Cardiovascular Disorders

How is the normal flow of adult heart (in terms of stoke volume) differ from newborn?

• Adult heart flow output is influenced by heart rate x stroke volume

• Neonates no change in stroke volume poorly complient- tachycardia

What are the prenatal screenings for cardiac abnormalities?

• Genetics, echo, MRI → cardiac issues can be prenatally diagnosed

• Favorable to deliver in a tertiary setting

• Prepare parents

• APGAR maybe low

• Available staff and equipment

• Fetal electronic monitoring

What are the risk factors for congenital cardiac disease?

• Prenatal History

• Family history of cardiac disease

• Viral illness: Rubella, 5th disease, Coxsackie\

• Chronic medical conditions lupus and diabetes

• Advanced maternal age >40 years of age

• Intrauterine or perinatal hypoxia; PPH

• Teratogenic exposure

  • Alcohol, recreational drugs, prescription drugs dilantin, lithium, hormones

Fetal Circulation

• Umbilical vein, 2 umbilical arteries → the vein brings the oxygenated blood to the fetus and the arteries bring deoxygenated blood and metabolic waste to the placenta to be cleaned by mothers circulation

• Foramen Ovale: a small, flap-like opening in the wall (atrial septum) between the upper chambers of the heart alowing blood to flow stright from right artium to left atrium bypasing lungs.

• Ductus Artriosus: Connects the pulmonary artery to the aorta thus allowing blood to bypass lungs. Prostoglandins keep this open in utero which is why we give them to keep it open in certain situations.

• Ductus Venosus: , allowing oxygen- and nutrient-rich blood from the placenta to bypass the liver as placenta does that job in utero.

• Shift of gas exchange from placenta to lungs after birth

• At first breathe: pulmonary vessels dilate; decrease pulmonary vascular resistance; increase systemic vascular resistance changes blood flow → the left side is higher pressure which is why they right side is considered preductal so the stat prob is put there → thios is why the fetal mecanisms close in addition to decrease of prstaglandins.

What are the S&S of newborn cardiac dysfuction?

• Physical exam

  • Poor purfusion, resp or cardiac failure

    • VS, BP & pulses; differences between upper & lower extremities; por perfusion → tachy

    • Ascultation for murmurs

    • CCHD screening (critical congenital heart disease)

      • Pulse Ox

      • Comparison of pre ductul to post ductul >95% at 24 hrs after birth

What is the cardiac asessment?

• Health hx

• General apperance

• Physical examination

  • Ascultation for murmurs

  • Pulse strength → would have thready pulse

  • Cap refil → would be delayed

How are murmurs defined?

• Heart sounds that reflect flow of blood within the heart

  • May occur in systole or diastole, or both

  • Can occur in a normal heart in periods of stress; anemia, fever, or rapid growth

  • Can reflect abnormalities in heart or vessels

• “Inocent murmurs”= mornal cardiac anatomy and cardiac function

  • Occur in up to 50% of all children at some time

Cardiac diagnostic tests

• CXR→ may see enlargment heart (cardiomegaly); fluid in lungs

• ECG

• Echocardiogram; echo can check for heart strength & shows HF

• CT/MRI

• Exercise stress test

• Cardiac catherization: Good way of checking pressure in heart & getting idea of what’s actually hapening

What is the management if congenital cardiac heart disease (CCHD) is suspected?

• Provide 100% oxygen and other respiratory support as indicated

• Evaluate for physical and laboratory signs of shock

• Following this evaluation if cardiac disease is suspected

  • O2 saturation remains less than 75% give Prostaglandin

• Carefully evaluate the neonate for any other causes of cyanosis

  • Pulmonary, sepsis, shock, neurologic issues

What are the two types of heart defects?

• Congenital (CHD)

  • Anatomic → abnormal function

• Acquired

  • Disease process

    • Infection

    • Autoimmune response

    • Environmental factors

    • Familial tendencies

What are some facts about CHD?

