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148 Cards in this Set

  • Front
  • Back
Normal MAP
70-100 mmHg
Normal MPAP
10-18 mmHg
BP needed for PH
greater than 25 mmHg
What can PAC measure?
*Right side pressure
*PA pressure
*RV pressure
*Mixed-venous Oxygen saturation
How will PCWP reflect the following?
1. PE
2. Mitral valve disease
4. Left heart failure
5. PAH
1. Normal
2. High
3. Normal
4. High
5. Normal
Reasons for Increased CO
1. Thyrotoxicosis
2. Sepsis
3. Anaphylaxis
4. Exercise
How does PVR change in the following settings?
1. PAH
2. PE
3. Early mitral valve disease
4. Hypoxia
5. Left heart failure
1. Increase
2. Increase
3. Normal
4. Increase
5. Normal
What are Left heart pressures like with PE?
Central Respiratory controllers modulate what?
1. Increase in PaCO2
2. Decrease in pH (Increase in H+)
Peripheral respiratory controllers respond to what?
Decrease in PaO2
What is the threshold of PaO2 which stimulates peripheral chemoreceptors?
60 mmHg
What is the effect of decreased PCO2 on the threshold of PaO2?
The threshold will be lower.
For example, if you increase PCO2, it will take less of a drop in PaO2 to stimulate the chemoreceptors.
What is the threshold of PaCO2 which stops stimulates chemoreceptors?
30 mmHg
What is Integral control?
Ventilation matched to metabolic rate
Ondine's Curse
patients have no chemical drive to breath, so when they sleep, they will not breath.
When awake, have wakeful stimulus
Obesity Hypoventilation Syndrome
Definition:An Obese person who doesn't breathe enough and so has hypercapnia and hypoxia
Cause: During sleep CO2 builds due to mechanical burden of obesity and low respiratory drive. Therefore they retain HCO3- to compensate during sleep, which blunts CO2 drive when awake.
Chronic hypoventilators
Compensate with elevated bicarb. Therefore if there is acute hypercapnea, they will not respond.
Respiratory failure in asthamatic presents with what kind of CO2
Increased PCO2.
Normally they can hyperventilate to compensate for obstructed airways. This should lead to lower than normal PCO2.
Cheyne-Stokes Breathing
Period of shallow breathing, that gets deeper, then shallow again. Then there is a period of apnea.
Commonly associated with Heart failure.
More common during sleep than wakefullness.
Carries with it bad prognosis.
Due to slow moving blood, chemoreceptors are presented with low PCO2 blood from previous episode of hyperventilation, therefore maintaining apnea.
SIDS and Ondine's Curse are related to what brain structure?
Respiratory controllers asking for more than you can give.
Length tension inappropriateness.
Signs of Shock
1. Tachypnea
2. Tachycardia
3. Hypotension
4. Skin changes (cyanosis, mottling, white/gray)
5. Confusion
6. Oliguria
Cardiogenic Shock
(CO, Filling pressures, SVR)
CO = Decreased
Filling pressures = pressure backs up behind pump
SVR = Increased due to vasoconstrict
Cardiogenic Shock Characteristics
Hx: Cardiac disease, acute chest pain
Physical: Tachycardia or bradycardia, hypotension
* Murmur or gallops
* Cool, clammy skin
*Crackles in lungs, dyspnea, sitting upright
CXR: Pulmonary edema - venous congestion and pleural effusions
Hypovolemic Shock
(CO, Filling pressures, SVR)
CO: Dec
Filling pressure: Dec (CVP & PCWP)
SVR: Inc
Hypovolemic Shock
Hx: Vomitting/diarrhea, blood stool, trauma
Physical: Cool clammy skin
Tachycardia, dry membranes, hypotension
Poor skin turgor
Labs: Low Hgb, high BUN/creatinine
Distributive Shock
(CO, Filling pressures, SVR)
CO: Increased
Filling pressure: Low to normal PCWP
SVR: Low (abnormal vasodilation)
Distributive Shock
*Direct AV connection: Macro or micro
*Mitochondrial poisoning
ie. cyanide poisoning or thiamine deficiency
*Abnormal oxygen release at capillary
Systemic Inflammatory Response Syndrome
2 or more of the following
1. Temp greater than 38 C or less than 36 C
2. RR > 20 breaths/min or PaCO2 <32 mmHg
3. WBC >12,000/mm3 or > 10% bands
4. HR >90 beats/min
Primary vs. Secondary
Primary: Directly attributed to insult itself
Secondary: Consequence of host response
Distributive Shock
Hx: Fever, confusion, abdominal pain
Physical: Warm extremities, flushed
Hypotension, tachycardia, tachypnea
Widened pulse pressure, low diastolic pressure
Hyper- or hypothermic
Labs: WBC high
Lactate out of proportion to BP
Respiratory alkalosis
Obstructive Shock
(CO, Filling pressures, SVR)
CO: Dec
Filling pressure: Increase, pressure backs up behind the pump
SVR: Increase

