hypoxic injury
loss of o2 at the cellular level
Single most common cause of cell injury/death
etiology
decreased oxygen delivery because of low cardiac output
Most common
Ischemia
It has decreased O2
decreased o2 in the atmosphere
Loss of hemoglobin
Carries 97% of oxygen
PAO2 is amount dissolved in arterial blood
Oxygen being carried on hemoglobin is what pulse ox measures
hypoxic injury mechanism + manifestation
mechanism
Lack of oxygen converts from aerobic to anaerobic metabolism
manifestation
Cannot maintain sodium potassium pump bc of lack of ATP
Cannot pump sodium out and draws water into the cell (K stays out)
Cell begins to swell
Without supplemental o2 membrane will rupture and cause cell death
reperfusion injury
Occurs after hypoxic injury
Occurs in the heart
Time=muscle
More cardio myocytes you can save
etiology
Heart doesn’t get oxygen
reperfusion injury mechanism + manifestation
Mechanisms
When blood supply is returned to the heart the cells form ROS and cause irritation that can cause arrythmias (v-tach and v-fib)
manifestations
signs of MI
chest pain
diaphoresis (sweating)
reactive oxygen species
Extra electrons in outer shell
Pulls electron from normal healthy cells and damages them
Body cannot rid them faster than they are made
Antioxidants
Vitamin E, C, beta carotene (precursor to vitamin A)
Kill off ROS
When oxygen is put back into the heart is causes ROS
Irritation of myocardium and causes cardiac arrest
Damages the heart muscle
etiology
cigarette smoke
infectious injury
bacterial and viral
bacterial injury
Pneumonia
Puss, mucus, inflammation (can make ROS) can all kill lung tissue and lead to cell death
Can regenerate interstitial cells in lungs
Tetanus
Releases exotoxins and damages cell
endotoxin
contained in cell wall of gram-negative bacteria
Releases cytokines, vasoconstriction,
In septic shock (mostly grama negative bacteria)
lipopolysaccharide
viral injury
Require permissive hosts
Do not produce exotoxins or endotoxins
DNA or RNA virus
Can damage the cell it replicates in to kill the cell
endocytosis
The cell surrounds substance and closes it off bringing it into the cell
Macrophages, phagocytes
Bacteria and infection will enter, and lysosomes will break it down and the cell will excrete it
(HIV) Virus will land on a cell and get pulled in and will replicate and retranspose RNA inside the cell and is released to infect more cells
exocytosis
The cell surrounds substance inside the cell and excretes it through cell membrane
Histamines
chemical injury
direct
Damages the cell wall
Resulting in cell death
Mercury, iron, lead
indirect
Because the metabolite that comes from a chemical
tylenol
When you take Tylenol (acetaminophen) and breaks down and becomes a metabolite that can kill hepatocytes
Only take max of 3g a day
physical injury
Temperature extremes
Frostbite – hypothermia
Can cause necrosis
Usually freezing of tissue
Trauma
Head injury
Primary injury (blunt force trauma)
48-72 hours (about 3 days) later
Inflammatory response
Can cause further injury and death of cells (physical cell injury)
cell swelling
Casual decrease in the amt of o2 being delivered to the cell tissue
Etiology
Hypoxic injury
Aerobic -> anaerobic metabolism
Water follows NA into the cell because of lack of ATP to function NA K Pump
Tumor compressing capillaries
Bacteria
Necrotizing fasciitis
Hyperthermia
Is reversible if o2 is brought to the tissue and water will be pumped out
If oxygen is not supplied
Cell will burst and die
Death occurs where swelling is
Becomes necrosis and tissue becomes necrotic
apoptosis
programmed cell death
DIFFERENT THAN NECROSIS
Scattered
necrosis
Etiology
Hypoxic injury
Mechanisms
Irreversible
