P2 Flashcards
Indication for continuous home O2 treatment in case of COPD?
1) Pa02=<55 and O2 saturation =<88 %
2) Pao2=<59 and o2 saturation= <89 % inpatient with the symptom of RSHF, Corpulmonala, and HCT>55%
Target and duration?
The target is to make o2 saturation >90, at rest, normal walking, and sleep.
Should be given for more than >15 hr/day
Sign of impending RF inpatient with Acute asthma exacerbation and COPD?
Elevated or normal PaCo2 despite hypoxia–Indicate respiratory fatigue
Marked decrease breath sound
Absent wheezing
Decrease mental status
Marked hypoxia with cyanosis
NB: This is an indication for ET intubation
Asthma exacerbation management?
Depend on severity?
Mild?
SABA
INO2
sever?
SABA
Systemic corticosteroid
Ipratropium bromide
No response with the above three-drug within 1 Hr give one dose of IV MGSO4.
Pulmonary embolism symptom?
Acute dyspnea and pleuritic chest pain–66-73%
Tachypnea–70%
Tachycardia-30 %
Low grade fever–<15%
Classic fingding of ECG in PE?
Prominent S wave in V1
Q wave on lead V3
Inverted T waves in lead V3
factor associated with poor outcome in PE?
Low O2 saturation
Atrial fibrillation
RV effect of massive PE?
Decrease LV preload that dec CO and increase wall stress in –R.Ventricular decrease O2 supply and increase O2 demand respectiveley–RV ischemia/infarction–shock,bradycardia,arrythemia,RV hypokinesis sparing apex and RVF
The initial criteria for extubation readiness?
PH>7.25
Adequate oxygenation with minimal suport(FiO2 <40% and PEEP<=5mm)
Intact inspiratory effort and sufficient mental status to protect the airway
What to do next to patient who fulfill above criterion?
Spontanous breathing trial
whay and how to do Spontanous breathing trial?
Short term risk of RF require intubation
Keep the ETT there
Turn off all respiratory support
See by making patient to breath by himself for 1-2 Hr
When to extubate?
Maintain normal ABG
Normal RSBI
RSBI?
Rapid shallow breathing index
RR to TV(in L) ratio
Should not be above 105
When we reduce TV in MV patients?
When there is respiratory alkalosis
Reduce the risk of barotrauma-If given mere than Recommended (Normal:7-8 ml/kg)
when we extubate w/o SBT?
When we intubate for elective surgery
When and why we do tracheostomy in an intubated patients?
Intubation >7-10 day
Prolonged intubation–Larengial and tracheal damage—-tracheal stenosis
Normal ABG in adults?
PH--7.35-7.45 PO2--60-100 PaCo2--35-45 HCO3--22-26 Sao2--95--100
Peak airway pressure?
Airway pressure measured at end of delivery of TV
Important for a patient on MV
How to calculate PAP?
Resistive presure + platu pressure
RP–flow rate + airway R
PP–Lung elatic pressure + PEEP
LEP–1/conpliance
When breathing stooped–RP equal to 0 as aresult PAP equal to platu pressure
Peak Pressure (Peak)?
This is the summation of pressure generated by the ventilator to overcome airway (ETT and bronchus) resistance and alveolar resistance to attain peak inspiratory flow and to deliver desired tidal volume.
Peak inspiratory pressure is typically 12 mm Hg. It is best if ventilation is adjusted according to the arterial or end-tidal carbon dioxide tensions.
Cause of elevated peak pressure?
Depend on the value of plateau pressure
Asses plateau pressure by making the patient pause breathing after inspiring TV–Wich makes RP zero.
If plateau pressure is normal?
Disease with increased airway resistance. Airway obstruction Bronchospasm Secretions or plugging Increased inspiratory flow rate coughing biting on ETT.
If there is an increase in PP?
Pneumonia Pneumothorax Pulmonary edema Atelectasis Right mainstem bronchus intubation
Treatment lists and their benefit In COPD?