There is a mechanical restriction to filling or emptying.
Obstructive Shock
*Tension pneumothorax
* PA obstruction (PE)
* Mechanical valve stuck closed
*Pericardial disease
Which has more of an effect on pulmonary microvascular fluid balance?
Protein Osmotic pressure or Permeability
CPWP in:
1. Cardiogenic
Cardiogenic --> Increased
ARDS --> Normal or low
What is ARDS?
Acute respiratory failure with:
1. Hypoxemia, refractory to supplemental O2
2. Diffuse pulmonary infiltrates, b/l
3. Pulm edema with absence of cardiogenic cause
4. Reduced pulmonary compliance (Dec FRC)
Risk Factors
*Multiple fractures (long bones, pelvis)
*Aspiration of gastric contents
*Massive blood transfusions
*Prolonged hypotension
*Acute pancreatitis
*Inhaltion of smoke or toxic gases
*Organ transplatns, esp allogenic bone marro recip
* Injured pulmonary vascular endothelium/epithelium
* Pulm edema, first insterstial, then alveolar flooding
*Hyaline membranes (made of albumin and fibrinogen) - from protein exudate
* Sequestration of granuloctyes
* Alveolar hemorrhage, lung hepatization
* Hyperplasia of Type II cells
Chest X-ray
Major Cause of people with ARDS
Organ Dysfxn Assement takes into account what systems?
*CNS (glasgow)
*Pulmonary (PaO2/FiO2)
*Renal (creatine)
*Cardiovascular (BP)
*Coagulation (platelets)
*Hepatic (bilirubin)
What does PEEP do?
Increases alveolar volume and improves arterial and tissue oxygenation
PEEP: side effects
1. Barotrauma - Dec Venous return and CO. Pneumothorax, pneumomediastinum
2. Volutrauma - Distension of lung induces or exacerbates ALI
Which position do you have a higher FRC, supine or standing?
Standing, because abdominal contents are out of the way.
What is abdominal paradox?
Abdomen pushes in during inspiration.
Due to b/l phrenic nerve damage.
What body parts are needed for coughing?
Rectus sheath
Compliance =
change in volume/change in pressure
(related to tension and radius)
Cell mediators of:
2. Asthma
1. macrophages and neutrophils
2. macrophages and eosinophils
Permanent Dilation of bronchi and bronchioles
Sx: Clubbing, coughing up phlegm, hemoptysis, dyspnea, cor pulmonale, febrile exacerpations
Causes: Infeciton, airway obstruction
Bronchial secretions: CF, ABPA, Primary ciliary dyskinesia
What is Varenicline?
Partial nAChR agonist
Relives craving and withdrawl
How to glucocorticoids exert their effect?
1. Dec cytokines release and production
2. Dec mucous production
3. Dec airway hyperresponsiveness

Trying to reduce inflammation
Mixed venous PO2
40 mmHg
4 key points on oxygen-dissociation curve
1. 27, 50%
2. 40, 75%
3. 60, 90%
4. 100, 97%
Oxygen consumption =
O2 consumed = oxygen delivered - oxygen leaving