Occurs in clump (where lack of blood flow was)
atrophy
Decrease in size and function of the cell
Can reverse
Etiology
Aging (brain atrophy)
Alzheimer's
Cannot reverse
Casts
Persistent cell injury
Insufficient nutrients
Muscle breaks down
Inadequate supply of oxygen
Can affect any organ
Most common
Skeletal muscle
Heart
Brain
Secondary sex organs
hypertrophy
Increase in size of cell
Augmented capacity of the cell (can work better if healthy increase)
Etiology
Weightlifting
Uterus in pregnant woman
Cells hypertrophy to grow and allow baby to grow
Maladaptive
Not physiologic = maladaptive
Pathologic does not increase function
Myocardial hypertrophy
Increased stress and workload
Gets bigger (ventricular remodeling)
hyperplasia
Increase in the number of cells in the organs tissue
When cells are capable in meiotic division
Can cause cell death
Etiology
Increased functional demand
Uterus when preparing for a baby
Persistent cell injury
Benign prosthetic hyperplasia (BPH )
Enlarged prostate gland
Men in 50s
Natural occurrence (NOT CANCER)
Organ donation
Donate lobe of liver
Lobe in recipient will begin to regenerate into entire new liver
Lobe in donor will grow back
metaplasia
Alteration in the type of cell
Chronic injury or irritation
Etiology
Smoking
Columnar cells go through metaplastic change and lay on the side (lose cilia)
Causes increased respiratory infections because cilia cannot push out contaminants
After quitting they switch back
dysplasia
Persistent severe injury or irritation
Alteration in size, shape, and organization of cell components
Can be seen on the cervix, respiratory tract
Precursor to cancer
Atypical hyperplasia
Most often in breast cancer
Etiology
Smoking
HPV
metabolic acidosis
pH - < 7.35 & HCO3 < 22 mEq/L
Etiology
Increased production of acids
DKA (diabetic keto acidosis)
Lactic acidosis
Alcohol
Breakdown of alcohol can develop metabolic acidosis
Decreased acid secretion by the kidney
Chronic renal failure
90% of the time results in metabolic acidosis
Excessive loss of bicarb
Severe diarrhea
Small bowel drainage
Lose bile in GI tract
Pancreatic fluid drainage
metabolic acidosis manifestations
Neuro
Patients are weak
Lethargic (very tired)
Confusion
Coma
No cerebral function
Cardiovascular
Dysrhythmias
Decrease in HR
GI
Anorexia
Loss of appetite (not the psych disorder)
Nausea and vomiting
Abdominal pain
metabolic alkalosis
pH - > 7.45 & HCO3 > 26 mEq/L
Etiology
Loss of hydrogen ions
Vomiting
Most common
NG tube
Suctioning too much stomach contents out
Can be prevented
Hyperaldosteronism
Too much aldosterone
Hangs onto sodium in exchange for K or H ions and excreted through the kidney
Endocrine disorder
Not common
Increased retention of bicarbonate
metabolic alkalosis manifestations
Neuro
Confusion
Hyperactive reflexes
Tetanus
spasm of muscles
Seizures
If pH is > 7.55
Causes hyperexcitability of neurons
Cardiovascular
Hypotension
Dysrhythmias
respiratory acidosis
Too much CO2
pH < 7.35 & pCO2 > 45 mm Hg
Etiology
Impaired function of the respiratory center
Chest injury
Rib fracture
Makes it difficult and painful to breath
Retains CO2
Weakness of respiratory muscle
ALS
Chronic degenerative neuro disorder
Eventually affects respiratory function
Acute Respiratory Failure – pneumonia, COPD
COPD
Chronic bronchitis piece causes CO2 retainment
Kyphoscoliosis
kyphosis is hunchback
Scoliosis – S curve
Cannot expand chest
Extreme obesity
Opiates, sedatives
Suppresses respiratory status
respiratory acidosis manifestations
Neuro
Impaired consciousness
Continue into coma
Headaches
Hypercapnia
Increased CO2 levels
Tremors
Weakness
Musculoskeletal
Weakness
Tremors
No cardiac manifestation
respiratory alkalosis
pH > 7.45 & pCO2 < 35 mm Hg
Etiology
