E&P II final

orthopnea

dyspnea that is triggered when patient is reclining

platypnea

dyspnea triggered by assuming upright position

orthodeoxia

oxygen desaturation on assuming upright position

trepopnea

laying on one side relieves dyspnea

pedal enema

swelling of lower extremeties due to heart failure most often

pleuritic chest pain

located internally or posteriorly, sharp and increases with deep breathing

nonpleuritic chest pain

located in center of chest and may radiate to shoulder or arm

pectus carinatum

abnormal protrusion of sternum

pectus excavatum

depression of part or entire sternum, can cause restrictive lung effect

apneustic breathing

deep, gasping inspiration with brief, partial expiration

ataxic breathing

completely irregular breathing pattern with variable periods of apnea

biot respiration

clustering of rapid, shallow breaths couples with regular or irregular periods of apnea

cheyne stokes respirations

breaths increase and decrease in depth and rate with periods of apnea

kussmauls respirations

deep and fast respirations

paradoxical breathing

abdominal wall moves inward on inspiration and outward on expiration, typically due to chest trauma

crepitus

air leaks into subcutaneous tissues causing this, sign of subcutaneous emphysema

bronchovesicular breath sounds

heard around sternum, softer and lower in pitch

vesicular breath sounds

heard over lung parenchyma, very soft and low pitch

coarse crackles

airflow moves secretions or fluid into airways

fine crackles

sudden opening of small airways in lung deep breathing

acrocyanosis

occurs in newborns, usually disappears within 24-72hrs after birth

FEV1

force exhalation volume, healthy adults should be able to exhale 80% of their inahle volume in the first second of a breath

FVC

forced vital capacity, amount one can forcibly exhale after taking in a deep breath

COPD mechanism

inflammation and obstruction of small airways, loss of elasticity (elastic destruction in alveolar walls), active bronchospasm, alveoli collapse on themselves causing air trapping

COPD symptoms

productive cough, wheezing or diminished breath sounds, SOB particularly on exertion, progressive dyspnea, barrel chest, accessory muscle use, edema (cor pulmonale)

acute COPD management

reestablish the patient to baseline status as quickly as possible, inhaled bronchodilators, oral antibiotics if purulent, short systemic corticosteroid course, O2, NIV if hypercapnic

emphysema

characterized by abnormal, permanent enlargement of the airspaces beyond the terminal bornchiole accompanied by destruction of the walls of the airspaces without fibrosis, loss of chest recoil, mucus plugs due to not being able to exit past collapse

chronic bronchitis

chronic cough is present for at least 3 months per year for at least 2 years, infection or inflammation of the large airways or bronchi, caused by virus, treated with antitussives

centriacinar vs panacinar (emphysema)

centriacinar occurs usually in upper lobes, with septal destruction in bronchioles and alveolar ducts, panacinar involves the entire acinus, damage is more randomly distributed (alpha 1)

late asthmatic response

4-8hrs after early response, recruitment of lymphocytes, eosinophils, basophils and neutrophil, airway scarring, increased bronchial hyperresponsiveness, mucous accumulation, airway remodeling

pulsus paradoxus

exaggerated drop in systolic blood pressure during inspiration, can indicate athma/acute COPD

status asthmaticus

bronchospasm not reversed by usual measures, life threatening (death signs: silent chest (no air movement) and a PaCO2 >70mmHg)

leukotriene inhibitors

mediate inflammation and bronchospasm, mild to moderate asthma control

anticholinergics

can be used as adjunct to first line brochohodilators if there is inadequete response, addictive effect

anti IgE therapy

omalizumab (xolair) blocks IgE biologic effects, allergic asthma with corticosteroids

asthma emergency management

early and frequent B2 agonists, high dose parenteral corticosteroids, magnesium sulfate, oxygen (heliox), antibiotics

bronchiectasis

abnormal, irreversible dilation of bronchi caused by chronic airway inflammation and destruction (common in CF), persistent abnormal bronchi dilation, hallmark: persistent purulent secretions

bronchiectasis treatment

sputum culture (antibiotics), bronchodilators, humidification and hyperosmolar substances, DPI mannitol, anti inflammatories, chest physiotherapy, O2, surgery

respirable mass

portion of inhaled mass that can reach lower airways

inertial impaction

>5 micrometers, occurs when aerosol in motion collides with and are deposited on surface, occur in first 10 airway generations

sedimentations

occurs when aerosol particles settle out of suspension and are deposited due to gravity (1-5micrometers)

brownian diffusion

very small particles, >3 micrometers, diffuse into alveolus, 1-.5 micrometers the particles may remain suspended until exhaled

