Exam 1

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