patho i - pneumonia and pulmonary embolism

process of pneumonia (general)

infection -> inflammation -> exudate

1. aspiration, inhalation, or hematogenous
2. bypass upper airway defenses (saliva, gag, secretory igA)
3. evade lower resp defenses (mucocilliary, surfactant, PMNs)
4. alveolar macrophages and PMN activated
5. capsules and toxins limit immune response and contribute to tissue injury
6. cytokine release and alveolar filling with inflammatory exudate
7. v/q mismatch and hypoxemia (shunt)
8. systemic spread may lead to sepsis

definition of penumonia

- Describes many diseases that cause pulmonary exudate
- Most commonly used to refer to infections of the lower respiratory tract that are associated with inflammation, reduced cilia function, and where secretions pool or alveoli exudate is present (can't fill with air to do gas exchange)

etiology of pneumonia

viral, bacterial, fungal, protozoal, parasitic

transmission of pneumonia

community acquired, nursing home acquired, hospital acquired

primary pneumonia

acute infection

secondary pneumonia

caused by underlying condition

Usually infected with virus first, then develop a secondary bacterial pneumonia (most common thing)

vasodilation and capillary leak (pneumonia)

(part of inflammation that is caused by infection), this allows bacteria to actually move from the alveoli to other areas, into your bloodstream (sepsis) → common way of patients dying from pneumonia

epidemiology of pneumonia

Overall incidence of CAP is 3% per year in people >65 years old

Mortality ranges from 5% to >30% depending on the etiologic organism

non-HAP: 13% mortality

HAP: second most common nosocomial infection, but has the greatestmortality (60% of deaths attributed to nosocomial infection)

VAP

Most common infection in intensive care units, especially in mechanicallyventilated patients (VAP)

HAP most common organisms

pseudomonas aeruginosa and Staphylococcus aureus

more resistant to drugs

greatest risk and highest mortality pneumonia

advanced age and immunocompromised

risk factors for pneumonia

- altered level of consciousness
- smoking
- underlying disease or infection
- endotracheal intrubation
- immobilization

altered level of consciousness -> pneumonia

aspiration (right lung more common) - inhale something that shouldn't be there into your lungs, risk for sepsis

right lung more common (branch is more steep, straight shot down into lung, whereas left lung has to make a turn down, recovery position is left lateral position which prevents aspiration in right lung)

not moving so secretions just pool

If you are unconscious, you cannot close off airway to not inhale vomit (can't protect airway)

Confused, then also less ability to cough away the things blocking the airway and protect the airway

smoking -> pneumonia

inhalation of chemicals (inflammation in the lungs too)

inhalation of burnt stuff (damages the lungs), also smoking equipment is not clean (so much bacteria from everywhere and inhaling all of that)

underlying disease -> pneumonia

hematogenous (travels through blood)

(translocation of bacteria due to capillary leak and vasodilation (inflammation process), spread via bloodstream into lungs to create pneumonia → same bacteria elsewhere can travel and can pop up in the lungs)

endotrach intubation -> pneumonia

direct exposure (if tube is not clean)

immobilization -> pneumonia

atelectasis (alveolar collapse so dec secretion mvmt) -> infection

hematogenous spread -> sepsis

pneumonia creates what v/q mismatch?

shunt (perfusion without ventilation)

dead space

ventilation without perfusion

shunt

perfusion without ventilation

pathogens that can cause pneumonia

- influenza
- streptococcus pneumonia
- legionella, pneumophila
- mycoplasma pneumoniae
- chlamydia pneumoniae
- pneumocystis jirovecii
- staphylococcus aureus

influenza -> pnuemonia

common viral CAP. Reoccurrence due to viral mutation

Can often have staph aureus pneumonia as secondary infection

cilia

help bring up secretions

where you get pneumonia tells you

about the nature of the organism that is causing the pneumonia (most likely pathogen or group of pathogens)

empirical treatment for pneumonia

Empirical treatment (guestimate the pathogen they have) while waiting for sputum cultures to come back with the specific result of pathogen

how does severe hypoxia develop with pneumonia

oxygen diffusion is impaired by congestion

physical locations of pneumonia

- lobar
- interstitial
- bronchial

lobar pneumonia

- often streptococcus pneumoniae
- Single lobe mass (consolidation)
- Alveolar inflammation with exudate
- Sudden onset: fever, chills, rales, rusty sputum

