Cardiac A & P Assessment

1. Cardiac A & P Assessment SOAR Session 4 Cathy Peterson, RN, BSN Clinical Educator NICU

2. Objectives • Describe basic cardiac anatomy • Describe basic cardiac physiology • Describe causes, pathophysiology, signs and symptoms, and management of CHF • Describe causes, pathophysiology, signs and symptoms, and management of PDA

3. Cardiac Anatomy • Four chambers • R & L atria • R & L ventricles • Aorta • Superior & Inferior vena cava • Pulmonary vein • Coronary arteries

4. Cardiovascular PhysiologyNormal Circulation • O2 poor blood enters the RA thru tricuspid valve to RV thru pulmonary artery to lungs • As flows thru lungs gives up CO2 and gains O2 • O2 rich blood from lungs thru PV to LA thru Mitral valve to LV thru aortic valve into aorta • Aorta delivers O2 blood to body’s organs and tissues

5. Concepts of Blood Flow • Blood flow will always take path of least resistance • If heart action (pressure) remains unchanged but vasoconstriction or dilation or obstruction to flow (resistance) changes, flow will change • PVR starts to fall after delivery and declines to levels > 50% of systemic arterial pressure • Influenced by prematurity, low birth wt and hypoxia

6. Congestive Heart Failure (CHF) • The inability of the heart to generate enough cardiac output to meet the body's demands.  • Set of clinical signs and symptoms that indicate a dysfunctional myocardium • Structural congenital heart defects most common cause of CHF

7. Causes of CHF • + Increase workload on an otherwise normal myocardium: • Increase blood volume such as with anemia. • Left to right shunting of blood, such as with AV fistula or septal defects (ASD, VSD, PDA and AVC defect).  This will cause already oxygenated blood in the left heart to return to the right heart.  The result is decrease in the left ventricular cardiac output and increase in the right ventricle cardiac output.  The decrease cardiac output from the left ventricle will cause poor blood supply to the body, while the increase cardiac output from the right ventricle will cause work overload of the right ventricular myocardium.  • An expanded right ventricle will also cause abnormal leftward deviation of the ventricular septum (flattening) resulting in abnormal left ventricular contour and further reduction of ejection capabilities. • Valvar regurgitation, causing volume overload of the ventricle.

8. Causes of CHF • + Pressure overload of one or both ventricles, such as with valvular diseases (pulmonary or aortic stenoses), coarctation of the aorta, pulmonary vascular obstructive disease or systemic hypertension.

9. Causes of CHF • + Cardiac myocardial disease such as with myocarditis and cardiomyopathy. •  + Coronary arterial insufficiency, such as with Kawasaki disease and hyperlipdemia. •  + Abnormal heart rhythm, typically tachycardia.Rapid heart rate will prevent proper filling of the ventricles as it shortens diastole, thus reducing cardiac output.

10. Pathopysiology of CHF

11. Signs and Symptoms of CHF • Symptoms • Regardless of the cause, children and particularly infants will be short of breath, feed poorly and fail to thrive.  With exertion, such as suckling, they will become pale and sweat profusely.  The heart will eventually dilate and the elevated LV and RV end-diastolic pressures will cause pulmonary edema and hepatomegaly respectively.  Pulmonary edema will result in tachypnea, while GI edema will lead to worsening absorption and further failure to thrive. • Signs • Inspection:  Pallor, respiratory distress, elevated JVP (not possible to assess in infants & young children). • Palpation:  edema, poor capillary refill, poor pulses, hepatomegaly, cardiomegaly, increase RV and/or LV impulses. • Auscultation: gallop rhythm, murmur if associated with CHD or AV valve insufficiency due to ventricular dilation.   

12. Medical Management • Semi-fowler’s or prone position • Decrease O2 consumption • Neutral Thermal Environment (NTE) • Avoid unnecessary stresses • Provide sedation • Consider assisted ventilation to decrease WOB • Provide supplemental oxygen • Correct acidosis

13. Fluid/nutritional support Reduce volume intake Enhance caloric content IV infusions of fat emulsion Pharmacologic Digoxin therapy Diuretic therapy Edecrin Diuril Medical Management

14. Patent Ductus Arteriosus (PDA) • Communication between pulmonary trunk and descending aorta • Common in preterm infants – 80% of infants less than 1200 grams • Blood flow through PDA commonly left to right (from the aorta to pulmonary artery) • 15% infants with PDA have additional cardiac defects

15. Surfactant treatment Perinatal asphyxia Excessive fluid treatment High altitude RDS requiringpip Congenital heart disease Genetic disposition Increased Incidence or Causes

17. Congestive heart failure due to left ventricle overload Widened pulse pressures Deterioration in ventilator status Cyanosis not present Audible murmur Peripheral pulses are bounding Signs and Symptoms of PDA

18. Medical Management • Asymptomatic • no treatment necessary • Monitor for congestive heart failure, failure to thrive, increasing O2 requirements

19. Medical Management • Symptomatic • Indomethacin - prostaglandin inhibitor • Side effects include transient oliguria, decreased platelet aggregation, risk GI bleed, risk IVH 2-3 hours after administration • NeoProfen – prostaglandin inhibitor • Same side effects as indomethacin but less severe • *Not compatible with TPN*

20. Surgical Management PDA Ligation • Closed heart surgery on the unit • Left lateral thoracotomy • Chest tube