respiratory labs Flashcards

1
Q

Causes of Respiratory Disease

A

Tumors:
Infections:
Airway diseases:
- emphysema
- bronchitis
-asthma
- RDS
Pulmonary vascular disease:
-PE
- P HTN
Interstitial lung disease:
- affect the tissue and space around the alveoli
- impaired diffusion of gases
- sarcoidosis, pneumoconiosis

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2
Q

Common Locations for an ABG: where do you palpate the arteries

A

Radial artery: *
- Palpated between the distal radius and the tendon of the flexor carpi radialis
- need to do modified allen test to make sure collateral circulation working

Femoral artery:
- Palpated below the midpoint of the inguinal ligament

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3
Q

Modified Allen Test

A
  • Tests for sufficient arterial blood flow to the hand prior to an ABG draw

1) hold hand high and make a fist while compressing ulnar and radial arteries (blanched hand)
2) lower hand and release fist
3) release pressure off ulnar artery
4) watch hand turn pink within 6s to indicate patent collateral blood flow
- patent ulnar artery
- intact superficial palmar arch
- -if flow is not restored to hand -> you cant do an ABG on this hand -> no collateral flow

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4
Q

components of typical arterial blood gas kit

A

-arterial blood gas syringe
-protective needle
-syringe cap
-iodine and alcohol preparation swabs
-gauze
-pt label
-biohazard ice bag
-adhesive bandage
-sample goes on ice

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5
Q

femoral artery anatomy/puncture

A

NAVEL:
-outside to inner- femoral nerve, artery, vein
-femoral artery can be palpated just below midpoint of inguinal ligament
-blood draw- 90 degree angle
-catheter: 45 degree angle -> “snaking a line:” threading a thin tube through the artery to reach various parts of the body

Code type situation: we all need to be able to check femoral pulse

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6
Q

Key Components of the Blood Gas Test Panel:

A

pO2 (Partial Pressure of Oxygen)
- low = hypoxemia
pCO2 (Partial Pressure of Carbon Dioxide)
- high = hypercapnia
pH
- Normal: 7.35 to 7.45

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7
Q

Body’s Response to Acid-Base Disturbances

A

Lungs respond within MINUTES:
-ex. if you put a pt on a ventilator, the lungs respond in mins, redraw ABG can be done within mins
-Respiratory Acidosis: can increase rate on ventilator to tx
-Respiratory Alkalosis: reduce ventilator

Renal response takes hours/DAYS:
-can’t check immediately
- response: can excrete H+ and retain HCO3-: INCREASE pH
- retain H+ and excrete HCO3-: lower pH

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8
Q

Respiratory Acidosis

A

ABG Findings:
- Low pH
- high pCO2

Cause: HYPOventilation*
- COPD exacerbations
- severe asthma
- airway obstruction

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9
Q

Metabolic Acidosis

A

Low pH (acidic) and low bicarbonate (HCO3−)

Examples:
- DKA: uncontrolled DM* tx with IV insulin
- lactic acidosis from shock
- severe dehydration

need to calculate ANION GAP
- normal anion gap: acidosis is due to a loss of bicarbonate, which could be from GI or renal causes
- elevated: due to additional acids in blood - MUDPILES (DKA, renal failure)

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10
Q

Respiratory alkalosis

A

High pH, low CO2

Causes: hyperventilation *
- severe anxiety/pain
- pneumonia
- PE
- high altitudes
- pregnancy

ALKalosis: “tALKative ppl need to hyperventilate to talk more”

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11
Q

Metabolic alkalosis

A

High pH, high HCO3

Causes: loss of H+ or HCO3- excess
- Severe chronic vomiting *: huge loss of H+ in stomach
- diarrhea
- laxatives
- loop diuretics
- hyperaldosteronism: mineralocorticoid excess

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12
Q

importance of Proper ABG Sample Handling

A

ABG blood draws must always be placed on ICE IMMEDIATELY after collection:
- at room temperature: metabolic processes continue within the blood sample -> consumption of O2 and production of CO2
- not on ice = alterations in pH*
- pO2 will decrease and pCO2 increases: pH will be skewed to be more acidic

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13
Q

Anion Gap: what electrolytes

A

Cations: Na+ and K+
Anions: Cl− and HCO3−

Normal anion gap: <12
Elevated: greater than 12-16
- indicates presence of additional acids in the blood (DKA!!)