interstitial pneumonia

- (usually viral): typically influenza (viral)
- Gradual or sudden onset
- Upper resp tract and spreads to lung tissue
- No alveolar exudate (inflammation and exudate in lung tissue not collected in alveoli)
- Pleuritic pain, aches (pleura rubbing together)
- Hallmark sign of unproductive cough
- Ground up glass kind of pattern in a predominantly central distribution (seen bilaterally)

bronchial pneumonia

- several species (opportunistic)
- Diffuse bilateral, lower lobes
- Bronchial mucosa and spreads to alveoli
- Pooled secretions become infected
- Gradual onset: low grade fever, crackles, colored sputum

clinical manifestations of pneumonia

- Headache, fever, chills (shaking chills - rigors → typically indicative of bacterial infections, trying to warm up the body by shaking), dec level of consciousness
- Dehydration, tachycardia (beats faster to try and circulate the low blood volume)
- Cough, dyspnea, cyanosis, pleuritic chest pain, tachypnea, use of accessory muscles, rhinitis (snot), postnasal drainage (down back of throat), discolored/thick sputum, hemoptysis (cough up blood)
- Crackles, rales on auscultation
- Radiological evidence of pulmonary infiltrate (consolidation present) and/or effusion (fluid collection)

Presentation and severity varies with the etiologic organism and underlying health of patient

diagnosis of pneumonia

Wbc with differential (numerous pmns consistent with bacterial infection)

Chest xray (sometimes can only hear it, not see it in the xray, sometimes helps if you give pt some fluid to fluff up the exudate so we see it in xray)

Sputum culture

sputum culture diagnosis of pneumonia

Numerous pmns consistent with bacterial infection

Numerous epithelial cells indicate oral contamination of specimen (came from mouth instead of infection)

clinical mgmt of pneumonia

Oxygenation
Hydration (if indicated)
Mobilization (increases breathing), deep breathing and cough (mobilizing secretions), I/S (incentive spirometer), chest PT, ambulation
Antibiotics

prevention of pneumonia

- Vaccination
- Isolation
- Positioning and mobilization
- Noninvasive ventilation (mask is preferred over invasive ventilation because pathogen could be introduced when inserting a tube in)
- Pharmacologic (mainly for immunocompromised individuals)

vaccination prevention of pneumonia

Defense against top common agents

Those with chronic cardiac, pulmonary disease, immune deficiencies, > 65 years old (recommended to get this vax)

tachypnea

Tachypnea- Rapid superficial breathing; regular or irregular rhythm

tachycardia

Tachycardia- Rapid heart rate (>100 BPM)

dyspnea

Dyspnea- subjective feeling of discomfort, occurs when a person feels unable to inhale enough air.

hypoxemia

insufficient oxygenation of the arterial blood (decreased Pa02)

hypoxia

inadequate oxygen supplies to the cells.

hypercapnia

an increase in carbon dioxide in the arterial blood (PaCO2)

ventilation

the flow of air into and out of the alveoli

Perfusion

(Q)- the flow of blood through alveolar capillaries

Infarct/infarction

- a small localized area of decreased or absent blood supply leading to tissue death

Sputum-

mucoid discharge

Hemoptysis-

Blood tinged (bright red) sputum

thrombus

blood clot that forms in a vein (yes can happen in artery, but veins are narrower so easily formed here)

embolus

anything that moves through the bvs until it reaches a bv that is too small to pass through

types of embolus

Fat embolus, amniotic fluid embolus, not just thrombus (thromboembolus)

pulmonary artery

All arteries in body carry oxygenated blood except for the pulmonary artery (pulmonary trunk to pulmonary arteries)

pulmonary embolism

no supply of oxygen brought to lungs and no co2 being removed from lungs (pulmonary artery obstruction)

pathophys of pulm embolism

1. Obstruction: embolism lodges in pulmonary arterial vessel (usually a blood clot -thromboembolism, but could be any kind of embolus)
2. inflammatory process: fluid floods alveoli (vasodilation and capillary leak)
3. Hypoxia and hypercapnia
4. Pulmonary arteriole constriction
5. Inc pulm pressure and dec perfusion (right side of heart has to work extra hard to push past that pressure → acute cor pulmonale)
6. Pulmonary embolism creates a v/q mismatch (ventilation without perfusion - dead space)

a completely intact, six-inch wide clot of human blood in the exact shape of the right bronchial tree

this did not come from the blood vessels, but the airway (this causes a shunt because obstructing ventilation)

