Acute Care Exam #2

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1
Acute Metabolic Response
-Alterations in metabolism that hospitalized children experience in response to injury or illness
-Increased production and release of catecholamines, cytokines, glucocorticoids and glucagon
-As the body regulates the impact of hormonal release, other metabolic changes occur, including hypermetabolism, hyperglycemia, catabolism, and dyslipidemia
2
Acute Metabolic Response: Degree Influence
-Preexisting conditions
-Malnutrition
-Underlying systemic disease
-Age
3
Acute Metabolic Response: Causes
-Catecholamine
-Cytokines
-Glucose
-Hyperglycemia
-Lipids
-Acute Phase Proteins
4
Catecholamine
Reduction of insulin secretion and peripheral insulin action stimulates the production of glucagon and adrenocorticotropic hormone (ACTH), causing increased corticosteroid production
5
Cytokines
Injured tissue causes the release of proinflammatory cytokines, causing growth hormone resistance, catabolism, and growth halt
6
Glucose
-The primary fuel source for the brain
-It is utilized to repair injured tissues and depletes quickly during acute illness and injury
7
Hyperglycemia
-A multifactorial stress response commonly seen in hospitalized pediatric patients
-It is important to evaluate and adjust exogenous sources of carbohydrates
8
Lipids
-Increased serum lipid levels are commonly seen in children who experience surgery, trauma, or critical illness
-Many factors contribute to this, including malnutrition, metabolic stress, organ dysfunction, and some medications
9
Acute Phase Proteins
-Inflammation during inflammatory responses causes hepatic protein synthesis
-Positive acute phase proteins include C-reactive protein (CRP), ceruloplasmin, and fibrinogen, which increase during inflammatory periods
-Negative acute-phase proteins include albumin, prealbumin, retinol-binding protein, and transferrin, which decrease during inflammatory periods
-Alterations in protein metabolism can predict mortality in children who have had surgery and those hospitalized in intensive care
10
Estimated Energy Requirements: Infants
-2-3 months:
102 calories/kg/day
-4-6 months:
82 calories/kg/day
-7-12 months:
80 calories/kg/day
-13-35 months
82 calories/kg/day
11
Estimated Protein Requirements: Infants
1.5 gm/kg/day
12
Estimated Energy Requirements: Children/Adolscents
-3 years:
boys: 85 calories/kg/day
girls: 82 calories/kg/day
-4-5 years:
boys: 70 calories/kg/day
girls: 65 calories/kg/day
-6-7 years:
boys: 64 calories/kg/day
girls: 61 calories/kg/day
-8 years:
boys: 59 calories/kg/day
girls: 59 calories/kg/day
13
Estimated Energy Requirements: Children/Adolscents Continued
-9-11 years:
boys: 49 calories/kg/day
girls: 42 calories/kg/day
-12-13 years:
boys: 44 calories/kg/day
girls: 40 calories/kg/day
-14-16 years:
boys: 39 calories/kg/day
girls: 33 calories/kg/day
-17-18 years:
boys: 37 calories/kg/day
girls: 31 calories/kg/day
->18 years:
boys: 36 calories/kg/day
girls: 34 calories/kg/day
14
Estimated Protein Requirements: Children/Adolscents
-3 years:
1.1 gm/kg/day
-4-13 years:
0.95 gm/kg/day
-14-18 years:
0.85 gm/kg/day
->18 years:
0.8 gm/kg/day
15
Overfeeding
Can cause:
hyperglycemia
lipogenesis
increased CO2 production
-Increasing the risk of morbidity and mortality
16
Underfeeding
-Commonly occurs in hospitalized children for various reasons, including:
NPO status
fluid restrictions
-Can cause:
protein-energy malnutrition
increased infections
poor wound healing
17
3 Goals of Parenteral Nutrition
1. Meet nutrient needs that cannot be met by enteral intake alone.
2. Avoid nutrient toxicity and/or deficiency.
3. Optimize nutritional status.
18
Parenteral Nutrition: Nonfunctional or Inaccessible Gastrointestinal Tract
-Intestinal failure (short bowel syndrome)
-Severe malabsorption
-Obstruction or ileus
-Intractable vomiting or diarrhea
-Necrotizing enterocolitis
-Congenital anomalies of the GI tract
-Bowel ischemia
19
Parenteral Nutrition: Extraintestinal Disorders/Therapy
-Malignancies
-Body surface burns
-Cardiac failure
-Kidney failure
-Chylothorax
-Extracorporeal membrane oxygenation (ECMO)
20
Parenteral Nutrittion: PIV Usage
-Limited to 10-14 days
-Limited to a dextrose concentration of <12.5%
-Osmolarity per liter is limited to 700-900 mOsm
21
When is PPN considered?
-Nutritional status is not adequate
-GI tract is not funcitonal
-<7-14 days needed
-Able to tolerate increased fluid volumes
-Needs dextrose <12.5%
22
When is TPN considered?
-Nutritional status is not adequate
-GI tract is not funcitonal
->7-14 days needed
-Not able to tolerate increased fluid volumes
-Needs dextrose >12.5%
23
When can you considered oral/enteral feedings versus parental nutrition?
-Infant NPO for 3-5 days
-Children NPO for 5-7 days
-Has a functional GI tract
-If oral feedings are inadequate, then consider enteral
-If goal feeds are not tolerated, then supplement with parentral nutrition
24
Osmolarity of Parenteral Nutrition Calculation
-Total grams of amino acids per liter of solution ___ gm × 10 = ___ mOsm
-Total grams of dextrose per liter of solution __ gm × 5 = __ mOsm
-Total mEq of sodium and potassium per liter of solution __ mEq × 2 = __ mOsm
-Total mEq of calcium per liter of solution __ mEq × 1.4 = __ mOsm
-Total mEq of magnesium per liter of solution __ mEq × 1 = __ mOsm
-Total osmolarity = __ mOm
25
Parenteral Nutrition Macronutrients
-Protein
-Carbohydrates
-Lipids
26
Protein
-Protein is supplied as crystalline amino acids
-Neonatal amino acid solutions are used for infants through one year of age
-After one year of age, adult amino acid products are typically used
-Minimum protein intake of 1.5 gm/kg/day is needed to prevent cumulative protein deficits in critically ill children
-Protein may be limited if kidney or liver dysfunction is present
27
Carbohydrates
-Carbohydrates are supplied as dextrose monohydrate and provide 3.4 Kcals per gram
-Carbohydrates are the primary source of calories in parenteral nutrition
-Complications of excessive carbohydrate infusion include phlebitis, refeeding syndrome, hepatosteatosis, cholestasis, CO2 retention, hypoglycemia, and hyperglycemia
28
Lipids
-Intravenous fat emulsions (IVFE) provide the essential fatty acids, linoleic acid and α-linoleic acid, which are isomolar and a concentrated source of energy
-IVFE can be given as a separate infusion, part of a total nutrient admixture, or as a 3-in-1 solution
29
Parenteral Nutrition Micronutrients
-Zinc
-Copper
-Chromium
-Manganese
-Selenium
30
Parenteral Nutrition Micronutrients Key Points
-Electrolytes can be ordered individually or in preset combinations
-Vitamins can be added to PN as a multivitamin preparation or as single vitamins
-Adding medications directly into PN is not recommended
31
Parenteral Nutrition: Complications
-Metabolic alkalosis and acidosis
-Electrolyte imbalance
-Volume overload
-Anemia
-Cholestatic jaundice
32
Parenteral Nutrition Monitoring Protocol: Weight
-Initial:
daily
-When Stable:
daily
33
Parenteral Nutrition Monitoring Protocol: Length and Head Circumference
-Initial:
weekly
-When Stable:
weekly
34
Parenteral Nutrition Monitoring Protocol: BMP with Magnesium and Phosphorus
-Initial:
daily
-When Stable:
2-3 times per week
35
Parenteral Nutrition Monitoring Protocol: CMP with Ionized Calcium
-Initial:
weekly
-When Stable:
weekly
36
Parenteral Nutrition Monitoring Protocol: Triglyceride Levels
-Initial:
2-3 days after starting
-When Stable:
2 times per week
37
Parenteral Nutrition Monitoring Protocol: Glucose
-Initial:
1-2 hours after initiation
changing glucose concentration
if cycled, midinfusion and one hour after stopping PN
-When Stable:
as needed
38
Parenteral Nutrition Monitoring Protocol: Trace Elements
-Initial:
1 month after initiating PN
-When Stable:
monthly
39
Who should be involved when initiating PN?
