Pathophysiology Exam: Cardiovascular & Respiratory Flashcards

Delivers oxygen & nutrients needed for metabolic processes to the tissues, carries waste products away from cellular metabolism to kidneys and other excretory organs for elimination, and circulates electrolytes & hormones needed to regulate body functions

Pulmonary Circulation (AKA central circulation)

Systemic circulation (AKA peripheral circulation)

Right side of heart, the pulmonary arteries, the pulmonary capillaries, and the pulmonary veins

(Moves blood thru the lungs and creates a link for gas exchange)

The left side of the heart, the aorta, and its branches, the capillaries that supply the brain and peripheral tissues, and the systemic venous system and vena cava.

(moves blood throughout all other tissues of the body)

Pressure, resistance, flow/velocity.

Outer cover of heart.

Visceral pericardium- faces the organ

parietal pericardium - faces away from organ.

The SA Node : functions as the pacemaker of the heart

The AV Node: connects the atrial and ventricular conductive systems

The ryhthmic pumping action of the heart. Divided into 2 parts: Systole & Diastole

Period when ventricles are contracting

Ventricles contract

blood pushes against AV valves & they shut

Blood pushes thru semilunar valves into aorta and pulmonary trunk

Cardiac emptying

Period when ventricles are relaxed and filling with blood

Ventricles relaxed

Blood enters atria

blood flows thru AV Valves into ventricles

Semilunar valves are closed.

Cardiac filling

EDV - ESV (End Diastolic volume - end systolic volume)

the amount of blood the heart pumps out in a single beat.

Stroke Volume X heart rate

Amount of blood pumped out of heart per minute

Cardiac Output X Peripheral resistance

Helps to understand blood pressure: if Peripheral resistance is high, then BP is high & vice versa

Stroke volume/ End diastolic volume

The percent of blood pumped out

Elevated levels of lipids or fats in the blood.

Cholesterol and triglycerides are insoluble in plasma and are encapsulated by special fat carrying proteins called lipoproteins for transport in blood

LDL is main carrier of cholesterol

Dietary lipids absorbed from intestines as chylomicrons, which adipose & muscle cells take up, but chylomicrons remnants are intermediate-density lipoproteins.

IDLs become LDL's and delivers fat to the liver and other tissues

Independent of other causes, no known cause

often genetic

Associated with other health conditions

• obesity
• Diabetes mellitus
• sedentary lifestyle, etc

Dietary, Therapeutic, medication ( decrease cholesterol production or absorption, remove cholesterol from blood stream)

Are blood vessels that carry oxygen and nutrients from your heart to the rest of your body, but when there is too much pressure the arteries become thick and harden, which can restrict flow

a type of arteriosclerosis, refers to build up of fats in and on artery walls (plaques) which can cause vessel stenosis and restrict blood flow.

It is considered a heart problem, but it can occur anywhere.

Lipids get into vascular endothelium (proportional to LDL Levels)

Macrophage tries to clear them away, then macrophage turns into a foam cell.

WBS & vascular endothelium release growth factors that promote plaque formation

Plaques block the arteries.

Fatty Streak

The fibrous atheromatous plaque

The complicated lesion

the earliest lesion, which is present in children, lesions result from collections of macrophage that phagocytize and accumulate fat within their cytoplasm (Foam Cells)

basic lesion of clinical atherosclerosis; characterized by accumulation of intracellular and extracellular lipids, proliferation of vascular smooth muscle cells, formation of scar tissue and calcification.

1. Stenosis of the vessel (Narrowing) and ischemia.

2. sudden vessel obstruction due to plaque hemorrhage or rupture

3. Thrombosis and formation of emboli resulting from damage to the vessel endothelium.

4. Aneurysm formation due to weakening of vessel wall.

The most important complication of atherosclerosis bc it causes acute blockage of arteries. It is caused by slow and turbulent blood flow in the region of the plaque and ulceration of the plaque.

