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Transcript
Cardiac emergancies for m students
Case Study 1
 Ali
is a 7 month old with Down Syndrome . His
birth weight was 3.5 kg; a week ago he weighed
5.5 kg.
 He is breathing 72 bpm with a HR of 190 and a
sat of 91%.
 He is diaphoretic and is not taking his usual 3
oz formula every 3-4 hours. He has had 4
moderately wet diapers in the past 24 hrs.
case study 1
 Identify
abnormal assessment data for ali
 What other data would you collect? (Hx and
examination)
 What is your priority medical action?
 What investigations' would you do for him?
 What other medical therapy& interventions
would you do for him.
Case Study 1
Air way support/management
 Oxygen
 fluids, as indicated( in CHF, fluids may be
restricted).
 increased calories or concentrated
formula(prescribed)
 rest and spacing of activity/rest periods

Case Study 1

Medication therapy

Digitalis
Digoxin

ACE inhibitors (Angiotensin-converting enzyme inhibitors)
captopril

Diuretics: Lasix, , aldactone.
Case Study 1
 surgery
during infancy to prevent PHT
 patches placed over septal defects; mitral valve
replacement
 arrhythmias and mitral valve insufficiency occur
postoperatively.
 no difference between short term survival rates in
infants with or without Down’s syndrome.
Case Study 2
You have responded for a 3 month old male infant because
the parent’s state he is having episodes of excessive crying
followed by limpness, cyanosis and passing out. He was born
at 41 weeks of gestation by C-section because of failure to
progress. Apgar scores of 7 and 8 at 1 and 5 minutes,
respectively. His cyanosis increases with crying.
 On Exam you note that he is alert and active in respiratory
distress, with visible cyanosis. His lungs are clear. He has
normal peripheral pulses with cyanotic nail beds and mucous
membranes. VS: T 37 (98.6), P164, RR 64, oxygen saturation
83% on blow-by oxygen.

Tetralogy of Fallot
 “Tet
spell”
 Hyperpnea
 Worsening
cyanosis
 Disappearance of
murmur
 RBBB pattern on ECG
Tetralogy of Fallot

Small to N cardiac
silhouette

pulmonary
vasculature
SVR
PVR
Treatment of Tet Spell


Quiet, calm environment
Knee-chest or squatting position
•


Oxygen
Morphine
•

increases afterload by promoting systemic vasoconstriction
Crystalloids
•

to reduce spasm and/or sympathetic stimulation
Phenylephrine
•

increases afterload thus increasing systemic resistance
consider small volume challenge (5-10 cc/kg) to increase preload and SVR
NaHCO3
•
to treat acidosis
Oxygenate to target
saturation levels
Squatting



Common with unrepaired TOF
Increases oxygen saturations
Angulation and kinking of femoral
arteries with increased SVR,
decreasing the R->L shunt
Hypercyanotic Spells ( TET spells)
Syncope
Morphine
Hypovolemia
 Agitation
Tachycardia
Oxygen
 Cyanosis
Knee-chest
Rt Lt
shunt
 PVR
Fluid
Impaired RV
filling
RVOT
obstruction
Phenylepherine
 Age
Cyanotic Spells

Increase systemic vascular resistance
Squat/Knee chest position
Ketamine 1-2mg/kg IV
Neosynephrine 0.02mg/kg IV

Tachycardia
Release of infundibular spasm
Propranolol 0.1mg/ Kg IV

Irritability
Morphine 0.2mg/ Kg S.C or IM

Hypoxia
Oxygen

Dehydration
Volume

Acidosis
NaHco3 1mEq/ Kg IV
Case study 3

A 5 hour old male newborn infant was born at 39 weeks gestation
via normal vaginal delivery to a 23 year old G2 P2 O+ mother with
unremarkable prenatal serology studies. Apgar scores were 8 and
9 at 1 and 5 minutes. His initial physical exam was normal. He
stayed in mother's room and breastfed shortly after delivery. At 5
hours of age, with the second feeding, the baby appears
tachypneic and cyanotic, and he is therefore taken to the nursery
for further evaluation.
Case study 3