Pulmonary embolism is clot in the pulmonary artery, not in the airways

pulmonary pressure inc ->

perfusion dec

- atelectasis (collapse)
- lung tissue infarction (typically segmented)

saddle embolus

Large obstruction known as a saddle embolus will infarct > 60% of lung tissue and associated with an acute cor pulmonale and sudden death (blood can't be ejected out of right ventricle bc how blocked the pulmonary arteries are since this embolus sits in the pulmonary trunk)

huge blood clot that blocks both pulmonary arteries (to both lungs)

risk factors for pulm embolism

Inc age
Surgery
Obesity
Trauma
Pregnancy
Genetics
Prolonged immobility (greater than 8 hours of sitting on a plane, walk around a bit, pump your legs)
Ocps (oral contraceptive pills) containing estrogen
Hormone therapy
Smoking related cancer (any cancer can inc risk)

DVT

PE due to a DVT is a leading cause of mortality while hospitalized (most often in legs - calves and popliteal space)

60k deaths per year

If survived, most will return to pre-illness level of functioning

DVT symptoms

Unilateral calf swelling, leg swelling

Warm skin in swollen area (blood pooling and not able to go up back towards heart)

Skin discoloration

Swollen, bulging veins

hypoxia occurring with pulmonary embolus bc of large obstruction in pulmonary artery ->

leading to atelectasis and lung tissue infarction

clinical manifestations of PE

- Chest pain, pleuritic pain (pain with deep breath)
- Tachycardia, hypotension, syncope (loss of consciousness)
- Dyspnea, tachypnea, cough, hemoptysis, crackles/rales to auscultation
- Apprehension and impending doom ("something's wrong, i feel like i'm going to die" → listen to them every time, even if vital signs look good)
- Diaphoresis (sweating), cyanosis
- Fever (physiologic rapid inflam response, no infection response)
- Evidence of dvt (most common origin of clot)

differentiating between bad or really bad PE

Depends on size and location

small emboli

can be silent

many small emboli together

Many small emboli known as a shower mimics large obstruction (a bunch of small clots in the cerebral circulation)

large emboli

can cause cor pulmonale and sudden death

hallmark of major or saddle PE

Hallmark of major/saddle PE: acute cor pulmonale, blood not able to get into lungs, so fills up superficial blood vessels (modeling from upper chest to up)

diagnosis of PE

- ABGs
- D-dimer
- ct angiogram
- doppler ultrasound or echocardiogram

ABGs for pulm embolism

85-90% have hypoxemia - Sometimes you can see hypocapnia at first (needing more air so blow off so much co2 when trying to quicken breathing, then gradually see hypercapnia bc can't bring air in anymore and co2 is not getting out)

Often have resp alkalosis (tachypnea due to air hunger and need for o2)

d-dimer

good negative predictive value for low-risk individuals for low-risk individuals (if < 500, PE unlikely)

If elevated, proceed to additional testing (you could have a dvt or pe, or something else)

Don't have to expose pt to radiation if d-dimer comes back negative (pretty sure it is not a dvt or pe)

ct angiogram

gold standard for diagnosing PE

v/q scan

v/q scan when supine positioning or weight prohibit cta (weighs more than table)
- alternative to ct angiogram
- look for a clot

doppler ultrasound for PE

Doppler ultrasound of extremities and/or echocardiogram to evaluate for dvt (source of clot)

clinical mgmt of PE

Oxygen
Positioning: upright/left
Iv fluids
thrombolytics/anticoagulants
Embolectomy (remove clot) if thrombolysis has failed or non-candidate for thrombolytics

prevention of PE

Maintain healthy bmi
Avoid prolonged immobility
Stop smoking
Prophylaxis

prophylaxis for pulm embolism in hospital

prophylaxis (lovenox, sequential compression devices, compression stockings, inferior vena cava filter to catch all the clots so that they don't get ejected from right ventricle into pulmonary vessels - this is done if pt forms clots very frequently)