The Child with a Cardiovascular Alteration Flashcards
Preload = volume of blood received by the heart.
Basically, preload is stretch. The amount of volume being returned to the heart.
Afterload = pressure or resistance the heart has to overcome to eject blood.
Afterload is squeeze. The amount of resistance that the heart has to overcome in order to eject blood.
?
Is the resistance the left ventricle must overcome to circulate blood.
Afterload
?
Is the volume of blood in ventricles at end of diastole (end diastolic pressure)
Preload
Prenatal Heart Circulation (Video)
https://www.stlouischildrens.org/health-resources/pulse/medical-animation-prenatal-heart-circulation
Congenital Heart Disease (CHD)
Classified according to structural abnormalities, functional alterations, or both
Subdivided into groups defined by blood flow patterns
> Increased pulmonary blood flow
> Normal to decreased pulmonary blood flow
> Obstructive lesions
> and other complex lesions
* Manifest during the newborn, infancy, or early childhood
* Degree of the symptoms = the need for medical, surgical, or transcatheter interventions
Important Terms
___ = abnormal blood flow from one part of the circulatory system to another
Can occur
> Abnormal opening or connection between cardiac chambers or great arteries
> Pressure increases on one side of the heart than the other side
> O2 saturation increases in blood flow that is normally desaturated or decreases in blood that is normally fully saturated
Shunt
___ or right side of the heart = a low/high (?) pressure and desaturated system @ 70%
___ or left side of the heart = a low/high (?) pressure and fully saturated system @ 95-98%
Venous; low
Arterial; high
Blood flow
* Amount of blood flow to lungs (pulmonary artery) = amount of blood flow to systemic circulation (aorta)
> Described as the pulmonary-to-systemic ratio QP/QS (ratio 1:1)
> CHD patients can have normal, increased, or decreased QP/QS blood flow ratios
Classification of Congenital Heart Disease (CHD)
Left-to-right shunting lesions (increase pulmonary blood flow)
* Defect in atrial septum or persistence of a patent ductus arteriosus (PDA)
* Saturated blood shunts from left-to-right → volume overload right side of the heart and pulmonary artery
* Cardiac workload ↑
* The abnormal increase in highly saturated blood along and the increased fluid volume in the lungs = ALTERED GAS EXCHANGE
* Major consequence of left-to-right shunting is HEART FAILURE
Examples
> ASD
> VSD
> PDA
> AVSD (endocardial cushion defect)
Obstructive or stenotic lesions (decrease cardiac outflow)
Stenosis = narrowing or constriction of an opening
* Can occur in a valve or a vessel - constricting or obstructing blood flow
* Pressure ↑ area behind the obstruction and blood flow distal to the obstruction ↓ or absent
* Stenotic lesions occur in the right or left side of the heart
* Obstruction on the left side of the heart ↓ amount of blood for systemic perfusion
* ↑ cardiac workload and ventricular strain
* Consequences: heart failure and ↓ cardiac output
Examples
> pulmonary stenosis
> aortic stenosis
> coarctation of the aorta
Cyanotic lesions with decreased pulmonary blood flow
* Problem in fetal development → hyperplasia or incomplete development, malalignment, or obstruction on the right side of the heart → decreased amount of blood flow to the lungs
