ccrn/ccrn k certification review course: … nursing actions ... heart disease ... hypoplastic left...

Neonatal CCRN/CCRN‐K Certification Review Course:

Cardiovascular

Nancy McNeillRNC‐NIC, MSN, CNS, CPNP

12/2015

Cardiovascular 1

Testable Nursing Actions

Apply leads for cardiac monitoring

Identify, interpret, and monitor cardiac rhythms

Monitor hemodynamic status and recognize signs and symptoms of hemodynamic instability

Recognize normal fetal circulation and transition to extrauterine life

Recognize indications for and manage patients requiring

12‐lead ECG

Arterial catheter

Cardiac catheterization

Cardioversion

Central venous pressure monitoring

Invasive hemodynamic monitoring

Umbilical catheter

Fetal Circulation

12/2015

Cardiovascular 2

Transitional Circulation

Closing of fetal shunts

Once the baby is delivered: The placenta no longer oxygenates the blood

The lungs facilitate gas exchange in the infant

Newborn Circulation

12/2015

Cardiovascular 3

Cardiac Output

Volume of blood ejected by the heart in 1 minute

Normal 120–200 mL/kg/min

CO=SV x HR

Preload

Volume of blood in ventricles before the heart contracts

Delayed cord clamping

12/2015

Cardiovascular 4

Afterload

The resistance of blood leaving the ventricle

Afterload is dependent on systemic vascular resistance and pulmonary vascular resistance

Shock

Hypovolemic

Distributive

Cardiogenic

12/2015

Cardiovascular 5

Most Common Dysrhythmias

Sinus tachycardia

Sinus bradycardia

Supraventricular tachycardia

Complete heart block

Atrial flutter

Hyperkalemia

Placement of Cardiac Leads

Lead 1 is best lead for changes in P waves

Pilcher J. Pocket Guide to Neonatal EKG Interpretation.NICU INK Book Publishers; 2004.

12/2015

Cardiovascular 6

Sinus Tachycardia

HR=180–220

Brief episodes can be normal

Common causes: Hypovolemia

Hyperthermia

Pain

Infection

Shock

Hydrops


No treatment if the condition is transient

Treat the underlying cause of shock or respiratory failure

Sinus Tachycardia Treatment

12/2015

Cardiovascular 7

Sinus Bradycardia

HR <90

Responsible for 30% of arrhythmias in infants

Most common in premature infants

Common causes: Immaturity of central nervous system

Vagal stimulation

Apnea

Medication

Heart disease

Sinus node disease

Srinivasan S, et al. HHS Public Access. Accessed June 19, 2015.

Sinus Bradycardia


12/2015

Cardiovascular 8

Important to assess infant’s respiratory status

Stimulate or provide respiratory support

If bradycardia continues, begin resuscitation based on NRPguidelines

Bradycardia is most often the result of hypoxia causing a depression of the myocardium or slowing of the heart rate

Sinus Bradycardia Treatment

HR >220

Most common dysrhythmia in newborns Occurs in 1.5–4/1,000 neonates

Causes Cardiac defects

Wolff‐Parkinson‐White Syndrome

Myocarditis

Supraventricular Tachycardia

Cloherty JP, et al. Manual of Neonatal Care.Moak JP. Prog Pediatr Cardiol. 2000;11(1):25–38.

Pilcher J. Pocket Guide to Neonatal EKG Interpretation. NICU INK Book Publishers; 2004.

12/2015

Cardiovascular 9

Supraventricular Tachycardia Treatment

Determine stable vs unstable supraventricular tachycardia (SVT)

If stable, consider vagal maneuver and/or adenosine

If unstable or vagal maneuver unsuccessful, treat with adenosine, propranolol, procainamide, or amiodarone

Infants who are in shock or congestive heart failure need rapid treatment of SVT IV adenosine if IV access

Synchronized cardioversion

Complete Heart Block

1 in 22,000 births

Mothers with lupus

Complete blockage of impulse between atria and ventricles

Friedman D, et al. Images Paediatr Cardiol. 2003;5(3):36–48.Pilcher J. Pocket Guide to Neonatal EKG Interpretation.