O2 consumed = CO*CaO2 - CO*CvO2
Cancer often associated with PE
Pulmonary Emoblism
Chest X-Ray
* Pleural effusion
* Dilated PA
* Hyperlucency
* Atelactasis
*Often normal
Clinical presentation
Chest pain
can have cough
Tension pneumothorax
Clinical presentation
Dec VR
Pleural Effusion
Clinical presentation
Chest pain
Pleural Effusion
Physical Exam
Dec breath sounds
Dullness to percussion
Egophony at upper level
Reduced excursion of diaphragm
Clinical Presentation
Hx: Insidious onset, 50-70 y/o
Physical: Velcro crackles, clubbing, loud P2, edema
CXR: Reticulonodular shadows, lower lobes, traction bronchiectasis, little ground glass, end stage honey-combing
Outcome: Poor prognosis
End stage honeycombing
Very little ground glass
Traction bronchiectasis
Patchy reticular densities at lung bases
CT plugs at terminal airways
Fume expsosures, viral infection, CT dz
Subacute onset of dyspnea and cough
CXR: Patchy consolidations
Good response to corticosteroids
Chronic eosinophilic pneumonia
Clinical presentation: Fever, weight loss, cough
NOT IgE mediated
Biopsy: Tissue infiltrate with eosinophils
CXR: Negative image of pulmonary Edema
Treatment: good response to corticosteroids
DDx: Ascaris, allergic granulomatosis, angitis, Nitrofurantoin, sulfa, carbamazepine
Young black females and Scandinavians
Non-caseating granuloma
CXR: b/l hilar and mediastinal adenopathy
Systems Affected
Lung: interstitial infiltrates and b/l hilar and mediastinal LNs
Nerves: bells palsy and peripheral neuropathy
Eye: anterior uveitis
Heart: Cardiomyopathy and AV block
Liver: cholestatic defect
Joints: diffuse arthralgias
Skin: erythema nodosum
Granulomata: hypercalcemia
Churg Strauss Vasculitis
1. Prodromal phase: Asthma; paranasal sinus disease
2. Blood eosinophilia: GI tract and lungs
3. Vasculitis:
Lung: Granulomatous vasculitis
Heart: pericarditis and coronary vasculitis
Neuro: Mononeuritis mulitplex
Skin: palpable purpura, ulcers, nodules

p-ANCA association 50% of time
Goodpasture's Syndrome
Clinical presentation: Acute lung hemorrhage and hematuria
Often follows influenza or exposure to toxic hydrocarbon
Muscles of Inspiration
External Intercostals
Emphysema has airflow obstruction during inhalation or exhalation
Why does abdominal paradox occur?
Neg pleural pressure due to the accessory muscles pull diaphragm up and this causes the abdomen to sink in
Ways to damage phrenic nerve
MVA (C3,4 5)
Mediastinal mass (cancer)
Neck trauma (carotid surgery)
Whats the main problem for quadriplegics?
Cannot expire
W/o rectus abdominis cannot generate positive pleural pressure
Required to cough
Rectus sheath
At what level does cartilage disappear?
why do things preferentially go to the right?
where in the right?
Right is more aligned with the trachea.

Upright - posterobasal segment of right lower lobe
Supine - superior portion of right lower lobe
Right side - right middle lobe or psoterior segment of RUL
Why do the small ariways contrible little to total airway resistance
aligned in parallel
At FRC, pressure in pleural space is...
compliance =
Change in volume/change in pressure

measure of distensibility
Pal during expiration
Types of work in resp system
Elastic work to overcome recoil pressure of chest wall and lung
-this is higher at higher lung volumes

Resistive work to overcome resistance to airflow
-higher during exhalation and low lung volumes
DLCO depends on
Hb present
Functioning alveolar capillary surface area
DLCO of emphysema
DLCO of chronic bronchitis
DLCO of asthma
normal or increased
Asthma classification
 Intermittent
• Sx less than 2/wk
 Persistent
• Mild
o Sx >2x /week
o Night sx >2x/mt
• Moderate
o Daily sx & Bagonist use
o >1x/wk night time
• Severe
o Continuous sx
o Frequent night sx
Cytokines important in asthma
IL-4 isotype switching
IL-5 make and activate eosinophils
Most common arterial blood gas in asthmatics
low po2 due to v/q mismatch
low pco2 due to hyperventilation

respiratory alkalosis
Histology of Asthma
Curschmann spirals --> mucuous plugs with shed epithelial cells. This is a pathologic effect of the major basic proteins and cationic proteins produced by eosinophils. They damage epithelium, leading to shed cells.

Charcot-leyden crystals: crystalline granules in eosinophils
Samter's syndrome
Nasal polyps
Stages of COPD
• Mild
o FEV1 >80%
• Moderate
o FEV1 50-80%
• Severe
o FEV1 30-50%
• Very Severe
o Fev1<30 or <50 plus chronic resp failure
What is first line COPD treatment
Short acting Anticholinergics
Nutritional requirements for COPD
Vit A, C, E and coenzyme Q
Adaquate Carbs
Most effective anti asthma drug
Main risk factor for TB
Unventilated Air
How long does it take for PPD to become positive after infection
2-3 weeks
% cases negative PPD:
newly active disease
pleural cases
miliary -- 50%
newly active case --20
pleuarl cases - 30%
What part of the PPD determines result?
Size of induration. The risk factors determine cut off for size.
How to treat latent TB?
conditions that increase risk of progression to TB disease
Diabetes mellitus
substance abuse
Recent infection with MTB
TB pleural disease
Follows primary infection
Where does TB reactivate
Apical posterior secion upper lobe
Superior segment of lower lobes
Ghon complex
caseous necrosis in hilar lymph nodes