* Left side of the heart low on oxygen saturation → hypoxemia, ↑ cardiac workload, and ventricular strain
* Manifestations
> Hypoxemia → cyanosis
> Upper respiratory infections
> Severely limited pulmonary blood flow
> Marked exercise intolerance
Examples
> Tetralogy of Fallot
> Tricuspid valve abnormalities
> Pulmonary atresia with intact ventricular system
Cyanotic lesions with increased pulmonary blood flow (mixing lesions)
* Fetal heart
> Fails to develop into separate pulmonary and systemic circulation
> Reversal of circulation = desaturated blood goes into systemic circulation and saturated blood goes into pulmonary circulation → cyanosis
* Cause increased cardiac workload, ventricular strain, and decreased cardiac output
Manifestations
- ruddy or cyanotic
- increased respiratory effort
- or systemic circulation is compromised - dusky or gray → cardiogenic shock
Examples
> truncus arteriosus
> hypoplastic left heart syndrome
> or transposition of the great arteries
Left-to-Right Shunt (Acyanotic)
↑ mixed blood flow; ↓ pulmonary blood flow
ASD
VSD
PDA
Coarctation of the aorta
Right-to-Left Shunt (Cyanotic) - Four T’s
↑ pulmonary blood flow; ↓ obstruction of blood from the ventricles
Tetralogy of Fallot
Truncus arteriosus
Transposition of the great vessels
Tricuspid atresia
Physiologic Consequences of CHD
Heart Failure (HF)
* Inability to circulate sufficient blood to maintain metabolic demands of the body
> Heart rate ↑ to increase the cardiac output
> Extra work → heart muscle to enlarge (hypertrophy) → enlarged heart - cardiomegaly
> Heart muscle walls - grow weak and inefficient → decreased blood volume → arteries constrict and force heart to work even harder
> Backup of blood flow → congestion in the body and lungs (pulmonary edema)
Etiology/Causes of heart failure (HF) in children
* Congenital cardiac defect
* Acquired heart disease
> cardiomyopathies
> dysrhythmias
> infections (such as endocarditis or myocarditis)
> tumors
Heart Failure - Manifestations
In infants
> Mild tachypnea at rest (70-100 breaths/min)
> Difficulty feeding (hungry and irritable soon after feeding)
> Failure to gain weight → failure to thrive
In older children
> Dyspnea w/exertion and tachypnea, orthopnea
> Diaphoresis, decreased appetite, chronic abdominal pain, failure to gain weight, jugular vein distention
* Cardiac rhythm gallop, periorbital and facial edema, hepatomegaly, splenomegaly, ↓ peripheral profusion, ↓ urine output, mottling, cyanosis, and pallor
* Watch for PULMONARY HYPERTENSION (PAH)
Heart Failure - Therapeutic Management
- ↓ cardiac workload and improving cardiac output
- Supplemental oxygen
Pharmacological agents
* Positive inotropes (digoxin), diuretics, angiotensin converting enzymes (ACE) inhibitors
Digoxin - cardiac glycoside
* Increases cardiac output and improves cardiac effectiveness
> Strengthens the force of myocardial contractions
> Slows the heart rate
> Improves blood flow to the kidneys and enhances diuresis
* Baseline ECG before initiating therapy
* Administered PO or IV
* Therapeutic serum drug level (0.8 - 2 ng/mL)
* Hypokalemia and hypomagnesemia increase risk for digoxin toxicity
Diuretics
* Eliminate excess water and sodium by increasing urine production → reducing systemic in pulmonary congestion
- Furosemide (loop diuretic)
- Thiazides less potent
- May lead to hypokalemia
- Potassium-sparing diuretics (spironolactone) may be used instead (! monitor K+ !)