* may cause acute vessel occlusion

• Ischemia
• infarction
• Gangrene

The Abdomen

Atherosclerosis changes that result in tissue ischemia (low blood)

Most common in men in 60s & 70s

Risk factors include: Smoking, diabetes

Gradual onset of intermittent claudication (pain in calf when walking)

Atrophic changes of the skin (pale bc skin is not getting oxygen)

Rest pain, only if severe, ulceration, and gangrene can develop (when blood flow no longer meets minimal needs)

avoidance of injury,walking program, reduce risk factors, antiplatelet agents, surgery,

Diagnose by: Inspection, check pulses(DP & PT), ankle brachial index

Functional disorder of arteries & arterioles of the skin - there are intense spasms of arteries & arterioles in the fingers and less often in the toes in response to stimuli. its aggravated by cold or emotional stress.

More common in feet and in middle-aged women

avoidance of triggering events, no smoking, use of vasodilator drugs.

An abnormal localized dilation of a blood vessel or wall of the heart., which may rupture or hemmorhage. Most common in abdominal aorta

can occur in arteries or veins

atherosclerotic plaque formation (most common)

congenital abnormality or arterial wall

Trauma

Infection

Aorta (most common)

• Abdominal aorta (bw renal arteries & iliac branches)
• Thoracic aorta (ascending, transverse, or descending)

Cerebral artery ( at circle of willis)

Femoral and popliteal arteries

Rupture - risk increases with increasing size

pressure on adjacent structures

* involving large vessels in critical locations

Saccular

• berry

Fusiform

Dissecting ( most common in ascending aorta)

can go undetected for long periods of time bc they are asymptomatic. A pulsating mass found on routine abdominal examination may be first evidence.

Develop in Men after 50

90% occur below renal artery

Diagnostic signs:

ultra sound, echocardiography, CT, MRI, surgical repair

an abrupt presence of excrutiating pain, described as tearing or ripping, high mortality rate.

the rythmic ejection of blood from the left ventricle into the aorta. It rises as left ventricle contracts and falls as it relaxes.

The highest pressure is systolic and the lowest is Diastolic

Systolic <120/ Diastolic <80

S 120-139

D 80-89

S 140-159

D 90-99

S >160

D>100

most common of all health problems in adults and leading risk factor for cardiovascular disorders and is usually asymptomatic. When symptons do occur its usually related to long-term afects on the organ systems.

90% of hyepertenssive patients

unknown cause

More frequent in Males, Black, Poor, Older, Obese

10% of hypertensive patients

Cause is known- most common cause is Renal Disease

Constitutional factors

• family history, race, sex

Lifestyle factors

• high sodium diet, excessive calories, excessive alcohol, physical inactivity, oral contraceptives, sleep apnea
• NOT stress (acute only), NOT High fat diets,
• Smoking unknown

Kidney- Renal Failure

Brain- Cerebral Vascular accident (stroke) CVA, TIA0 transient ischemic accident (a smaller stroke)

Heart - chest pain (angina), LVH (left ventricle hypertrophy), CAD, CHF

Eyes - retinopathy

blood vessels - peripheral vascular disease(PVD), arteriosclerosis

you treat patients to live longer, not feel better. Must take repeated BP measurements to be diagnosed with HT

AKA postural Hypotension, an abnormal drop in BP upon standing.

Symptoms: Dizziness & Syncope (fainting)

Causes: Reduce blood volume, Drug induced, aging, immobility

Diagnosis: sitting and standing BP measurements

Tilt Table

Treatment: alleviate the cause(ie if it is due to dehydradtion, then rehydrate), education, adjusting meds, support hose

Low-pressure system, pumped by skeletal muscles to return blood to hear

and has venous valves to prevent retrograde flow

2 components: Deep Veins ( these return blood to the heart) & Superficial Veins

Varicose Veins

Venous Insufficiency

Venous Thrombosis

Dilated, tortuous veins, engorged with blood resulting from improper venous valve function.

