lecture 10: peds Flashcards
gas exchange
- lungs
- pulmonary arteries from RV
- arteries from LV
Gets blood supply from right and left ventricles
Lungs: Gas exchange
- Primary goal of lung: Co2 elimination + O2 uptake during respiratory cycle
- Gas exchange occurs @ alveoli through diffusion
Systemic and pulmonary circulations are “in series”
- CO from RV to lung = CO from LV to the rest of the body
- Therefore, resistance to blood flow must be low in the lungs (lower pressure)**
route from heart to lungs is shorter than heart to rest of body
less stops along the way when comparing pulmonary vs systemic circulation
Pulmonary arteries from RV: branch into pulmonary capillaries, which intertwine alveoli
Main role: gas exchange – CO2 & O2
Arteries from LV: branch with bronchial tree
Main role: provide O2 to bronchi/ resp system
Acid Base Balance
Utility:
- Measurement of oxygenation and ventilation
- Measurement of acid/base status
Indications:
- Symptoms of oxygenation, ventilation, or acid/base imbalance
- Used to monitor patients requiring respiratory support measures
Arterial or capillary blood gases:
pH indicates the acid-base balance
- Acidosis is pH < 7.35
- Alkalosis is pH > 7.45
PaCO2 reflects the adequacy of alveolar ventilation
- PaCO2 > 55 mmHg = hypercarbia
PaO2 reflects the oxygenation
- PaO2 < 60 mmHg = hypoxemia
lactate!!
End Tidal Monitoring
Reflects CO2 at end of exhalation
How is this monitored ? NC, vent
Alterations in ETCO2
1) Increases ETCO2
Hypoventilation
Increased Pulmonary Capillary blood flow
Increased CO
Increased CO2 production
Sodium Bicarb administration
2) Decreases in ETCO2
Hyperventilation
Decreased Pulmonary capillary blood flow
Pulmonary HTN
Pulmonary embolus (thrombus or air)
Decreased CO
Impairment of Respiration
Under neural and chemical control
Hypoventilation should always raise concern for neuronal anomaly
Hyperventilation often caused by conditions outside the lung (metabolic acidosis, neurologic process, anxiety)
tip:
Respiration is controlled by CNS -> negative feedback system
Central neuronal processing and integration in the brainstem is hierarchical - (e.g. drug effect, underlying intracranial process, others)
Brainstem neurons can “beat” or cycle spontaneously to generate respiratory rhythm
Afferent information is not essential for generation and maintenance of breathing
review: Pediatric Airway
Upper Respiratory tract:
Nose, pharynx, larynx, upper trachea
Lower Respiratory tract:
Lower trachea, bronchi and bronchioles, alveoli
Respiratory Syncytial Virus (RSV)
1) Single-stranded RNA virus
2) Leading cause of hospitalization in children < 1 year old
3) Cause of the majority of bronchiolitis cases
4) Seasonal outbreaks
Onset: November
Peak: January – February
End: May
5) Increased morbidity and mortality in premature infants and infants with chronic lung disease
tip:
Nearly all children are infected at least once by 2 years of age
Two subtypes: A & B
Peak incidence is 2-3 months
RSV clinical manifestations
1) Mucosal inflammation
- Congestion, rhinorrhea, sneezing
2) Lower respiratory tract involvement
- Cough, increased work of breathing, accessory muscle use
3) Auscultation
- Vibration of conducting airways, prolonged expiratory phase, diffuse polyphonic wheezing, coarse crackles scattered throughout bilateral lungs
4) Hypoxia
- Ventilation-perfusion mismatch secondary to mucous plugging
5) Carbon dioxide retention
6) Respiratory acidosis
RSV Management Fluid Management
Asthma
Most common chronic illness in childhood
7.5% of children
Chronic reversible disorder resulting in inflammation, bronchoconstriction, airway hyperresponsiveness
Characterized by episodes of cough, wheeze, dyspnea, chest tightness
Asthma Triggers
Extrinsic: Allergic/immunologic factors
Intrinsic: Infectious
Exercise induced
Status Asthmaticus Symptoms
- Cough, especially at night
- Tachypnea
- Shortness of breath
- Wheezing, forced and prolonged expiratory phase
- Accessory muscle use
- Tachycardia
- Hypoxia
- Pulsus paradoxus (moderate/severe exacerbations)
*Fever, if associated with infectious trigger
tip:
Pulmonary Mechanics:
Bronchial smooth muscle contraction, mucosal edema, increased mucous production -> smaller airway diameter and increased airflow resistance
Inspiration: negative pleural pressure -> intrathoracic airway dilation
Expiration: pleural pressure approaches zero -> airway narrowing
Gas-Exchange: Abnormalities
V-Q mismatch
Cardiopulmonary Interactions:
Hyperinflation increases pulmonary vascular resistance and right ventricular afterload compromised right ventricular function
what does Status Asthmaticus look like on a CT
Hyperinflation, narrowed cardiac silhouette
Status Asthmaticus Management
1) Inhaled Beta2 agonists (albuterol, levalbuterol)