Vasodilators - hydralazine
ACE inhibitors - captopril or enalapril
Feeding an infant or child with heart failure (HF)
* Relaxed environment
* Time feedings before other activities
* Frequent, small feedings less tiring
* Hold in an upright position - less stomach compression and improves respiratory effort
* May need nasal gastric or nasal duodenal feedings
* Assess for tachypnea, diaphoresis, feeding intolerance vomiting
* Increase caloric intake by concentrating formula 30 kcal/oz
Pulmonary Hypertension
* Elevated BP in lung blood vessels
* Diagnosed when mean pulmonary arterial pressure exceeds 25 mmHg at rest for children >3 mos age (normal at rest 15 mmHg)
Treatment
* Treating symptoms of HF
> Digitalis, calcium channel blockers, diuretics, warfarin, oxygen
> Avoid strenuous exercise and high altitudes
Cyanosis
* Cyanotic cardiac lesions lead to cyanosis
* Bluish discoloration of the skin, nailbeds, and mucous membranes
* Visible when unbound hemoglobin reaches 5 g/dL and O2 sat drops <85%
* Crying intensifies cyanosis and is not alleviated by the administration of 100% O2
Consequences of Cyanosis
* Polycythemia
* Anemia
* Clotting abnormalities
* Hypercyanotic episodes
* Central nervous system injury
* PAH
* Endocarditis
* Dehydration
* Hyperthermia
* Fever
* Poor oral intake
* Vomiting
* Diarrhea
Hypercyanotic episode (“tet spells”)
* Dramatic decrease in pulmonary blood flow → hypoxia & metabolic acidosis
* Episodes may last a few minutes to a few hours
* Manifestations
> Rapid and deep respirations, irritability and crying, peripheral vasodilation, increased systemic venous return, increasing cyanosis, decrease in systolic murmur, tachypnea, and hyperpnea
* Episode may be preceded by crying, feeding, or defecation
Treatment
* Calming the infant
* Placing the infant in the knee-chest position - ↑ systemic vascular resistance and force blood to pulmonary system
* Oxygen
* Morphine sulfate
* Phenylphedrine (vasoconstrictive)
* Propanolol
Cardiac Assessment of CHD
Health History
> Obtain data on maternal past history & prenatal care
> Obtain data on pregnancy, birth, and any birth defects or genetic anomalies
> Obtain data on feeding difficulties, weight gain, color changes with crying
Inspection
> Color of the skin, oral mucous membranes, nailbeds, conjunctiva
> Activity level while sitting and laying down
> Observe for color changes with activity, feeding, or crying
> Observe for exercise tolerance
> Observe chest movements for symmetry and chest shape
> Observe respiratory pattern
> Observe for signs of respiratory distress (tachypnea, retractions, nasal flaring, crackles, grunting, head bobbing)
Auscultation
> S1 and S2 heart sounds
> Assess for “gallops” - extra heart sound S3 or S4
> Assess for murmurs, clicks or precordial friction rubs
Palpation
> Compare temperature of torso with extremities
> Compare central and distal pulses
> Assess for capillary refill, PMI
> Assess for hepatomegaly - locate liver border
Cardiovascular Diagnostic Evaluation - Cardiac Catheterization
* Invasive procedure
* Catheter inserted via vein or artery (femoral or radial) directly into the heart
* Angiography - detailed images of structures and blood flow patterns
* Diagnostic, interventional, and therapeutic
> angioplasty
> pulmonary valvuloplasty
> aortic valve balloon angioplasty
> stent placements
> valve replacements
> closure of septal defects
Complications
* Dysrhythmias, hemorrhage, vascular damage
* Vasospasms of the catheterized vessel
* Thrombus or embolus formation, infection
* Reaction to the dye and catheter perforation
Cardiac Catheterization - Nursing Care
Prior to Cardiac Cath
* 12-lead EKG, chest x-ray, coagulation studies
* Locate and mark distal pulses
Post-Cardiac Cath
* Affected leg straight 4-6 hours
* Bed rest; IV fluid administration
* Vital signs; insertion site dressing observed every 5-15 minutes
* Assess for bleeding; check peripheral perfusion of the affected extremity
* Avoid strenuous exercise; return to school on 3rd day after procedure