Hyperventilation
Breathe in a bag can breathe CO2 in
Usually from panic attack
Fever
Anemia
Hemoglobin too low causes increased respiration
Encephalitis
Inflammation of the brain
Usually, unconscious
respiratory alkalosis manifestations
Neuro
Numbness and tingling in fingers and toes
Seizures
Light headedness
Tetani
Changes in calcium levels (hypocalcemia)
Cardiovascular
Dysrhythmias
Respiratory control mechanisms
Increased respiratory rate can blow off CO2
Diabetic keto acidosis
Do not have insulin to move glucose into cell
Break down free fatty acids -> creates ketones (acid)
Creates metabolic acidosis
Deep and fast respirations will lower CO2 to counter metabolic acidosis
Can respond in minutes
Manifestations
Fruity smell in breath
precursor
Renal control mechanisms
Responds in hours (3-4)
In elderly or renal disease 3-4 days
Can reabsorb more bicarb to bind w H ions and create carbonic acid to be broken down and excreted (metabolic acidosis)
Secrete H ions
Secrete them out (removes from blood and puts it into tubule)
Excreted out of the body
fastest buffering system
lungs
increase RR to blow off acid
protein buffering system
Protein that latches onto H ion
Hemoglobin
Can bind with carbon dioxide
bicarb buffering system
Can bind with H ions
Makes carbonic acid that shifts into CO2 and H2O
Can bind to fixed ions
normal pH
7.35-7.45
< 7.35 acidotic
7.45 alkalotic
Can survive between 6.8 and 7.8
Outside range will result in death
normal PaCO2
35-45 mm Hg
Respiratory acid
normal PaO2
80-100 mm Hg
Dissolved in arterial blood
normal HCO3
Can go up to 26
Metabolic acidosis (too little bicarb)
Metabolic alkalosis (too much bicarb)
oxygenation
Oxygen saturatioon
Hemoglobin level
Oxygen delivery
Cardiac output
analyzing blood gases
Examine pH, O2 & saturation (will be normal for now), CO2, HCO3
CO2 will tell you if its respiratory acidosis or alkalosis
HCO3 will tell you if its metabolic acidosis or alkalosis
upper airway
Nose down to the trachea (carina cartilage)
Warm filters humidify air
If respiratory rate increases, you can lose water
Diaphoretic – sweating
Insensible water loss 10%
Not a lot but can make a difference when on the verge of dehydration
airway circulation
Pulmonary artery
Comes off the heart and splits into right and left lung
If the patient is hypoxemic or hypoxic
Pulmonary vasculature vasoconstricts
Creates pulmonary hypertension
Can cause heart failure
Pressures are a lot lower than systemic pressure
Normal systolic 25-30mmHg
90-119 is normal systemic systolic
minute ventilation
Amount of air moved in 60 seconds
Tidal volume x RR (Vt = tidal volume)
CO2 increases if RR decreases
CO2 decreases if RR increases
Minute volume decreases = CO2 retainment
More or deeper breaths to counteract
tidal volume
air in each breath
vital capacity
all the air you can inhale and exhale
inspiratory reserve
anything you can breathe on top of tidal volume
atelectasis
alveolar collapse
expiratory reserve
Everything you can exhale in forceful exhale
Does not empty lungs completely
Residual volume is left
1L left to keep lungs open
functional residual capacity
Expiratory reserve + residual volume
Positive end expiratory pressure
PEEP
Increased FRC pumps alveoli open and promotes gas exchange
sitting up
Blood flow is at the bottom of the lungs
E.g., Right sided pneumonia decreases the amount of O2
laying down
Perfusion changes
Pneumonia oxygenation will not be good (turned to the right)
Turned to the left (gravity takes perfusion to the left side and increase perfusion because right-sided pneumonia
good lung down
Lung without disease should be down towards gravity to increase perfusion
ventilatory failure
Don’t have mechanics to breathe
Can happen with drugs