-Provider
-Dietitian
-Pharmacist
40
Calcium Functions
-Intracellular processes
-Bone formation
-Neuronal activity
-Muscular contraction
-Blood coagulation
41
How is calcium regulated?
-Regulation of calcium concentration is primarily controlled by the parathyroid hormone
-Increased the concentration of PTH causes an increase in serum calcium concentration
42
Cause: Hypocalcemia
-Caused by the binding of ionized calcium to the citrate of banked blood during or following cardiac bypass, with massive transfusion after trauma, or during plasmapheresis
-Renal replacement therapy
-Tumor Lysis Syndrome
-Pancreatitis
-Syndromic etiology
-Medications
-Other electrolyte abnormalities
43
Presentation: Hypocalcermia
-Numbness
-Tingling
-Muscle cramps
-Irritability
-Confusion
-Trosseau sign
-Positive Chvostek sign
-Prolonged QT interval on ECG
-Laryngospasm
-Seizures
-Tetany
44
Management: Hypocalcemia
-IV replacement with careful monitoring during infusion
-Chronic hypocalcemia-oral supplements such as:
calcium carbonate
calcium citrate
45
Cause: Hypercalcemia
-Associated with malignancy
-Can result from:
immobility
leg fractures
spinal cord damage
critical illness
-Syndromic etiology:
familial hypocalciuric hypercalcemia
hyyperparathyroidism
46
Presentation: Hypercalcemia
-Vague symptoms
-Mild to moderate is typically asymptomatic
-Constipation
-Anorexia
-Headache
-Depression
-Hypotonia
-Nephrolithiasis
-Nephrocalcinosis
-Coma
-Anxiety
-Shortened QT interval on ECG
-Renal tubular dysfunction
47
Management: Hypercalcemia
-Hydration with normal saline
-Avoid thiazide diuretics
-For rapid treatment:
glucocorticoids
calcitonin
bisphosphonates
48
Potassium
-Excreted by the kidneys
-Balance is hormonally regulated
this appears when the cell appears
-Homeostasis is impacted by acid-base imbalance and osmolarity
-Acidosis can cause a rise in serum potassium
-Alkalosis can cause a decrease in serum potassium
49
Cause: Hypokalemia
-Most often drug induced:
laxatives
diuretics
penicillin
enemas
-Drugs that have B sympathetic activity:
bronchodilators
decongestants
dopamine
dobutamine
50
Presentation: Hypokalemia
-Generally asymptomatic
it may present as ventricular arrythmias in individuals with underlying cardiac issues
these individuals should maintain a potassium level >4.5
-It can cause hypertension and increases the risk of digoxin toxicity
51
Management: Hypokalemia
-Treated with potassium replacement, usually supplemental potassium in hospitalized patients
-Oral supplementation can be given in non-emergent situations
3 Formulations
potassium chloride
potassium phosphate
potassium bicarbonate
52
Management: Hypokalemia Continued
-Emergency treatment may include IV supplementation with potassium chloride at 0.5 to 1 mEq/kg with a max dose of 20 mEq:
cardiac monitoring should occur throughout infusion
preferable through a central vein when possible
never given IV bolus
53
Hyperkalemia
-Hemolysis of the sample should first be considered in any lab value revealing hyperkalemia, and another lab should be drawn, while also preparing to treat the condition
-Most common cause in a hospitalized patient is the use of potassium sparing diuretics
-Hyperkalemia may also be found in impaired renal conditions
54
Cause: Hyperkalemia
-Acute rise in potassium:
individual may be in an acidotic state
-Chronic hyperkalemia:
associated with kidney excretion impairment
55
Presentation: Hyperkalemia
-May be life threatening
-Can present with cardiac arrythmias
56
ECG Changes: Hyperkalemia
-First: Peaked T waves
-Progressing to prolonged PR and QRS intervals
-Leading to a loss of the PR interval
And, merging of the QRS and T wave to produce a sine wave pattern
-Hyperkalemia with ECG changes is an emergency and should be treated immediately
Stop all exogenous forms of potassium and confounding medications
57
Hyperkalemia Management
-Calcium chloride (10 mg/kg) or calcium gluconate (100 mg/kg)
-Insulin and glucose therapy
-Bicarbonate
-Beta agonists IV or aerosolized
-Kayexalate administered rectally
-Hemodialysis
58
Phosphorus
-Involved in most metabolic processes
-Important part of glycolysis
-Kidneys primarily control phosphate excretion
-Levels vary according to circadian rhythms
-Most variable electrolyte by age
59
Hypophosphatemia Causes
-DKA
-Rapidly growing tumors
-Respiratory alkalosis
-Hyperventilation
-Panic attacks
-Sepsis
-Salicylate poisoning
-Mechanical ventilation
-Chronic use of aluminum-containing antacids
-Extensive burns
-Chronic phosphorus depletion can cause rickets
60
Hypophosphatemia Presentation
-Muscle weakness (including diaphragmatic weakness)
-Rhabdomyolysis
-Decreased respiratory function
-Rickets
-Malformation of the skull
-Bowing of the arms and legs
-Delayed tooth eruption with enamel defects
-Long bone fractures
-Abnormalities of the spine and pelvis
61
Hypophosphatemia Management
-IV phosphorus supplementation for severe hypophosphatemia
-Oral phosphorus supplementation for mild or chronic hypophosphatemia
-Give oral supplementation in divided doses to avoid diarrhea or GI distress
62
Hyperphosphatemia Causes
-Kidney failure
-Tumor lysis syndrome
-DKA
-Disorders causing lactic acidosis
63
Hyperphosphatemia Presentation
-Hypocalcemia
-Tetany
-Increased osteoblastic activity
-Abnormal bone formation
64
Hyperphosphatemia Management
-Dietary phosphate restriction for mild cases with normal kidney function
-Reduce protein intake
-IV fluids
-Calcium carbonate
-Calcium acetate
65
Chloride
-Most abundant anion in the extracellular fluid
-Regulated by the kidneys and intestine
-Maintains electrical neutrality
-Has an inverse relationship with bicarbonate
66
Hypochloremia Causes
-Metabolic alkalosis
-Emesis
-Nasogastric suctioning
-Diuretic use
-Respiratory failure
-Cardiac failure
-Chronic hypercarbia
-Cystic fibrosis
-Chloride-losing diarrhea
67
Hypochloremia Presentation
-Symptoms of metabolic alkalosis and underlying disorder
-Thirst
-Lethargy
-Tachycardia
-Tachypnea
-Delayed capillary refill
-Seizures (severe)
68
Hypochloremia Management
-Treat the underlying cause
-Volume repletion (except in heart failure)
-Sodium chloride or potassium chloride replacement
-Use sodium chloride cautiously in congestive heart failure
