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Cardiac A & P Assessment. SOAR Session 4 Cathy Peterson, RN, BSN Clinical Educator NICU. Objectives. Describe basic cardiac anatomy Describe basic cardiac physiology Describe causes, pathophysiology, signs and symptoms, and management of CHF - PowerPoint PPT Presentation
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Cardiac A & P Assessment
SOAR Session 4
Cathy Peterson, RN, BSN
Clinical Educator NICU
Objectives• Describe basic cardiac anatomyDescribe basic cardiac anatomy• Describe basic cardiac physiologyDescribe basic cardiac physiology• Describe causes, pathophysiology, Describe causes, pathophysiology,
signs and symptoms, and signs and symptoms, and management of CHF management of CHF
• Describe causes, pathophysiology, Describe causes, pathophysiology, signs and symptoms, and signs and symptoms, and management of PDAmanagement of PDA
Cardiac Anatomy• Four chambersFour chambers
– R & L atriaR & L atria– R & L ventriclesR & L ventricles
• AortaAorta• Superior & Superior &
Inferior vena cavaInferior vena cava• Pulmonary veinPulmonary vein• Coronary arteriesCoronary arteries
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
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
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
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.
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.
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.
Pathopysiology of CHF
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.
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
Medical Management • Fluid/nutritional
support– Reduce
volume intake– Enhance
caloric content– IV infusions of
fat emulsion
• Pharmacologic– Digoxin
therapy– Diuretic
therapy– Edecrin– Diuril
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
Increased Incidence or Causes
• Surfactant treatment
• Perinatal asphyxia
• Excessive fluid treatment
• High altitude
• RDS requiringpip
• Congenital heart disease
• Genetic disposition
Signs and Symptoms of PDA• Congestive heart
failure due to left ventricle overload
• Widened pulse pressures
• Deterioration in ventilator status
• Cyanosis not present
• Audible murmur• Peripheral pulses
are bounding
Medical Management• Asymptomatic
• no treatment necessary– Monitor for congestive heart
failure, failure to thrive, increasing O2 requirements
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*
Surgical Management PDA Ligation
• Closed heart surgery on the unit
• Left lateral thoracotomy
• Chest tube
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