Intubation or Narcan
Can be fixed with mechanical ventilation
oxygenation failure
Problem with gas exchange
Disease can affect perfusion or not enough hemoglobin to carry it
central chemoreceptors
controlled by brain and pH of the blood
PH decreases RR increases
To blow off acid
PH increases RR decreases
peripheral chemoreceptors
Carotid artery and aortic arch
Responds to o2 levels
If O2 decrease and CO2 increase, then RR increases
respiratory mechanics
More narrow airway resistance increases
Big with asthma and other obstructive pulmonary disorders
Broncho spasm can narrow airway
Compliance
Sponginess of the lung
How well it expands and contracts
Very compliant = moves easily when breathing
Poor compliance = stiff lungs
Interstitial lung disease
Over compliant
Emphysema
Floppy lungs
Lose elasticity and alveolar wall breaks down
bronchiolitis
Inflammation of the bronchioles
Airway becomes obstructed from swelling of the bronchiole walls
Causes bronchiole edema (swelling)
Causes
RSV
Respiratory syncytial virus
Used to be disease of young children
Now is seen in adults and vaccine for 60+
Influenza
signs and symptoms
Symptom
What the patient experience
Cough
Sign
Nurse observes
Vitals
bronchiolitis manifestations
Exudate in airways
Medical term for pus
Dead neutrophils
Increase in lymphocytes in airways
Causes inflammation
Wheezing
Because of narrowing of airway
Crackles
Sounds from FLUID in the lungs
Fine
Heart failure
Coarse
Loud popping
Gonna be coarse
Retractions
See in children and adults
If stomach is pulling in or clavicle area is sucking in
Muscles are working very hard
Elevated WBC
Because of infection
Slight bump bc caused by a virus
XRAY
Can look like atelectasis
asthma
obstructive disorder
Recurring attack of wheezing, dyspnea, and coughing
Occurs because of inflammation and bronchospasms
Broncho spams trigger cough
Heightened airway responsiveness
Two types
Extrinsic
Etiology
Allergic asthma
Usually, children but can be in adults
Intrinsic
Etiology
Respiratory infection
Usually, middle age or children
NSAIDS
Can trigger asthma
Arachidonic acid cascade
Can have an allergic response with it
DO NOT give asthma patients NSAIDS
Can exacerbate asthma
asthma manifestations
Wheezing
Diffused wheezing = throughout the whole chest
Feeling of tightness in chest
Dyspnea
Confusion
If O2 falls
Productive cough
Coughs up sputum
Nonproductive cough
Dry cough
Usually with broncho spasms
Decreased peak expiratory flow rate or (FEV1)
How much air can they actually get out
Measures FEV in one second
How much air they can force out in one second
chronic bronchitis
obstructive disorder
Usually in older adults
Etiology
smoking
95% of the time it is the cause
Smoking yourself or secondary smoke
Repeated viral or bacterial infections
Acute bronchitis is viral
Chemical irritants
Mechanisms
Chronic inflammation
Lining of bronchioles is inflamed
Scarring and swelling of bronchiole mucosa
Impaired mucociliary escalator function
Due to metaplasia
Cilia is not removing debris
Chronic thick secretions
From inflammatory response
chronic bronchitis manifestations
obstructive disorder
Productive cough
Fatigue
Lower levels of O2
Retain CO2
Hypercapnia
Elevated PACO2
As CO2 level increases increase RR
Tend to breathe by levels of oxygen instead
Do not put on high levels of oxygen bc it can stop breathing
Breathing by hypoxic drive
Loss of libido
Insomnia
Decrease FEV1
emphysema
obstructive disorder
Destructive changes in alveolar walls without fibrosis (scarring)
Abnormal enlargement of distal sacs
Air gets trapped
Results in fewer capillaries that interact with alveoli
Residual volume increases
Because of trapped air
Etiology
Smoking
Asbestos
Air pollution