-Arginine hydrochloride or hydrochloric acid for rapid correction in emergent situations with monitoring
69
Hyperchloremia Causes
-Metabolic acidosis
-Diarrhea
-Excessive chloride-containing substances
70
Hyperchloremia Presentation
-No specific symptoms
-Commonly occurs with hypernatremia and hyperkalemia
-Kussmaul respirations
-Lethargy
-Headache
-Confusion
-Coma (severe)
71
Hyperchloremia Management
-Treat the underlying cause
-Treat associated acidosis
-IV bicarbonate for severe acidosis
72
Magnesium
-Half of body stores are in bone
-Involved in ATP generation
-DNA transcription
-Protein synthesis
-40% of dietary magnesium is absorbed in the upper small intestine
73
Hypomagnesemia Causes
-Medications (amphotericin, cisplatin, potassium-sparing diuretics, calcium)
-GI losses
-Renal losses
-Diarrhea
-Steatorrhea
-Treatment of DKA
-Fluid administration
-Infants of diabetic mothers
74
Hypomagnesemia Presentation
-Associated with hypocalcemia and hypokalemia
-Seizures
-Paresthesia
-Ataxia
-Tetany
-Muscle weakness
-Delirium
-Hyperglycemia
-Arrhythmias
75
Hypomagnesemia Management
-IV magnesium sulfate or magnesium chloride
-Slow IV infusion is preferred
-IV magnesium may treat torsades de pointes, ventricular arrhythmias, preeclampsia, and status asthmaticus
-Emergent bolus for symptomatic seizures or arrhythmias with monitoring
-Oral magnesium in divided doses for mild cases
76
Hypermagnesemia Causes
-Excessive magnesium intake
-Magnesium-containing laxatives
-Antacids
-Inappropriate magnesium concentration in TPN
-Infants of mothers treated with magnesium for preeclampsia
-Chronic kidney failure
-Tumor lysis syndrome
-Milk-alkali syndrome
-Lithium ingestion
-DKA
77
Hypermagnesemia Presentation
-Lethargy
-CNS depression
-Hypotension
-Flushing
-Prolonged PR, QRS, and QT intervals
-Abdominal cramping
-Nausea and vomiting
78
Hypermagnesemia Management
-Basic stabilization
-Inotropes and ventilatory support for severe muscle weakness
-Exchange transfusion
-Loop diuretics
-Dialysis for life-threatening cases
-Stop magnesium intake for mild cases with normal kidney function
79
Sodium
-Associated with skeletal muscle, nerve, and myocardial action potentials
-Maintains acid-base balance
-Normal range: 135-145 mEq/L
80
Hyponatremia Types
-Hypervolemic
-Hypovolemic
-Normovolemic
81
Hypervolemic Hyponatremia Causes
-Congestive heart failure
-Acute or chronic kidney failure
-Nephrotic syndrome
-Water intoxication
-Cirrhosis
82
Hypovolemic Hyponatremia Causes
-Renal losses
-Diarrhea
-Vomiting
-Burns
-Pancreatitis
83
Normovolemic Hyponatremia Causes
-SIADH
-Adrenal insufficiency
-CNS disease
-Pulmonary disease
-Excessive diuretic use
84
Hyponatremia Presentation
-Irritability
-Poor feeding
-Nausea and vomiting
-Lethargy
-Seizures
-Coma
-Death
-Chronic hyponatremia may be asymptomatic until sodium is very low
-Acute hyponatremia increases risk of cerebral edema
85
Pseudohyponatremia
-Associated with hyperlipidemia
-Hyperproteinemia
-Hyperglycemia
-Serum sodium appears low but total body sodium may be normal
86
Hyponatremia Management
-Restore intravascular volume
-Replace sodium deficit
-Treat underlying cause
-Monitor serum sodium closely
-Urgently treat neurologic symptoms
-Raise sodium to 125 mEq/L if seizures are present
-Use hypertonic saline if available
-If unavailable, give 20 mL/kg NS bolus
-Avoid rapid correction to prevent neurologic injury
87
Hypernatremia Causes
-Excessive sodium intake
-Free water loss
-Concentrated formula
-Breastfeeding without supplementation
-Salt supplements
-Sodium bicarbonate
-Diarrhea
-Diabetes insipidus
-Renal tubular disorders
-Post-obstructive diuresis
88
Hypernatremia Presentation
-Irritability
-High-pitched cry
-Lethargy
-Seizures
-Renal failure
-Rhabdomyolysis
-Permanent CNS dysfunction may occur with sodium >165-170 mEq/L
89
Hypernatremia Management
-Correct sodium slowly to prevent cerebral edema
-If shock is present, give 20 mL/kg isotonic crystalloid boluses until perfusion is restored
-Replace fluid deficit over 48-72 hours after shock is corrected
-Provide maintenance fluids and replace ongoing losses
-Hypovolemic hypernatremia may require loop diuretics and decreased sodium
90
Failure to Thrive
-Symptom resulting from medical, psychosocial, and environmental conditions that lead to poor growth
-Also called faltering growth
-State of inadequate weight gain velocity
-If untreated, results in poor health outcomes
91
When to Consider Failure to Thrive
-Growth measurements below the 3rd-5th percentile
-2 or more standard deviations below baseline on the growth chart
92
Failure to Thrive Risk Factors
-Environmental factors
-Chronic comorbidities
-Social challenges
-Poverty
93
Malnutrition
-Imbalance between energy, protein, and micronutrient requirements and consumption or utilization
-Can be undernutrition or overnutrition
94
Malnutrition Classification
-Illness-related
-Environmental causes
-Behavioral causes
-Acute or chronic
95
Acute Malnutrition
Significant decline in weight-for-height occurring within 3 months
96
Chronic Malnutrition
-Length/height deficit lasting 3 months or longer
-Common in chronic illnesses
-Neurologic disorders
-Cystic fibrosis
-Childhood cancer
-Cardiovascular disease
-GI disease
97
Malnutrition Diagnosis
Evaluate growth charts using weight and height
98
Obesity
Weight-for-length >95th percentile
99
Obesity Risks During Acute Illness
-Anemia
-Decreased vitamin levels
-Altered lipid metabolism
-Insulin resistance
-Altered glucose control
100
Complications of Malnutrition
-Decreased skin integrity
-Increased infection risk
-Reduced GI function
-Prolonged hospitalization
-Muscular dysfunction
-Vitamin and micronutrient deficiencies
101
Malnutrition Management
-Recognition, assessment, and accurate classification
-Hospitalization for severe malnutrition
-Ongoing assessment of weight gain
-Monitor cognitive and motor development
-Assess social and emotional environment
102
Goal of Care for Malnutrition
-Individualized care
-Catch-up growth
-Target weight gain 2-3 times the average rate
103
Growth Charts
-Used as part of nutrition assessment
-Preterm infant growth charts
-Term infant and child (<2 years) growth charts
-Children 2-20 years growth charts
-Condition-specific growth charts
104
Percentiles
-Compare a child to the reference population