Exam: VS T 37.0, HR 145, RR 78, BP 67/38, oxygen saturation
82% in room air. Length 53 cm (50%ile), weight 3.7 kg (50%ile),
HC 34 cm (50%ile). He is an alert active, nondysmorphic and
mildly cyanotic term male. Tachypnea and mild nasal flaring are
present. His heart is regular with a grade 2/6 soft systolic murmur
at the upper left sternal border. The precordium is quiet. Lungs are
clear bilaterally. No hepatosplenomegaly is noted.
Case study 3

He is placed in an oxygen hood with a fraction of inspired oxygen
(FiO2) of 0.7 (70%) with no appreciable rise in his oxygen
saturation. A radial arterial blood gas shows pH 7.44, pCO2 35,
paO2 39, bicarb 22 in FiO2 0.7 (70%) by hood.

A chest radiograph : cardiomegaly , narrow mediastinum and
increased pulmonary vasculature. ECG: RAD and RVH
Case study 3

Echocardiography reveals D-transposition of the great vessels
with a 5mm ventricular septal defect and patent ductus
arteriosus. A prostaglandin E1 infusion is started. The infant is
mechanically ventilated and subsequently transported to a
pediatric cardiac surgical specialty center. An arterial switch
procedure is performed successfully. He is discharged home 3
weeks later.
Initial Stabilization





ABC’s: Volume resuscitation, ionotorpic support, correction of
metabolic acidosis, r/o sepsis
Intubate if needed, titrate Fi02 to keep Sp02 80%-85% to prevent
pulmonary overcirculation
Placement of umbilical lines
Infants who present in shock within the first 3 weeks of life, consider
ductal dependent lesions
Use of PGE1 (0.025 to 0.1mcg/kg/min)
Stabilization for Transport





Reliable vascular access
Intubation if on PGE1, OG placement
Oxygen delivery, Sp02
Monitor HR, tissue perfusion, blood
pressure, temp and acid-base status
Calcium and glucose status .
Case study 3

Neonates and infants with central
cyanosis or cardiac failure are an
emergency – irrespective of their
clinical state.
Case study 4



•
•
•
•
6 years old girl presented with fever for 8 days ,skin rash for 4
days associated with red strawberry tongue .
She was seen at private clinic 3 days earlier and diagnosed as
scarlet fever, treated with ospen since then but without any
improvement.
On examination :
normal vital signs apart from fever
Enlarged right anterior cervical lymph nodes , strawberry tongue .
Maculopapular skin rash over the chest and back
Normal systemic examination
Case Study 4




Tests :
CBC, CRP, ESR
EKG, ECHO
Ultrasound of abdomen
Case Study 4


•
•
•
•
On the 2nd day after admission to hospital she had peeling of the
fingers ,nausea, vomiting , diaphoresis, pallor and irritability .
Examination:
HR: 120 .RR :42 .BP: 100/60 . Oxygen sat: 92%
She is irritable ,sick looking with respiratory distress
Enlarged right anterior cervical lymph nodes .
peeling of fingers
Kawasaki Disease


She had an attack of syncope for 2 minutes in the 2nd day
evening so transferred to ICU .
She also complained from chest pain ,shortness of breath and
weakness. She was very anxious.
Kawasaki Disease

ECG:
o
Q waves (>3 mm)
•
In lead III, aVF
o
ST segment changes of >2 mm

ST depression in lead V5, V6 with T wave inversion
Troponin Level was high
•
Kawasaki Disease
Case Study 5
You have responded for a 5 month old female who has been
lethargic, not feeding well, and appears to be in respiratory
distress. She was sick 2 weeks ago . At that time she had a fever,
cough, and a runny nose. She was also seen 2 days ago in
private clinic for respiratory distress ,diagnosed as bronchiolitis
and started on steroids and bronchodilators.
 She is the product of a G3P2, full term, uncomplicated pregnancy.
Delivery was unremarkable except for meconium stained fluid. She
did well at delivery and in the nursery. Her pediatric follow-up has
been poor.