Most common in legs; edema of calves, leg heaviness, dull aching of lets

• Weakening in valve allows backflow of blood
• Increase pressure in the veins causing walls to stretch

2 types: Primary & Secondary

Complications include: Chronic Venous insufficiency & blood clots secondary to venous stasis

Treatment: Treat underlying cause, anti-embolism socks, exercise, surgical stripping

Originates in superficial veins

Result from impaired flow in the deep venous channels

The most common cause is DVT Deep Vein Thrombosis

a condition in which the incompetent venous valves result in an ineffective venous pump. THe pump causes tissue congestion and impaired nutrition resulting in atrophy of the skin and fat necrosis. Brown pigmentation occurs bc of hemosiderin deposits resulting from the break down of RBCs

Stasis dermatitis & ulcers

acute development of a blood clot that may cause vessel occlusion or embolization

• causes vessel irritation, which results in inflammation & contributes to occlusion or embolization
• may occur in deep(more serious) or superficial (more common)
• aka thrombophlebitis

Venous Stasis: bed rest, immobility, shock, airplane rides, long car rides, AMI (Acute Mycardial infarction)

Hypercoagulability of blood - pregnancy, child birth, BCPs, dehydration, cancer

Vascular Trauma - venous catheters, surgery, massive trauma, hip fracture, orthopedic surgery

Inflammation of the pericardium as a result of systemic or cardiac diseases

• Viral infections (most common)
• Bacterial infection, trauma, radiation, & autoimmune

Associated with fluid collection within the pericardial space ( pericardial effusion)

when the pericardial becomes inflammed the serous fluid becomes inflammed as well

Pericardial friction run & sharp substernal pain

shallow rapid respirations due to associated pleurisy

mild fever from inflammation

dyspnea, orthopnea, tachycardia

accumulation of fluid in pericardial cavity;

may occur as a result of inflammatory processes, infection, neoplasms, cardiac surgery, trauma. Major threat is compression of the heart chambers with resultant reduction in ventricular filling and cardiac output.

Testing: CXR shows a widened mediastinum & echnocardiogram shows pericardial fluid

Treatment: Pericardiocentesis; Pericardial window; Pericardiectomy

Rapid compression of the heart due to accumulation of fluid, pus, or blood in pericardiarl space. Could be due to infection, inflammation, trauma, or rupture of ventricular wall.

THe compression of the heart results in a decrease in ventricular filling, which ultimately results in a decrease stroke volume & a diminished or absent pulse

a rapid, accurate and widely used method of evaluating pericardial effusion.

Impaired Coronary blood flow

• Narrowing of coronary arteries due to atherosclerosis resulting in:
  • Heart disease secondary to mycocardial ishcemia
  • strength of myocardial contractions is reduced
  • wall motion is abnormal resulting in lower cardiac output
  • conduction deficits
• Imbalance in blood supply & the hearts demands for oxygen
  • Less blood
    • Atherosclerosis
    • Vasospasm
    • Thrombosis
  • Higher Oxygen Demand
    • stress, exercise, cold

acute ischemic heart diseases

Unstable Angina

Acute Myocardial Infarction (aka, heart attack)

Intermediate of stable angina and myocardial infarction. Often ischemia is not severe enough to cause permanent myocardial damage

Worst than stable angine, but not quite MI

Due to atherosclerotic plque disruption --> platelet aggregation --> Hemostasis

Occurs when a portion of the myocardium loses its blood supply and the tissue infarcts(dies)

The onset is usually abrupt pain at significant symptom, GI complaints common

The extend depends on location & extent of occlusion, amount of heart tissue supplied by the vessel, duration of the occlusion, metabolic needs of the affected tissue, extent of collateral circulation, & other factors like heart rate.

Ischemic death of myocardial tissue

sudden onset --> pain

reduced blood flow thru one or more coronary arteries causing myocardial ischemia & necrosis

heart failure

• AMI is most common cause of left HF

Cardiogenic Shock

Pericarditis

thromboembolism

rupture of heart

ventricular aneurysms

cardiac arrthythmias

• most common cause of sudden death with AMI

occurs when the ability of the coronary arteries to supply oxygen is inadequate to meet the metabolic demands of the heart.

