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CCP 350 Cardiovascular Emergencies Flashcards

1
Q

Classify and differentiate between Cyanotic and Acyanotic heart defects

A

If the defect lowers the amount of oxygen in the body, it is called cyanotic. In infants with cyanotic lesions, hypoxia is more of a problem than congestive heart failure. Cardiac causes of cyanosis include congenital lesions with right-to-left shunts and cardiac lesions with decreased or increased pulmonary blood flow.

If the defect doesn’t affect oxygen in the body, it is called acyanotic. Congestive heart failure is the primary concern in infants with acyanotic lesions. acyanotic lesions usually present within the first 6 months of life with symptoms of CHF; however, ASDs can remain asymptomatic until adulthood

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2
Q

when should one consider a a congenital heart defect in an infant

A

Suspicion of a congenital heart defect should be raised by the presence of feeding difficulties in association with tachypnea, sweating and subcostal recession, or severe growth impairment

The possibility of a congenital heart defect should be considered in an infant who presents with central cyanosis that does not respond to 100% supplemental oxygen (hyperoxia challenge)

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3
Q

When do Neonates with ductal-dependent cardiac lesions typically present, and how?

A

Neonates with ductal-dependent cardiac lesions typically present within the first 2 to 3 weeks of life with either acute cyanosis or shock

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4
Q

what is the lifesaving intervention for Neonates who present with ductal-dependent cardiac lesions?

A

Initiation of a prostaglandin E1 (PGE1) infusion will be lifesaving in these neonates

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5
Q

The most common acyanotic lesions

A 
ventricular septal defect
atrial septal defect
atrioventricular canal
pulmonary stenosis
patent ductus arteriosus
aortic stenosis
coarctation of the aorta
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6
Q

The most common cyanotic lesions

A

tetralogy of Fallot

transposition of the great arteries

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7
Q

The epidemiological incidence of congenital heart disease (CHD) in Canada

A

approx 8 cases per 1,000 live births

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8
Q

initial treatment of a hypoxic tet spell

A
  1. placement of an infant in the knee-to-chest position or of an older child in a squatting position to increase systemic vascular resistance (SVR)
  2. provision of supplemental oxygen
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9
Q

child with a known congenital heart defect or an acquired cardiac defect who presents with fever of unknown origin, acute neurologic deficits, new-onset microscopic hematuria, myalgias, splenomegaly, petechiae

A

Acute bacterial endocarditis

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10
Q

main emergency treatment of infants and children who present with congestive heart failure (CHF)

A
  1. Oxygen
  2. positive pressure ventilation (noninvasive or invasive)
  3. diuretics
  4. possibly inotropes
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11
Q

treatment of choice for stable SVT in children If vagal maneuvers fail

A

adenosine administration (0.1 mg/kg for the first dose, followed by 0.2 mg/kg on repeated doses)

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12
Q

cardiac differentials for sudden collapse in Young athletes

A 
hypertrophic cardiomyopathy (HOCM)
prolonged QT syndromes
commotio cordis
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13
Q

Trace the path of the RBC during foetal circulation, and describe the changes that occur following delivery

💣💣💣PATHO BOMB💣💣💣

A

during foetal circulation:

  1. Oxygen flow: mom’s lungs/body/placenta → umbilical vein → ductus venosus → fetal heart (through IVC) → right atrium → shunted to the left atrium by the patent foramen ovale → left ventricle → aorta → directed to the fetal coronary and cerebral circulations.
  2. Deoxygenated blood: SVC → RA → RV → pulmonary artery → patent ductus arteriosus* (PVR > SVR) → mixes with well oxygenated blood in the descending aorta
  3. Fetal pulmonary vascular resistance (PVR) is higher than fetal systemic vascular resistance (SVR); this forces deoxygenated blood to mostly bypass the fetal lungs.
  4. This poorly oxygenated blood enters the aorta through the patent ductus arteriosus and mixes with the well-oxygenated blood in the descending aorta. The mixed blood in the descending aorta then returns to the placenta for oxygenation through the two umbilical arteries.”

following delivery:

  1. Decrease in pulmonary vascular resistance (increased pulm. Blood flow)
  2. Increase in global 02 enhances closure of umbilical arteries, umbilical vein, ductus venosus, ductus arteriosus (complete closure by 2-3 weeks) – functional closure by 15-18 hours.
  3. Increase in pulmonary artery flow creates a higher pressure system on the left side of the heart and closes the flap of the foramen ovale (closes completely by 3 months)
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14
Q

What are the ductal dependent (PDA) heart lesions?

think of the ANATOMY

A

Acyanotic: We need the duct (PDA) to get blood to the body because of an obstruction in the left side of the heart or aortic arch

  1. aortic stenosis / aortic atresia
  2. Coarctation of the aorta
  3. Hypoplastic left heart syndrome (HLHS) (the LV is weak)

Cyanotic: We need to get blood to the lungs because the kid has a weird structural abnormality on the right side (or otherwise) that won’t allow them to oxygenate blood
That’s a bit tougher but you have this!

  1. Tetralogy of Fallot
  2. Transposition of the great arteries
  3. Tricuspid atresia
  4. pulmonic stenosis / pulmonic atresia
  5. Hypoplastic right heart syndrome
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15
Q

List types of CHD which are most likely to present outside of the neonatal period

A

Mixing lesions – leading to CHF

  1. VSD
  2. Patent ductus arteriosus (encourages foramen ovale to stay open)
  3. Tetralogy of Fallot

Obstructive lesions – leading to decreased CO/shock

  1. Coarctation of the aorta
  2. Aortic stenosis
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16
Q

What are the anatomic anomalies seen in Tetralogy of Fallot?

A
  1. Right ventricular outflow tract obstruction
  2. large, unrestrictive, malaligned VSD
  3. over-riding aorta that receives blood flow from both ventricles
  4. right ventricular hypertrophy secondary to the high pressure load placed on the RV by the right ventricular outflow tract obstruction
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17
Q

What is the pathophysiology of a Tet spell

💵💵💵MONEY SLIDE💵💵💵

A
  1. Event causes sudden ↓ in SVR (such as crying/defecation) → a large right-to-left shunt across the VSD
  2. Shunt through the VSD bypasses the lungs and → hypercarbia, hypoxemia, acidosis
  3. Respiratory centres are stimulated → hyperventilation
  4. More negative intrathoracic pressure ↑ the amount of blood returning to the right side of the heart
  5. The systemic blood shunts across the VSD → further hypoxia
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18
Q

Management priorities of a Tet spell

A
  1. Increase the SVR to push blood back towards the right ventricle
    - Knee to chest position
    - Ketamine
    - Phenylephrine
  2. Decrease the PVR to promote forward flow to the lungs
    - Supplemental O2
    - Calm the child
  3. Relax the structures around the pulmonary outflow tract
    - Morphine/Fentanyl
    - Beta Blockade (esmolol / propranolol)
  4. Reverse the acidosis
    - IV fluids
    - NaHCO3
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19
Q

What is ductal-dependant ToF?

A

ToF with severe pulmonic stenosis / atresia

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20
Q

what is the danger with venodilators like nitroglycerin as first line agents in pediatric CHF?

A
  1. kids are more sensitive to the drug’s potent vasodilatory effects than adults
  2. can experience profound and rapid hypotension
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21
Q

primary causes for dysrhythmias in kids (SVT is the most common dysrhythmia!)

A

Plumbing problem

  1. RHD
  2. Kawasaki’s
  3. CHD
  4. Anomalous left coronary artery from the pulmonary artery (ALCAPA)

Muscle problem

  1. Myocarditis
  2. Cardiomyopathy

Electrical problem

  1. Long QT
  2. Heart blocks
  3. Conduction pathway – WPW, ARVD

Critical substrate problem
1. K, Mg, Ca, hypoxia, hypothermia

Other:

  1. Progression of shock or respiratory failure
  2. Drug of abuse/OD (cocaine, crystal meth, TCAs)
  3. Trauma – commotio cordis
  4. Electrocution
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22
Q

ECG characteristics for SVT in kids

A
  1. Usually narrow QRS (<0.08)
  2. HR > 220 (infants)
  3. HR > 180 (children)
  4. Constant R-R interval
  5. No variability with activity
  6. No P waves
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23
Q

Describe the management of SVT in the infant/child

A

IF UNSTABLE (poor perfusion, AMS, long cap refill, pallor, cyanosis, hypotension) → SYNCHRONIZED CARDIOVERSION! 0.5 - 1 J/kg; if no success then ↑ to 2 J/kg

Stable?