NICU INK Book Publishers; 2004.

12/2015

Cardiovascular 10


Causes

Infections

Congenital heart defects

Myocarditis

Trauma

Lupus

Genetic


Treatment Temporary or permanent pacing

Isoproterenol

12/2015

Cardiovascular 11

Atrial Flutter

Sawtooth appearance on EKG

Causes Damage to sinus node

Congenital heart disease

Cardiac catheterization

Digoxin toxicity

Occurs most often in structurally normal heart


Atrial Flutter

Treatment Digoxin

Propranolol

If unstable, then cardioversion

12/2015

Cardiovascular 12

Hyperkalemia

Serum potassium >6.5 meq/L

Causes Hemorrhage

Bruising

Prematurity

Acidosis

Renal failure

Verklan MT, et al. Core Curriculum for Neonatal IntensiveCare Nursing. Elsevier Saunders; 2015.

Hyperkalemia

Causes tall tented T wave and disappearance of P wave and widening of the QRS This is abnormal conduction through the ventricle

Appears like v tach but is NOT

Treatment Diuretic depletes potassium; secretion of potassium from urine

IV calcium

Glucose/insulin infusion to push potassium into cell

Sodium bicarbonate to correct acidosis

Albuterol pushes potassium into cell

Sodium polystyrene sulfonate (Kayexalate) removes potassium

CARDIOVERSION DOES NOT WORK

Merenstein GB, et al. Handbook of Neonatal Intensive Care.Mosby; 2011.

12/2015

Cardiovascular 13

Cardiac Defects

Cyanotic Tetralogy of Fallot (TOF)

Transposition of the greater arteries (TGA) or vessels (TGV)

Truncus arteriosus

Tricuspid Atresia

Hypoplastic Left Heart Syndrome (HLHS)

Acyanotic Patent ductus arteriosus (PDA)

Atrial septal defect (ASD)

Ventricular septal defect (VSD)

Atrioventricular canal (AVC)

Pulmonic stenosis (PS)

Aortic stenosis (AS)

Coarctation of the aorta

Cardiac Defects

12/2015

Cardiovascular 14

Tetralogy of Fallot

1 in 5,000 live births

Accounts for 10% of all

defects

Combination of four defects: Pulmonary stenosis

VSD

Overriding aorta

Right ventricular hypertrophy

Centers for Disease Control and Prevention. Accessed June 19, 2015.

Tetralogy of Fallot

Presentation depends on the degree of pulmonary stenosis (pink TOF vs blue TOF)

Cyanosis, hypoxia, and dyspnea present with severe obstruction

Tachypneic

Murmur detected

CXR will show a “boot‐shaped heart”

12/2015

Cardiovascular 15

Tetralogy of Fallot

Treatment Propranolol

PGE1 infusion to maintain duct patency

Careful use of oxygen therapy

Blalock‐Taussig procedure—palliative surgery

Corrective surgery Prognosis is poor without surgery

Verklan MT, et al. Core Curriculum for Neonatal IntensiveCare Nursing. Elsevier Saunders; 2015.

Occurs in 1 per 5,000 births

(predominantly male)

Most common cause of cyanosis

Position of the main arteries is reversed

Ductal dependent defect

Diagnosis usually made within the first week of life


Transposition of the Greater Arteries or Vessels

12/2015

Cardiovascular 16


Cyanosis is present and becomes more prevalent

No murmur unless VSD is present

CXR may show “egg on a string” appearance

Echocardiogram is the standard diagnostic tool

This is a cardiac emergency


Treatment/management

Correction on metabolic acidosis

Prostaglandin (PGE1) to maintain duct patency (mixing)

Balloon septostomy

Blade septostomy

Pulmonary artery banding

Corrective surgery Arterial switch operation (Dr. Jatene and Dr. Yacoub)

Mustard and Senning procedure

Rastelli procedure

12/2015

Cardiovascular 17

Truncus Arteriosus

1 per 33,000 births

Artery arises from both ventricles and overrides VSD

Three types Type I: Most common; short pulmonary artery from base of the trunk which divides to the right and left arteries