Possibility with normal aging
Mechanisms
Inflammation of lung tissue
Loss of alveolar walls
Loss of elastic tissue in lung
emphysema manifestations
Progressive exertional dyspnea
Shorter of breath with more movement
Retractions
Increased AP Diameter
Barrel chested
Pursed lip breathing
Trying to make their own alveoli open
PEEP
Positive end expiratory pressure
Decrease in FEV1
Air gets stuck
Increase in residual volume
Do not retain CO2 like chronic bronchitis
pulmonary fibrosis
restrictive disorder
Stiff
interstitial lung disease
Non-compliant lungs
Thickening of alveolar interstitial
Etiology
scarring
Oxygen toxicity
Seen with ARDS
Acute respiratory distress syndrome
Immune reaction
Mechanisms
Infiltration of lung tissue
Lymphocytes, macrophages and plasma cells
Cause scarring
pulmonary fibrosis manifestations
Rapid shallow breathing
Dyspnea
A non-productive cough
Clubbing
When your nail bed changes
Finger flattens and nail bed rounds up
From low levels of O2
Decrease in FVC (Functional Vital Capacity)
Functional vital capacity
Normal FEV1
status asthmaticus
Severe asthma attack
Repetitive broncho spasms
Unresponsive to any therapy
Can die
Steroids can help break the spasms
Silent chest
Want to hear people wheezing
Then they're moving air
No wheezing
Air is trapped and not moving
Need to dial 911
cystic fibrosis
Hereditary disorder
Lung congestion and infection
Malabsorption of nutrients by the pancreas
Mucus build up
Autosomal recessive disorder
Both parents need to have gene for child to get it
Most often infected with pseudomonas
Often get lung infections
Mechanisms
Problem with chloride channel in the airways
Cannot move in sodium and water
cystic fibrosis manifestations
Thick tenacious sputum
Recurrent bronchitis
Hemoptysis
Coughing up blood
Pancreatic enzymes
Thick secretions in the pancreas
Enzymes cannot empty into the duodenum
Take digestive enzymes in capsules before eating to break down food
Tachypnea
Fast breathing
Dyspnea
Difficulty breathing
Retractions
Coarse crackles
pneumothroax
Air in the pleural space
Affects oxygenations
Any can turn into tension pneumothorax
Mechanism
Air in pleural space causing collapse
Manifestations
Absent breath sounds over collapse long
SOB
Dyspnea
Hypoxemia
O2 sats decreased
Tachypnea
RR increase
open pneumothroax
Sometimes called sucking chest wound
Etiology
Penetrating trauma
Bullet, knife, impaled object
DO NOT PULL IT OUT
Hole in parietal pleura
Hear sucking sound in inspiration
Problems w oxygenation and ventilation
HR (Heart Rate) goes up with struggle to breathe
Can put a chest dressing over it
Only tape on 3 sides
Allows air to get out
If tape on all 4 you close off wound and cause worsening pneumothorax that can turn into tension pneumothorax
Medical emergency
tension pneumothorax
Everything shifts and compresses the heart
Manifestations
Tachypnea
Tachycardia
Dyspnea
Hypoxemia
Absent breath sounds
Decreased/absent cardiac output
Hypotension
Faint pulse
Urine output decreases
Prolonged capillary refill (3+ seconds)
Due to vasoconstriction
Tracheal deviation
The side that gets compressed (right side)
The trachea pulls to the right
Needle thoracotomy can save the patient until a chest tube is inserted
hemopneumothorax
Blood built up in pleural space
Traumatic event
Etiology
Knife would
Blunt chest trauma that ruptures vessels
Iatrogenic
Central line placement can cause it
Manifestations
SOB
Hypoxemia
Tachypnea
Decreases cardiac output
Dyspnea
Hematocrit decreases
pleural effusion
fluid in pleural space
Etiology
Cancer
Malignant pleural effusion
Chronic renal failure
Manifestations
SOB
Hypoxemia
Decreased O2
Tachypnea
Dyspnea
Muffled or decreased breath sounds
Thoracentesis