- Bronchial smooth muscle relaxation
- Reduce antigen induced histamine release
- Increase mucociliary transport
- Intermittent dosing (MDI or nebulize); typically every 20 minutes for one hour. Continuous for refractory exacerbation
2) Corticosteroids
- Decreases inflammation associated with chronic and acute airway inflammation
- May be given intravenously or enterally
- 2-4 hours to take effect
- Therapy > 5-7 days requires tape
3) Anticholinergics (e.g. ipratropium bromide)
- Promotes bronchodilation
- Used most frequently in the Emergency Department to prevent hospitalization
4) Magnesium sulfate
- Physiologic calcium antagonist; causes smooth muscle relaxation
- May be administered continuously or intermittently, IV
- Most common adverse reaction is hypotension
5) Intravenous beta agonist (e.g Terbutaline)
- Bolus, +/- continuous infusion
- ECG monitoring
6) Methylxanthines (e.g aminophylline, theophylline)
- Promotes smooth muscle relaxation through unknown mechanism
- Narrow therapeutic index; requires serum drug level monitoring
- High side effect profile (nausea, vomiting, seizures, abdominal discomfort)
Status Asthmaticus Management: Corticosteroids
Improves airway edema and inflammatory processes
Administer IV, oral once tolerated
Continue through resolution of exacerbation
Side effects: hyperglycemia, hypertension, agitation
Status Asthmaticus Management:Inhaled Beta-Agonists
Cause smooth muscle relaxation
Administer via continuous nebulization, then intermittent nebulizer or metered-dose inhaler
ommon side effects: sinus tachycardia, palpitations, hypertension, diastolic hypotension, hyperactivity, tremors, nausea/vomiting, hypokalemia, hyperglycemia
Status Asthmaticus Management: Intravenous / Subcutaneous Beta-Agonists
Ideal when airflow is minimal
Monitoring may show elevation of troponin I levels; monitor ST on continuous EKG and CPK to trend
Status Asthmaticus Management: Methylxanthines
Relax bronchial smooth muscles, mechanism controversial
Monitor serum levels
- >20 is associated with nausea, jitters, restlessness, tachycardia, irritability
- >35 is associated with seizures and dysrhythmias
Status Asthmaticus Management: Anticholinergics
Relaxes bronchial smooth muscles
May be helpful as an adjunct therapy
Adverse effects: dry mouth, bitter taste, flushing, tachycardia, dizziness
Status Asthmaticus Management: Magnesium Sulfate
Bronchodilator
Target level of 4mg/dL may achieve maximal effect
Side-effects: hypotension, CNS depression, muscle weakness, flushing
Status Asthmaticus Management: Helium-Oxygen/ non-invasive mechanical ventilation
Low-density gas enhanced laminar gas flow reduced airflow resistance in small airways
Limited by oxygen requirement
Pediatric data without definitive conclusion
Used in 3-5% of critically ill asthmatics
Status Asthmaticus Management: Mechanical Ventilation
Risks: initial care at a community hospital (3x’s more likely)
Indications: cardiac arrest, refractory acidosis, refractory hypoxemia
Goals: maintain adequate oxygenation, permissive hypercarbia allowed, minute ventilation adjusted to maintain arterial pH >7.2
- Slow rate, prolonged expiratory phase, short inspiratory time
Complications: increased risk for pulmonary barotrauma, nosocomial infection, pulmonary edema, circulatory dysfunction, steroid/muscle relaxant-related myopathy, and death
tip:
- these patients will require sedation and muscle relaxation (medication: ketamine)
pARDS: Classically (1994)
Bilateral opacities on CXR
PaO2/FiO2
<300 for ALI
<200 for ARDS,
Pulmonary capillary wedge pressure of <18 mmHg (or no suspicion of cardiac disease)
pARDS: Berlin Definition (2012)
PaO2/FiO2 ratio:
<100= severe
100-200= moderate
200-300= mild
Requires minimum PEEP of 5
Bilateral infiltrates
pARDS: Acute Phase
Pulmonary edema:Increased permeability of alveolar/capillary membrane leads to protein rich edema fluid entering the alveoli
Surfactant deficiency:Alveolar type II cell injury reduces production
Inflammatory exudateas cytokines (IL-1, IL-6, TNF-a) are released and activate neutrophils
pARDS: Resolution Phase
Active transport of fluid from alveoli to interstitium
Removal of proteins
Restoration of normal alveolar epithelial membrane
Angiogenesis
pARDS: Fibrosing Phase
Occurs approximately 5-10 days after initial lung injury
Marked by fibroblasts fibrosing alveolitis
Lung disease is heterogeneous:
- regions are atelectatic while others may be overdistended -> dead space ventilation
pARDS - Treatment
Minimize oxygen toxicity
Allow permissive hypercapnia
Maintain optimal PEEP
Set appropriate iTime (ventilator)
Find appropriate driving pressure (plateau < 30)
Monitor End tidal CO2
Prone Positioning
Fluid Management
Neuromuscular Blockade