3 types of chronic ischemic heart disease

Pain when hearts oxygen demand increases

Fixed coronary artery obstruction that produces a disparity b/w coronary blood flow and the metabolic demands of the myocardium.

Pain is described as constricting, squeezing, suffocation.

pain relieved by anti-platelet aspirin or nitroglycerin

Pain when coronary arteries spasm

Prinzmetals angina (vasopastic angina)

Intermittent coronary vasospasms (at rest)

myocardial ischemia without pain

unknown eitology but found in diabetic patients

a group of disorders that affect the myocardium & are usually associated with disorders of myocardial performance which may be mechanical(heart failure) or electrical (arrhythmias)

They can be primary or secondary

disorders of the heart muscle that are confined to the myocardium.

conditions in which there is a cardiac muscle disease in the presence of a multisystem disorder

Genetic

Mixed

Acquired

Hypertrophic cardiomyopathy, most common, genetic, ppl dont' know they have it

• autosomal dominant disorder
• Hypertrophied ventricle becomes stiff and noncompliant and unable to relax causing a reduction in ventricular filling
• 1 out of 500 in general population
• common cause of sudden cardiac death in athletes
• signs & symptoms vary

Dilated Cardiomyopathy: extensively damaged myocardium reduces contractility causing a decline in systolic function and cardiac output (heart failure). There is left ventricular dysfuncion characterized by thinning of the ventricular wall. (still hypertrophied, but it's stretched out)

Restrictive Cardiomyopathy: Fibrosis and stiffening of the ventricle reducing the ability to relax and fill during diastole resulting in a decrease in cardiac output. Least common

Termed myocarditis or inflammatory cardiomyopathy. Its inflammation of the heart muscle and conducting systemw/o evidence of myocardial infarction

Focal or diffuse inflammation of the cardiac muscle which may be acute or chronic

• Inflammatory cardiomyopathy
• inflammation may lead to hypertrophy, fibrosis or inflammatory changes of the conduction system
• usually resolves spontaneously
• heart muscle weakens and contractility is reduced(during acute)

Infection(bacterial, viral); radiation therapy, hypersensitivity immune reaction, toxins such as lead, chemicals, & cocaine, chronic alcoholism

most common cause is viral

Treatment- most cases are transient and resolve within several months

Arrhythmias & sudden death

Chronic valvulititis

dilated cardiomyopathy

heart failure

pericarditis

cardiac rupture

thromboembolism

infection of the endocardium, heart valves or cardiac prosthesis.

relatively uncommon, life-threatening

• causing deformities & destruction of valvular tissue & chordae tendineae causing rupture & valvular insufficiency
• collection of microorganisms, fibrin & platelets from vegetations that can cover the valve surface
• vegetations may break off and form septic emboli
• aka bacterial endocarditis

Bacterial (most common) or fungal invasion

predisposing factors

• Portal of Entry
  • IV Drug abuse
• Damaged endocardial surface
  • Presence of prosthetic heart valve
  • Rheumatic heart disease

S/Sx: fever, chills due to bacterial infection

heart murmur due to turbulent blood flow (over valves that have been damaged by endocarditis)

diagnosis:

positive blood cultures (most definitive & essential guide to treatment) blood cultures can identify causitive agent & sensitivity testing to make antibiotics

elevated WBC Count

acute renal failure

brain abscess (from septic emboli)

cardiac arrhythmia

cerebral emboli

heart failure

meningitis

death

an acute immune mediated, systemic, inflammatory disease of childhood that develops after infections with group A streptococcus.