Case Study 5
 On
Exam you note that she is an acyanotic infant
who is pale, lethargic, and tachypneic, with mild to
moderate subcostal and intercostal retractions. VS
T 36.8, RR 72, HR 160, BP 72/48, with capillary refill
of 4 to 5 seconds.. Oxygen saturation in room air is
94%. Her lungs have scattered crackles with slightly
decreased aeration in the left lower lobe.
Case Study 5
 Her
heart is of regular rate and rhythm, with a
normal S1 and S2. An S4 gallop is noted at the
cardiac apex.
 A 12 lead electrocardiogram shows a sinus
tachycardia, low voltage QRS complexes. Qwaves in L2 &L3 and T wave inversion in V5 & V6
are noted.
Case Study 6
Case Study 6
MYOCARDITIS
MYOCARDITIS
Symptomatic
•
o
o
o
Correction of etiology
Immunosupression
•
•
o
o
o
o
•
inotropes
Diuretics
afterload reduction
Steroids
Anti-virals
Cyclosporin
Interferon
Transplantation
Case study 6
 11-year-old
girl passed out during reading;
awoke after 3 min.
 She was stiff with eyes rolled back ~
approx. 3 min.
 Three
similar episodes; Preceded by palpitations
,one of them associated with exercise.
 Family History : Negative
Case study 6
 Now
awake and alert; skin color is normal , normal
breathing. normal appearance
 Vital
signs: HR 70; RR 20; BP 90/60; T 37.7 C Wt 39
kg; O2 sat 99%
 Systemic examination ; normal
Case study 6
 What
is your general impression of this
patient?
Clinical Features: Your First Clue
 Loss
of consciousness
 Lasted only a few minutes
 Minimal or no postictal state
 No stigmata of seizure: Urinary incontinence,
bitten tongue, witnessed tonic-clonic activity
Syncope: Key questions to address with initial
evaluation
 Is
the loss of consciousness attributable to
syncope or not?
 Is
heart disease present or absent?
 Are
there important clinical features in the history
that suggest the diagnosis?
Case study 6
•



Stable
Patient with syncope
In no distress; normal exam
Concerning/ominous history
What are your initial management priorities?
Diagnostic Studies
Laboratory is often normal but may include:
 Electrolytes / Ca++, Mg++, PO4. Blood glucose
 CBC with differential
 cardiac enzyme
 Radiology:
 CXR offers little.
 CT or MRI of the brain and neck may be indicated if
considering seizures or injury

Diagnostic Studies
ECG/Holter.
 Echocardiography
 Cardiac MRI
 Continuous cardiac monitoring
 EEG
 Genetic testing
 Stress ECG

Case study 6
Differntial diagnosis :
 Structural heart defect :
• Known Congenital heart disease (Ebstein’s anomaly,LTGA,ASD)
• Hypertrophic cardiomyopathy
• Anomalous origin of the LCA
• Myocarditis
• Arrhythmogenic RV dysplasia
• Coronary artery disease
• Primary or secondary pulmonary hypertension.
Case study 6
 Normal




heart structure
WPW syndrome.
Long or short QT
syndrome.
Brugada syndrome
CPVT
Case Study 5
Long QT syndrome (Jervell-Nielson-Lange)
QT (corrected)
QTc= QT (msec)
√R-R (sec)
= 640/ 1.05
= 610 msec
> 450 m sec is
long
Syncope in Children
– transient loss of
consciousness and postural tone due to
generalized cerebral ischemia with
rapid and spontaneous recovery
Presyncope - no complete loss of
consciousness occurs
Syncope
Syncope in Children
Affects 15% of children between 8-18
 Uncommon under age 7 therefore think about:

Seizure disorders
 Breath holding
 Primary cardiac dysrhythmias


Cardiovascular causes unusual but life-threatening
anatomic abnormalities
 congenital malformations
 valvular disease
 electrical abnormalities

Syncope in Children
 Vasovagal
Events
 32% to 50% of cases
 Decreased PVR
 Decreased venous return
 Decreased cardiac output
 Hypotension
 Bradycardia
Syncope Mimics
Disorders
without impairment of consciousness
Falls
Drop attacks
Cataplexy
Psychogenic pseudo-syncope
Transient ischemic attacks
Disorders
with loss of consciousness
Metabolic disorders
Epilepsy
Intoxications
Vertebrobasilar transient ischemic attacks
Differential Diagnosis of Syncope: Seizures vs Hypotension
Observation
Onset
Duration
Jerks
Headache
Confusion after
Incontinence
Eye deviation
Tongue biting
Prodrome
EEG
Seizure
Inadequate Perfusion
Sudden
More gradual
Minutes
Frequent
Seconds
Rare
Frequent (after)
Frequent
Frequent
Occasional (before)
Rare
Rare
Horizontal
Frequent
Vertical (or none)
Rare
Aura
Often abnormal
Dizziness
Usually normal
Causes of True Syncope
NeurallyMediated
Orthostatic
Cardiac
Arrhythmia
Structural
CardioPulmonary
1
2
3
4
• Vasovagal
• Carotid Sinus
• Situational
Cough
PostMicturition
• Drug-Induced
• Autonomic
Nervous
System Failure
• Brady
Primary
Secondary
• Tachy
SN
Dysfunction
AV Block
VT
SVT
• Long QT
Syndrome
Unexplained Causes = Approximately 1/3
• Acute
Myocardial
Ischemia
• Aortic Stenosis
• HCM
• Pulmonary
Hypertension
• Aortic
Dissection
Likely Causes In Children
 Vasovagal
 Situational
 Psychiatric
 Long QT*
 WPW syndrome
 RV dysplasia
 Hypertrophic cardiomyopathy
 Catecholaminergic VT
 Other genetic syndromes
Risk Factors for Serious Cause of Syncope
•history of cardiac disease in patient
•FH of sudden death, cardiac disease, or deafness
•recurrent episodes
•recumbent episode
•exertional
•prolonged loss of consciousness
•associated chest pain or palpitations
•medications that can alter cardiac conduction
Syncope: Important Historical Features
Questions about circumstances just prior to attack
 Position (supine, sitting , standing)
 Activity (rest, change in posture, during or immediately
after exercise, during or immediately after urination,
defecation or swallowing)
 Predisposing factors (crowded or warm place, prolonged
standing post-prandial period) and of precipitating events
(fear, intense pain, neck movements)
Questions about onset of the attack
 Nausea, vomiting, feeling cold, sweating, pain in chest
Syncope: Important Historical Features
Questions about attack (eye witness)
 Skin color (pallor, cyanotic)
 Duration of loss of consciousness
 Movements ( tonic-clonic, etc.)
 Tongue biting
Questions about the end of the attack
 Nausea, vomiting, diaphoresis, feeling cold, muscle
aches, confusion, skin color, wounds
Syncope: Important Historical Feature
Questions about background
 Number and duration of syncope spells
 Family history of arrhythmic disease or sudden
death
 Presence of cardiac disease
 Neurological disease
 Medications (Hypotensive, negative chronotropic
and antidepressant agents)
Clinical Features Suggesting Specific Cause of Syncope
Neurally-Mediated Syncope
 Absence of cardiac disease
 Long history of syncope
 After sudden unexpected, unpleasant sensation
 Prolonged standing in crowded, hot places
 Nausea vomiting associated with syncope
 During or after a meal
 With head rotation or pressure on carotid sinus
 After exertion
Clinical Features Suggesting Specific Cause of Syncope
Syncope due to orthostatic hypotension
 After standing up
 Temporal relationship to taking a
medication that can cause hypotension
 Prolonged standing
 Presence of autonomic neuropathy
 After exertion
Clinical Features Suggestion Cause of Syncope
Cardiac Syncope
 Presence of structural heart disease
 With exertion or supine
 Preceded by palpitations
 Family history of sudden death
Initial Exam: Thorough Physical
 Vital signs
 Heart rate
 Orthostatic blood pressure change
 Cardiovascular exam: Is heart disease present?
 ECG: Long QT, pre-excitation, conduction
system disease
 Echo: LV function, valve status, HCM
 Neurological exam
Orthostatic Measurements
 Classically,
abnormal if systolic BP decreases
by more than 20 points and/or pulse increases in
pulse rate of more than 20 beats per minute after
a change from supine to standing
 If there is only a pulse increase but no drop in
blood pressure, the test is less significant
Diagnostic Objectives
Distinguish true syncope from syncope
mimics
 Determine presence of heart disease and risk
for sudden death
 Establish the cause of syncope with
sufficient certainty to:
• Assess prognosis confidently
• Initiate effective preventive treatment