HFOV
ECMO
I/NI positive pressure ventilation Benefits
Reduce work of breathing
Redistribute alveolar water
Improve V/Q mismatching
Minimize airway collapse
Preserve spontaneous respiration
KEY: ** Patient selection and proper mask/interface fit is crucial **
When not to use I/NI positive pressure ventilation
Cardiac/respiratory arrest
Severe encephalopathy
Hemodynamic instability
Facial surgery, trauma, or deformity
Inability to protect airway
vent Settings
High-Low approach: PIP ~ 20-25 cm H2O and PEEP ~ 5 -8
Low-High approach: PIP ~ 8-10 cm H2O and 3-5 for PEEP 3 -5
Respiratory Failure
Due to:
- Parenchymal
- Upper Airway obstruction
- Neuromuscular weakness
- Failure of respiratory drive
Airway protection due to insufficient airway protective reflexes (severe brain injury, GCS <8 in trauma patients, lack of sufficient cough or gag)
Hemodynamic instability (shock, CPR)
Therapeutic control of ventilation (Intracranial hypertension, pulmonary hypertension, metabolic acidosis with insufficient compensation)
Pulmonary Toilet (airway clearance, inability to handle secretion)
Progression of respiratory distress
Inability to adequately oxygenate and ventilate despite compensatory mechanisms
PaO2 < 60 mmHg
PaCO2 > 50 mmHg
Intubation
Tube Selection:
- Tube size formulas include: 4 + age/4
half size down for a cuffed tube
- Same diameter as the 5th finger of the patient
Tube depth:
- Generally, 3X the inner diameter of the tube
MSOAP: Monitors/Meds,Suction,Oxygen,Airway equipment (blades, ETT’s, Mapelson anesthesia bag, etc),Personnel (RT, nursing, physician)
Mechanical Ventilation
Level of support:
SIMV vs Assist control
Variables to control:
Pressure or volume control
Mechanical Ventilation Complications
Barotrauma: result of excess distending pressures; maintain Plateau Pressures (pPlat) < 30cmH2O
Volutrauma: ARDSnet trials 6cc/kg Vt vs. 12cc/kg
Atelectrauma: result of shearing forces when the alveoli are allowed to collapse and re-expand
Oxygen Toxicity - FiO2 > 60%: contributing to lung injury due to free radical production
Cellular Biotrauma: ‘upregulation’ of the inflammatory response
What are other complications of mechanical ventilation
Pts with existing intracranial or neurovascular problems are at risk with mod – high ventilation pressures. Increased ventilatory pressures will result in increased ICP
If CPP drops too low due too dec. blood flow low then cerebral hypoxia can result
Due to decreased cardiac output, redistribution of renal blood flow in abdoman and hormonal alterations (release of ADH). Therefore creating less urine
GI Bleed occurs in 25% of pts due to stress ulcers
Oral/Nasal ET tube can cause ulcerations, dental trauma, may cause dysphagia
Tracheal intubation for longer than 8 hr can cause transient injury to the larynx resulting in swallowing disorders (Critical Care Medicine, 39 (12) Dec. 2011)
Acute Deterioration of patient
D = Dislodgement
O = Obstruction
P = Pneumothorax or other air leak
E = Equipment failure
Hemodynamic Monitoring
EKG
PE: Altered mental status, prolonged capillary refill time, central and peripheral pulses, core to peripheral temperature gradient
Capnography: Partial pressure of CO2 measured in inhaled and exhaled gases over time
Blood pressure monitoring
Central Venous Pressure
Blood gases
Pulse ox
ECHO: Provides information about cardiovascular function
Fractional shortening: change in LV short-axis diameter
Ejection fraction: quantifies changes in ventricular volume during the cardiac cycle
Heart Patho
4 chambers: 2 upper/2 lower
Upper chambers – atria
Lower chambers – ventricles
4 Valves: Tricuspid, pulmonary, mitral, aortic
Normal blood flow: SVC/IVC > RA > Tricuspid > RV > Pulmonary valve > pulmonary artery > lungs > Pulmonary veins > LA > mitral valve > LV > aortic valve > aorta
Congenital Heart Disease: Acyanotic shunts
atrial septal defect
ventricular septal defect
patent ductal arteriosus
Congenital Heart Disease: Cyanotic shunts
tetralogy of Fallot
truncus arteriosus
total anomalous pulmonary venous return (TAPVR)
pulmonary atresia with ventricular septal defect tricuspid atresia
hypoplastic left heart syndrome
transposition of great arteries double-outlet right ventricle
tip: Incomplete separation of right and left-sided structures leads to defects like ASD, VSD, and PDA. Since left-sided cardiac pressures are higher, defects in atrial or ventricular septums or patency of ductus arteriosus lead to blood shunting into the right side where pressures are lower. Since all deoxygenated blood from systemic circulation makes its way to the lungs, oxygenation is not a problem. Shunting only sends additional blood into the lungs; this blood is already oxygenated. Therefore, these lesions are called acyanotic shunts.