• inflammation of heart, joints, CNS, skin, subcutaneous tissues

The cardiac and valvular manifestations of rheumatic fever & is associated w acute inflammation of the myocardium, pericardium, and heart valves

• includes pericarditis, myocarditis, and endocarditis during early phase
• chronic valve disease in the later phase

Patients who develop acute rheumatic heart disease are not actively infected w Group A Streptococci but rather develop S/Sx weeks after infection has cleared

GAS infection leads to autoimmune reaction in which antibodies produced to combat GAS affect connective tissues of the body

Antibodies may attack healthy body cells by mistake bc the bacterial antigens are similar to the bodys own cells

molecular mimicry

polyarthritis caused by inflammation

firm movable subcutaneous nodules

Erythema marginatum skin rash found on trunk

Carditis with dyspnea and chest pain

sydenhams chorea is a CNS manisfestation

destruction of mitral and aortic valves

pancarditis (Inflammation of heart)

heart failure

infection

prompt treatment of GAS with antibiotics

salicylates(aspirin) to relieve fever & pain

corticosteroids for carditis

corrective surgery

Narrowing of heart valve opening

• blood accumulates in chamber preceding stenosed valve
• results in increased chamber pressure due to resistance to flow thru the valve
• may cause hypertrophy of cardiac wall on chamber preceding the stenosed heart valve

often results in decreased cardiac output and left ventricular hypertrophy. there is a heart murmur as blood is forced thru the narrow opening

occurs when heart valve leaflets don't completely close

• incompetent heart valves allow blood to flow both directions
• volume of pumped blood increases
• involved chambers dilate to accommodate increased volume

blood going thru a valve

syndrome that occurs when the heart cannot pump enough blood to meet the bodys needs (pump failure)

• results in intravascular and interstitial volume overload and poor tissue perfusion
• classified as Left sided or Right sided

Pumping ability of left ventricle fails

cardiac output falls

blood backs up into left atrium

Pumping ability of right ventricle fails

blood backs up into right atrium and peripheral circuation

peripheral edema develops

Hypertension

myocardial infarction

most dramatic symptom of left heart failure.

A life-threatening condition in which capillary fluid moves into the interstitial and causes lung stffness, makes lung expansion more difficult & decreases gas exchange in lungs

an acute failure of the circulatory system to supply the peripheral tissues and organs of the body with an adequate blood supply resulting in cellular hypoxia

Diminished cardiac output that severely impairs tissue perfusion (pump failure)

• the left ventricle initiates a series of compensatory mechanisms that attempt to increase cardiac output
• the actions initially stabilize and later deteriorates as oxygen demands increase on an already compromised heart

acute myocardial infarction (most common)

end stage cardiomyopathy

cardiac tamponade

myocardial ischemia

Ventricular arrhythmias

Circulatory dysfunction and inadequate tissue perfusion caused by reduced intravascular blood volume.

venous return is reduced and cardiac output fails

• acute loss of 15%-20% of blood volume

blood loss; burns; GI fluid loss

pathophysiologic changes:

tachycardia restlessness; reduced urine output; hypotension; cyanosis

treatment:

oxygen, fluids, blood replacement

Mechanical obstruction of blood flow

• great veins
• heart
• lungs

causes:

aortic aneurysm; pneumothorax; pulmonary embolism (most common)

inqadequate tissue perfusion and circulatory collapse in response to infection

caused by loss of blood vessel tone and enlargement of vascular compartment

capacity of vascular compartment expands such that normal blood volume will not fill the circulatory system

decreased sympathetic activity: neurogenic

• brain or spine injury, anesthetics,, insulin shock, emotion

vasodilator substances in blood

• type 1 hypersensitivity (anaphylactic shock)
• inflammatory response to infection (sepsis)
  • gram negative sepsis (70%)

chills & fever due to infection

tachycardia

reduced urine output

cyanosis

death, heart failure, renal failure

test with blood cultures

treatment: antibiotics therapy, medications to increase cardiac output oxygen

Oxygenation of blood

Removal of CO2 Carbon Dioxide

Protection (ciliary blanket, macrophage0

Metabolism

Conducting Airways - consists of nasal passage, mouth, & pharynx, larynx, trachea, bronchi, bronchioles

Respiratory tissue - area distal to the terminal bronchi and consists of respiratory bronchioles, alveolar ducts and alveoli

