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NICU Board Review Cards > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Determinant of cardiac output

A

heart rate (HR) and stroke volume (SV). It is expressed as follows:

CO = HR × SV

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2
Q

What is stroke volume and its determinants

A

Stroke volume is the difference between end-diastolic volume (EDV) and end-systolic volume (ESV)

Affected by preload, contractility and afterload.

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3
Q

What is the definition of physiologic hypotension

A

Cerebrovascular autoregulation is lost leading to cerebral function compromise and tissue ischemia

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4
Q

What is expected MBP after 72 hours regardless of gestional age

A

MBP > 30 mmHg

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5
Q

Factors in the fetus that ensures most oxygentated blood goes to the heart and brain (4)

A
  1. Low SVR
  2. High PVR
  3. PDA
  4. PFO
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6
Q

What are the transition from fetal to neonate circulation (4)

A
  1. Cord clamping: removal of placenta result in inc in SVR
  2. First breath: reduce PVR, inc pulm blood flow
  3. Inc LA pressure: functional closure of PFO
  4. Inc PaO2: PDA closes
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7
Q

Factors contributing to hypotension in preterm neonates (7)

A
  1. Immature myocardium: dec contractility
  2. Maladaptive transition: may not overcome the inc SVR (common in neonates <30 wks)
  3. PDA: steal syndrome
  4. Perinatal hypoxia/ asyphyxia: inc catecholamine, RAA axis, vasopressin, myocardial dysfunction
  5. PPV: inc intrathoracic pressure
  6. Sepsis and inflamatory response: TNF and IL-1: vasodilation and permeability
  7. Relative adrenal insufficiency
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8
Q

Adverse effect of hypotension

A
  1. Impaired cerbral blood flow (immature autoregulation)
    • Ischemia: low BP
    • Hemorrhage: high BP

Avoid fluctations in BP to prevent IVH

Permissive hypotension: MAP less than gestational age but good perfusion (CRT, HR, UO, no acidosis)

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9
Q

Indication to treat hypotension

A
  1. prolonged
  2. associated with:
    • metabolic acidosis
    • hypoxia
    • hypocapnia/ hypercapnia
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10
Q

Treatment for hypotension (8)

A
  1. Volume expander: PRBC for anemia, crystalloid
  2. Dopamine
  3. Dobutamine
  4. Epinephrine
  5. Vasopressin
  6. Milirone
  7. Hydrocortisone
  8. Dexamethasone
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11
Q

What is the MOA of dopamine

A

Release of stored norepinephirne from terminal nerve ending (stores last for 8-12 hrs)

  • for hypotension cause by vasodilation- inc afterload
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12
Q

What are the dose and effect of dopamine

A
  1. Low dose (2-4): dopaminergic receptor- dilate renal and splanchnic vessels
  2. moderate (5-10): beta1&2, alpha 1 and dopa- inc cardiac contractility and HR
  3. high (>10-20) alpha 2 receptor- inc SVR
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13
Q

MOA of dobutamine

A

cardioselective inotrope (limited chronotrope)

  • limited effect on BP and afterload
  • preferred for myocardial dysfunction
  • not dependent on endogenous catecholamine
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14
Q

What are dose and effect of epinephrine drip

A
  • Low dose (0.01-0.1 ug/kg/min)- (beta) myocardial contractility and peripheral vasodialtion
  • Higher dose: >0.1 ug/kg/min)- (alpha) increase heart rate, peripheral vasoconstriction and inc PVR
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15
Q

Side effect of epinephrine

A
  • risk for hyperglycemia and inc lactate
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16
Q

Indication for vasopressin in hypotension

A
  • vasodilatory shock resistant to catecholamine
  • to be used as infusion

Dopa vs vasopressin: lower pCO2, received fewer doses surf, no tachycardia

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17
Q

MOA of milrinone

A
  • inc cAMP (via phosphodiesterase III inhibitor)
    • enhances myocardial contractility without inc mycardial O2 or inc afterload
    • dec vas tone both systemic and pulm
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18
Q

Adverse effect of milrinone

A

thrombocytopenia and hypotension

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19
Q

Cardiovascular action of hydrocortisone (5)

A
  1. Upregulation of cardiovascular adrenergic receptor
  2. upregulation angiotensin II
  3. Inhibition of NO synthase and vasodilatory PG
  4. Inhibition of catecholamine metab
  5. Inc intracellular Ca
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20
Q

Concentration reduced hemoglobin for cyanosis to be visible

A

3-5 g/dl

Ex:

Hgb 15, de-ox 10/15= 70-80% O2 sat

Hgb 20, de-ox 15/20= 80-85% O2 sat

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21
Q

True or false Hgb F has a lower p50

A

true- bec Hgb F is more avid to O2

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22
Q

What amino acid is substituted in Hgb F

A

histidine to serine

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23
Q

True or false central cyanosis in Hgb F is seen at a lower pO2

A

True- cyanosis a pO2 40 vs pO2 50 with adult Hgb

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24
Q

Factor that Hgb love O2 (shift to the left)

A
  1. Low H (alkalosis)
  2. Low CO2
  3. Low temp
  4. Low 2,3BPG- as in fetal Hgb
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25
Q

Cyanosis presenting at rest and improves with crying

A

Choanal atresia

  • inability to pass catheter thru the nares
  • Confirm CT
  • Improve: oral airway
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26
Q

Cyanosis more pronounced in supine

A

Micrognathia, retrognathia, pierre robin

    • Obtruction from tongue
  • reduce at prone
  • may require tracheostomy
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27
Q

Cyanosis that worsens with crying, feeding, supine or resp infection

A

Laryngomalacia/ tracheomalacia

  • inspiratory stridor
  • presents at several weeks
  • temporary elevation of head
  • Improves with time
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28
Q

Presents as expiratory stridor, resp distress, wheezing, persistent cough

A

Tracheal stenosis

  • dx: direct bronchoscopy
  • assoc with complete tracheal rings
  • Tx: surgical repair
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29
Q

Stridor associated with birth or surgical injury

A

Vocal cord paralysis

  • Unilarteral: hoarse cry
  • Bilateral respiratory distress and cyanosis
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30
Q

What are the congenital lung abnormalities presenting with resp distress and cyanosis unresponsive to standard vent

A
  1. diaphragmatic hernia
  2. CPAM
  3. Pulm sequest
  4. Lobar emphysema
  5. Arteriovenous fistula
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31
Q

Condition with hypoventilation, apnea, cyanosis

A

ICH, seizure, encephalopathy

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32
Q

Diagnosis: infant with cyanosis without resp distress, dec O2 sats but N PaO2

A

Methemoglobinemia

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33
Q

Differential dx after O2 admi based pO2

A
  • <100- cardiac with parallel circ/mixing lesion with restricted PBF
  • 100-150- PPHN, mixing lesion with inc PBF
  • 150-300- Pulm d/o, CNS, meth
  • >300 N
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34
Q

Primary screening target of CCHD (12)

A
  1. Truncus
  2. TGA
  3. Tricupsid atresia
  4. TOF
  5. Total anomalous pulmonary venous return
  6. Hypoplastic left heart syndrome
  7. Double outlet right ventricle
  8. Ebstein anomaly
  9. Interrupted aortic arch
  10. Single ventricle complex
  11. Coarctation of the aorta
  12. pulm atresia with intact septum
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35
Q

The most common neonatal cardaic tumor

A

Rhabdomyoma

  • associated with tuberous sclerosis
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36
Q

Most common type TAPVR

A

Supracardiac

  • enters via veritcal vein, azygous vein or superior vena cava
37
Q

Most common type TAPVR that presents with obstruction

A

Infracardiac

Presents with

  • Cyanosis
  • CHF with pulm edema
  • resp distress
  • dec systemic perfusion
38
Q

Most common cause of complete vascular ring

A

Double aortic arch

  • from the right and left 4th brachial arch
39
Q

A heart block that present with progressive prolonged PR interval

A

2nd degree AV block Mobitz type I

  • also known as Wenkebach
  • disease within AV node (inc vagal tone)
  • benign
40
Q

A heart block that presents sudden non conduction

A

Mobitz type II

  • defect distal to AV node
  • precede complete heart block

Code: second (II)- sudden

41
Q

Causes of third degree AV Block

A
  1. autoimmune: SLE
  2. idiopathic
  3. after cardiac surgery
  4. associated with CHD
  • Congenitally corrected TGA: abN dev of AV node and distal conduction system
42
Q

Indication for pacemaker

A
  1. 2nd degree AV block- Mobitz II
  2. symptomatic 3rd degree AV block
  3. Rest HR <55
  4. HR< 70 + CHD
43
Q

How to terminate SVT (7)

A
  • Termination
  1. Ice to the face
  2. Adenosine
  3. DC CardioVersion
  4. Transesophageal pacing
  • Infusion:
    1. amiodarone
    2. Esmolol
    3. Procainamide

Avoid verapamil- causes hemodynamic collapse

sVt

44
Q

Things to consider for refractory SVT to adenosine and cardioversion

A
  1. Focal atrial tachycardia (FAT)/AF (remember adenosine block AV node)
  2. deep central line (triggers accessory pathway)
  3. Call cardiology (procainamide, esmolol)
45
Q