In these disorders, there are anatomic defects that impede the flow of deoxygenated blood to the lungs. Oxygenation is impaired in these disorders, and partial pressure of oxygen in arterial circulation is low. Tissues do not get enough oxygen supply, and characteristic bluish discoloration of the skin called cyanosis is seen.
Goal is to maintain the patency of the ductus, as that is the conduit for systemic blood flow that bypasses the obstruction
Immediate prostaglandin E1
Ventilatory support, supplemental oxygen
Consultation to cardiology/cardiac surgery
Echocardiogram to establish diagnosis
Inotropic agents to improve contractility
IV fluids to improve cardiac output
Correction of metabolic derrangements
Myocardial Heart Disease: Dilated cardiomyopathy
Risk factors: male gender, African-American heritage,
age < 1 year
Dilated, poorly functioning left ventricle without compensatory left ventricular wall hypertrophy
2/3 of cases are idiopathic
tip:
Most common (50%)
most common known causes include myocarditis and neuromuscular disorders
Myocardial Heart Disease: Hypertrophic cardiomyopathy
Hypertrophied, nondilated ventricle in the absence of other disease processes
1/3 of cardiomyopathies, usually diagnosed in the first year of life
Most cases are idiopathic
Presentation: chest pain, arrhythmias, exercise intolerance
Myocardial Heart Disease: Restrictive cardiomyopathy
Significant diastolic dysfunction, marked bi-atrial enlargement due to elevated ventricular filling pressures
Genetic, acquired, or mixed etiologies
Myocardial Heart Disease: Tachycardia-induced cardiomyopathy
Prolonged rapid heart rate can result in presentation similar to cardiomyopathy
Sustained ventricular arrhythmias precipitate heart failure
Presentation: sudden death or malignant ventricular arrhythmias
Myocardial Heart Disease: Arrhythmogenic right ventricular cardiomyopathy
Fatty infiltration of the right ventricular free wall
1/3 of cases are familial
Presentation: decreased right ventricular function, arrhythmias, sudden death
Myocardial ischemia
Myocardial Heart Disease: systemic disease
Sepsis / septic shock
Post-arrest myocardial dysfunction
Systemic HTN
Pulmonary HTN
Thyrotoxicosis
Transient dysfunction after cardiopulmonary bypass
Heart Failure Treatment
Reduce fluid overload
- Diuretics
Reduce systemic vascular resistance
- Vasodilators
- First line: dobutamine or milrinone
Assist work of breathing, lower left ventricular afterload, improve energy balance
Cardiogenic shock with acidosis: goal to increase cardiac output
low-dose epinephrine, dopamine, dobutamine increase contractile state of myocardium
Myocarditis treatment:
- IVIG
- Steroids (autoimmune disorders, vasculitis, eosinophilic disorders)
Aggressive treatment of arrhythmias
Anticoagulation if LV shortening fraction is <20%
Systemic heparin, aspirin, warfarin
Chronic heart failure treatment
ACE inhibitors, Beta blockers, aldosterone agonists, furosemide
Based on adult protocols
Cardiac transplantation
Extracorporeal Membrane Oxygenation
Removes blood out of the body, CO2 is filtered out, oxygenates, returns blood to RA or aorta
VV ECMO: VenoVenous
- does work of lungs
- Helpful to remove CO2 in asthmatics who are air trapping
- Helpful in ARDS to allow rest of lungs
VA ECMO: VenoArterial
- does work of lungs and heart
- For cardiac failure (with or without respiratory)
- Extreme sepsis and hypotension not responsive to vasopressors
Ventricular Assist Device (VAD)
Mode of blood flow: continuous or pulsatile
Position of pump: extra-, para- or intracorporeal
Duration of intended use: temporary, short-term, long-term
Heart Failure Complications: Neurologic
stroke
