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Neontal boards J > 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 (7) before cyanosis sets in

A
  1. Truncus
  2. TGA
  3. Tricupsid atresia
  4. TOF
  5. Total anomalous pulmonary venous return
  6. Hypoplastic left heart syndrome
  7. pulm atresia with intact septum
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35
Q

The most common neonatal cardiac 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
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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
  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 (elfin features)
  • 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
  • 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

most common etiology of hypertension

A

renal parenchymal and vascular anomalies- majority

79
Q

Common nonrenal cause of hypertension

80
Q

When to treat hypertension

81
Q

Factors that close the PDA (6)

A
  • 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

90
Q

Newborn presents with:
* cyanosis
* CXR: dec pulm marking
* ECG: left superior axis deviation with small RV forces

Whats the Dx:

A

Tricuspid atresia

Buzz: Left superios axis deviation, LVH on ECG

Signs occur when PDA closes
vs TOF/ TGA: ECG RAD and RVH

Neontal boards J (19 decks)

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