Respiratory Flashcards
Components of Upper Respiratory Tract
Sinus, nasal cavity, external nose, nostril, tongue, larynx, esophagus, trachea, pharynx, glottis, epiglottis, opening of eustachian tube
Components of Lower Respiratory Tract
Larynx, Trachea, Bronchi, Lungs
Central Chemoreceptors
In brain, respond to changes in H and arterial Co2 in CSF
Positive feedback loop
Dorsal and ventral respiratory neurons
In medulla
Control rhythm of respiration
Apneustic and Pneumotaxic centres
In pons
Affect rate and depth of respiration
Activation of muscles of respiration
Phrenic nerve
Peripheral Chemoreceptors
In carotid and aortic bodies, respond to changes in CO2, pH and O2 levels
Secondary drive
Low pO2 in peripheral chemoreceptors
Increase ventilation
Inspiratory muscles
Increase thoracic cage volume –> decreased intrathoracic pressure
Expiratory muscles
Decrease thoracic cage volume –> increased intrathoracic pressure
Tidal volume
500mL
Amount of air moved in or out each breath
Inspiratory Reserve Volume
3000mL
Max volume inspired above normal inspiration
Expiratory Reserve Volume
1100mL
Max volume expired below normal expiration
Residual Volume
Volume of air left in the lungs after maximum expiratory effort
Surfactant
Produced by type II alveolar epithelial cells
Reduces surface tension by forming a layer between aqueouss fluid lining alveoli and air
Bronchial Sounds
Heard over trachea
I:E ratio 2:3 or 1:3
Loud, harsh, high pitched
Broncho-vesicular sound
Anteriorly near 1st and 2nd IC space
Soft/breezy
Vesicular Sounds
Lungs, peripheral
Lower pitch
Adventitious sounds
Crackles, wheeze, stridor, pleural rub
Pulmonary Oxygen Toxicity
Cellular injury to lung parenchyma and airway epithelium
O2 causes thickening of intra-cellular space, loss or inhibition of surfactant
Results in ARDS, fluid leaking, and atelectasis
Depends on O2 concentration, length of exposure, underlying condition
Nitrogen Washout
Damage from deficiency of nitrogen. High concentrations of O2 causes nitrogen to be exhaled and replaced by O2 in the alveoli. Removal of O2 causes alveolar collapse and hypoxemia
Oxygen Induced Hypercarbia/Apnea
Extended time to occur
Affects pts that utilize peripheral chemoreceptors to breath
Affects hypoxic drive
COPD pts
Retinopathy of Prematurity
Insult to developing retinal vasculature from elevated PaO2 leading to abnormal blood vessel growth
Leads to separation of retina, visual impairments, blindness
Oxygen radical attack incompletely developed retinal tissue
Premature infants
Factors influencing affinity of HgB for O2
Acidity
Partial pressure of CO2
Temperature
2,3 BPG
Right Shift
Acidosis
Hyperthermia
Hypercapnia
Hypoxia
Anemia
Increased 2,3 BPG
More oxygen available to the tissues, high affinity at lungs
Shift Left
Alkalosis
Hypothermia
Hypocapnia
Decreased 2,3 BPG
Carboxyhemaglobin
V<Q
Wasted perfusion
Anything that decreases or completely stops O2 from reaching alveoli
Pulmonary oedema, COPD, asthma, FBAO
V>Q
Dead space, wasted ventilation
Oxygen present but no pulmonary capillaries/blood for diffusion
Hypoxic Hypoxia
Lack of oxygen diffusion into pulmonary circulation
Decreased amount inhaled
Pulmonary oedema, COPD, ARDS, FBAO, drowning, high altitude
Anemic Hypoxia
Lack of RBC to transport O2
Will not respond to O2 therapy
Low HgB, sickle cell anemia, hemorrhage, CO poisoning
Histotoxic Hypoxia
Inability to offload oxygen from hemoglobin
Inability for cells to utilize oxygen
Requires treatment of underlying cause to respond to O2
Metabolic alkalosis, cyanide poisoning
Stagnant Hypoxia
lack of circulating O2
Blood flow insufficient to supply tissues
Treat the cause
Angina, MI, crush injury, poor circulation
Asthma
Hyper-reactive airway to stimuli resulting in inflammation, swelling, and narrowing of trachea and bronchi
3 main insults causing asthmatic respiratory distress
Inflammation
Bronchoconstriction
Excess mucus Secretion
Asthma Triggers
Allergens
Exercise
Respiratory infeciton
Nose + sinus problems
Drug and food additives
GERD
Emotional stress
Early Phase Asthma
30-60 min post exposure, subsides 30-90 min late
Bronchospasm
Release of histamine and leukotrienes
Release of inflammatory cytokines
Wheezing, cough, chest tightness, dyspnea
Late Phase Asthma
Inflammation
Histamine causes hyper-responsive airways
Increased resistance causes air trapping and hyperinflation of lungs
Can cause lung damage
Peaks in 5-6 hours with infiltration of eosinophils, and neutrophils
Within 1-2 day infiltration with monocytes and lymphocytes occurs
Medication Therapy of Asthma
Bronchodilators
Longer acting bronchodilator
Anti-inflammatory drugs
Leukotriene Modifiers
Dexamethasone Indications
Hx of asthma/COPD or 20 pack/year Hx of smoking
Contraindications dexamethasone
Allergy to steroids
Steroids in last 48 hours
Treatment Dexamethasone
PO/IM/IV
0.5mg/kg up to 8mg
1 dose
Permissive Hypercapnia
Tolerating higher ETCO2 instead of attempting to decrease value with aggressive ventilation
COPD
Chronic inflammatory lung disease causing obstructed airflow from lung
