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