Outer layer- supporting connective tissue layer- provides support and protection

Middle Layer - Smooth muscle layer that circle the airway

Inner Layer - Mucosal Lining, pseudostratified columnar epithelium with hair like projections called cilia intermingled are goblet cells that secrete mucus. mucus forms ciliary blanket

95% of surface, primary function is gas exchange

secrete surfactant

1. lowers surface tension within the alveoli therby keeping the alveoli open

2. Increases lung compliance or the ease of inflation

3. Provides stability and more even inflation of the alveoli

4. assists in preventing pulmonary edema by keeping alveoli dry

encases the lungs; the pleura is thin, transparent, double layered serous membrane,

Functions to reduce friction during breathing

Ventilation, perfusion, diffusion

The movement of air bw the atmosphere and the alveoli of the lungs

Process of blood flowing thru lungs

The actual movement of gas b/w alveoli & blood

Oxygen: can be carried as a dissolved gas in plasma

or in combination with hemoglobin (98%)

CO2 - carried in blood but is converted to bicarbonate and transported in that form

when oxygen and CO2 are dissolved in plasma.

Normal partial pressure for Oxygen is 80-100 mmhg

Normal partial pressure for CO2 is 35-45 mmhg

has become preferred method to measure PO2 in arterial blood gas.

It measures total percent of O2 that is saturated with oxygen (SpO2)and the PO2 is determined using the Oxygen-Hemoglobin Dissociation Curve. This is an INDIRECT measure of PO2 and PO2 must be calculated.

As dissolved CO2 (10%)

Attached to Hemoglobin (30%)

As Bicarbonate, HCO3 (60%)

PO2 <60 mmHg

Cyanosis

Impaired function of vital centers

• agitated or combative behaviour, euphoria, convulsions, delirium
• retinal hemorrhage
• hypotension & bradycardia

Activation of Compensatory mechanisms

• sympathetic system activation

PCO2 > 50 mmHg

Respiratory Acidosis

• increased respiration
• decreased nerve firing
  • CO2 narcosis
  • Disorientation
• Decreased muscle contraction
  • vasodilation
  • headache, conjunctival hyperemia, warm flushed skin

Medulla (the rate) & Pons (how deep your breath is)

monitor oxygen & cabon dioxide & pH

Central Chemoreceptors - hypercapnic drive- located in brain stem

• monitors PCO2 levels
• the primary stimulus for respiration

Peripheral Chemoreceptors - hypoxemic drive

• located in carotid arteries and aorta
• monitors PO2 levels (oxygen)
• a back up system for respiration

monitors breathing patterns and lung function

Lung receptors:

Stretch Receptors: located in smooth muscle of conducting airways & responds to changes in airway pressure

Irritant receptors: Located bw the airway epithelial cells, stimulated by irritants, like smoking

Juxtacapillary: J Receptors: located in alveolar wall & sense lung congestion

caused by a virus & has 3 distinct types: A B or C

36,000 deaths annually in US

A&B can cause epedemics bc they can mutate C cannot

Antigenic Drift- minor mutation (epedemic)

Antigenic Shift - Major Mutation (pandemic)

an acute inflammation of the parenchyma of the lungs (alveoli & bronchioles). Leading cause of morbidity & mortality world wide.

The interstitial tissues & alveolar spaces become infiltrated & filled with exudative fluid, leukocytes, and local macrophages

1. Virulence of organism

2. size of innoculum

3. effectiveness of host defense

Type of Agent

• Typical Vs Atypical

Anatomic Pattern (distribution)

• Lobar vs bronchopneumonia

Setting

• community acquired vs hospital

Bacteria in the alveoli

• mulitply extracellulary
• cause inflammation
• fluid in alveoli (decreases diffusion & affects respiration)

Viral, mycoplasma and chlamydia

infections of alveolar septum or interstitium

Affects entire Lung

Affections patchy distributions over more than one lobe

Streptococcus or Pneumococcal

gram positive

virulence factors- capsule prevents or delays digestions by phagocytes

Spleen is helpful in clearing bacteria from blood

Immunization for preventioin

Bacteria, Acquired from the environment

gram negative rod

warm stagnant waters

incubation period is 2-10 days, abrupt onset of malaise, weakness, diarrhea, high fever & cough

Treatment- quick antibiotics

Worlds foremost cause of deat from a single infectious agent.