Tube drains fluid
pulmonary embolus
Clot that is lodged in pulmonary arteries
Can be in a capillary
Further in it gets the more likely you're able to survive
Big clots that plug big arteries can block blood flow to half the lung or more
Etiology
Blood clots in legs
DVT
If clot breaks off goes into the heart right into the lung
Increase in dead space
Air is in the lung but no perfusion
mechanism
Increase in dead space
Bronchoconstriction
Compensatory shunting
Can shunt blood into other vessels to bypass clot
Hemodynamic consequences
Affects pressures in the heart
pulmonary embolus manifestations
Dyspnea
Chest pain
Cough
Tachypnea
Tachycardia
Palpitations
Apprehension
Nervousness/panic
Diaphoresis
Hypoxemia
Low grade feve
acute bronchitis
productive cough
secretions
fever
spontaneous pneumothroax
seen in young people
Young men
Etiology
Weightlifting
Very small in apex area
Usually heal on their own
pneumonia
Inflammatory reaction in alveoli and interstitium of the lung
Immunosuppressed pt
Cancer and elderly
Etiology
Aspiration
Especially w stroke patients
MI (Myocardial Infarction)
Vomit and aspirate vomit
Inhaling bacteria or virus
Contamination from systemic circulation
E coli can translocate into blood stream
Travels into the lungs and infects lung
Pathology/mechanism
Bacterial
Worse
Buildup of exudate (pus) in alveoli
Consolidates
Decreases gas exchange
Viral
Less severe
No exudate
pneumonia manifestations
Crackles
Coarse
Fluid will be softer noises
Fever
Cough
Purulent sputum
Weird color and thick
Decreased breath sounds in consolidated area
acute respiratory failure
Problems with gas exchange affecting oxygenation and CO2 removal (PAO2 < 60 PACO2 > 50 )
Etiology
Head injury
Neuromuscular disease
Giambarre ascending paralysis
Can paralyze diaphragm
ALS
Affects moto neurons
Chest wall problem
kyphoscoliosis
Cracked rib
Airway problem
Collapse
Clothesline injury
Crushes trachea
Infection in lungs
Pneumonia
ARDS
Vascular disorder
Pulmonary embolus
Blood clot prevents perfusion
Heart failure
Fluid overload can end up in the lung
Pulmonary edema
COVID
Mechanism
Mucus
Infection
Fluid
Traumatic injury
VQ mismatch
acute respiratory failure manifestations
Dyspnea
Tachypnea
Hypoxemia
Decreased pulse ox
SOB
Cyanosis
Only seen at 78-80%
Can look ashen or gray before cyanotic
acute respiratory distress syndrome
Worst form of acute respiratory failure
Etiology
Trauma
Pulmonary contusions
Fracture of lung bone?
Shock states
Septic shock
Aspiration
Mechanism
Damage to alveolar-capillary membrane
Inflammatory response
Interstitial edema
Decrease in FRC
Functional residual capacity
Due to atelectasis
Infiltrates
Fluid buildup in the lungs/alveoli
Patchy areas of fluid
Neutrophils cross into alveoli
Release inflammatory markers
Surfactant gets inactivated
Causes Atelectasis
Decreased gas exchange
Intrapulmonary shunting
Blood goes through the lung but does not pick up any gas
Refractory hypoxemia
Can give pt high levels of o2 but won't see change in O2 levels
MAJOR PROBLEM W ARDS
ARDS manifestations
Tachycardia
Tachypnea
Shallow respirations
Hypotension
Do not have angiotensin conversion working
Vasodilation
Restlessness
Decrease in mental status
Confusion
Hypoxemia
Hypercapnia
Mortality rate is 40%
Ones that survive can recover fully
infant respiratory distress syndrome
Neonates
Esp delivered before 25 weeks
Do not have enough surfactant
Women with gestational diabetes
Higher risk
RH incompatibility
Mom is rh- has a baby is rh+
Doesn’t get rogam
Antibodies from mom attack baby that is rh+
Pathology
Do not produce enough surfactant
Manifestations
Intercostal retractions
Nasal flaring
Early signs of respiratory arrest
Tachypneic
Respirations fast and shallow