-Range from 0-99%
-Always positive values
105
Z-Scores
-Number of standard deviations from the mean
-More precise measure of abnormal growth
-Useful when above or below the growth chart limits
-More negative = more severe malnutrition
-Used to quantify malnutrition
106
Preterm Growth Charts
-Compare infant growth to intrauterine growth
-Fenton Growth Chart: 22-50 weeks gestational age
-Olsen Growth Chart: 22-42 weeks gestational age
-Olsen includes racially diverse children
107
WHO Growth Charts
-Used for term infants and children 0-2 years
-Includes length, weight, head circumference, and weight-for-length
-Length measured lying down until age 2
-Head circumference measured until age 2
-Correct preterm infants for gestational age until 2 years corrected age
-Assess growth by corrected gestational age rather than chronological age
108
CDC Growth Charts
-Used for children 2-20 years
-Includes height, weight, and BMI
109
BMI Classification
-Underweight: <5th percentile
-Normal weight: 5th-84th percentile
-Overweight: 85th-94th percentile
-Obese: >95th percentile
110
Condition-Specific Growth Charts
-Cerebral palsy
-Down syndrome
-Turner syndrome
-Marfan syndrome
111
Mid Upper Arm Circumference
-Measures muscle, fat, and bone
-Independent marker for mortality
-Correlates with BMI
-Used to diagnose and document malnutrition
112
Refeeding Syndrome
-Occurs when previously malnourished children are aggressively fed
-Carbohydrates stimulate insulin secretion causing fluid and electrolyte shifts
-Hypophosphatemia is most common
-May also cause hypokalemia and hypomagnesemia
113
Refeeding Syndrome Risk Factors
-Recent weight loss
-Prolonged poor nutritional intake
-Malnutrition
114
Refeeding Syndrome Prevention
-Start oral, enteral, or parenteral nutrition slowly
-Gradually increase feeds
-Closely monitor serum electrolytes
-Monitor fluid status
-Monitor cardiopulmonary function
115
Water Distribution: Infants and Malnourished Children
-25% extracellular
-19% interstitial
-6% plasma, protein, and lipids
-45% intracellular
-Higher water-to-lean body mass ratio increases dehydration risk
116
Water Distribution: 5-Year-Old to Adult
-20% extracellular
-50% intracellular
117
Daily Maintenance Fluid Requirements
Include physiologic losses from urine, stool, and insensible losses
118
Holliday-Segar Maintenance Fluids: 3-10 kg
-100 mL/kg/day
-4 mL/kg/hr
119
Holliday-Segar Maintenance Fluids: 10-20 kg
-1,000 mL + 50 mL/kg for each kg over 10
-40 mL/hr + 2 mL/hr for each kg over 10
120
Holliday-Segar Maintenance Fluids: 20-70 kg
-1,500 mL + 20 mL/kg for each kg over 20
-60 mL/hr + 1 mL/hr for each kg over 20
121
Infectious Causes of Dehydration
-Viral
-Bacterial
122
Noninfectious Causes of Dehydration
-Antibiotic therapy
-Malnutrition
-Overfeeding
-Protein allergies
-Chronic diarrhea
-DKA
-Capillary leak (sepsis)
-Burns
-Hemorrhage
-Inadequate fluid intake
123
Dehydration Assessment
-Etiology of fluid loss
-Chronic illness
-Close contacts with similar symptoms
-Heat or sun exposure
-Fever
-Oral intake compared to baseline
-Activity level
-Medications or treatments
-Duration of illness
-Wet diapers in last 24 hours
-Toxic ingestion
-Metabolic disorders
-Prior surgeries
-Normal diet
124
Signs of Dehydration
-Poor skin turgor
-Tachycardia
-Delayed capillary refill
-Weight loss
-Mottled skin
-Sunken fontanel
-Sunken eyes
-Increased respiratory and heart rate
-Hypovolemic shock
125
Mild Dehydration
-Infants: 5% (50 mL/kg)
-Older children: 3% (30 mL/kg)
-Normal skin turgor
-Normal or sticky mucous membranes
-Normal eyes
-Tears present
-Flat fontanel
-Alert
-Normal pulse
-Normal capillary refill
-Normal urine output or mild oliguria
126
Moderate Dehydration
-Infants: 6-10% (100 mL/kg)
-Older children: 4-6% (60 mL/kg)
-Mildly decreased skin turgor
-Dry skin and mucous membranes
-Deep-set eyes
-Decreased tears
-Sunken fontanel
-Irritable or lethargic
-Slightly increased pulse
-Weak pulse
-Delayed capillary refill (>1.5 sec)
-Mild oliguria
127
Severe Dehydration
-Infants: >10%
-Older children: >6%
-Delayed skin elasticity
-Cold, mottled skin
-Parched, cracked lips
-Sunken eyes
-No tears
-Sunken fontanel
-Lethargic or obtunded
-Increased pulse
-Weak or absent pulse
-Capillary refill >3 seconds
-Severe oliguria
128
Isonatremic Dehydration
-Most common type
-Normal sodium (135-145 mEq/L)
-Usually secondary to gastroenteritis
129
Hyponatremic Dehydration
-Sodium <135 mEq/L
-Seizures
-Noncardiogenic pulmonary edema
-Respiratory arrest
-Brain herniation
130
Hypernatremic Dehydration
-Sodium >145 mEq/L
-Often secondary to vomiting
-May cause rapid brain volume reduction
-Subarachnoid hemorrhage
-Subdural hematoma
-Hyperreflexia
-Confusion
-Seizures
-Coma
131
Dehydration Management
-BUN increases with dehydration
-Assess sodium level
-Follow daily weights
-Monitor intake and output
-Monitor blood pressure
-Assess for edema
132
Oral Rehydration Therapy (ORT)
-Used for mild to moderate dehydration
-Goal: 15 mL/kg/hr or 60 mL/kg over 4 hours
133
ORT Contraindications
-Severe dehydration or shock
-Severe vomiting or ileus
-Lack of caregiver supervision
134
Moderate Dehydration Management
-Reassess every hour
-Hospital admission not always necessary
-Restart feeds after hydration
-Outpatient follow-up the next day
135
Initial IV Fluid Management
-20 mL/kg isotonic fluid bolus
-Use NS or LR
-Repeat until perfusion improves
-Up to 60 mL/kg in the first hour
136
Signs of Adequate Fluid Resuscitation
-Improved level of consciousness
-Improved pulses
-Decreased capillary refill time
137
Repletion Management
-Replace deficits based on type of dehydration
-Use NS or LR
-Avoid glucose-containing or hypotonic fluids initially
138
Isonatremic Dehydration Management
-Replace deficits, maintenance, and ongoing losses
-Complete over 24 hours
-Base replacement on fluid, sodium, and potassium deficits
-Subtract initial boluses from 24-hour total
-Reassess ongoing losses every 4-6 hours
139
Hypernatremic Dehydration Management
-Most dangerous type
-Improve perfusion
-Lower sodium to ~155 mEq/L
-Decrease sodium no faster than 10-12 mEq/L per 24 hours
-Replace fluids over 48 hours or longer
-Subtract initial boluses from total fluids
-Reassess ongoing losses every 4-6 hours
140
Hyponatremic Dehydration Management