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14
Q

Causes of Increased Anion Gap

A

“MUDPILES”
M methanol
U uremia
D DKA
P Propylene glycol
I iron tablets or INH
L lactic acidosis
E ethylene glycol
S salicylates (aspirin)

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15
Q

Causes of normal Anion Gap

A

HARDASS

H hyperalimentation
A addison’s ds
R renal tubular acidosis
D diarrhea
A acetazolamide
S spironolactone
S saline infusion

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16
Q

thoracentesis: asesses what

A

asses:
-color
-characteristics
-odor
-exudate vs transudate

17
Q

transudative vs exudative

A

Transudative:
-low protein and LDH
-increased hydrostatic pressure or low osmotic pressure (lack of proteins)
-water/fluid (CLEAR) in lungs
- integrity of capillary walls is maintained
-ex. CHF, cirrhosis, nephrotic syndrome, PE, hypoalbuminemia

Exudative:
-high protein and LDH
-inflammation and INCREASED capillary permeability
-ex. pneumonia, cancer, TB, viral infection, PE, autoimmune
-pus, yellow color, odor, thick

18
Q

Light’s criteria for pleural effusions

A

Transudate causes:
- hypoalbuminuria: cirrhosis, nephrotic syndrome
- CHF
- pericarditis

Exudate causes:
- autoimmune ds
- esophageal rupture
- infection
- malignancy
-pancreatitis
- post-CABG
- PE

19
Q

Bronchoalveolar Lavage Fluid Analysis: diagnostic for what

A

Pulmonary infection
Acquired Pneumonia
Interstitial Lung Diseases-SARCOIDOSIS
Lung Cancer
Lung Transplant monitoring

20
Q

Bronchoalveolar Lavage Fluid Analysis: testing

A

Can: culture, WBC count, Gram stain
- Bloody BAL → diffuse alveolar hemorrhage
- Cloudy → pulmonary alveolar proteinosis
- process BAL: microscopy and find biomarkers,

21
Q

Bronchoalveolar Lavage Fluid Analysis: procedure

A
  • Several aliquots of warmed saline are instilled in different areas of the lungs
  • At least 30% of the instilled fluid is carefully aspirated
  • BAL fluid is collected with the aid of a bronchoscope
22
Q

Asthma

A

Spirometry:
- helping in the diagnosis and monitoring of asthma
Pulmonary function test
Chest X-Ray
Allergy testing

23
Q

COPD

A

Pulmonary Function Tests:
- Obstructive pattern: decrease in FEV1 and FVC, FEV1/FVC lower than 1, decrease DLCO

-CBC: secondary polycythemia from chronic hypoxemia
-Rule out infections: can exacerbate COPD sx
-Symptoms: chronic cough, sputum production, and SOB
-r/o Alpha-1 antitrypsin Deficiency, elastin degradation

24
Q

Community acquired Pneumonia organisms

A

Streptococcus pneumoniae
Mycoplasma pneumoniae
Haemophilus influenzae
Legionella species
Bordetella pertussis

25
Q

Viral Pneumonia Causes:

A

Influenza
COVID-19

26
Q

Ventilator-Associated Pneumonia (VAP)
Drug-Resistant Organisms:

A

Klebsiella pneumoniae
P. aeruginosa
Acinetobacter baumannii
Methicillin-resistant Staphylococcus aureus (MRSA)

27
Q

immunocompromised hosts pneumonia

A

HIV-Associated:
- Pneumocystis pneumonia
- Cytomegalovirus (CMV)
Neutropenic Patients:
- Aspergillus species

28
Q

Travel-Related pneumonia pathogens

A

Tuberculosis (TB)
Fungal Infections

29
Q

Pneumonia Testing

A

Bacterial:
- Gram stain
- sputum culture

Fungal:
- KOH preps
- culture.