priming

pMDI, shake for at least 5 seconds prior than releasing one or more sprays into the air if it is new or has not been used in awhile, required to provide adequate dose

blow by technique

used if patient cannot tolerate mask treatment, directs aerosol from nebulizer towards patients nose or mouth several inches away

mucous blanket

consists of a gel layer and a sol layer, produced by the goblet cells and bronchial glands, sol layer allow cilia movement, gel layer traps particles

sol layer

can be replenished by drinking water, blank aerosol therapy, coughing

cough stages

inrritation (stimulating nerve endings), inspiration, compression, expulsion (high velocities pick up particle laden mucus)

chest PT contraindications

distended abdomen, recent esophageal surgery, uncontrolled airway risk for aspiration, subcutaneous emphysema, would, bronchospasm, osteoporosis, chest wall pain, lung contusion

vibration

stimulates the cilia and the cough mechanism, should be done on every site where percussion occurred, done on exhalation usually 3x at one site

active cycle of breathing technique

relaxation and breathing control, 3-4 thoracic expansion exercises, relax, repeat 3-4, relax, perform one or two FETs (huffs), relax

autogenic drainage

patient uses diaphragmatic breathing to mobilize secretions by varying lung volumes and expiratory airflow in three phases, should be sitting, coughing suppressed until complete (CF) can be done in place of. PDPV/CPT

mechical insufflation-exsufflation

apply positive pressure of 30-50cm H2O to airway for 1-3 seconds then abruptly reverses airway pressure to -30 to -50cm H2O for 2-3 seconds, five cycles of this followed by normal breathing, mimics a cough (neuromuscular disease patients)

positive airway pressure therapy

mimics pursed lip breathing (pursed lip prevents airway collapse on exhalation, increases expiratory flow) increases expiratory flow in large airways and collateral flow in smaller airways

threshold PEP

mimics pursed lip breathing, numbers increase the pressure the device is putting back on the lungs, promotes bronchial hygiene, exhale into it

therapep

gives visual representation to keep blue dial between the arrows while exhaling, breathing treatment can be incorporated

aero pep

holding chamber, can do inhaler through it and PEP

aerobeca / acapella

increases expiratory flow and collateral flow, it creates oscillations which vibrate the airway walls and loosen mucus, shakes the airway

intra alveolar pressure

decreases on inspiration, increases on expiration

pulmonary surfactant

decreases surface tension which increases pulmonary compliance (reduces effort needed to expand lungs), reduces tendency for alveoli to collapse

adhesive atelectasis

from lack of surfactant, air exchanged is labored without surfactant resulting in collapse

gas absorption atelectasis

occurs when there is a complete interruption of ventilation to a section of lung or when there is significant shift in V/Q, also known as nitrogen washout

lobar atelectasis

can occur when ventilation is compromised in a larger airway or bronchus

compression atelectasis

when something presses against lungs to let out the air in the alveoli, this occurs. an obstruction in the area between the lungs and chest wall due to a mass, fluid or air

incentive spirometry

provides visual cues to patient when desired inspiratory volume of flow is reaches, provided to be effective in high risk patients, mimics sigh

IS indications

presence of pulmonary atelectasis, presence of conditions predisposing to atelectasis (abdominal/thoracic surgery, COPD pt surgery), presence of restrictive lung defect associated w/ quadriplegic or dysfunctional disphragm (10 breaths per hour)

intermittent positive pressure breathing

uses positive airway pressure to expand lung during inhalation, lasts 15=20min, useful in treatment of pulmonary complications or exacerbations of lung disease

IPPB indications

preventing or expanding atelectasis, atelectasis not responsive to other modalities such as IS, patient high risk for atelectasis and cannot perform IS

EzPAP

when IS alone wont open airways, connect device to flowmeter and adjust to 5-15lpm, patient exhales into it and breathes against a pressure on exhale

PAP effects

recruitment of collapsed alveoli via FRC increase, decreased WOB secondary to increased compliance elimination, improved ventilation distribution, secretion removal increase

PAP indications

atelectasis treatment/cardiogenic pulmonary edema (fluid in lungs secondary to R sided HF), contraindications → hemodynamic instability, hypoventilation

CPAP

continuous positive airway pressure, spontaneous ventilation with a positive airway pressure being maintained throughout the whole respiratory cycle