  1. Vagal maneuvers (eg ice bag to face, REVERT in older kids)
  2. Adenosine (0.1-0.2 mg/kg) – max 12 mg
  3. 3rd line drugs for stable SVT: Amiodarone or Procainamide
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24
Q

what four medications should be avoided in kids with known WPW

A

A-B-C-D medications (adenosine, beta-blockers, calcium channel blockers, and digoxin)

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25
Q

What is the most common cause of myocarditis in children?

A

The most common cause is viral; coxsackievirus B and enteroviruses account for the majority of cases

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26
Q

conditions predisposing kids to bacterial endocarditis

A
  1. Hx of previous bacterial endocarditis
  2. Indwelling IV lines
  3. Underlying CHD
  4. VSD, TOF, Aortic stenosis, single ventricle, bicuspid aortic valve, prosthetic valve, post-op shunts
  5. Acquired heart disease (ARF)
  6. ALL dental procedures
  7. Any manipulation or perforation of the gingival or oral mucosal tissue
  8. Resp, MSK procedures
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27
Q

clinical diagnostic criteria for Kawasaki’s disease?

A

Fever for 5 days plus 4 of CREAM

Conjunctivitis
Rash
Extremity changes
Adenopathy
Mucous membrane changes
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28
Q

What is the hyperoxia test? How is it clinically useful?

A
  1. Thought to help determine cardiac and pulmonary causes of CENTRAL CYANOSIS. Assessment of the rise in arterial oxygenation with the administration of 100% oxygen. An arterial blood gas is measured after several minutes on high-flow oxygen (100% oxygen)
  2. After breathing high flow O2 – the PaO2 (you need to use an ABG) should be more than 250 mmHg; if NOT you should suspect a congenital heart disease.
  3. Pulse oximetry is not an appropriate substitute for an arterial blood gas analysis; it is not sensitive enough to determine “pass or fail” of the test because a child breathing high-flow oxygen and registering 100% on pulse oximetry may actually have a Pao2 anywhere between 80 and 680 mm Hg
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29
Q

a common cause of sudden cardiac death in the young athlete (usually undiagnosed)

A

hypertrophic cardiomyopathy (HOCM)

30
Q

List 9 causes of sudden death in young athletes

A
  1. Hypertrophic cardiomyopathy
  2. electrocution
  3. Drug related arrhythmias
  4. LGL syndrome / WPW / Brugada
  5. Trauma – commotio cordis
  6. Aortic rupture – Marfan’s
  7. Long QT syndrome
  8. Coronary artery abnormality - ALCAPA, post Kawasaki’s, myocardial bridge
  9. Idiopathic dilated cardiomyopathy
31
Q

List 8 ductal dependent cardiac lesions in the neonate.

A
  1. Aortic Stenosis
  2. Hypoplastic left heart
  3. Coarctation of the Aorta
  4. Tricuspid Atresia
  5. Transposition of the Great Arteries
  6. Tetralogy of Fallot
  7. Pulmonic Atresia
  8. Hypoplastic Right Heart
32
Q

When does the ductus arteriosus close functionally? Physically?

A
  1. Ductus arteriosus functionally closes at about 10 to 15 hours of life
  2. Complete anatomic closure does not occur until 2 to 3 weeks of life.
33
Q

When does the foramen ovale close?

A

Complete anatomic closure of the foramen ovale does not occur until about 3 months of age.

34
Q

In what percentage of the population does the foramen ovale remain open?

A

Around 10% of the population has a patent foramen ovale.

35
Q

classic complication/emergency from an adult with a PFO

A

Embolic phenomenon – diving emergencies, strokes, mesenteric ischemia, limb ischemia, MI.