* Notify physician for any S&S of infection
Acyanotic Congenital Heart Defects: L → R Shunts
* PDA, ASD, VSD, AVSD [endocardial cushion deficit]
↑ fatigue
Heart murmur
↑ risk endocarditis
CHF
Growth retardation
Patent Ductus Arteriosus (PDA)
- Left-to-right shunting lesion
* Failure of the fetal ductus arteriosus to completely close after birth
* Normally closes 24-72 hours after birth d/t ↓ prostaglandin levels and ↓ BP in ductus lumen
Manifestations
* Heart failure signs
* Continuous murmur
* Widened pulse pressure
* Bounding pulses
* Cardiomegaly
Therapeutic Management
* Treat heart failure
* Administer indomethacin (indocin)
* Monitor respiratory status, renal function, and growth
* Cardiac catheterization with coil placement
* Surgical management - ligation of the ductus
Atrial Septal Defect (ASD)
- Left-to-right shunting lesion
* Abnormal opening between the atria
* Right atrium is enlarged and pulmonary blood flow ↑
Manifestations
* May be asymptomatic
* Fatigue, dyspnea on exertion, palpitations, atrial dysrhythmias, recurrent respiratory infections, systolic murmur, mitral valve regurgitation, heart failure if not repaired
Ventricular Septal Defect (VSD)
- Left-to-right shunting lesion
* Abnormal opening between the ventricles
* Most common cardiac defect
* Increase pulmonary blood flow → pulmonary HTN → progressive pulmonary vascular disease
Manifestations
* May be asymptomatic
* Loud harsh systolic murmur, palpable thrill, diastolic murmur, and gallop
* Heart failure - moderate to large defect
Atrioventricular Septal Defect (AVSD) (Endocardial Cushion Deficit)
- Left-to-right shunting lesion
* Abnormal endocardial tissue development
- atrial and ventricular septum and mitral and tricuspid valves (AV valves)
* Usually associated with Down Syndrome
* May be partial or complete
Manifestations
* Heart failure
* Systolic pulmonary flow murmur
* Intermittent cyanosis
Pulmonary Stenosis
- Obstructive or stenotic lesion
* Narrowing of the entrance to the pulmonary artery
* Obstruction causes resistance to the blood flow at the right ventricular outflow track
> ↑ pressure in the right ventricle → right ventricular hypertrophy
> Blood may regurgitate into the right atrium
Manifestations
* May be asymptomatic
* Exercise intolerance
* Signs of right-sided heart failure
* Systolic murmur
* Cardiomegaly
* Severe cases cyanosis
Aortic Stenosis
- Obstructive or stenotic lesion
* Narrowing of the entrance to the aorta
* Difficult blood flow through aortic valve
> ↑ pressure and hypertrophy of the left ventricle, ↓ cardiac output, ↓ blood supply to the coronary arteries
Manifestations
Mild-to-moderate
> May be asymptomatic
> Exercise intolerance, cardiomegaly, systolic murmur
Severe
> Heart failure
> ↓ cardiac output with ↓ peripheral perfusion
> Chest pain, dizziness, syncope
Therapeutic Management
* Restriction from competitive sports
* Cardiac catheterization
> Aortic balloon valvuloplasty
* Surgical valvulotomy
* Aortic valve replacement
* Mechanical valve replacement requires warfarin
Coarctation of the Aorta (COA)
- Obstructive or stenotic lesion
* Aorta is constricted near the ductus arteriosus insertion site → may cause aortic valve stenosis → obstructs the left ventricle output
↓ blood supply to the abdominal organs and lower extremities
↑ left ventricular pressure - PULMONARY EDEMA
Tetralogy of Fallot - TOF or TET
- Cyanotic lesion with decreased pulmonary blood flow
* Most frequent cyanotic lesion
* Malalignment of the ventricular septum during fetal development
> VSD
> Right ventricular outflow tract obstruction (ex pulmonary stenosis)
> Overriding of the aorta
> Right ventricular hypertrophy
Manifestations
* If mild leads to “pink tet” with mild saturation changes
* Cyanosis, extreme fatigue, hypercyanotic episodes, chronic hypoxemia, systolic murmur, boot shaped heart on x-ray
Therapeutic Management
* Prostaglandins
* Cardiac catheterization
- Balloon atrial septostomy (create opening in septum)
