lecture 10: peds Flashcards

Question

pARDS: Acute Phase

Answer 1

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 exudate as cytokines (IL-1, IL-6, TNF-a) are released and activate neutrophils

Answer 2

Active transport of fluid from alveoli to interstitium Removal of proteins Restoration of normal alveolar epithelial membrane Angiogenesis

Answer 3

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

Answer 4

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

Answer 5

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 **

Answer 6

Cardiac/respiratory arrest Severe encephalopathy Hemodynamic instability Facial surgery, trauma, or deformity Inability to protect airway

Answer 7

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

Answer 8

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

Answer 9

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)

Answer 10

Level of support: SIMV vs Assist control Variables to control: Pressure or volume control

Answer 11

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

Answer 12

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)

Answer 13

D = Dislodgement O = Obstruction P = Pneumothorax or other air leak E = Equipment failure

Answer 14

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

Answer 15

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

Answer 16

atrial septal defect ventricular septal defect patent ductal arteriosus

Answer 17

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

Answer 18

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

Answer 19

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

Answer 20

Significant diastolic dysfunction, marked bi-atrial enlargement due to elevated ventricular filling pressures Genetic, acquired, or mixed etiologies

Answer 21

Prolonged rapid heart rate can result in presentation similar to cardiomyopathy Sustained ventricular arrhythmias precipitate heart failure Presentation: sudden death or malignant ventricular arrhythmias

Answer 22

Fatty infiltration of the right ventricular free wall 1/3 of cases are familial Presentation: decreased right ventricular function, arrhythmias, sudden death Myocardial ischemia

Answer 23

Sepsis / septic shock Post-arrest myocardial dysfunction Systemic HTN Pulmonary HTN Thyrotoxicosis Transient dysfunction after cardiopulmonary bypass

Answer 24

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

Answer 25

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

Answer 26

Mode of blood flow: continuous or pulsatile Position of pump: extra-, para- or intracorporeal Duration of intended use: temporary, short-term, long-term

Answer 27

stroke 29% incidence with pulsatile VAD <10% in adults with continuous-flow devices

Answer 28

bleeding Major bleeding May require surgical re-exploration Release of free hemoglobin secondary -> cause renal dysfunction

Answer 29

unpredictable complication following LVAD implantation

Answer 30

Respiratory failure (29%) Renal dysfunction (12%) Hepatic dysfunction (9%) Arrhythmias (9%)

Answer 31

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

Answer 32

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

Answer 33

Oxygen delivery (DO2): supply of oxygen per unit of time to tissue Oxygen consumption (VO2): oxygen utilized per unit of time by tissue

Answer 34

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)

Answer 35

Endotracheal intubation (takes away work of breathing which can be substantial) Sedation Paralytic Cooling (or maintaining normothermia and avoiding fever at least)

Answer 36

Imbalance of O2 delivery & demand Inadequate oxygen delivery to meet metabolic demand Does not equal hypotension

Answer 37

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

Answer 38

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

Answer 39

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

Answer 40

Crystalloid > albumin Balanced crystalloid > 0.9% NS

Answer 41

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

Answer 42

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