-Treat like isonatremic dehydration if no neurologic symptoms
-Raise sodium to ~125 mEq/L
-Increase sodium no faster than 10-12 mEq/L per 24 hours
-Rapid correction can cause osmotic demyelination syndrome
-Subtract initial boluses from total fluids
-Reassess ongoing losses every 4-6 hours
141
Discharge Criteria for Dehydration
-Mild to moderate dehydration can be discharged after completing 3-4 hours of ORT
-If IV fluids were given, complete ORT before discharge
-Follow up the next day after urgent care or ED evaluation
142
Arterial Line Placement
-Provides continuous blood pressure monitoring
-Allows frequent blood sampling
-Ultrasound guidance is recommended
143
Arterial Line Indications
-Continuous blood pressure monitoring
-Hemodynamic instability
-Vasoactive medication administration
-Active volume resuscitation
-Unreliable or unobtainable noninvasive blood pressure
-Frequent arterial blood gases
-Significant respiratory support
144
Arterial Line Risks
-Infection
-Trauma to the artery
-Thrombosis
-Hematoma
145
Arterial Line Contraindications
-Infection at insertion site
-Traumatic injury proximal to insertion site
-Inadequate collateral circulation
-Failed Allen's test
146
Arterial Line Techniques
-Slide-off (Thread-off): shallow angle, easier catheter advancement
-Through-and-through: steep angle, uses guidewire
-Do not switch techniques after starting
-If unable to thread catheter, remove it, hold pressure, and reattempt
147
Peripheral Arterial Line Sites
-Radial artery (preferred)
-Ulnar artery
-Brachial artery (not recommended)
-Dorsalis pedis artery
-Posterior tibial artery
148
Why is the Radial Artery the Preferred Arterial Line Site?
-Easily accessible
-Pulse easily palpated
-Good collateral circulation
149
Why is the Brachial Artery Not Recommended for Arterial Line Placement?
-Sole blood supply to the distal arm
-Compromise may decrease blood flow to the lower arm
150
Central Arterial Line Placement
-Sterile procedure
-Used when distal pulses cannot be palpated
-Indicated in profound shock or severe extremity trauma
151
Central Arterial Line Sites
-Femoral artery
-Axillary artery
152
Allen's Test
-Patient clenches fist
-Occlude radial and ulnar arteries
-Allow palm to become pale
-Release one artery and assess return of color
-Repeat on opposite side
-Determines adequate collateral circulation
153
Arterial Line Catheter Sizes
-24G: Infant
-22G: Toddler
-22-20G: Small children
-20-18G: Larger children and adults
154
Arterial Line Monitoring
-Assess distal perfusion
-Monitor insertion site for infection
-Monitor arterial waveform
-Monitor blood pressure values
155
Central Venous Line
-Used in acutely ill children
-Strict protocols for medications, blood sampling, and dressing changes
156
Central Venous Pressure (CVP)
-Pressure in the intrathoracic vena cava
-Approximates right atrial pressure
-Depends on cardiac output and venous return
157
Factors Affecting CVP
-Blood volume
-Vascular tone
-Heart rate
-Ventricular contractility
158
CVP Changes
-Decreases with hypovolemia
-Increases with increased circulating volume
159
CVP Uses
-Assess cardiac function
-Assess central circulation pressure
-Monitor fluid therapy
-Prevent fluid overload
-Assess intravascular volume status
-Evaluate right atrial compliance
160
CVP A Wave
-Occurs late in diastole
-Corresponds with the P wave
-Represents atrial contraction
161
CVP C Wave
-Occurs during early systole
-Corresponds with the R wave
-Represents tricuspid valve bulging into the right atrium
-May merge with the A wave during tachycardia
162
CVP X Descent
-Occurs during mid systole
-Corresponds with the QRS complex
-Represents atrial relaxation and downward movement of the tricuspid valve
163
CVP V Wave
-Occurs during late systole
-Corresponds with the T wave
-Represents right atrial filling during ventricular systole
-Large V wave suggests tricuspid regurgitation or a noncompliant right atrium
164
CVP Y Descent
-Occurs during early diastole
-Represents emptying of the right atrium into the ventricle
165
Chest Tube Size
>16 French
166
Thoracostomy Catheter Size
<14 French
167
Chest Tube Indications
-Pneumothorax
-Pneumomediastinum
-Air leak after pulmonary resection
-Bronchopleural fistula
-Hemothorax
-Chest trauma
-Postoperative complications
-Pleural effusion
-Empyema
-Parapneumonic effusion
-Chylothorax
-Compression from air, fluid, or blood
168
Chest Tube Contraindications
-Skin infection at insertion site
-Use caution with coagulopathy
-Platelet count <50,000
-Pulmonary bullae
-Pleural adhesions
-Diaphragmatic adhesions
169
Chest Tube Placement
-Insert at the anterior axillary line
-Level of the 4th-5th intercostal space (nipple landmark)
-Placing too low risks entering the peritoneal cavity
170
Chest Tube Post Placement
-Occlusive dressing
-Atrium collection system
-20 cm H2O suction
-2 cm H2O water seal
171
Chest Tube Removal
-No further air or fluid leak
-Place to water seal
-Obtain chest x-ray
-Remove if no reaccumulation of air or fluid
172
Chest Tube Complications
-Injury to lungs
-Injury to heart
-Injury to liver
-Injury to other organs
-Bleeding
-Pneumothorax
-Infection
173
Chest Tube Monitoring
-Monitor vital signs
-Monitor oxygen saturation
-Monitor amount of air, fluid, or blood drained
-Assess patient comfort
174
PICC Line
-Central line inserted through a peripheral vein into the SVC or IVC
-Reduces repeated needle sticks
175
PICC Line Insertion Sites
-Basilic vein
-Median cubital vein
-Cephalic vein
-Axillary vein
-Superficial temporal vein
-Retroarticular vein
-Great saphenous vein
-Small saphenous vein
-Popliteal vein
-Femoral vein
176
Cardiac Cycle: Diastole
-Active relaxation phase
-Ventricles relax creating negative pressure that pulls blood from atria
-Atrial kick occurs at end of diastole and contributes 20-30% of ventricular filling
-Mitral and tricuspid valves open
-Aortic and pulmonary valves closed
177
Cardiac Cycle: Systole
-Active contraction phase
-Ventricles contract and eject blood
-Aortic and pulmonary valves open
-Mitral and tricuspid valves closed
-Ends with ventricular relaxation and return to diastole
178
4 Principles of Hemodynamics
-Heart grows as blood flows
-Blood follows the path of least resistance
-Pressure leads to hypertrophy
-Volume leads to dilation