What is Atrial flutter

A
  • functional reentrant circuit within the right atrium
  • Atrial rate 300-600
  • r/o structural heart (ECHO), deep central line
  • Tx:
    • Stable: digoxin
    • Unstable: cardioversion
  • Reoccurence is rare
46
Q

Characteristic of normal sinus rhythm

A
  • Upright P wave in lead I and aVF
  • P wave follwed by narrow QRS
47
Q

What is the normal PR interval

A

70 to 140 msec

Best measured in lead II

48
Q

What is the normal QRS

A
  • Duration 20-80 msec on lead V5
  • N QRS axis: 100-150 (use I, II, AVF)
  • R axis N until 1 month
49
Q

What is the normal QT interval

A
  • mean QTC 400+/- 20 msec
  • best measure lead II, V5, V6
  • mild prolonged in newborn: <470 msec (resolves in 48-72 hours
50
Q

True or false T wave in V1 is upright during the first week of life

A

True

  • T wave is positive on V5 and V6
51
Q

True or False:

PACs are

(1) benign
(2) decline in frequency within frist few week
(3) highly associated with SVT

A

(1) True
(2) True
(3) False

52
Q

Causes of sinus bradycardia (8)

A
  1. oversedation
  2. maternal meds
  3. hypothermia
  4. CNS abN
  5. inc ICP
  6. inc vagal tone
  7. obstructive jaundice
  8. hypothyroidism
53
Q

It is a change in P wave axis and morphology

A

Wandering atrial pacemaker

54
Q

Most common mechanism of SVT

A

Orthdromic reciprocating AVRT

  • Delta wave = WPW (ventricular preexcitation)
55
Q

Cardiac drug and toxicity
1.nitropruside
2.digoxin
3. norepi
4.dopamine

A
  1. Nitropruside: cyanide poisoning
  2. Digoxin: GI, AV block/ bradycardia (greater with hypoK)
  3. Norepi: hypocalcemia and hypoglycemia
  4. Dopamine: hypothyroid (transient)
56
Q

A neonate presents with

  • a systolic murmur located along the left sternal border, radiating to the neck
  • dysmorphic features
  • EKG: left atrial enlargement and high voltages representing biventricular hypertrophy

What is the diagnosis?

A

Hypertrophic cardiomyopathy

  • Murmur from LVOT obstruction
  • Echo: biventricular hypertrophy, hypercontractile and has diastolic dysfunction
57
Q

Syndromes associated with hypertrophic cardiomyopathy

A
  1. Noonan syndrome is the most common cause in neonates and children younger than age
  2. Beckwith-Wiedemann syndrome
  3. Pompe disease
  4. mitchondiral d/o
  5. FAO
58
Q

True or false:

Medical management of hypertrophic cardiomyopathy changes prognosis

A

False

  • Goal of medical management is relief of symptoms
  • Tx: B-blocker (propanolol)
    • slowing of the heart rate and prolongation of diastole, which allows for an increase in ventricular filling.

  • Avoid: Inotropic agents and diuretics
    Rationale: may decrease stroke volume and thus cardiac output in HCM
59
Q

What is the ECHO finding in dilated cardiomyopathy?

A
  • dilation and impaired contraction of the left ventricle or both ventricles.
  • LVEF less than 40%
  • fractional shortening less than 25%
60
Q

What is the most common cause of myocarditis?

A

Viral infection

  • may lead to dilated cardiomyopathy
  • parvovirus B19
  • human herpesvirus 6
  • coxsackievirus
  • influenza virus
  • adenovirus
  • echovirus
  • CMV
  • HIV
61
Q

Management of dilated cardiomyopathy

A
  • Diuretics (Spironolactone)
    • avoid an excessive decrease in preload.
  • Inotropic (milrinone, epinephrine, and dopamine)
    • to improve myocardial contractility
    • afterload reducing agent.
  • B-blockers
    • blockade of RAA
    • blocking the excessive sympathetic activity that contributes to cardiac failure.
62
Q

What is p-wave

A

Atrial contraction

  • peaked= RAE
  • wide= LAE
  • N duration 0.1-0.12sec
  • N height 3 sm boxes
63
Q

What QRS wave?