• Incidence: 1 in 4 babies

• who will need surgery in the first year of life

  • Major cause of death in the first year of life (after prematurity)

  • Most common anomaly is VSD (ventricular septum defect)

  • 30% of children with CHD have a genetic syndrome

    • Examples: Down syndrome, Turner syndrome, 22q11 deletion syndrome, Williams syndrome, and Noonan syndrome

What are the types of cardiac defects (acyanotic; cyanotic)

• Acyanotic (O2 not affected)

  • Increased pulmonary flow

    • Atrial septal defect (ASD)

    • Ventricular Septal defect (VSD)

    • Patent ductus arteriosus (PDA)

  • Obstructive defects

    • Coarctation of the aorta

• Cyanotic (O2 is affected)

  • Decreased pulmonary flow

    • Tetralogy of Fallot

  • Mixed defects

    • Transportation of great vessels; two seperate circuits

      • Oxygen-poor blood returning from the body is pumped right back out to the body without picking up oxygen in the lungs. Oxygen-rich blood from the lungs just goes back to the lungs

What are the things that cause increased pulmonary blood flow defects (PDA, ASD, VSD)? (plus what does this mean in terms of curculation)

• Abnormal connection between two sides of heart

  • Either the septum or the great vessels

• Increased blood volume on right side of heart

• Increased pulmonary blood flow

• Decreased sytemic blood flow

What is Patent Ductus Arteriosus (PDA)?

• Fetal shut fails to close

• More common among premature infants → bc heart muscle is not strong enough to cause it to shut

• Allows blood to flow from the aorta (area of high pressure) through the PDA and into the main pulmonary artery (area of low pressure)

  • Can lead to pulmonary hemmorhage

• Blood floods the lungs and go back into left artium via pulmonary veins

• A occusion device may be used to close this opening via cathater

What is Atrial Septal Defect (ASD)?

• Occurs when a portion of the atrial septal tissue does not completely form

• Blood flows from the higher pressure in the left atrium to the lower pressure in the right atrium → blood flow goes back to RA leading to RA hypertension

• Many times, no murmur is noted due to low atrial pressure

• Leads to pulmonary overcirculation

• Less likely to cause HF

What is Ventricular Septal Defect (VSD)?

• Most common congenital defect in newborns

• VSD is part of other diagnoses

• Happens when a portion of the ventricular septum does not completely close

• Blood flows from the left side (high pressure) to the right side (lower pressure)

• Most close on their own, but some need surgical closure due to heart failure

• Confirmed by echo, treated with diuretics and increased calories to prevent FTT (failure to thrive)

• Would have RV hypertrophy; backs into lungs → pulmonary edema

Tetrology of Fallot (4 components, management)

• 4 Components

  • RV outflow tract obstruction r/t pulmonary stenosis

  • VSD

  • Overriding Aorta (PDA)

  • RV Hypertrophy

• Pulmonary artery gets the extra blood flow → lungs get beat up

• Aorta gets least oxygenated blood

• Aorta gets the least oxygenated blood

• Tet Spells:shuts down ability to get blood to lungs b/c RV tract gets closed when child gets upset

  • Spasm below the pulmonary valve…

  • Increases resistance to blood flow

  • Increased (deoxygenated) blood shunts from right to left across the VSD, causing a cyanotic spell

• Treatment of Tet spell

  • Knees to chest / O₂ / sedation = increased systemic vascular resistance, and O₂ dilates the pulmonary bed'

  • *Pushes blood back through the pulmonic valve

Heart Failure (presentation in children, clinical manifestations)

• The inability of the heart to supply adequate oxygenated blood to meet the metabolic demands of the body

• Cardiac output: volume of blood pumped by ventricles each minute

• Preload: volume of blood in the ventricle at the point just before contraction → Lasix helps with preload (offloads fluid)

• Contractility: the rate and force of fiber shortening → digoxin increases contractility