Parasitic:
- Based on exposure risk, special stains, and serology

Viral:
- PCR assays
- NAAT for specific viruses
- rapid antigen tests (ex: influenza)

Specialized Testing:
- Acid-fast staining: culture or nucleic acid amplification test for TB.
- NAAT (nucleic acid amplification test) for viral infections

30
Q

acute respiratory distress syndrome (ARDS)

A

Definition:
-Rapid onset respiratory failure
-caused by systemic inflammation, trauma, or severe infection
-Significant morbidity & mortality from diffuse alveolar damage
- pts have perfusion but no ventilation

Sx:
-Hypoxia
- bilateral infiltrates
- respiratory failure without cardiovascular insult or pulmonary HTN

Dx: Hx, CXR, CT, ABG, Echo, Cardio biomarkers,

Tx:
- Oxygen, IV fluids, treat underlying disease
-if in preterm labor- give steroids to increase lung maturity in baby

31
Q

neonatal respiratory distress syndrome

A

Definition:
-Incomplete lung development in preterm infants = surfactant deficiency!!!*
-deficiency in SURFACTANT which prevents alveolar collapse during exhalation
-Have perfusion but lack VENTILATION

Signs: no ventilation
- hypoxia
- respiratory acidosis

Tx:
-Steroids 48hrs before birth.

Dx:
- Lamellar body count test: indicates fetal lung maturity in amniotic fluid
- LBCs >50,000/µL suggest maturity

32
Q

Sepsis

A

Definition:
-Severe physiological and biochemical response to a global infection
-Response to infection is SYSTEMIC

Systemic Inflammatory Response Syndrome (SIRS): proinflammatory cytokines cause:
- fever
- leukocytosis
- activation of endothelial cell function
- hypercoagulation
-LEFT SHIFT- neutrophils (banded), leukocytosis

Complications:
-Shock hypotension and organ failure
-70 % mortality
-bad signs: Lactate elevation, WBC with neutrophil elevation (left shift)

33
Q

Signs of SIRS, sepsis, severe sepsis, septic shock

A

Signs: need 2 signs for SIRS
- Temperature >38C (100.4) or <36C (96.8
- WBC >12,000 or <4,000; >10% bands
- RR>20 /min,
- HR>90 bpm
- PCO2: <32

Sepsis: confirmed/suspected infection with SIRS

Severe:
- evidence of organ damage
- hypotension
- lactate >4 mmol

septic shock:
- same as severe but with PERSISTENT SIGNS

34
Q

Lung cancer

A

Dx work up:
- Chest xray
- CT
-MRI

Dx: needs TISSUE ANALYSIS
- histological and immunohistochemical analysis

Molecular testing:
- mutations crucial for directed therapy

Biomarkers:
- cytokeratin 19 in serum may be used in prognosis

35
Q

Immunohistochemical (IHC) and histochemical staining profiles for different types of carcinomas

A

Bx techniques used in pathology laboratories to help identify the types of cells present in a tissue sample

Adenocarcinoma:
- TTF-1 (Thyroid Transcription Factor-1)
-napsin A
- CK 7
- Mucicarmine
- PAS-D (Periodic Acid-Schiff with diastase)

Squamous Cell Carcinoma: -p40, p63
- CK 5/6
- Desmoglein:
- Negative for TTF-1 and CK 7

Small-cell Carcinoma:
- TTF-1 and markers associated with a high proliferative rate (such as Ki-67, MIB-1)

36
Q

what is banded? what is left shift?

A

Left shift:
- “left shift”: immature neutrophils in the bloodstream
- severe infections/sepsis: bone marrow releases immature neutrophils to fight infection

Banded:
- immature neutrophils look different under microscope
- have a banded nucleus appearance

“left shift” originates from the historical practice of plotting immature cells to the left on a chart and mature cells to the right.