Caused by myobacterium which are acid fast with a waxy cell wall.

Lesions that contain macrophage, T Cells and INACTIVE TB.

Definitive Diagnosis:

Bacterial culture (can take up to 12 weeks)

M. TUberculsosis DNA amplification technique

Sputum identification (nonspecific)

skin test (PPD) - cannot distinguish bw active & latent

4 drugs:

isoniazid, rifamycin, pyrazinamide, ethambutol

Adenocarcinoma

Squamous cell carcinonma

Small Cell Carcinoma

Large cell carcinoma

Small cell carcinoma & non-small cell carcinoma

Metastasizes early

infiltrate widely

rarely resectable

death within 3 months w/o treatment

cant do surgery usually, only chemo

Adenocarcinoma- most common (in women & non smokers)

Squamous cell- most common in men, smokers

Parainfluenza virus,

in children under 5,

a "cold gone bad"

upper airway infection, primarily with vocal chords

barking cough, worsens at night

Upper airway infection;

etiologic agent: historically- haemophilus influenza

now: streptococcus or staphylococcus

Very sudden onset that can be life threatening bc airways become occluded

Cherry-red epiglottis, drooling, chin thrust forward, sick looking

Lower airway infection, occurs in children less than 2 yrs old

etological agent: Respiratory Syncytial Virus (RSV)

Preceede by stuffy nose, cold symptoms

may progress to respiratory failure but usually slower onset

Inflammation of the pleura

Parietal Pleura - abrupt onset, unilateral

Causes: neoplasm, Inflammation (pneumonia)

Must differentiate: Musculoskeletal Pain and Heart pain (angina)

fluid accumulation in pleural space

Serous, water like fluid

Pus cells & infectious fluids

milky fluid

bloody fluid

Air in pleural space

partial or complete collapse of the affected lung

Types: spontaneous, traumatic (open or tension)

Penetrating chest injury or surgery, air flows into pleural space

Intrapleural pressure exceeds atmospheric pressure.

air enters pleural space but cannot exit

Bleb ruptures (or a blister0

Bronchial Asthma (acute)

Chronic Obstructive airway disease

• Chronic Bronchitis
• Emphysema
• Bronchiectasis

Episodic acute airway narrowing

• cough, bronchospasm
• Dyspnea (shortness of breath)
• Anxiety
• Tachypnea (rapid breathing)
• Tachycardia (rapid heart rate)

Basically- inflammatory airway disease, causes spasm, excessive mucous production & edema causes obstruction

type 1 hyersensitivities (childhood, allergies)

Mast cells inflammatory mediators cause acute response within 10-20 minutes

Airway inflammation causes late phase response in 4-8 hrs.

Caused by External factors- pollen,

Respiratory infections (epitheleal damage, IgE production)

Caused by internal factors- exercise, cold air

inflammation and fibrosis of bronchial wall

hypertrophied mucus glands, excess mucus (obstructs airway flow)

loss of alveolar tissue (decreased surface area for gas exchange)

Loss of elastic lung fibers (airway collapse, obstructed exhalation)

4th leading cuase of death in US

Enlargement of air spaces and destruction of lung tissue

defined anatomically:

abnormal permanent enlargement of airspaces distal to the terminal bronchioles, accompanied by destruction of the walls of the alveoli w/o fibrosis

Increased mucus production and obstruction of small airways

clinical terms:

condition in which chronic productive cough is present for 3 months per year for at least 2 consectutive years and the absence of other causes of chronic cough

uncommon, secondary condidtion

infection and inflammation destroy smooth muscle airways, causing permanent dilation of airways