Long term supplemental O2–Increase survival(the only management that increases survival)
Influenza Vaccination–Decrease exacerbation
Beta 2 agonist–Central to management
Systemic steroid: Acute exacerbation
Periodic phlebotomy: When a patient has polycythemia symptom(usually occur when HCT >65%)
Mucoactive agent(acetylcysteine)–Pt with mucous plugging
Prophylactic Ab: rarely used but show a decrease in acute exacerbation.
Long term systemic corticosteroid in COPD?
Not recommended B/C of side effects and increase mortality.
Common causes of chronic cogh?
upper airway cough syndrome(postnatal drip)
asthma
GERD
UACS feaucher?
Also called postnasal drip
Is due to mechanical(due to discharge) stimulant cough reflex in the upper airway
Diagnosis confirmed by improvement to first-generation antihistamine( Block H1 receptors–anti-inflammatory and block histamine release from mast cell –Decrease secretion(a major mechanism)
a side effect of o2 treatment in patients with COPD?
CO2 retention by 3 mechanism due to increase Po2
Mechanism?
Vasodilation — V/Q mismach
Haldal effect on hemoglobin—Decrease Co2 affinity of HgB
Decrease RR–Deacrese minute ventilation
Benefits of pulmonary vasoconstriction in COPD?
Decrease B/F to Hypoventlated area –Correct the V/Q mismatch(prevent Co2 retention and hypoxia due to V/Q mismach)
symptoms?
Decrease LOC(Due to a reduction of aspartate and glutamate and increment of GABA and Glutamine) Seizure due to reflex cerebral vasodilation Acidosis
Prevention and management?
Target o2 saturation b/n 90-93 and pao2 b/n 60-70
Put on MV if have sever acidosis and decrease LOC
OSA feaucher?
Obesity
HTN
Day time drowsiness
Diagnose with polysomnography
Typical feather of bronchiectasis due to CF from other causes?
Crackle and infiltration in the upper lobe
Sign and symptoms of ankylosing spondylitis?
Low back pain improves with exercise and worsens at night
Hip or buttock pain
Limited chest expansion and spinal mobility(PFT–show restrictive lung pattern with normal or increase RV/FRC due to chest wall stiffness)
Enthesitis
Systemic symptoms
Acute anterior uvitis
How to differentiate RLD from lung fibrosis from chest wall stiffness on PFT?
In the case of CWS the RV/FRC will be normal or high but low in the case of ILD.
Cough related to ACE inhibitors?
Mainley stary whithin weeks of start/increament of drug dose
Occur upto 20% of patient
Is due to increasing level of inflammatory mediators(bradikinin,substance P ,thromboxane and prostaglandine)–bronchial irritation and constriction
Aproch to plural effusion?
Do diagnostic thoracyntesis whether you suspect or not.
treatment of non allergic rhenitis?
Mild:Intranasal antihistamin and corticosteroids
sever:combination
Sinus X-Ray indication in sinusitis?
lpersistent symptom–chronic sinusitis
CXR feather of PE?
Wage shaped infarction(shallow wedge-shaped opacity in the periphery of the lung with its base against the pleural surface)
Unilateral plural effusion
Aproch to hyponatremia(<275meq/l)
Cheek blood volume status
Cheek urine osmolarity
If hypovolemic do Una?
Una>40–renal loss(Diuretic,PAI)
Una<40–nonrenal(vomiting,diharoa ,DHN)
If normovolumic check Uosm?
Uosm>100-SIADH
Uosm<100-Psychogenic polydipsia, beer potomania
Beer potomania?
It is described as the excessive intake of alcohol, particularly beer, together with a poor dietary solute intake that leads to fatigue, dizziness, and muscular weakness.
Hypervolemic?
CHF
Nephrotic syndrome
Hepatic failure
PCP endocrine complication?
SIADH
worsen by normal saline
How NS worsen it?