179
Heart Grows as Blood Flows
-Blood flow stimulates growth of the heart and vessels
-Example: HLHS with PDA allows aortic arch growth despite small left heart
180
Pressure Leads to Hypertrophy
-Increased pressure or resistance causes ventricular muscle thickening
-Example: Hypertension
181
Volume Leads to Dilation
-Increased volume causes ventricular dilation
-Occurs with poor ventricular function or shunting lesions
182
Fetal Circulation
-1 umbilical vein carries oxygenated blood from placenta
-2 umbilical arteries carry deoxygenated blood to placenta
-Right ventricle does little work
-Left ventricle performs most systemic work
183
Fetal Circulation Shunts
-Patent foramen ovale (PFO): Right atrium → Left atrium
-Patent ductus arteriosus (PDA): Pulmonary artery → Aorta
184
Fetal Circulation Pathway
-Umbilical vein enters fetus
-50% flows through ductus venosus to liver
-50% enters IVC and right atrium
-Most blood crosses PFO to left atrium
-<5% reaches lungs
-PDA shunts blood from pulmonary artery to aorta
-60% of descending aortic blood returns to placenta
185
Transitional Circulation
-Begins at birth
-Oxygen causes pulmonary vasodilation
-Pulmonary vascular resistance decreases
-PDA flow reverses from aorta to pulmonary artery
-PDA gradually closes
186
Pulmonary Catheter Measurements
-Right atrium = CVP
-Right ventricle = Tall systolic waveform
-Pulmonary artery = High pressure waveform
-Pulmonary capillary wedge = Reflects left-sided heart pressure
187
Right Atrium (CVP)
-Normal pressure: 2-6 mmHg
-Mean: 3 mmHg
-Target 8-12 mmHg in vasodilatory shock
188
Right Ventricle
-Pressure: 25/3 mmHg
-RV pressure is normally 1/4 to 1/5 of LV pressure
-Systemic RV pressure suggests pulmonary hypertension
189
Pulmonary Artery
-Pressure: 25/10 mmHg
-Mean: 16 mmHg
-Mean >25 mmHg suggests pulmonary hypertension
-RV pressure > PA pressure suggests pulmonary stenosis
190
Pulmonary Capillary Wedge Pressure
-Normal: 6-12 mmHg
-Reflects left-sided filling pressure
-Assesses left ventricular diastolic function
191
Left Atrium
Mean pressure: 8 mmHg
192
Left Ventricle
-Pressure: 100/8 mmHg
-Mean: 16 mmHg
193
Left Ventricular End-Diastolic Pressure
-Normal: 3-12 mmHg
-Pressure at end of diastole before systole
-Assesses diastolic function
-Elevated in diastolic cardiomyopathy
194
Aorta
-Pressure: 100/83 mmHg
-Mean: 83 mmHg
-LV pressure > aortic pressure suggests aortic stenosis or coarctation
195
Normal Cardiac Saturations
-Right atrium: 75%
-Right ventricle: 75%
-Pulmonary artery: 75%
-Left atrium: 100%
-Left ventricle: 100%
-Aorta: 100%
196
ASD Hemodynamics
-Step-up in oxygen saturation from right atrium to right ventricle
-Oxygenated blood shunts from left atrium to right atrium
197
VSD Hemodynamics
-Step-up in oxygen saturation from right ventricle to pulmonary artery
-Oxygenated blood shunts from left ventricle to right ventricle
198
Cardiac Output
-Amount of blood pumped into systemic circulation each minute
-Assessed clinically and in the cath lab
199
Preload
-CVP
-Volume status
-Ventricular filling at end diastole
200
Contractility
-Strength of ventricular contraction
-Measure of cardiac pump performance
201
Stroke Volume
-Amount of blood ejected with each beat
-Normal: 50-80 mL
202
Afterload
-Systemic vascular resistance
-Resistance ventricle must overcome to eject blood
203
Cardiac Index
-Cardiac output corrected for body surface area
-Normal: 3.5-5.5 L/min/m²
204
Qp:Qs Ratio
-Ratio of pulmonary to systemic blood flow
-Normal: 1:1
205
Small Shunt Qp:Qs
<1.5:1
206
Moderate Shunt Qp:Qs
1.5-2:1
207
Large Shunt Qp:Qs
>2:1
208
Decreased Pulmonary Vascular Resistance
-Relaxed pulmonary vessels
-Oxygen
-Nitric oxide
-Sildenafil
-Acetylcholine
-Prostaglandins
-Milrinone
-Calm state
209
Increased Pulmonary Vascular Resistance
-Sympathetic stimulation
-Stress
-Agitation
-Hyperinflation
-Hypoxemia
-Hypercarbia
-Acidosis
-Increased blood viscosity
210
Factors Affecting Systemic Vascular Resistance
-Autonomic nervous system
-Hormones
-Catecholamines
-Vasoactive medications
-Inotropes
-Environmental temperature
-Exercise
-Blood viscosity
211
Shock in the First Month of Life
-Neonates often present with nonspecific signs and symptoms
-Parents may underestimate illness severity
-Presentation may progress rapidly
-Sepsis is the most common cause of shock
-Early consideration of a broad differential is essential
212
Pediatric Assessment Triangle
-Appearance
-Work of breathing
-Circulation to skin
-Helps identify the affected organ system
213
ABCDE Assessment
-Airway
-Breathing
-Circulation
-Disability (neurologic exam)
-Dextrose (glucose) in infants
214
Problem List
-Identify major problems before creating a differential
-Example: Respiratory distress, shock, lethargy, hypothermia
215
Shock Differential: "THE MISFITS"
-Trauma
-Heart
-Endocrine
-Metabolic
-Inborn errors of metabolism
-Sepsis
-Formula dilution/overconcentration
-Intestinal catastrophes/dehydration
-Toxins
-Seizures
216
Common Differentials for Neonatal Shock
-Sepsis
-Viral infection
-Cardiac disease
-GI disorders
-Dehydration
-Feeding problems
-Metabolic disorders
-Endocrine disorders
-Hematologic disorders
-Neurologic disorders
-Trauma
217
Airway Management
-Intubate early if indicated
-Use sedatives cautiously
-ETT size: 3.0-3.5 mm
-Depth: 10-10.5 cm at the lip
-Confirm placement with CO₂ and CXR
218
Breathing Management
-Rate approximately 20 breaths/min
-Try to ventilate in phase with the child's breathing
219
Circulation Management
-Obtain IV or IO access
-UV line or saphenous cutdown if needed
-NS 20 mL/kg IV push
-Avoid LR in neonates
-Consider epinephrine, norepinephrine, or dobutamine
220
Intraosseous (IO) Line
-Preferred site: Tibial plateau
-Distal femur may be used in neonates
-Can administer anything given through an IV
-Rare complications: Osteomyelitis, fractures, epiphyseal injury
-In cardiac arrest, place IO while IV is attempted
221
Hypoglycemia Management
-Check bedside glucose
-D10 4 mL/kg IV push if low
-Recheck glucose frequently
222
Initial Laboratory Evaluation
-ABG
-CBC
-Blood cultures
-BMP
-LFTs
-Urinalysis with Gram stain
223
Empiric Antibiotics
-Ampicillin
-Gentamicin
-Ceftazidime preferred over ceftriaxone
-Vancomycin if meningitis suspected
224
Why Avoid Ceftriaxone in Neonates?