Chronic Bronchitis
Mucus plugging/inflammatory edema
Increased airflow resistance leads to alveolar hypoventilation
Increased secretions due to ongoing mucus + phlegm
Hypoxemia and Hypercarbia
Hypoxemia
Increased RBCs without oxygen
Cyanosis (blue bloater)
Hypercarbia
Pulmonary vascular constriction
Increased RV work
Right heart failure
For Pulmonale
Emphysema
Excess loss of elastin causing lung tissue to lose elastic recoil
Destruction of alveolar septum
Neutrophils produce elastase that destroy elastin
Pink Puffer
Pathology of Emphysema
Destruction of alveolar walls/septum
Destruction of gas exchange surface area
Distension or pulmonary air space
Loss of elastic recoil
Emphysema vs Bronchitis
Bronchitis: irritation + inflammation of upper and lower air tracts
Emphysema: alveoli, destruction of elastin, loss of ability to recoil
Factors affecting CO
HR
Preload
Afterload
Contractility
Preload
Volume of blood in LV at diastole
Starlings Law
Greater the stretch, greater the contraction
Increases of preload
Fluid increase
Vasoconstriction
Decreases of Preload
Fluid loss
Vasodilation
Loss of atrial kick
Afterload
Resistance LV must pump against
Increases of Afterload
HTN
Vasoconstriction
Decreases of Afterload
Vasodilation
Contractility
Ability of heart to squeeze, strength of contraction and ejection fraction
Ejection fraction
Amount of blood as percent that LV pushes
50-70%
Decreases of Contractility
Infected tissue
Ischemic tissue
Acid-base imbalance
Negative inotropes
Increases of Contractility
Sympathetic stimulation
Positive inotropes (digoxin)
Compensatory mechanisms of CHF
SNS stimulation
Myocardial hypertrophy
Hormonal response
Left sided heart failure
Blood backs up through left atrium and into pulmonary system
Pulmonary HTN
Biventricular failure
Causes of LSHF
HTN
MI
Dysrhythmias
Valvular disorder
Right Sided Heart Failure
Dereased RV
Blood backs up into right atrium and venous circulation
Can lead to venous congestion
Causes of RSHF
LVF
For pulmonal
RV infarction
Clinical Manifestations of Acute CHF
Pulmonary edema
Agitation
Pale/cyanosis
Cold, clammy skin
Severe dyspnea
Tachypnea
Pink, frothy sputum
Clinical Manifestations of Chronic CHF
Fatigue
Dyspnea
Tachycardia
Edema
Nocturia
Behavioural changes
Chest pain
Weight change
Skin changes
Drug Therapy Chronic CHF
ACE inhibitors
Diuretics
Inotropic drugs
B-adrenergic drugs
Goal of Initial CHF therapy
Decrease intravascular volume
Decrease venous return
Decrease afterload
Increase gas exchange and oxygenation
Increase cardiac function
Decrease anxiety
Nitroglycerin
Relaxes vascular smooth muscle
Peripheral venodilation
Dilation of arteriolar resistance vessels of peripheral circulation
Decrease MVO2
Side effects of Nitro
Headache
Dizziness
Weakness
Tachycardia
Hypotension
Orthostasis
Skin rash
Dry mouth
N/V
Causes of PE
Trauma/travel
Hypercoagulability or hormone replacement
Recreational drugs
Older
Malignancy
Birth control
Obesity/obstetrical
Surgery
Immobilization
Sickness
3 Types of PE
Massive
Submassive
Low Risk
Etiology of PE
DVT moves to pulmonary arterial tree causing V/Q mismatch. Increase pulmonary artery resistance leads to right ventricular failure
Clinical Manifestation PE
Tachypnea
SOB
Hypotension
Tachycardia
Altered LOC
Anxiety
Pale
Cough
Central cyanosis
Leg pain
Cardiovascular collapse
S1Q3T3
S1Q3T3
S Wave in lead 1
Q wave in lead 3
T wave inversion lead 3
Immunologic Anaphylaxis
Allergen enters system and interacts with B cells, creating antibodies for the allergen
Non-Immunologic Anaphylaxis
Allergen interacts directly with receptors on mast cells
Epinephrine
Antagonist for Histamine
Alpha and Beta effects
Relaxes smooth muscle in GI and GU
Benadryl
H1 receptor antihistamine
Competes for histamine receptors in CNS and PNS
Sedative properties due to competitive antagonism in CNS
Also acts as anti-muscarinic
Epiglottitis
Swelling of supraglottic area of epiglottis and pharyngeal structures
Often bacterial
S/Sx epiglottitis
Sniffing position with inability to swallow, high fever, inspiratory stridor, retractions
Children 2-6yo
Quick progression
Croup
Inflammation of entire airway, edema in subglottic area
Bacterial or viral, usually viral
Croup S/Sx
URTI, barking cough, low fever
Children 6mth to 3 years
Spontaneous Pneumothorax
Sub-pleural bleb ruptures allowing air to enter pleural space
Simple Pneumothorax
No communication with atmosphere
No mediastinum shift or hemi-diaphragm
Mechanism of Simple Pneumothorax
Fracture rib
Increased intrathoracic pressure with closed glottis
Open Pneumothorax
Open defect in chest wall
If >2/3 diameter of trachea then path of least resistance
Paradoxical motion of affected lung
Large dead space
Tension Pneumothorax
Trapping of air created by one way valve
S/Sx of Tension Pneumothorax
Decreased BS or hyper-resonance on one side
Distended neck veins
Hypotension
tachycardia
Needle decompression current site
2nd intercostal space, superior aspect of 3rd rib mid clavicular line
PCS 5 Needle decompression
Patch removed
Site anterior axilla