36
Q

define and describe Atrial septal defect (ASD)

A
  1. ASD = one of the most common congenital heart defects
  2. occurs when there is a failure to close the communication between the right and left atria
  3. five types of ASD ranging from most frequent to least:

a. patent foramen ovale
b. ostium secundum defect
c. ostium primum defect
d. sinus venosus defect
e. coronary sinus defect

37
Q

Detail the pathophysiology of Atrial septal defect (ASD), specifically the pathway towards the development of pulmonary hypertension

A
  1. Normally, the pressure in the RA is significantly lower than the LA; therefore, blood flows from the LA to the RA causing a left-to-right shunt.
  2. The size of the defect determines how significant the shunt is.
  3. Significant shunts have a ratio of pulmonary (Qp) to systemic flow (Qs) that is greater than 1.5:1 (Qp/Qs > 1.5)
  4. Chronic volume overload d/t ↑ pulmonary blood flow → remodeling of the pulmonary vasculature. As pulmonary vessels remodel, the layer of smooth muscle ↑ in the vascular wall.
  5. Because the muscle layer in the vascular wall increases, resistance to flow in the pulmonary circuit increases. Due to the ↑ vascular resistance and pulmonary pressures increase, PH develops.
  6. Once pulmonary pressures = systemic pressures, the shunt across the ASD reverses, and deoxygenated blood flows into the LA and systemically. When the reversal of the shunt across an ASD occurs due to PH, a condition known as Eisenmenger syndrome develops
38
Q

define and describe Ventricular septal defect (VSD)

A
  1. VSD are the most common congenital cardiac anomaly in children
  2. The main mechanism of hemodynamic compromise in VSD occurs d/t an abnormal communication between the RV/LV and shunt formation
  3. VSD develops when there is a developmental abnormality or an interruption of the interventricular septum formation during embryologic development
39
Q

Detail the pathophysiology of Ventricular septal defect (VSD)

A
  1. The main pathophysiologic mechanism of VSD is shunt creation between the right and left ventricles.
  2. The amount of blood shunted and the direction of the shunted blood determine the hemodynamic significance of the VSD.
  3. These factors are governed by the size, location of the VSD and pulmonary vascular resistance.
  4. In the setting of long-standing large left-to-right shunts, the pulmonary vascular endothelium undergoes irreversible changes resulting in persistent PAH.
  5. When the pressure in the pulmonary circulation exceeds the pressure in the systemic circulation, the shunt direction reverses and becomes a right-to-left shunt. This is known as Eisenmenger syndrome, and it occurs in 10% to 15% of patients with VSD
  6. Small VSDs only lead to the minimal left-to-right shunt without left ventricular (LV) fluid overload or PAH
  7. Medium size VSDs result in a moderate LV volume overload and absent to mild PAH; they present late in childhood with mild congestive heart failure (CHF)
  8. Those with large defects develop CHF early in childhood due to the severe LV overload and severe PAH
40
Q

define and describe Atrioventricular septal defect (AVSD)

A
  1. The atrioventricular septal defect is a congenital cardiac malformation that is characterized by a variable degree of the atrial and ventricular septal defect along with a common or partially separate atrioventricular orifice
  2. A partial atrioventricular septal defect is characterized by an ostium primum atrial septal defect, separate atrioventricular valves with a common junction, an inlet ventricular septal defect, and a cleft mitral valve
  3. the complete form of the atrioventricular septal defect (AVSD) is characterized by a common atrioventricular valve with ostium primum atrial septal defect and an unrestricted ventricular septal defect of inlet type
41
Q

define and describe the anatomy/physiology of a normal ductus arteriosus

A
  1. During fetal life, <10% of blood enters the pulmonary circulation
  2. the DA is a structure that permits blood leaving the RV to bypass pulmonary circulation and enter the aorta.
  3. The DA connects the proximal descending aorta to the main PA
  4. During fetal life, ↓ PaO2 + ↑ prostaglandins from placenta keep the DA patent
  5. At birth, placenta is removed and prostaglandins ↓, this → ↑ pulmonary blood flow. as infant takes its first breaths, the oxygen tension ↑ which drops the PVR
  6. these changes → closing of the DA
42
Q

describe the pathophysiology of Patent ductus arteriosus (PDA)