29% incidence with pulsatile VAD
<10% in adults with continuous-flow devices
Heart Failure Complications: Hematologic
bleeding
Major bleeding
May require surgical re-exploration
Release of free hemoglobin secondary -> cause renal dysfunction
Heart Failure Complications: Right-ventricular failure
unpredictable complication following LVAD implantation
Heart Failure Complications: infections
30-50%
Heart Failure Complications: Other adverse events
Respiratory failure (29%)
Renal dysfunction (12%)
Hepatic dysfunction (9%)
Arrhythmias (9%)
Heart Failure Nursing Dx
Alteration in cardiac output due to inadequate tissue perfusion and arrhythmias
Activity intolerance
Potential for thrombus formation
Potential fluid-volume excess
Potential for hypotension related to diuretic therapy
Supraventricular Tachycardia
Stable
IV adenosine, RAPID BOLUS
Unstable
Synchronized Cardioversion
Shock delivered to coincide with the R wave
0.5-1.0 J/kg for first dose
Increase to 1-2 J/kg for second dose
Oxygen Delivery and Consumption (VO2 /DO2)
Oxygen delivery (DO2): supply of oxygen per unit of time to tissue
Oxygen consumption (VO2): oxygen utilized per unit of time by tissue
What improves O2 demand ?
Increase oxygen content by increasing hemoglobin or oxygen saturation
Increase cardiac output by improving contractility, reducing afterload, or increasing heart rate (already increased in most patients with impaired oxygen delivery)
What decreases O2 demand ?
Endotracheal intubation (takes away work of breathing which can be substantial)
Sedation
Paralytic
Cooling (or maintaining normothermia and avoiding fever at least)
What is Shock?
Imbalance of O2 delivery & demand
Inadequate oxygen delivery to meet metabolic demand
Does not equal hypotension
Types of Shock
Hypovolemic: Fluid depletion secondary to hemorrhagic or nonhemorrhagic causes
- Hemorrhagic, dehydration
Distributive
- Anaphylactic, septic, neurogenic
Cardiogenic: Cardiac compensatory mechanisms fail
- CHD, myocarditis
Obstructive: Increased afterload of the right or left ventricle
- Pneumothorax, PE
Dissociative: Peripheral vasodilation, pooling of venous blood, decreased venous return to the heart
- Anemia, hypothyroid
Stages of Shock
Clinical Manifestations
Tachycardia (unless hypothermic)
Decreased organ or peripheral perfusion:
- Decreased peripheral pulses compared to central pulses
- Decreased level of consciousness
- Flash capillary refill or capillary refill > 2 seconds
- Mottled/cool extremities
- Decreased urine output
difference between warm shock and cold shock
Shock Treatment: warm vs cold
warm: norepinephrine
cold: epinephrine
Recognize decrease mental status and perfusion. Begin O2. Establish IV/IO access
Initial resuscitation:
Boluses of 20 mL/kg isotonic fluid up to & over 60 mL/kg until perfusion improves or unless rales or hepatomegaly develop – THEN WHAT ??
Correct hypoglycemia & hypocalcemia.
Blood gas – LACTATE
Begin antibiotics – esp if septic shock – new pSSC guidelines say 1 hour to get them in
Type of Fluid
Crystalloid > albumin
Balanced crystalloid > 0.9% NS
Goldstein Criteria for Sepsis
SIRS- 2 or more of the following:
Core Temperature >38.5 or <36 C
Tachycardia or Bradycardia (>2 SD above age or <10%ile)
Tachypnea (RR >90th %ile) or need for mechanical ventilation
WBC elevated or decreased for age (or >10% immature neutrophils)
SEPSIS
SIRS + infection (or suspected infection)
SEVERE SEPSIS
Sepsis + CV dysfunction or ARDS or 2 other dysfunctional organs
SEPTIC SHOCK
Sepsis + CV dysfunction
fluids for sepsis
icu available: 40-60 mL/kg over first hour
icu not available, no hTN: NO BOLUS
icu not available, hTN: up yo 40mL/kg (10-20mL/kg) in bolus fluid over first hour