-Often require calcium
-Ceftriaxone and calcium can crystallize and damage the kidneys
225
Antiviral Therapy
-Acyclovir 30 mg/kg/day every 8 hours
-Consider HSV infection
226
Risk Factors for Neonatal Sepsis
-Prolonged rupture of membranes (>18-24 hours)
-Maternal Group B strep
-Nosocomial exposure after 7 days
227
Common Neonatal Sepsis Organisms
-E. coli
-Other gram-negative bacteria
-Group B Streptococcus
-Listeria monocytogenes
-Staphylococcus aureus
-Streptococcus pneumoniae
-Haemophilus influenzae
228
Neonatal Sepsis Presentation
-Fever or hypothermia
-Lethargy or irritability
-Poor feeding
-Vomiting
-Diarrhea
-Tachypnea
-Tachycardia
-Poor perfusion
-Petechiae
-Purpura
229
Neonatal Sepsis Laboratory Findings
-Leukocytosis or leukopenia
-Bandemia
-Acidosis
-Hypo- or hyperglycemia
-Pyuria or bacteriuria
-CXR infiltrates
230
HSV Findings
-Elevated hepatic transaminases
-Hepatic failure
-Positive Tzanck prep or immunofluorescence
-Severe pneumonitis on CXR
-PCR testing
231
Enterovirus Findings
-Elevated hepatic transaminases
-Hepatic failure
-PCR testing
232
RSV Findings
-Rapid RSV testing
-Patchy infiltrates
-Atelectasis
-Hyperinflation
233
Common Viral Causes of Neonatal Shock
-HSV
-Enterovirus
-RSV
234
HSV Presentation
-Vesicles
-Hepatomegaly
-Icterus
-Petechiae
-Purpura
235
Enterovirus Presentation
-Myocarditis
-Diffuse maculopapular rash
236
RSV Presentation
-Apnea
-Hypothermia
-May initially lack lower respiratory symptoms
237
Viral Infection Management
-Supportive care
-Aggressive fluids
-Vasopressors if needed
-Empiric acyclovir if HSV suspected
238
GI Causes of Neonatal Shock
-Gastroenteritis
-Volvulus
-Pyloric stenosis
-Hirschsprung disease
-Necrotizing enterocolitis
239
GI Presentation
-Vomiting
-Diarrhea
-Poor feeding
-Decreased urine output
-Bloody stools
-Bilious vomiting
-Abdominal distention
-Palpable olive (pyloric stenosis)
-Visible peristaltic waves
240
GI Laboratory Evaluation
-CBC
-Stool leukocytes
-Abdominal x-ray
-Abdominal ultrasound
-Upper GI study
-Barium/Gastrografin enema
-Metabolic alkalosis in pyloric stenosis
241
GI Management
-Fluid resuscitation
-NG decompression for obstruction
-Antibiotics if indicated
-Early surgical consultation
242
Feeding Problems
-Poor breastfeeding may cause hypernatremic dehydration
-Formula over-dilution causes hyponatremia
-Formula over-concentration causes hypernatremia
243
Feeding Problem Management
-Restore intravascular volume
-Slow correction of electrolyte abnormalities
244
Metabolic Disorders Presentation
-Vomiting
-High-pitched cry
-Lethargy
-Irritability
-Seizures
-Coma
-Unusual urine odor
-Hepatomegaly
-Jaundice
-Hypothermia
-Bulging fontanel
245
Metabolic Disorder Laboratory Findings
-Hypoglycemia
-Abnormal electrolytes
-Severe acidosis
-Hyperammonemia
246
Metabolic Disorder Management
-Fluid resuscitation
-D10 2.5-10 mL/kg IV push
-D10 at 1.5-2x maintenance
-Treat electrolyte abnormalities
-Early metabolic specialist consultation
247
Congenital Adrenal Hyperplasia (CAH)
-Enzyme defect in cortisol production
-Usually presents during the second week of life
248
CAH Presentation
-Poor feeding
-Vomiting
-Irritability
-Lethargy
-Dehydration
-Hyperkalemic arrhythmias
-Females: Ambiguous genitalia
-Males: Small phallus or hyperpigmented scrotum
249
CAH Laboratory Findings
-Severe hyponatremia
-Severe hyperkalemia
-Hypoglycemia
-Peaked T waves
250
CAH Management
-NS resuscitation
-Treat severe hyperkalemia
-Stress-dose hydrocortisone
-Later fludrocortisone
251
Neonatal Thyrotoxicosis
-Maternal hyperthyroid antibodies cross the placenta
-May present after 10 days of life
252
Neonatal Thyrotoxicosis Presentation
-Marked tachycardia
-CHF
-Arrhythmias
-Irritability
-Respiratory distress
-Hyperthermia
-Shock
253
Neonatal Thyrotoxicosis Management
-Careful fluid resuscitation
-ABCs
-Propylthiouracil
-Potassium iodide
-Propranolol
-NICU/PICU monitoring
254
Infant Botulism
-Occurs in infants <1 year
-Spores colonize the gut
255
Infant Botulism Presentation
-Constipation
-Weak cry
-Lethargy
-Dehydration
-Afebrile
-Hypotonia
-Hyporeflexia
-Mask-like facies
-Increased oral secretions
-Decreased gag reflex
-Respiratory failure
256
Infant Botulism Management
-Supportive care
-Avoid aminoglycosides
-BabyBIG antitoxin
257
Trauma Presentation
-Respiratory distress
-Apnea
-Irritability
-Vomiting
-Lethargy
-Bulging fontanel
-Seizures
-Retinal hemorrhages
258
Trauma Evaluation
-Dilated retinal exam
-Head CT
-MRI
-LP
-CXR
-Skeletal survey
-Coagulation studies
-Abdominal CT if unstable
259
Trauma Management
-Fluid resuscitation
-Drug-assisted intubation
-Treat seizures
-Notify CPS and law enforcement
260
Cardiac Disease Presentation
-Tachycardia
-Tachypnea
-Pallor
-Cyanosis
-Poor perfusion
-Slow feeding
-Murmur
-Gallop
-Hepatomegaly
-Rales or wheezing
261
Cardiac Disease Evaluation
-Metabolic acidosis
-Hypoxia
-CXR
-ECG
262
Cardiac Disease Management
-Supportive care
-Fluid boluses
-Prostaglandin E1 for left-sided obstructive lesions
263
Prostaglandin E1
-Potent vasodilator
-0.05-0.1 mcg/kg/min
-May increase to 0.2-0.4 mcg/kg/min
-Dilute in D5W or NS
-Administer through a large vein
264
Prostaglandin E1 Monitoring
-Monitor oxygen saturation
-Perfusion
-Blood pressure
-pH
265
Prostaglandin E1 Complications
-Hyperpyrexia
-Flushing
-Hypotension
-Seizures
-Hypocalcemia
-Bleeding
-Diarrhea
-Apnea
266
Syncope
-Abrupt transient loss of consciousness and postural tone due to decreased cerebral blood flow
-Sudden and temporary
-Self-terminating with rapid recovery
267
Pre-Syncope