A
  1. DA functional closure within 12-24 hours of life. anatomic closure takes several weeks.
  2. patency of the ductus is promoted by prostaglandin E2. PDA after birth is assoc. w/ pulmonary edema, pulmonary hemorrhage, NEC, IVH, CHF, AKI, and BPD.
  3. A PDA can → blood flowing from the descending aorta across the patent ductus arteriosus into the pulmonary circulation (“left-to-right”) → pulmonary edema
  4. Extremely premature infants have limited ability to ↑ SV and thus use ↑ HR to ↑ CO. Decreased blood flow to the lower body results in ↑ risk for NEC + renal failure.
  5. The magnitude of the right → left shunt depends on many factors but the most important is the ratio of the PVR to SVR. If the PVR is low and the SVR is ↑, the flow through the shunt to the lungs will be ↑. This will also → more blood returning to the LA and LV, which later → LA + LV hypertrophy
43
Q

define and describe Pulmonary valve stenosis

A
  1. Pulmonic stenosis is a defect of the pulmonic valve in which the valve is stiffened, causing an obstruction to flow.
  2. This disease is typically congenital, and diagnosed in pediatric patients
  3. Pulmonic stenosis is commonly associated with congenital structural cardiac syndromes, including ToF and Noonan syndrome
44
Q

define and describe Coarctation of the Aorta

A
  1. Coarctation of the aorta is a narrowing of the aorta, most commonly occurring just beyond the left subclavian artery
  2. The narrowing of the aorta ↑ the upper body blood pressure → extremity HTN.
  3. Unrepaired coarctation → premature CAD, ventricular dysfunction, aortic aneurysm/dissection, and cerebral vascular disease by the third or fourth decade of life.
45
Q

detail the pathophysiology of Coarctation of the Aorta

A
  1. Coarctation of the aorta causes an ↑ in the upper extremity blood pressure, resulting in two common presentations.
  2. The first is the neonatal presentation that is associated with LV dysfunction and shock from the neonatal myocardium’s intolerance of the sudden ↑ in afterload that occurs with closure of the ductus arteriosus. This presentation often occurs within the first 1-2 weeks after birth.
  3. In patients with neonatal coarctation evolving while the patent ductus arteriosus is closing, the lower extremity saturation can be low as perfusion to the lower body can be maintained by ductal patency.
  4. The second presentation occurs in older children and adults. Coarctation of the aorta in this scenario results in upper extremity HTN, → early CAD, aortic aneurysm, and cerebrovascular disease.
46
Q

define and describe Transposition of the great arteries (TGA)

A
  1. congenital cardiac defect arising from an embryological discordance between the aorta and pulmonary trunk.
  2. aorta arises from the RV and the pulmonary trunk arises from the LV → parallel circuits incompatible with life
47
Q

detail the pathophysiology of Transposition of the great arteries (TGA)

A
  1. The most common form of TGA is referred to as dextro-TGA (D-TGA) which is characterized by the RV being positioned to the right of the LV and the aorta arising anterior and rightward to the PA thus forming two parallel circuits
  2. In the systemic circuit, deoxygenated blood returns to the RA pass through the tricuspid valve and is then forced back into systemic circulation by contraction of the RV and passage into the aberrantly developed aorta. 3. The second circuit is a pulmonary circuit in which oxygenated blood from the pulmonary veins drains into the LA, passes through the mitral valve, and is then forced back into the lungs via contraction of the LV and through the pulmonary arteries.
  3. Patients typically present with cyanosis during the first 30 days of life.
  4. Complete parallel circuits are incompatible with life and thus require a PDA and VSD that allows mixing of oxygen-rich and oxygen-poor blood
48
Q

define and describe Tetralogy of Fallot (TOF)

A
  1. congenital anomaly → pulmonary stenosis, interventricular defect, biventricular aortal origin, and right ventricular hypertrophy.
  2. most common cyanotic heart condition in kids
49
Q

detail the pathophysiology of Tetralogy of Fallot (TOF)

