductus and foramen ovale closes, the infant develops extreme cyanosis, tachycardia and dyspnea --Surgery - construction of a subclavian to pulmonary artery shunt, or Fontan procedure

Failure of embryonic arterial trunk to separate into aorta and pulmonary artery. Resulting single vessel overrides ventricles and carries blood for both pulmonary and systemic circulation.

Truncus Arteriosus Characteristics --Ventricular septal defect (VSD) always present --Common trunk may have 2 to 6 valve cusps --Usually fatal within 6 months if untreated Signs and Symptoms Cyanosis Systolic murmur about 1 months after birth Fatigue Dyspnea Failure to thrive Parasternal lift Loud decrescendo diastolic murmur possible Ejection click S2 has only one component, because of single valve in common trunk Tachypnea Rales Recurrent respiratory infections Wide pulse pressure possible Congestive heart failure, usually indicating rapid physical decline Hepatomegaly possible

Describe the function and use of Vasopressin.

Vasopressin: 40 units IV bolus, potent vasoconstrictor, shown to be equal to Epi for tx of VF and pulseless VT Long half-life, given one time Monitor rhythm Monitor for returning pulse

Implanted pump powered by an external controller that takes over the workload of the failing left ventricle and can be programmed to generate a fixed or variable rate.

Ventricular Assist Device How the pump works --At the end of the systolic phase, blood flows from the LV, through the LVAD's inflow conduit into the pump. --Pump pushes the blood through the outflow conduit into the patient's aorta. From there it follows the normal circulatory pattern **Patients on VAD have no pulses**