-No loss of postural tone or consciousness
-Nausea/vomiting
-Lightheadedness
-Visual disturbances
-Sweating
-Flushing
268
Forms of TLOC
-Traumatic
-Non-traumatic syncope
-Reflex syncope
-Orthostatic hypotension
-Cardiac (arrhythmia or structural)
-Epileptic seizures
-Functional/Psychogenic
269
Benign Causes of Syncope
-Vasovagal syncope
-Carotid sinus syndrome
-Situational (cough, post-micturition, pain)
-Orthostatic hypotension
-ANS failure
-Drug-induced (diuretics)
270
Malignant Causes of Syncope
-Aortic stenosis
-Cardiomyopathy (HCM, DCM, ARVC)
-Coronary artery anomalies
-Pulmonary hypertension
-CHD
-LQTS
-SQTS
-Brugada
-CPVT
-Idiopathic VF
-WPW with RVR
-Bradyarrhythmias
271
Syncope Etiology
-Brief interruption of cerebral blood flow
-Most common pediatric cause is vasovagal syncope
-Vasovagal syncope accounts for ~50% of ED cases
-Usually does not require testing
272
Reflex Syncope Pathophysiology
-Exaggerated vasovagal reflex
-Sympathetic response causes hypotension
-Parasympathetic response causes sinus bradycardia or varying degrees of heart block
273
VASIS Type I
-Mixed response
-Blood pressure falls before heart rate
-Heart rate does not fall below 40 bpm
-Most common type in children
274
VASIS Type 2A
-Cardioinhibitory without asystole
-Heart rate <40 bpm for >10 seconds
-No pauses >3 seconds
275
VASIS Type 2B
-Cardioinhibitory with asystole
-Heart rate <40 bpm for >10 seconds
-Pauses >3 seconds
276
VASIS Type 3
-Vasodepressor
-No significant heart rate decrease (>10% from peak)
277
Social History for Syncope
-Alcohol
-Illicit drugs
-Psychosocial stressors
-Psychogenic syncope may begin as true vasovagal syncope
278
Medication History for Syncope
-Prescription medications
-Non-prescription medications
-QT-prolonging drugs
279
Syncope Physical Exam
-Orthostatic blood pressure and heart rate
-Neurologic examination
-Cardiac examination
280
Heart Sounds on Exam
-Evaluate for murmurs and structural disease
-Most cardiac causes will not be detected on auscultation alone
281
Syncope Red Flags
-ECG abnormalities
-Known heart disease
-Family history of sudden unexplained death
-Supine or seated syncope
-Palpitations before syncope
-Syncope while driving
-Syncope during exercise
-Chest pain or shortness of breath
-Anemia or electrolyte abnormalities
-Stokes-Adams attacks
282
Initial Syncope Evaluation
-History
-Physical examination
-Lying and standing blood pressure
-ECG
283
High Risk Syncope Evaluation
-Echocardiogram
-ECG monitoring
-Carotid sinus massage
-Exercise tolerance test
-Implantable loop recorder if initial workup is negative
284
Low Risk Syncope Evaluation
-Stop evaluation if syncope is rare
-Recurrent syncope likely due to neurally mediated syncope: ECG monitoring
-If not likely neurally mediated: Head-up tilt test
-If tilt test negative: ECG monitoring
285
Screening ECG
-Most useful initial test
-Assess rhythm
-Assess hypertrophy
-Assess ischemia/strain
-Calculate QTc manually
-Look for Brugada pattern
-Epsilon waves
-Abnormal T waves
286
Emergency Department Syncope Workup
-Blood tests (BNP, troponin)
-EEG
-CT
-MRI
-Imaging has low yield and is overused
287
Tilt Table Test
-Recreates postural change
-Evaluates heart rate and blood pressure
-Poor reproducibility
-Poor sensitivity and specificity
-Time consuming
288
Echocardiogram in Syncope
-Limited indications
-Useful when structural heart disease is suspected
289
Implantable Loop Recorder (ILR)
-Recurrent unexplained syncope
-High-risk CHD
-Severe syncope with injury
-Vasovagal syncope with concern for heart block or pacing need
290
Vasovagal Syncope Management
-Increase salt and water intake
-Education
-Avoid triggers
-Hydrate before exercise
-Tilt training
-Compression stockings
-Exercise training
-Counter-pressure maneuvers
-Symptom recognition
-Psychotherapy if needed
291
Fludrocortisone
-Mineralocorticoid
-Increases sodium and water retention
-Use with increased salt and water intake
-Side effects: Weight gain, hypertension, hypokalemia
-May take 2-3 months to work
292
Midodrine
-Peripheral alpha-1 agonist
-Increases PVR and cardiac output
-Side effects: Supine hypertension, nausea, urinary retention, rash
-Dose: 2.5-10 mg
293
Glycopyrrolate
-Anticholinergic
-Used for breath-holding spells causing vasovagal syncope
-Side effects: Dry mouth, urinary retention
-Dose: 50-200 mcg/kg/dose TID-QID
294
Extracorporeal Membrane Oxygenation (ECMO)
-Extracorporeal support that removes blood from the patient, oxygenates it, removes CO₂, and returns it to the patient
-Provides temporary life support for reversible pulmonary or cardiac failure
-Bridge to recovery
-Bridge to decision
-Bridge to transplant
295
ECMO Principle
-Desaturated blood is drained through a venous cannula
-CO₂ is removed
-O₂ is added through the oxygenator
-Blood is returned through a vein (VV ECMO) or artery (VA ECMO)
296
Goals of ECMO
-Ensure adequate oxygen delivery to organs
-Allows time for heart/lung recovery
-Decrease ventilator-induced lung injury
-Allow weaning of vasoactive medications
297
VA ECMO
-Blood drained from venous circulation and returned to arterial circulation
-Provides cardiac and respiratory support
298
VV ECMO
-Blood drained from venous circulation and returned to venous circulation
-Requires preserved native cardiac function
-Used for isolated respiratory failure
299
ECMO Components
-Centrifugal pump
-Oxygenator
-Controller
300
Centrifugal Pump
-Replaces roller pumps
-RPM controlled (0-4000 RPM)
-Flow up to 8 L/min
-Reliable up to 21 days

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