Respiratory Diseases Flashcards
The 4 acid-base disorders
Normal pH range of blood, acidosis range an alkalosis range
Respiratory acidosis: high CO2
Respiratory alkalosis: low CO2
Metabolic acidosis: high HCO3-
Metabolic alkalosis: low HCO3
Normal: 7.35-7.45
Acidosis: 7-7.35
Alkalosis: 7.45-7.8
Death beyond these ranges
Carbonic acid
Acidic products excreted from respiration
Carbonic acid (H2CO3) easily dissociates into bicarbonate ion (HCO3-) in dissolved plasma or as a gas as CO2 + H2O
CO2 –> lungs for excretion
H+/HCO3- –> excreted by kidneys
Bicarbonate-carbonic acid buffer system
How do kidneys prepare for compensation of acidosis
H2CO3 (acid) easily dissociates into CO2
- controlled by hyper/hypoventilation (fast)
Bicarbonate/HCO3- (base) can be reabsorbed/conserved by kidneys or excreted as bicarbonate or H+ for pH regulation (slow)
Kidneys generate sodium bicarbonate to create a reserve
How does buffer system compensation work?
Increased acid: more H+ –> more CO2
Lungs increase rate/depth of breathing to expire more CO2
Faster compensation than excretion through kidneys
What happens to pH balance when the lungs don’t function properly?
Hypoventilation conditions
More CO2 buildup –> more carbonic acid –> more H+ –> respiratory acidosis
Kidneys increase net H+ excretion and retain Na/K-HCO3
Hypoventilation conditions: impaired CNS respiratory drive, neuromuscular transmission, muscular weakness, obstructive or pulmonary disorders
Mechanism of respiratory alkalosis
Hyperventiliation due to panic, anxiety or lung conditions w/ SOB
↑ CO2 exhaled and ↓ CO2 in blood/↓ H+
Kidneys conserve H+ and excrete Na/K
Definition of metabolic acidosis/alkalosis
Rate of compensation for metabolic vs. respiratory issues
Any acidosis caused NOT by excessive CO2 in the blood (ex. severe diarrhea)
Any alkalosis NOT caused by lower levels of CO2 in plasma (ex. severe vomiting)
Lungs compensate faster to a metabolic problem while kidneys take longer to compensate for an acute respiratory problem
Normal ranges for blood pH, pCO2, pO2, O2 saturation, HCO3- and base excess
pCO2: 35-45 mmHg
pO2: 80-100 mmHg
O2 saturation: 95-100%
HCO3-: 22-26 mEq/L
Base excess: [-2, +2]
6 steps of ABG analysis (arterial blood gases)
- Analyze pH
If normal, label which side: Normal/acidic <7.4 or normal/alkalotic >7.4 - Analyze CO2 (higher = acidic)
- Analyze HCO3 (higher = basic)
- Match CO2 or HCO3 w/ pH to determine respiratory vs. metabolic acidosis/alkalosis
- Does CO2 or HCO3 counter pH? –> compensation by system
Ex. acidotic pH/CO2 but alkalotic HCO3 - Analyze pO2 and O2 saturation (low = hypoxemia)
Chronic obstructive pulmonary disease (COPD) or maladie pulmonaire obstructive chronique (MPOC) definition and common causes
Definition: group of lung conditions which make breathing difficult by blocking airflow in lungs
–> ↓ O2 in blood due to restriction and/or inflammatory causing damage over time
Smoking, 2nd hand smoke or wood fire are common causes
Define dyspnea, DOE, hypercapnia and hypoxia
Dyspnea = SOB
DOE dyspnea on exertion (or SOBOE)
Hypercapnia = excessive accumulation of CO2 in blood
Hypoxia = low O2 in blood
Co-morbidities with COPD
T2D/MetS
Cancer
CVD
Osteoporosis/osteopenia
Depression/anxiety
Smoking, lifestyle, lack of exercise, alcohol, obesity
3 Physical types/nutritional needs in COPD
- Cachexia: disease driven loss of skeletal muscle and fat (increased osteoporosis risk)
- Obesity: increased CVD/diabetes risk w/ sleep apnea
- Sarcopenic obesity: loss of muscle mass + more abdominal WAT w/ high CVD risk
*Mild/moderate COPD may have no physical signs
Spirometry definition and values
Lung function test to measure Forced Expiry Volume (FEV)
FEV1 = volume of air that can be forcibly blown out in 1 second following full inspiration
GOLD 1: mild, FEV1 ≥ 80% predicted
GOLD 2: moderate, FEV1 50-<80% predicted
GOLD 3: severe, FEV1 30-<50% predicted
GOLD 4: very severe, FEV 1 <30% predicted
Why might someone w/ COPD have GI symptoms?
GI symptoms may occur due to impaired peristalsis from hypoxic GI tract
Pink puffer type of COPD and nutritional recommendations
Rapid breathing, enlarged alveolar airspaces, cough with or without mucous
- barrel-shaped chest
- thin + muscle wasting
Ex. emphysema, alveoli level
–> less elasticity, fewer capillaries or less SA
Nutritional recs:
1. E to maintain or gain weight (30-35 kcal/BW)
1-1.5g/kg protein (1.2-1.7g/kg during stress/infection/exacerbation)
2. Small (6x/d), frequent, nutrient dense high kcal meals/snacks (oral nutritional supplements like MedPass or Sip Supp)
3. soft foods, easy to chew
4. add kcal and limit low nutrient dense foods
Blue bloater type of COPD
GI changes and risk of sarcopenic obesity
Nutritional rec
Blue bloater: productive cough with mucous, cyanosis due to O2 deprivation, edema/bloating, digital clubbing
- overlap with heart failure showing distended neck veins
- progressive cardiac failure over time
Ex. chronic bronchitis, bronchiole level
GI changes: hyperinflation pressure on diaphragm, limited O2 to GI, constipation, early satiety and sense of fullness
Decrease appetite from fatigue/coughing/SOB/depression/anxiety
High risk of sarcopenic obesity (difficulty exercising and loss of muscle mass) –> high risk of malnutrition
Diet rec: limit Na, limit fluids possibly, 6x small, soft texture meals per day
–> severe prognosis = less restrictive diet
Critical care feeding in COPD
Intubation via oral route (unconscious or heavily sedated)
Tracheostomy to ventilator - may require tube feeding, some textures can be allowed
Avoid overfeeding in critical care- more food requires more work from lungs to expel CO2
- except if already malnourished