Type II: The left and right pulmonary arteries arise from the posterior side of the trunk

Type III: The right and left pulmonary arteries arise from different origins of the lateral side of the trunk


Truncus Arteriosus

Clinical manifestations Bounding pulses

Widened pulse pressure

Signs and symptoms of CHF

Harsh murmur

CXR will show cardiomegaly and pulmonary markings

Echocardiogram and Doppler are the standard diagnostic tools

12/2015

Cardiovascular 18

Truncus Arteriosus

Treatment

Manage CHF Diuretics

Digoxin

ACE inhibitors

Surgical repair Homograft

Patch to close VSD

Separation of the arteries from the trunk

Tricuspid Atresia

1 per 18,000 live births

Failure of the development of the tricuspid valve

Associated with a PFO or VSD

Pulmonary stenosis or atresia may also be present


12/2015

Cardiovascular 19

Tricuspid Atresia

Clinical manifestations

Cyanosis

Dyspnea

CHF

Murmur if associated with VSD, PDA, or stenosis

Tricuspid Atresia

Management Balloon septostomy to improve mixing of blood

Oxygen

Bicarbonate

PGE1

Blalock‐Taussig procedure


Fontan or modified Fontan procedure

Bidirectional Glenn procedure on or off bypass

12/2015

Cardiovascular 20

Hypoplastic Left Heart Syndrome

2–2.6 per 10,000 births

Obstruction of blood to left side of the heart

Hypoplastic left ventricle

Absent or small mitral valve

Absent or small aortic valve

Ascending aorta is small

May have ASD

Pulmonary congestion and edema



Clinical manifestations Tachypnea

Dyspnea

CHF

Become rapidly ill as the PDA begins to close Mottling

Gray pallor

Diminishing pulses

Shock

CXR will show cardiomegaly

Echocardiogram done to diagnose; detected prenatally

12/2015

Cardiovascular 21


Management/treatment

Initial Management includes:

PGE1

Managing acidosis

Sedation

Balloon septostomy

Ventilation management

Staged surgical repair (Norwood 3–5 years to complete)

Cardiac transplant

Acyanotic

12/2015

Cardiovascular 22

Patent Ductus Arteriosus

Fourth most common cardiac lesion

8 of 1,000 premature births, 2 of 1,000 full term births

Persistent patency of the duct or failure of it to close

Prostaglandins inhibit the closure of this duct

Maintains fetal circulation in utero and meant to close after birth

National Heart, Blood, and Lung Institute. Accessed June 19, 2015.


Clinical manifestations Cardiomegaly

Bounding peripheral pulses

Widening pulse pressure

Low diastolic blood pressure

Metabolic acidosis

Continuous murmur may be auscultated in upper left sternal border

12/2015

Cardiovascular 23


Echocardiograph is the gold standard for diagnosis

B‐type natriuretic peptide levels of 70–100 pg/mL can be used to identify a PDA


Treatment/management Fluid restriction

Diuretics

Ventilation therapy

NSAIDs (indomethacin and ibuprofen)

Surgical management (ligation)

12/2015

Cardiovascular 24


Lipooxygenasepathway

Leukotrienes

Cyclooxygenasepathway

Prostaglandins

Cyclooxygenase inhibitors

Indomethacin (NeoProfen)

Prostaglandin synthase inhibitors

Arachidonic Acid Pathways

Atrial Septal Defect

1 per 5,000 births

More common in females

Defect in the formation of the

septum or patent foramen ovale

Usually asymptomatic

Systolic murmur may be detectable

Failure to thrive

Recurrent respiratory infections may occur


12/2015

Cardiovascular 25

Atrial Septal Defect

Defect may close on its own

Manage CHF if present

Surgical repair

Transcatheter closure

Ventricular Septal Defect

2 per 1,000 births

Most common of all defects (about 50%)

Abnormal opening of the septum between the right and left ventricle

Centers for Disease Control and Prevention. Accessed June 19, 2015.Reller MD, et al. J Pediatr. 2008;153(6):807–813.