A
  1. The VSD’s seen in patients with ToF are usually perimembranous that can extend into the muscular septum.
  2. Different factors can contribute with the RV outflow obstruction, including the pulmonary valve that is usually bicuspid and stenotic, the hypoplastic pulmonary valve annulus, the deviation of the infundibular septum that causes a subvalvular obstruction, and the hypertrophy of the muscular bands in this region.
  3. The degree of the overriding aorta usually varies and receives blood flow from both ventricles. The physiological process surrounding the hypercyanotic episodes or “Tet spells” in tetralogy of Fallot consist of either a ↓ in SVR or an ↑ in PVR contributing to a right-to-left shunt across the VSD, causing marked desaturation
50
Q

define and describe Total anomalous pulmonary venous return

A

Total anomalous pulmonary venous connection (TAPVC) is a form of cyanotic congenital heart disease in which the four pulmonary veins fail to make their normal connection to the left atrium and all drain into the systemic venous circulation through various anatomic pathways

51
Q

detail the pathophysiology of total anomalous pulmonary venous connection (TAPVC)

A
  1. In TAPVC, the entire oxygenated pulmonary venous return mixes with the systemic venous system.
  2. A portion of this mixed, partially oxygenated blood is then shunted right-to-left at the atrial level (or infrequently through a patent ductus arteriosus) into the systemic arterial circulation, causing cyanosis.
  3. The clinical presentation varies and is dependent upon the presence and degree of pulmonary venous obstruction (PVO)
  4. Patients with severe obstruction generally present as critically ill newborn infants with cyanosis, respiratory distress, and signs of shock
52
Q

define and describe Hypoplastic left heart syndrome (HLHS)

A
  1. variant of congenital heart disease that → underdevelopment of the left-sided structures of the heart, including the mitral valve, LV, aortic valve, the ascending aorta, and aortic arch.
  2. The factors leading to this defect can be categorized into two groups, obstruction of outflow from the LV (obstruction of the LVOT, aortic valve atresia or stenosis) or obstruction of flow into the LV (mitral valve atresia or stenosis, restrictive foramen ovale).
  3. Aortic valve stenosis is the most common cause of underdevelopment of the left ventricle
53
Q

detail the pathophysiology of Hypoplastic left heart syndrome (HLHS)

A
  1. During fetal development, obstruction to LV outflow 2nd to AS ↑ LV afterload and → LV hypertrophy, eventually → LV dilatation and ↓ LV contractility
  2. Additionally, ↓ blood flow through the LV inhibits the growth of the ventricle leading to hypoplasia
  3. As a result, the pressure in the LA ↑ leading to bidirectional blood flow or flow reversal through the foramen ovale. The physiologic sequela is a further ↓ in blood flow to the LV
  4. Obstruction of flow into the LV d/t mitral stenosis or mitral atresia will also cause hypoplasia of the LV due to ↓ preload and pressure in the LV. A reduction in blood flow to any developing cardiac structure will lead to abnormal development in-utero
  5. Neonates with HLHS are dependent on a patent ductus arteriosus (PDA) to provide a blood source for the systemic circulation and coronary arteries
  6. The LV in an infant with HLHS does not serve any function. In neonates with HLHS and a patent ductus arteriosus, blood is ejected from the heart through the pulmonary valve and into the main PA to provide a source of blood for the pulmonary circulation. After the main PA, blood flows into the right and left branch pulmonary arteries, and from the left pulmonary artery, a portion of the blood flows through the ductus arteriosus.
  7. Blood flow through the ductus arteriosus supplies the aortic arch, ascending aorta and coronary arteries in a retrograde fashion and the descending aorta in an antegrade direction, thereby supplying blood to the systemic circulation
54
Q

describe Total anomalous pulmonary venous return (TAPVR)

A
  1. uncommon congenital heart defect that may present after nursery discharge in rare cases
  2. Oxygenated pulmonary venous blood returns to the right atrium rather than the left atrium; a mixing lesion, such as an ASD or PFO, is needed for survival.
  3. A small subset of TAPVR may result in pulmonary venous obstruction, leading to pulmonary hypertension, right heart failure, and hypoxia
55
Q