- Catheter blader septostomy (cut septum tissue)
* Surgical management
Goal to separate the saturated and unsaturated blood
Three stage surgery
* Palliative systemic-to-pulmonic artery shunt
* Creation of a connection between the SVC and pulmonary arteries
* Modified Fontan procedure: connection created from the inferior vena cava to the pulmonary arteries
Truncus Arteriosus
- Cyanotic lesion with increased pulmonary blood flow
* Non-division of common great vessel (truncus arteriosus) into pulmonary artery and pulmonary valve and aorta and aortic valve during fetal development - results in a single vessel and valve → rise to pulmonary systemic and coronary circulations
Manifestations
- HF and cyanosis in neonates
- Systolic murmur with thrill
- Diastolic murmur of truncal valve insufficiency (bounding pulse and widened pulse pressure)
Therapeutic management
- ACE inhibitors and diuretics
- Polycythemia prevention
- Infection prevention (assess calcium and magnesium levels)
- Surgery
Transposition of the Great Arteries
- Cyanotic lesion with increased pulmonary blood flow
* Abnormal separation and rotation of the fetal common truncal vessel causes aorta to arise from the right ventricle and pulmonary artery to arise from left ventricle
* Associated VSD
Manifestations
- Cyanosis at birth
- Hypoxemia despite O2 delivery
- Progressive desaturation and acidosis, developing HF
Therapeutic management
- Emergency PGE infusion
- O2 administration
- Balloon atrial septostomy
- Arterial switch
- Complications include low cardiac output, dysrhythmias
Manifestations
- Fear, anorexia, nausea, fatigue, malaise, arthralgias, chest pain, heart failure, petechiae, neurological impairment due to embolus, heart murmur
Diagnostic evaluation
- Blood cultures
- Echocardiogram
- CBC, ESR, ECG, and rheumatoid factor (RF)
Therapeutic management
Fast pulse rate (tachydysrhythmias)
?
> __ is a narrow QRS tachycardia
> Rates between 220-300 bpm
> Vagal manuevers - to stop episodes of __
> Constant monitoring and emergency medical equipment should be available
> Antidysrhythmic drug therapy
> Adenosine
> Synchronized cardioversion
Supra ventricular tachycardia (SVT)
?
Wide complex tachycardia
Treatment for an unconscious child is synchronized cardioversion
Wide complex tachycardia and absent pulse = CPR
Ventricular tachycardia
?
* Autoimmune inflammatory condition
* Affects connective tissue
> Primarily heart, joints, subcutaneous tissues, brain, and blood vessels
> May lead to permanent damage of cardiac valves (mitral and aortic valve)
Causes
> Manifests 2-6 weeks after untreated group A beta-hemolytic streptococcal infection of the upper respiratory tract (strep throat)
Rheumatic fever
Kawasaki disease
- Mucocutaneous lymph node syndrome is an acute febrile exanthematous illness
- Immune response to an infectious or toxic trigger affecting medium-sized arteries (coronary arteries)
- T-lymphocytes and B-lymphocytes - infiltrate smooth muscle cells of vascular walls → edema and inflammation → weakens the vascular walls → leads to aneurysm → vascular walls thicken and scar
- Weakened vascular walls and increased platelets = formation of thrombus, myocardial infarction, and eventually death
Causes
> Unknown
Cardiomyopathies
- Disease of the heart muscle
Dilated
> Decreased contractility and dilation of ventricles without an increase in wall thickness - hypertrophy
Restrictive
> Impaired ventricular filling caused by infiltration of the muscle with abnormal material
> Ventricular size and contractility are normal
Hypertrophic cardiomyopathy (HCM)
- Hypertrophy of the ventricles = contractility is normal but ventricular filling is not due to ↑ stiffness of the ventricular walls
- Left ventricular outflow tract may be obstructed → sudden death
- S/S = dyspnea, chest pain with exertion, palpitations, syncope, systolic murmur
- Restrict from strenuous exertion and competitive sports
- Beta blockers or calcium channel blockers (verapamil)
- Surgery may be needed - septal myomectomy