12/2015

Cardiovascular 26


Clinical manifestations

Small VSD Asymptomatic with a murmur

Moderate VSD Asymptomatic with a murmur, fatigue, and respiratory infections

Large VSD Signs and symptoms of CHF

Loud murmur

Cardiomegaly on CXR

Echocardiograph done to diagnose


Treatment 50%–75% of small VSD will close spontaneously (muscular)

Surgical banding of pulmonary artery

Surgical suturing of defect

Surgical patching of defect

Transcatheter device

Prognosis is excellent

Topol EJ, ed. Textbook of Cardiovascular Medicine. Lippincott Williams & Wilkins; 2007.

12/2015

Cardiovascular 27

Atrioventricular Canal

Also known as endocardial cushion defect

1 per 9,000 births

Common in Down syndrome

Craig B. Heart. 2006;92(12):1879 – 1885.

National Institutes of Health. Accessed June 19, 2015.

Clinical manifestations Respiratory distress

Active precordium

Murmur

Respiratory infections



12/2015

Cardiovascular 28

Treatment

Treat CHF with digoxin and diuretics


Primary repair closure


1 in every 14,000 live births

Narrowing in or below the pulmonary valve

Depending on the degree of stenosis, may be ductal‐dependent or ductal‐independent

Murmur

Hepatomegaly


Echocardiography is used to diagnose

Pulmonic Stenosis

American Heart Association. Accessed June 19, 2015.

12/2015

Cardiovascular 29

Pulmonic Stenosis

Treatment:

Oxygen, bicarbonate, PGE1

Balloon valvuloplasty

Surgical valvotomy if valvuloplasty is not effective

Aortic Stenosis

1 in 24,000 births

More likely in males

Anatomy includes: Valvular (most common)

Subvalvular

Supravalvular (least common)

Increased left ventricular pressure

Excess blood to the lungs

Sadowski SL. Crit Care Nurs Clin North Am. 2009;21(1):37–48.


12/2015

Cardiovascular 30

Aortic Stenosis

Clinical findings

Asymptomatic at birth

Murmur detected

Congestive heart failure symptoms


Aortic Stenosis

Treatment Acidosis management and fluid restriction

If critical, use PGE1

Balloon valvuloplasty

Valvotomy or valve replacement

Ross‐Konno procedure

12/2015

Cardiovascular 31

Coarctation of the Aorta

Accounts for 7% of cardiac lesions

More common in males

Most common form is juxtaductal

Common in Turner syndrome

Constriction of the aorta

Kenny D, et al. Cardiol J. 2011:18(5):487–495.



Congestive heart failure due to high afterload

Pulses decreased or absent in the lower extremities

Blood pressure higher in upper extremities

CXR will show enlarged heart and pulmonary vascular markings

Echocardiogram is the standard tool to detect, but cannot rule out coarctation in patients with PDA

MRI can determine location of coarctation

12/2015

Cardiovascular 32


Treatment

CHF management

PGE1

Palliative balloon angioplasty to open narrowing

Stent placement

Surgical correction (resection, reanastomosis, or patch)

Vascular Rings and Slings

Occur secondary to abnormal development of aortic arch

Can cause compression to the trachea and esophagus

Symptoms include respiratory distress and stridor

The Children’s Hospital of Philadelphia. Accessed June 19, 2015.

12/2015

Cardiovascular 33

Management After Cardiac Surgery

Noninvasive monitoring

ECG

Blood pressure

Continuous pulse oximetry

Urine output

Cerebral near‐infrared spectroscopy

Management After Cardiac Surgery

Invasive monitoring Arterial pressures

Right‐sided cardiac pressures

Pulmonary artery pressure

Left‐sided cardiac pressure

Epicardial pacing

Hemodynamic monitoring

12/2015

Cardiovascular 34

Review Questions

A. SVT

B. Complete heart block

C. Junctional ectopic tachycardia

D. Hyperkalemia

Question 1

What is the most common neonatal dysrhythmia?