A

Venticular contraction

64
Q

Determinant of development of hydrops fetalis in fetus with SVT

A
  • Duration of SVT
  • degree of immaturity

SVT usually presents at 28-32 weeks

65
Q

Intrauterine mgt of
SVT

A
  1. digoxin- admin IV due to poor Po availability
  2. Flecainide
  3. amoidarone- takes several days to be effective, used to lower dose of digoxin
  • Monitor: hyperbili, anemia, NEC
  • needed for 6 months
66
Q

Management of fetal AF

A
  1. digoxin
  2. sotalol

Amiodarone not effective

67
Q

Etiology of prolonged QTc

A
  • hypocalcemia
  • myocarditis
  • Long QT sydrome

Tx: propanolol (first line)

68
Q

True or false

LVOT obstruction has a higher genetic predisposition vs RVOT

A

True

10% increase with stronger link if the mother is affected

69
Q

It is the most common LVOT obstruction

A

Aortic Valve stenosis

  • PE:
    • harsh systolic murmur RUSB
    • Poor or absent peripheral pulses
  • Concern:
    • cardiogenic shock
  • Mgt
    • consider PGE for ductal patency and RV to augment systemic CO
  • Link to HLHS
70
Q

This syndrome is associated with supravalvular aortic stenosis

A

Williams-Beuren sydrome

  • Elastin gene mutation
  • Assoc with stenosis of the branch pulmonary arteries and coronary ostia
71
Q

Syndrome Associated with Coarctation of the aorta

A

Turner’s syndrome

  • CoArc usually at insertion of PDA
  • Male predominance
  • Repair indication:
    • hemodynamic compromise
    • sBP diff >20 bet UE and LE
72
Q

Goal of management of hypertrophic obstructive cardiomyopathy

A
  • prevent dehydration
  • prevent systemic hypotension
  • Lower HR to allow ventricular filling and preload
73
Q

Why is heart failure less common in PV stenosis vs Aortic stenosis

A
  • intrinsic hyeprtrophy of the RV from elev PVR and its rapid decline postnatally
74
Q

Associated syndromes with pulmonary valve stenosis

A
  • Noonans
  • LEOPARD
  • 22q11 del
  • alagille
  • Williams
  • congenital rubella
75
Q

Neonates at risk for hypertension

A
  • UAC
  • BPD
  • IVH
  • renal failure
  • anomalies of the kidneys and urinary tract
76
Q

Standardize method for measuring BP

A
  • prone/supine
  • cuff size: cuff width: arm circumference ration 0.45-0.7
  • right arm
  • timing
    • asleep or awake should be quiet
    • not disturbed 15 mins after cuff is placed
    • feed/medical intervention 1.5 hrs before BP
  • 3 readings 2 mins apart
77
Q

Definition of hypertension

A

systolic/diastolic BP > 95th percentile on 3 separate occasions

  • if above 99th percentil investigate
78
Q

Etiology of hypertension

A

renal parenchymal and vascular anomalies- majority

79
Q

Common nonrenal cause of hypertension

A

BPD/CLD

80
Q

When to treat hypertension

A

>95 p

81
Q

Factors that close the PDA (6)

A
    1. stimulated by:
      1. rising oxygen tension
      2. withdrawal of vasodilatory mediators (prostaglandins, nitric oxide, adenosine)
      3. vasoconstrictors (endothelin-1, catecholamines, contractile prostanoids),
      4. platelets
      5. morphologic maturity
      6. genetic predisposition
82
Q

What the common heart lesion in Pentalogy of Cantrell

A

VSD

Defect in Pentalogy of Cantrell: defects of the heart, pericardium, diaphragm, sternum, and abdominal wall.

83
Q

What the other name of Holt-Oram syndrome

A

Heart-hand syndrome

  • Autosomal dominant- complete penetrance: Chromosome 12q2
  • Genes TBX5 and TBX3: embryonic prevelance of ASD,VSD, left sided heart malformation
  • PE: hand and upper limb abnormalities (triphalangeal thumb and radial dysplasia)
84
Q

what valve may develop insuffciency in VSD

A

Aortic valve

85
Q

What is pathonomonic finding in truncus arteriosus?

A

absence of aorticopulmonary septum (21%)

most frequent form of TA: partially formed aorticopulmonary septum

86
Q

Which parameter of BP is reflective of cardia contractility and cardiac output

A

Systolic blood pressure

87
Q

Which BP parameter is reflective of systemic vascular resistance (SVR)

A

Diastolic blood pressure

88
Q

What are markers for cardiovascular dysfunction

A
  • Cap refill time
  • HR
  • UO
  • Lactic acid

cardiac output is inadequate when it is unable to:
1. to perfuse tissue capillary beds
2. maintain oxygen delivery
3. meet end-organ metabolic demand

89
Q

Most common congenital heart disease of Turner’s syndrome

A
  1. Bicupsid aortic valve
  2. CoArc

Inc risk for PPHN and Aortic dissection

NICU Board Review Cards (19 decks)

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