**Calcified focus of infeciton + associated lymph node
Pott's Disease
TB in vertebra
Extrapulm sites of TB infection
Adrenal - Addisons disease
Cervical lymph nodes --> Crofula
Vertebra --> potts diseaes
Meningeal - meningitis
kidney is most common
What kind of people get MOTT
People with underlying lung disease or immuno comproised
Can have skin involvement
Inflammation of the bronchial tree (no evidence of alveolar space infection)
3 most common resp infections by aspiration
Viral infections, TB, legionella
What kind of people are more at risk for H. influenzae?
COPD and alcoholics
CXR often shows pleural effusion
When deprived of sleep, the first things to recover are...
S3/S4 of NREM
Two key changes in sleep as we age:
Increase in Wakefulness after sleep onset
Ded in SWS
75% sat O2 = x mmHg
40 mmHg
Hypoxia - lack of o2 supply to tissues
Hypoxemia - Dec PO2 or SO2 in the blood
50% sat O2 = x mmHg
27 mmHg
Causes of Hypoxia w/o hypoxemia
Anemia (blood is saturated, just Hb isnt)
Abnormal tissue demand
Hypoxia w/ hypoxemia
Low PiO2
Diseases of the lungs or chest bellows
Physiologic dead space equation
Vd/Vt =(PaCO2-PeCO2)/PaCO2
90% sat = x mmHg
60 mmHg
97% sat = x mmHg
Right shift of Hb dissociation curve
Inc temperature
Decreased pH
Inc 2,3 DPG
tissue oxygen delivery =
O2content ml/dl x CO dl/min
Effects of Anemia on:
oxygen content
aterial po2
o2 sat
Dec oxygen content (b/c dec in Hb amount conc)
Aterial PO2 normal
O2 sat is normal
Effects of CO on:
oxygen content
aterial po2
o2 sat
oxygen content: dec
aterial po2: normal
o2 sat: normal
Most common people to get iPH
young, healthy, women
Most common cause of PH
Autoregulation causing vasoconstriciton
Bone morphometric protein receptor related to...
Levels of various things in PH:
NO, thromboxane, Prostcyclin, endothelin
NO dec (normally vasodilates)
Prostacyclin dec (protects against vascrular injury)
Endothelin inc (mitogen that contributes to vasoconstrion and clel prolif)
Thromboxane Inc
Treatment for Pulm HTN
Endothelin antagonists
Prostacyclin analogues
Calcium channel blockers
Progressive systemic sclerosis
Interstitial fibrosis
Raynauds phenomena
pursing of lips
Common organisms causing bronchiectasis
H influenzae
Staphylococcus aureus
Size restriciton of particles that can enter resp tract
>10 microns --> nasopharynx
5-10 microns --> trachea
<4 microns --> terminal bronchi
Percent of cells that are macrophages in normal BAL
85% (10% lymphs)
Master switch for immune response in the lung
NK-kB; due to LPS, IL-1, or TNF
What is the action of IL-10
Inhibits actions of activated T cells
Chemo/luekemia predisposes to what infecitons
S aureus

gram neg
Lupus or CML predisposes to what lung infections
punemococcus or H flu
HIV, Hodgkins, Sarcoid --> T cell defects predispose to what infections
PCP, HSV, candida, crypto, TB, MAI, varicella, aspergillus, VZ, listeria
B cell defects mimic what sort of defect?
Asplenia. cannot make Abs to target encapsulated organisms
Common molds include:
These appear with B or T cell defects

B cell defects
Where can candida spread to systemically?
Urine, eye
Clinical presentation of Histo
Flu like syndrome
Hilar adenopathy
Nodular inflitrates in upper lobes

fibrosisng mediastinits
Blastomycoses presentation
75% are just lung
Can have skin, bone, prostate involvement as well
Diffue infiltrates, fibronodular or mass infiltrates, cavitaiton
Predispose to disseminated coccidoies disease
HIV viral load and related risks of diseases
CD4 >500: TB and bacteria
CD4 200-500: oral thrush, zoster, hairy leukoplakia
100-200: PCP
less than 100, toxo, crypto
less than 50 CMV, AI, PML
how does PCP patient present
Fever, wasting, cough, dyspnea
CXR: diffuse interstital and bilateral infiltrates
Bacteria that is increasing in prevalance in nosocomial pneumonia
most common cause of bronchiectasis worldwide