12/2015

Cardiovascular 35

Question 1—Rationale

A. SVT—This is the most common neonatal dysrhythmia

Complete heart block—Typically associated with lupus, which isn’t very common

Junctional ectopic tachycardia—Typically occurs in neonates after cardiac repair, not the most common

Hyperkalemia—Usually found in premature babies who are critically ill and acidotic. This is a unique situation

What is the most common neonatal dysrhythmia?

A. Hypoxia

B. Pain

C. Fever

D. NICU admission

Question 2

The most common cause of bradycardia in the newborn population is:

12/2015

Cardiovascular 36


A. Hypoxia—The most common cause of bradycardia in a newborn. Most infants have bradycardia for the same reasons they have apnea; often, bradycardia results from the baby having apnea. Apnea is defined as a pause >15–20 seconds in a baby’s regular breathing

Pain—A sympathetic response which causes heart rate acceleration

Fever—A sympathetic response which causes heart rate acceleration

Hypercapnia—May be responsible for tachypnea but not bradycardia

The most common cause of bradycardia in the newborn population is:

A. Placenta

B. Heart

C. Lung

D. Kidney

Question 3

The organ responsible for gas exchange in utero is the:

12/2015

Cardiovascular 37


A. Placenta—The placenta is responsible for all gas exchange in utero

Heart—Not responsible for gas exchange; responsible for pumping blood around in utero

Lung—Once baby is born, the lung is responsible; only function in utero is to practice breathing and to grow

Kidney—Function of the kidney in utero is to produce amniotic fluid

The organ responsible for gas exchange in utero is the:

A. Ductus arteriosus

B. Foramen ovale

C. Ductus venosus

D. VSD

Question 4

The fetal vessel connecting the pulmonary artery to the descending aorta is:

12/2015

Cardiovascular 38


A. Ductus arteriosus—A short vessel that shunts blood from the pulmonary artery directly to the ascending aorta, bypassing the lungs, before birth

Foramen ovale—The connection at the atrial septum opening; it connects the left atria to the right atria

Ductus venosus—The fetal vein that passes through the liver to the inferior vena cava

VSD—Early opening in the embryologic heart. The VSD is a hole in the wall separating the two lower chambers of the heart

The fetal vessel connecting the pulmonary artery to the descending aorta is:

A. Resuscitation equipment

B. Cooling mattress

C. Inotropes

D. Chest tube

Question 5

Your patient in the NICU has cyanotic heart disease and was started on PGE. The most important thing for the nurse to have available at the bedside is:

12/2015

Cardiovascular 39


A. Resuscitation equipment—bag valve mask. The nurse should be prepared to treat the apnea that may occur as a side effect of administering PGE

Cooling mattress—An infant may become flush and have a fever from administration of PGE, but placing a cooling mattress is not the treatment of choice for this symptom and is not the most important intervention

Inotropes—PGE administration does not cause hypotension

Chest tube—PGE is not known to cause air leaks

Your patient in the NICU has cyanotic heart disease and was started on PGE. The most important thing for the nurse to have available at the bedside is:

References

American Heart Association. Aortic valve stenosis (AVS). Available at: American Heart Association. Available at: http://www.heart.org/HEARTORG/Conditions/CongenitalHeartDefects/AboutCongenital

HeartDefects/Aortic‐Valve‐Stenosis‐AVS_UCM_307020_Article.jsp. Accessed June 19, 2015.

American Heart Association. Pulmonary valve stenosis. Available at: http://www.heart.org/HEARTORG/Conditions/CongenitalHeartDefects/AboutCongenitalHeartDefects/Pulmonary‐Valve‐Stenosis_UCM_307034_Article.jsp. Accessed June 17, 2015.

Centers for Disease Control and Prevention. Available at: http://www.cdc.gov. Accessed June 17, 2015.

Centers for Disease Control and Prevention. Facts about atrial septal defects. Available at: http://www.cdc.gov/ncbddd/heartdefects/atrialseptaldefect.html. Accessed June 19, 2015.