• Afterload: amount of resistance met by the ventricles upon ejection

• Volume overload

• Pressure overload

• Decreased contractility

• High cardiac output demands

• Pathophysiology

  • Right-sided failure

    • Reduced function

    • Back up to body would see ascites (liver would move down bc of excess fluid back up)

  • Left-sided failure

    • Increased pressure; lung congestion

• Tachypnea & hypoxia are first

• Clinical manifestations

  • Impaired myocardial function

    • Tachycardia; fatigue; weakness; restlessness; pale, cool extremities; decreased BP; decreased urine output

      • Poor feeding, decreased UO meand blood is not getting to kidney → if at RR of like 100 means something is wrong

  • Pulmonary congestion

    • Tachypnea, dyspnea, respiratory distress, exercise intolerance, cyanosis

  • Systemic venous congestion

    • Peripheral and periorbital edema, weight gain, ascites, hepatomegaly, neck vein distention

What are the goals of management in children?

• Improve cardiac function

• Decrease preload — how? → diuretics

• Decrease cardiac demands

• Improve tissue oxygenation → w/ O2

• Decrease oxygen consumption

• VAD; Ventricular Assist Device- allow for blood flow to be perserved while waiting for heart

Transposition of the Great Arteries (TGA) ( clinical presentation/management)

• Cyanotic defect

• Second most common congenital defect

• ”reversal of the great arteries”

• Aorta arises from the RV

• Pulmonary artery arises from the LV

• 2 separate circulations

  • Oxygenated blood returns from the lungs to the LA, goes to the LV and goes back through the PA and to the lungs again

  • Deoxygenated blood returns from the body to the RA, to the RV and back out the aorta providing deoxygenated blood to the systemic circulation

• Infant typically tachypneic

• Prostaglandin (PGE) needed to maintain PDA and ”mix” blood→ relaxes muscle to allow for oxygenation to still occur

  • S/E: It vasodilates as a result facial flushing can occur but the s/e are Apnea and hypotension

• Complications of PGE: apnea, hyperthermia

• Balloon septostomy will allow mixing through ASD/PFO → Surgical Plan: “Arterial Switch”

• Surgically corrected within first 14days of life

Hypoxemia

• Hypoxemia

  • Lower than normal arterial oxygen tension

• Hypoxia

  • Reduction in tissue oxygenation

• Cyanosis

• Clinical manifestations

  • Polycythemia

  • Clubbing

  • Hyper-cyanotic spells (TET spells)

Coarctation of the Aorta (Diagnosis & Management)

• Narrowing anywhere in the aorta

• Increased pressure proximal to the defect

• Restricts amount of oxygenated blood to lower part

• LV has to work harder= LV hypertrophy

• Infancy diagnosis most commonly an emergency

• Kidney would not get blood flow, lactate acidosis, hypoxia

• If you have PDA may be able to get blood flow

• Diagnosis & Management

  • ECHO

  • 4 point BP’s (gradient >10points) → BP in arms would be high & in legs would be low

  • Bloodwork (lactate)

  • PGE initiation immediately will open PDA

  • Balloon/ Stent/ Surgical correction

  • CCHD screening for prevention

Kawasaki disease (Etiology, management)

• Leading cause of acquired heart disease

• Acute systemic vasculitis, unknown cause

• Duration 6 to 8 weeks, self-limiting

• Without treatment of KD, 20%-25% have cardiac complications

• Dilation of coronary arteries Coronary artery aneurysms (giant aneurysms >8 mm)

• Acute (WEEK 1), subacute (WEEK 2+3)

• TREATMENT WITH IVIG

• Etiology

  • Etiology unconfirmed

  • Peak incidence in toddler ages

  • Seasonal variations (late winter/early spring)

  • Widespread inflammation of small and medium- size arteries

• Clinical Manifestations

  • High fever—unresponsive to antipyretics/ antibiotics

  • “Strawberry” tongue

  • Edema hands and feet

  • Extreme irritability (inconsolability) desquamation (SKIN SLOUGH)