Normal saline administration(water in >water out)–net water retention
Serum osmolarity calculation?
2x NA+ G + BUN
The normal serum osmolality?
should range from 275 to 295 mOsm/kg.
Psycogenic polydypsia and hyponatremia?
ADH suppression
Overwhelmed renal H2O excretion
Cause of hyperinflation in COPD?
Static and dynamic phenomena
Static phenomena?
NEW high FRC(created by low alveolar collapsing pressure and decrease CW expansion)
Dynamic phenomena?
more important
airway resistance–more air retention due to expiratory difficulty
Exercise and COPD?
Decrease time-lapse b/n respiration due to increase RR to increase MV–Decrease time for expiration–more inflation–Increase work of breathing due to diaphragmatic flattening and respiratory muscle shortening.
Acute COPD exacerbation cardinal symptoms?
Dyspnea
Cough exacerbation
Change in color or volume of sputum
Diagnostic tool?
Hyperinflation on CXR
Low O2 and CO2 retention
management of AECOPD?
O2(Target 88-92 %) Inhaled bronchodilator(beta-agonist and anticholinergics) Systemic glucocorticoid(short course) Antibiotic if >=2 cardinal symptom Oseltamivir if evidence of influnza NPPV-if ventilatory failure Tracheostomy if NPPV failed
Systemic glucocorticoid?
5 day of oral prednisolone or IV methylprednisolone
Improve hypoxia, lung function, relapse, hospital stay, and treatment failure.
No mortality benifit
Risk factors for ARDS?
Infection
Trauma
massive transfusion
acute pancreatitis
pathophysiology?
fluid and cytokine leakage to alveoli
decrease gas exchange, decrease lunge compliance, and P.HTN.
diagnosis?
New/worsen RD < 1 week
Bilateral lung opacity(Pulmonary edema)not due to CHF or fluid overload
Hypoxia with Pa02/Fio2 ratio < 300mmhg
The formula for calculating FiO2 percentage?
. FiO2= 20% + (4 X oxygen liter flow)
management?
mostly need MV
oxygen delivery
Tx underline cause
MV principle in ARDS?
LOW TV–prevent baritrauma-decrease mortality
PEEP–prevent alveolar collapse and improve O2 delivery
mortality benefiting treatment in COPD?
Smoking session–By reducing the rate of FEV1 decline
Long term 02 supplementation inpatient have an indication for LTOT)
Surgery
longterm treatment sequale after HL?
Cardiac complication
Radiation induced hypothyroidism
Life time 2nd malignancy >30%,mostley occur after 10 year of inithal NHL treatment.
Classification of plural effusion?
Based on PFA
PF LDH
PF/S protien ratio
PF LDH for exudative?
1) >2/3 of upper normal serum level(which is 90)
2) PF/S ratio >0.6
PF/S protien level for exudative?
1)>0.5
If plural fluid lymphocyte predominant?
TB
Obesity hypoventlation syndrome(OHS)?
Obesity (BMI>30)
Awake daytime hypercapnia(>45)
No alternative diagnosis
workup?
ABG on room air(Hypercapnia with normal A_a gradient No interesic pulmonary disease on x-ray Restrictive pattern PFT Normal TSH polysomnography(ass.OSA is common)
treatment?
nocturnal PPV
wight loss
avoidant of sedative medication
respiratory stimulant(Acetazolamide) last resort
Other future OHS?
Dyspnea Polycytemia Respiratory acidosis with metabolic alkalosis Pulmonary HTN Corpulmonale
pathophysiology?
Low CW and lung cpmpliance-dec TV and TLC and increase airway resistance–persistent nocturnal hypercapnia exacerbated by decrease central chemosensetivity for co2 and renal hco3 los for response of respiratory acidosis.
which heparin form is good to use in renal insufficiency?
unfracctionate heparine
effect of high Fi02>
Free radical injurt
athelectasis
