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Case Management: Acute Respiratory Failure. Santos, Jennifer Joy Santos, Ma. Socorro Tiongson , Denver. Y.d. 57 year old Female Widow Born Again Christian Right-handed from Baclaran , Paranaque. Patient Profile. Chief Complaint : Dyspnea

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case management acute respiratory failure

Case Management:Acute Respiratory Failure

Santos, Jennifer Joy

Santos, Ma. Socorro

Tiongson, Denver

slide2
Y.d.
  • 57 year old
  • Female
  • Widow
  • Born Again Christian
  • Right-handed
  • from Baclaran, Paranaque
patient profile
Patient Profile
  • Chief Complaint : Dyspnea
  • Non-hypertensive, non-diabetic, non-asthmatic
  • No history of PTB
  • With a finding of an intracranial mass (temporal lobe) in CT scan c/o PGH (2005)
family history
Family history
  • (+) HPN- mother
  • (+) CVD- siblings
  • (+) MI- brother
  • (-) known Cancer of any type
  • (-) PTB, DM
personal social history
Personal /social history
  • Non-smoker
  • Non alcoholic beverages
  • Denies illicit drug use
  • Works in buy and sell business
  • Church worship leader
  • High school graduate
  • Lives with youngest daughter aged 16 y/o in their old house, while the other 2 daughters are now living with their respective families
slide18
PTB extensive disease with possible cavitation

Pneumonia with consolidation

Subsegmentalatelectasis, L

  • WAT IS OUR aditional READING of this XRAY?
  • Elevated Right diaphragm can mean pulmonary contraction
  • - cardiac reading?
other pertinent laboratory results
Other pertinent laboratory results

3/11

  • ETA GS: 0-2 gram (-) bacilli; 0-2 yeast cells
  • KAYA KAYA NATING MAHANAP YUNG CULTURE STUDIES NYA PARA MALAMAN UNG ETIOLOGIC AGENT? =)
physical examination on admission
Physical examination on admission
  • Awake, conscious, responsive, intubated @ET 7.5 L18, NICRD
  • BP= 120/80 HR=120 RR=40s T=37.6
  • HEENT: pale palpebral conjunctivae, anictericsclerae, pupils 2mm EBRTL, (+) NVE, (+) Anterior neck mass 3x4 cm firm, nodular, movable. (-) CLAD
  • Chest: Equal chest expansion, harsh breath sounds,

(+) crackles bilateral LF mid to base, (-) wheezes.

  • Heart: DHS, tachycardic, regular rhythm, apex beat at 5th ICS anterior axillary line. (-) murmurs.
  • Abdomen: soft, flabby, normoactive bowel sounds, (-) masses/tenderness
  • Extremities: pink nailbeds, full and equal pulses, CRT<2 sec. (-) edema/cyanosis, (+) grade I sacral ulcer, Right
other pertinent laboratory findings
Other pertinent laboratory findings

3/12

  • CKMB 23.5
  • CK total 42

Rules out ACS

course in the ward

3/11/2010, 9 AM

Course in the ward
  • noted BP 70/50
  • A> ARDS 2’ CAP HR
  • Sepsis secondary to CAP HR
  • PTB cat I
  • Intracranial mass, R lobe
  • DTG in storm, s/p RAI
  • IFG
  • Dyslipidemia
  • Anemia prob secondary to chronic disease.
  • Dopamine drip started
slide39
ARDS
  • Severe dyspnea of acute onset (< 2 weeks)
  • Hypoxemia
  • Diffuse bilateral pulmonary infiltrate on CXR
  • PaO2/FiO2 < 200 mmHg
  • No elevated left atrial pressure (PCWP <18 mm Hg)
  • Respiratory
  • Failure
three phases
Three Phases

Recovery

Exudative

Proliferative

Fibrotic

0 7 14 21 6 mos

slide42

Diffuse alveolar and endothelial damage

Increase pulmonary vascular permeability

Atelectasis and increase work of breathing:

Dyspnea

Tachypnea

Hypoxemia

Microvascular occlusion, pulmonary hypertension, increase in dead space:

Hypercapnia

Alveolar edema

PMN infiltration of lungs Hyaline membrane formation

Inactivation of surfactant due to exudates

Accumulation in dependent portions

Atelectasis

proliferative phase
Proliferative Phase
  • Time of Lung repair
  • Layering of exudates
  • Lymphocytic infiltration
  • Type II pneumocytes reproduce surfactant
fibrotic phase
Fibrotic Phase
  • Fibrosis
  • Emphysema like changes (bullae)
  • Vascular occlusion
  • Complications:
  • Pulmonary Hypertension
  • Pneumothorax
  • Increase in dead space
mechanical ventilation
Mechanical Ventilation
  • Augments the increase in work of breathing
  • But can aggravate lung injury via repeated Alveolar Overdistention and Recurrent Alveolar Collapse
  • Set MV at lower tidal volumes
    • 6 ml/kgBW( vs standard 12ml/kgBW)
  • Optimal PEEP for alveolar recruitment :
    • 12-15 cmHg
  • Target RR < 35
  • ARDS net protocol: Low volume, High frequency ventilation
management1
Management
  • Manage Respiratory Acidosis
  • Fluid restriction and diuretic
    • to reduce left atrial filling pressure
    • Dry Lungs are Happy Lungs!
  • Steroids
    • anti-inflammatory  No role!
mortality
Mortality
  • 41-65%
  • Mostly from non-pulmonary causes (Sepsis, organ failure)
  • Recovery of lung function within 6 months
slide49