  • Arthritis (JOINT PAIN)

  • Coronary complications

Rheumatic fever & Rheumatic heart disease manifestations

• Inflammatory disease occurs after strep infection

• Infrequently seen in United States; big problem in Third World

• Self-limiting

• Affects joints, skin, brain, serous surfaces, and heart

• Most common complication of RF

• Damage to valves as result of RF

• Clinical manifestations

  • Carditis—affects muscle layers of heart and most commonly the mitral valve

  • Polyarthritis—reversible affecting large joints of the body

  • Erythema; Transitory rash on trunk and proximal extremities

What is the care of the family and child with congenital heart disease?

• Help family adjust to the disorder

• Educate family

• Help family cope with effects of the disorder

• Prepare child and family for surgery

• Surgical interventions:

  • Open heart

  • Closed heart procedures

  • Staged procedures

  • Prepare child and family for procedures

Cardiac catherization (pre and post op)

• Preprocedural care

  • Preparation/explanation geared toward developmental level

  • Perform a nursing history and physical exam

  • Check for allergies

  • Locate and mark dorsalis pedis and posterior tibial pulses

  • Sedation management

  • NPO

• Postprocedural care

  • Cardiac and pulse oximetry monitoring

  • Vital signs X 15 min

  • Assess puncture site for bleeding or

  • hematoma

  • Monitor pulses, temperature, color of extremity → ensure cap refill & pedal pulses are intact

  • I/O

  • Parent teaching

What is the postop care for child for correction of cardiac issues?

• Monitor vital signs and arterial/venous pressures

• Intra-arterial monitoring of BP

• Intracardiac monitoring

• Respiratory needs

• Rest, comfort, and pain management

• Fluid management

• Progression of activity

How should fluid status be monitered post cardiac procedure?

• Intake

  • From all sources

  • All flushes, other intake

• Output

  • From all sources

    • Chest tube, urine, NG, surgical drains; also include blood drawn for lab work

  • Urine output <1 ml/kg/hr = possible renal failure

    • Concern r/t decreased cardiac output

What are the pharmacological approach with cardic disorders?

• IV IgG → support immune

• Digoxin (Lanoxin)—improve contractility

• ACE inhibitors—reduce afterload

• ASA, NSAIDs

• Lasix—loop diuretic—causes diuresis—monitor potassium

• Spironolactone (Aldactone) —K+ sparing diuretic

How are chest tubes monitored after cardiac surgery?

• Monitor chest tube drainage q hour for COLOR

• Immediate postoperative may be bright red, but changing to serous

• Monitor chest tube drainage for quantity

• Notify surgeon if chest tube drainage is frank blood or increases

• Be alert for cardiac tamponade (rapid onset; life threatening)

What are the postop complications after cardiac surgery?

• CHF

• Dysrhythmias

  • Sinus Bradycardia

  • Sinus Tachycardia

  • Supraventricular Tachycardia

  • Lethal Dysrhythmias

    • Ventricular tachycardia

    • Ventricular Fibrillation

• Decreased cardiac output syndrome

• Decreased peripheral perfusion

• Pulmonary changes

• Neurologic changes

Cardiac transplant

• Most common need for transplant related to CHD and Cardiomyopathy

• Not an easy decision

• VAD’s and ECMO as bridge

• Survival improved

  • If transplanted before 10yr of age= 83% survival

  • Immunosuppressants for life

Systemic HTN

• Primary = no known cause

• Secondary = identifiable cause

• Pediatrics: HTN is generally secondary to a structural abnormality or underlying pathology

  • Renal disease

  • CV disease

  • Endocrine or neurologic disorders

Dyslipidemia

• Identify children at risk and treat early

• Treatment = dietary

  • Restrict intake of cholesterol and fats

• If no response to diet → Rx

  • Colestipol (Colestid)

  • Cholestyramine (Questran)