Centers for Disease Control and Prevention. Facts about coarctation of the aorta. Available at: http://www.cdc.gov/ncbddd/heartdefects/coarctationofaorta.html. Accessed June 19, 2015.

Centers for Disease Control and Prevention. Facts about hypoplastic left heart syndrome. Available at: http://www.cdc.gov/ncbddd/heartdefects/hlhs.html. Accessed June 19, 2015.

Centers for Disease Control and Prevention. Facts about dextro‐transposition of the great arteries (d‐TGA). Available at: http://www.cdc.gov/ncbddd/heartdefects/d‐tga.html. Accessed June 19, 2015.

12/2015

Cardiovascular 40

References

Centers for Disease Control and Prevention. Facts about triscupid atresia. Available at: http://www.cdc.gov/ncbddd/heartdefects/tricuspid‐atresia.html. Accessed June 19, 2015.

Centers for Disease Control and Prevention. Facts about truncus arteriosus. Available at: http://www.cdc.gov/ncbddd/heartdefects/truncusarteriosus.html. Accessed June 19, 2015.

Cloherty JP, Eichenwald EC, Hansen AR, Stark AR, eds. Manual of Neonatal Care. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2012.

Craig B. Atrioventricular septal defect: from fetus to adult. Heart. 2006;92(12):1879–1885.

Friedman D, Duncanson L, Glickstein J, Buyon J. A review of congenital heart block. Images Paediatr Cardiol. 2003;5(3):36–48.

Kenny D, Hijazi ZM. Coarctation of the aorta: from fetal life to adulthood. Cardiol J. 2011;18(5):487–495.

Klabunde RE. Cardiovascular Physiology Concepts. 2nd ed. Baltimore, MD: Lippincott Williams & Wilkins; 2011.

Martin RJ, Fanaroff AA, Walch MC. Fanaroff and Martin’s Neonatal‐Perinatal Medicine. 10th ed. Philadelphia, PA: Elsevier Inc.; 2015.

Merenstein GB, Gardner SL, eds. Handbook of Neonatal Intensive Care. 7th ed. St. Louis, MO: Mosby; 2011.

References

Moak JP. Supraventricular tachycardia in the neonate and infant. Prog Pediatr Cardiol. 2000;11(1):25–38.

National Heart, Blood, and Lung Institute. What is patent ductus arteriosus? Available at: http://www.nhlbi.nih.gov/health/health‐topics/topics/pda/. Accessed June 19, 2015.

National Institutes of Health. Atrioventricular canal (endocardial cushion defect). Available at: http://www.nlm.nih.gov/medlineplus/ency/imagepages/19877.htm. Accessed June 19, 2015.

Pilcher J. Pocket Guide to Neonatal EKG Interpretation. 2nd ed. Petaluma, CA: NICU INK Book Publishers; 2004.

Reller MD, Strickland MJ, Riehle‐Colarusso, Mahle WT, Correa A. Prevalence of congenital heart defects in metropolitan Atlanta, 1998–2005. J Pediatr. 2008;153(6):807–813.

Sadowski SL. Congenital cardiac disease in the newborn infant: past, present, and future. Crit Care Nurs Clin North Am. 2009;21(1):37–48.

Srinivasan S, Strasburger J. Overview of fetal arrhythmias. HHS Public Access. Available at: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3326657/. Accessed June 19, 2015.

12/2015

Cardiovascular 41

References

The Children’s Hospital of Philadelphia. About vascular ring. Available at: http://www.chop.edu/conditions‐diseases/vascular‐ring/about#.VYSSFZDJBIJ. Accessed June 19, 2015.

Topol EJ, ed. Textbook of Cardiovascular Medicine. 3rd ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2007.

Verklan MT, Walden M. Core Curriculum for Neonatal Intensive Care Nursing. 5th ed. Philadelphia, PA: Elsevier Saunders; 2015.

12/2015

Cardiovascular 42

ccrn/ccrn k certification review course: … nursing actions ... heart disease ... hypoplastic left...

Documents