PEEP

positive end expiratory pressure, maintained airway pressure above atmospheric at the end of expiration and may be used with mechanical ventilation or spontaneous breathing

hilar region

great vessels and mediastinum

lateral neck x ray

helpful in differentiating between croup and cute epiglottitis

pleura

thin membrane surrounding the lung parenchyma, two thin membranes - outer parietal and inner visceral

pleural effusion

hydrothorax, accumulation of excess fluid within pleural space, best.x ray for detecting is lateral, blunted costophrenic angles

pneumothorax

collection of air in pleural space, may occur spontaneously (bled rupture), with trauma or invasive procedure or mechanical ventilation (barotrauma), causes lung margins to pull from chest wall

tension pneumothorax

occurs when air in the pleural space in under pressure, air accumulates in pleural space on inhalation but cannot exit on exhale, requires immediate decompression, pushes organs to the other side

pulmonary edema

alveoli are filled with a watery fluid that contains few cells, parenchymal disease, pink, frothy secretions, BIPAP indicated

bacterial pneumonia

alveoli are filled with an exudative fluid containing numerous white blood cells (pus), parenchymal disease

pulmonary hemorrhage

alveoli fill with blood, parenchymal disease, ICU patients mechanically ventilated → given heparin on high FiO2 breaking down alveolar capillary membrane → drank blood exits membranes into lungs

airspace opacity or infiltrates

indentical - appear patchy, increased density shadows that tend to coalesce over time on chest radiograph, infiltrates → fluid filling of alveolus (pneumonia, pus)

air bronchograms

lucent tubular structures that course through dense airspace opacities or infiltrates on both chest radiographs and chest CT images, air filled airways surrounded by infiltrates will cause these, hallmark of infiltrates that fill alveoli (air space disease)

pulmonary edema

due to left heart failure usually, kerly B lines (thin lines seen near pleural edge on chest film as a result of increased pulmonary capillary pressures) bat wing appearance (predominance of edema in hilar regions of lungs)

radiograph signs of cardiac decomp

(pulmonary edema) cardiac enlargement, pleural effusions - bilateral, resdistribution of blood flow to upper lobes, poor definition of the central blood vessels, kerley B lines, alveolar filling

interstitial lung disease

(idiopathic pulmonary fibrosis, sarcoidosis) radiograph shows diffuse, bitaletal infiltrates, opacities may resemble scattered, poorly defined nodules

plate atelectasis

when atelectasis is localized to subsegmental portion of lung, makes a plate shape where good lung function remains in center

volume loss (x-ray)

unilateral diaphragmatic elevation, mediastinal shift towards atelectasis, narrowing of the pace between ribs, hilar displacement towards atelectasis

hyperinflation (x-ray)

commonly seen with emphysema, more than sever anterior ribs are seen above the diaphragm, flattening of hemidiaphragms, large retrosternal airspace, narrowed mediastinum, increased AP diameter

solitary pulmonary nodules

seen via CT, smooth edge, malignant, star jagged edge, parenchymal opacity smaller than 3cm in diameter surrounded by aerated lung

pneumomediastinum

barotrauma, may result from movement of air into mediastinum, esophageal rupture - occurs in distal esophagus, chest trauma- may cause trachea / mainstem bornchus rupture

hypertension treatment

ACE inhibitors, ARBs, aldosterone agents, calcium channel blockers, thiazide diuretics and other antihypertensives

aneurysm

local dilation or outpouching of a vessel wall or cardiac chamber, true (fusiform-bilateral, fusiform-saccular one side, dissecting-saccular medical emergency) vs false

dilated cardiomyopathy

impaired systolic function (LV) leading to increases in intracardiac volume, ventricular dilation and systolic heart failure, caused by ischemic heart disease, hyperthyroidism, niacin deficiency, treatment involve reducing blood volume and increasing contractility

hypertrophic obstructive cardiomyopathy

inherited thick septal wall causing angine, syncope, palpitations, MI symptoms, L sided HF symptoms, treat w/ beta blockers/ACE inhibitors, surgery, septal ablation, implantable cardioverter-defibs

hypertensive/vavular hypertrophic cardiomyopathy

hypertrophy of the myocytes, attempts to compensate increased myocardial workload causing angina, syncope, dypnea on exertions & palpitations

restrictive cardiomyopathy

myocardium becomes rigid and noncompliant, impeding ventricular filling and raising filling pressures (diastole) causing R sided HF, venous congestion

acute HF

symptoms result from any structural or functional impairment of ventricular filling or ejection of blood (ischemic, MI, valvular heart disease, HTN)

ejection fraction

50-70% or less is HF, how much blood the left ventricle pushes out on exertion

AHF may result from…

impaired ventricular filling (preserved EF), impairment of ejection of blood (reduced EF), triggers a catecholaminergic response aimed to improve heart function by increased HR and muscle contractility