Inability of the lung to meet the metabolic demands of the body

  • Dysfunction in lung’s main function:
    • Oxygenation
    • Carbon Dioxide elimination
  • PaO2 <60 mmHg
  • PaCO2 >50 mmHg
  • Develops 4-48 hours
signs
Signs
  • Tachypnea
  • Exaggerated use of accessory muscles
  • Intercostal, supraclavicular and subcostal retractions
  • Neuromuscular disease: signs of respiratory distress may not be obvious
  • CNS disease: bradypnea + shallow breathing
slide51

Respiratory Tract

  • CNS (medulla)
  • Peripheral nervous system (phrenic nerve)
  • Respiratory muscles
  • Chest wall
  • Lung
  • Upper airway
  • Bronchial tree
  • Alveoli
  • Pulmonary vasculature
hypoxemic rf
Hypoxemic RF
  • SaO2 < 90% despite

FiO2 > 0.6

  • Interference with O2 exchange, but overall ventilation is maintained
  • Goal of MV: provide adequate SaO2 to improve VP matching and reduce IP shunt
  • Most common
causes of hypoxemic arf
Causes of hypoxemic ARF

1. FiO2

2. Hypoventilation

( PaCO2)

3. V/Q mismatch (eg.COPD)

4. Diffusion limitation

5. Intrapulmonary shunt - Pneumonia - Atelectasis - CHF (high pressure pulmonary edema) - ARDS (low pressure pulmonary edema)

slide55

Focal infiltrates on CXR

Atelectasis

Pneumonia

  • Diffuse infiltrates on CXR

Cardiogenic Pulmonary Edema

Non cardiogenic pulmonary edema (ARDS)

Interstitial pneumonitis or fibrosis

Infections

hypoxemic respiratory failure
Hypoxemic respiratory failure
  • The major problem is PaO2.
  • If due to low V/Q mismatch: O2 therapy
  • If due to pulmonary intra-parenchymal shunts (ARDS):Assisted ventilation with PEEP
  • If due to intracardiac R-L shunt: Surgical
hypercarbic rf
Hypercarbic RF
  • Hypoxemia is always present
  • pH depends on level of HCO3
  • HCO3 depends on duration of hypercapnia
  • Renal response occurs over days to weeks
hypercarbic rf causes
Hypercarbic RF: Causes
  • Impaired CNS central drive :
    • Dug overdose, Brainstem injury, Sleep-disordered breathing, Hypothyroidism
  • Impaired neuromuscular transmission
    • MG, GBS, Phrenic injury
  • Respiratory muscle weakness and fatigue
  • Increase load in respiratory system
    • Increase resistive load/bronchospasmie Asthma and COPD
  • Reduced lung compliance
    • Atelectasis, Edema
  • Reduced chest wall compliance
    • Pneumothorax, Pleural effusion, Abdominal distention
  • Increase minute ventilation
    • Pulmomary Embolus with incr dead space, Sepsis
acute hypercarbic rf
Acute Hypercarbic RF
  • Arterial pH is < 7.35
  • Acute on Chronic:
  • This occurs in patients with chronic CO2 retention who worsen and have rising CO2 and low pH.
  • Mechanism: respiratory muscle fatigue
hypercarbic rf1
Hypercarbic RF
  • Goal: Normalize arterial pH through CO2 elimination
  • Respiratory muscle fatigue ssx:
    • Inability to speak full sentences
    • Use of accessory muscle
    • Paradoxical abdominal muscle activity
    • Extreme tachypnea (>40bpm)
    • Decrease RR despite increase in drive to breath
  • Tx must be directed at reversing cause of ventilatory failure: NIPPV
  • Contraindications: hemodynamic instability, inability to protect airway, respiratory arrest
hypercapnic respiratory failure
Hypercapnic Respiratory failure
  • ToMechVent or Not to MechVent ?
  • In Acute respiratory acidosis: Mechanical ventilation!
  • Chronic Respiratory acidosis: Close monitoring, mechanical ventilation is rarely required.
  • In acute-on-chronic respiratory failure, the trend of acidosis over time is a crucial factor.
type iii rf
Type III RF
  • Lung atelectasis
  • A.k.a Perioperative RF
type iii rf tx
Type III RF : Tx
  • frequent change in position
  • chest physiotherapy
  • upright positioning
  • aggressive control of postop pain
  • NIPPV
type iv rf
Type IV RF
  • Systemic hypoperfusion
  • Occurs in Shock (pulmonary edema, lactic acidosis, anemia)
  • Normally, muscles consume < 5% total CO and O2 delivery  40% CO
  • Tx: Intubation and MV
    • to allow redistribution of CO away from respiratory muscles and into vital organs
diagnostics
Diagnostics
  • ABG
  • PaO2
  • PaCO2
  • Compute Alveolar-Arterial PO2 Gradient

P(A-a)O2 Gradient = PIO2 – PaCO2 / R

where PiO2 = partial pressure of inspired air, R = 0.8

Normal range: 5-10 mm of Hg

  • Hyperoxia Test
    • Give 100% O2 and assess improvement
cap 2010 guideline
CAP 2010 Guideline
  • CAP HR criteria
  • CAP HR treatment options
  • Risk factors for Pseudomonas
  • Risk factors for Anaerobes
  • Ceftazidime
    • With gram negative and anti-pseudomonas coverage
    • Clindamycin
      • Covers for anaerobes
  • Pip-Tazo
mechanical ventilation indications
Mechanical Ventilation: Indications
  • PaO2< 55 mm Hg or PaCO2 > 60 mm Hg despite 100% oxygen therapy.
  • Deteriorating respiratory status despite O2 and Nebulization
  • Anxious patient with deteriorating mental status.
  • Respiratory fatigue: for relief of metabolic stress of the work of breathing