Case study 7
 12
year old girls presented to ED with history of
sever headache for last 2 weeks . The headache
was intermittent ,diffuse and bilateral .
 She was seen in different private clinic and
treated with regular analgesics but without
effect.
 Not regular in the school. no menses yet
Case study 7
On exam: T 37, HR 86, RR 20, BP 90/60, oxygen
saturation 99% in room air. height 159 cm (50%ile),
weight 43.7 kg (50%ile). She is alert ,no signs of
respiratory distress , pallor , cyanosis.
 Normal E.N.T ,chest ,CNS ,abdomen and skin
examination.
 Cardiac exam: normal heart sounds ,short systolic
murmur grade 2/6 at ULSB, good volume pulses.
 Normal puberty stages .

Case study 7

What is your general impression of this
patient?
Case study 7
 Laboratory:
all normal
Electrolytes
CBC with differential
Hepatic and renal profile.
 Head CT was postponed
Case study 7






On exam by the 2nd shift in ER: T 37, HR 80, RR 18, BP in RA
130/90, oxygen saturation 100% in room air. She is alert ,no
signs of respiratory distress , pallor , cyanosis.
Normal neurological examination .
Normal E.N.T ,chest ,abdomen and skin examination.
Cardiac exam: normal heart sounds ,short systolic murmur grade
3/6 at ULSB with radiation to the back between the scapulae.
Extremities: Femoral pulses are slightly diminished to palpation;
no peripheral edema, clubbing or cyanosis of the nail beds.
Normal puberty stages , normal female genitalia.
Case study 7

Laboratory Evaluation:
 CBC & ABG/VBG
 Ca, Magnesium & Phos
 Renal profile
 CXR & 12 lead ECG
 Hormonal assay
 Ultrasound of abdomen/ Echocardiography
 Urinary VMA
Case study 7


Chest radiograph : cardiac/thoracic ratio of 0.55, normal cardiac
configuration, and normal pulmonary vasculature and notching at
lower margins of upper ribs
ECG:

sinus tachycardia

LVH apparent (left lateral leads)
Deep S waves in the right chest
Large R waves in lateral leads


Case study 7
Case study 7
 The
echocardiogram demonstrates
narrowing of the distal aortic arch with
increased velocities on pulsed and color
Doppler and bicuspid aortic valve
 She was diagonesd as Coarctation of the
aorta , bicuspid aortic valve.
Coarctation of Aorta
Case study 7

Management :
Coarctation of Aorta
 Upper
arm vs lower extremity BP discrepancy
>10-20 mmHg systolic upper vs. lower
20-30% develop CHF by 2-3 months
 Hx of lower extremity weakness or pain after
exercise
 50% will have no murmur
Hypertension
1-3% of the pediatric population
 unknown cause = essential or primary HTN
 underlying kidney or cardiac disease=secondary HTN
 children’s BP in >90th at increase risk for adult HTN
 HTN in adolescent correlates with obesity and elevated
serum lipid level