Physical exam clues for congenital heart defect

A

cyanosis, poor perfusion, respiratory distress, murmur, hepatomegaly, and a pulse/blood pressure differential between the right upper extremity and the lower extremities

56
Q

Common adverse effects of prostaglandin E1

A

apnea and hypotension

57
Q

The rare patient who may worsen on prostaglandin E1

A

Patients with obstructed TAPVR, since prostaglandin E1 dilates the pulmonary vasculature and worsens the left to right shunt through the ductus

58
Q

rate of fluid bolus (mL/kg) If cardiac disease is suspected

A

5-10 mL/kg crystalloid, with reassessment afterwards.

59
Q

physical exam for congenital heart defect

A

Vital signs: Increased respiratory rate, tachycardia
BP in all 4 limbs: Increased concern for CHD if systolic BP in upper extremities ≥20 mm Hg greater than in lower extremities

Assess for murmur, crackles in lungs, and hepatomegaly
Brachial and femoral pulse comparison
Pulse oximetry; assess character of peripheral pulse
Skin: Assess capillary refill, central cyanosis, sweating

60
Q

Neonatal CVS Key Pearls

A
  1. Shock, Cyanosis despite Oxygen Therapy or tachycardia are indicators of CVS instability
  2. Respiratory distress may be a presenting sign of cardiac instability
  3. Babies with serious CHD may appear well initially
  4. Shock may be the initial presentation of sepsis
  5. The classic presentation of a duct dependent lesion is cyanosis and or shock
  6. Prostaglandin E1 is the life saving treatment in duct dependent CHD
  7. SVT should be considered when HR > 220
61
Q

primary driver of neonatal CVS instability

A

oxygenation and ventilation

62
Q

secondary drivers of neonatal CVS instability

A

Insuffiscient volume
Myocardial dysfunction
Structural abnormalities
Arrthymias

63
Q

alerting signs of neonatal CVS instability

A

Pale, mottled or Grey
Weak pulses or low BP
Cyanosis unresponsive to O2
HR greater than 220

64
Q

CCP approach to neonatal CVS assessment

🧙🧙🧙Esoteric Wisdom🧙🧙🧙

A 
LOC, Activity, Tone
Skin Color
Temperature (Central vs peripheral)
Capillary refill (Central vs peripheral)
Pulses (x4)
Blood Pressure
HR
Urine Output
65
Q

When does the ductus arteriosus normally close?

A
  1. Within 12 hours of birth

2. Closure is primarily caused by redirection of blood flow to the pulmonary vasculature

66
Q

What medication is used to maintain PDA patency when cyanotic congenital heart defects are present?

A

Prostaglandin (PGE). Alprostadil exerts direct vasodilatory effects on venous and ductus arteriosus smooth muscle.

67
Q

Where are pre- and post-ductal measurements obtained from?

A

Pre-ductal right hand.

Post-ductal left foot (left hand can be pre-ductal in some circulation anomalies)

68
Q

List some of the cardiovascular differences seen in children

A
  1. Stroke volume is fixed, therefore HR is the only way to ↑ CO
  2. SVT is more common in the first few weeks of life because of the immaturity of the AV septum
69
Q

Outline the drug profile of milrinone

A
  1. Classification: Phosphodiesterase inhibitor

2. MOA: ↑ intracellular cAMP → increased cardiac inotropy, chronotropy, dromotropy, lusitropy

70
Q

Why is epinephrine generally preferred versus norepinephrine in the paediatric population?

A
  1. Paediatric patients are less sensitive to the B1 effects of epinephrine and norepinephrine.
  2. Norepinephrine stimulation of B1 and A1 are unproportionate in the paediatric population.
  3. Adults are more sensitive to the B1 effects of norepinephrine
71
Q

Why does epinephrine cause hyperlactatemia?

A

Thought to be caused by peripheral vasoconstriction of distal capillaries, with some degree of distal limb ischemia

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