Exam #1 ( Ch. 9, 11, 26, 27, 29, & 31 ) Flashcards
incision
cutting or sharp instrument; wound edges in close approximation & aligned
contusion
blunt instrument, overlying skin remains intact, with injury to underlying soft tissue; possible resultant bruising and/or hematoma
abrasion
friction; rubbing or scraping epidermal layers of skin; top layer of skin abraded
laceration
tearing of skin & tissue with blunt or irregular instrument; tissue not aligned, often with loose flaps of skin & tissue
puncture
blunt or sharp instrument puncturing the skin; intentional ( such as venipuncture ) or accidental
penetrating
foreign object entering the skin or mucous membrane & lodging in underlying tissue; fragments scattering throughout tissues
avulsion
tearing a structure from normal anatomic position; possible damage to blood vessels, nerves, & other structures
chemical
toxic agents such as drugs, alcohols, metals & substances released from cellular necrosis
thermal
high or low temperatures; cellular necrosis as a possible result
irradiation
ultraviolet light or radiation exposure
tissue repair
a response to tissue injury & represents an attempt to maintain normal body structure & region
tissue regeneration
replacement of injured tissue with cells of the same type
fibrous tissue repair
repair by replacement with connective tissue & scar formation
granulation tissue
- glistening red, moist connective tissue that contains newly formed capillaries, proliferating fibroblasts, & residual inflammatory cells
- scar formation builds on the granulation tissue framework of new vessels & loose ECM
1st stage of wound healing
inflammatory phase: begins at the time of injury; blood clot forms, migration of phagocytic WBCs into the wound site
2nd stage of wound healing
proliferative phase: new tissue fills the wound
➡️ fibroblasts: a connective tissue that synthesizes & secretes collagen, proteoglycans, & glycoproteins needed for wound healing
3rd stage of wound healing
wound contraction & remodeling phase: about 3 weeks after injury; fibrous scar develops; remodeling of scar tissue
causes of impaired wound healing:
- malnutrition
- impaired blood flow & oxygen delivery
- impaired inflammation & immune responses
- infection
- wound separation
- foreign bodies
- age effects
serous
watery fluid low in protein
hemorrhagic
leakage of RBCs from the capillaries
fibrinous
large amounts of fibrinogen, forms a thick & sticky meshwork
membranous
develops on mucous membranes surfaces & are composed of necrotic cells enmeshed in fibro-purulent exudate
abscess
localized area of inflammation containing purulent exudate
ulceration
epithelial surface becomes necrotic
bone marrow
b cells are produced & develop then migrate to lymph nodes
thymus
located in the mediastinum, secretes hormones enabling lymphocytes to develop into mature T cells
lymph nodes
distributed along lymphatic vessels to filter fluids, which drains from the body & returns to the blood as plasma
➡️ removes bacteria & toxins from the circulatory system
➡️ spleen is the largest lymphoid organs ( macrophages clear cellular debris & produce hemoglobin )
➡️ tonsils consist of lymphoid tissue & produces lymphocytes
immune response
the collective, coordinated responses of the cells & molecules of the immune system
types of immune defenses
innate or nonspecific immunity: the natural resistance with which a person is born with
adaptive or specific immunity: the second line of defense, responding less rapidly than innate immunity but more effectively
active immunity
specific protection induced following exposure to antigens
passive immunity
specific production induced through transfer of protective antibodies against an antigen; transferred from another source
lymphocytes
cells that specifically recognize & respond to foreign antigens
accessory cells
macrophages & dendritic cells ( function as antigen-presenting cells by the processing of a complex antigen into epitopes required for the activation of lymphocytes )
myeloid phagocytic cells ( innate immunity )
macrophages/monocytes, granulocytes, & dendritic cells
lymphoid & natural killer cells
b lymphocyte cells: produce antibodies
t lymphocyte cells: cell-mediated immunity
➡️ helper t cells: helps b lymphocytes produces antibodies
➡️ cytotoxic t cells: kill or lyse intracellular microbes
functions of innate immunity ( natural immunity )
- first line of defense
- able to distinguish self from non-self
- does not distinguish between different microbes
- response is rapid
- prevents establishment of infection & deeper tissue penetration
- major components includes:
➡️ skin & mucous membrane
➡️ phagocytic leukocytes ( neutrophils & macrophages )
➡️ plasma proteins
➡️ natural killer cells
Complement System of Immunity
- found in the blood
- essential for the activity of antibodies
- mediator of the inflammatory response
- inflammation is caused by increasing:
➡️ vascular permeability
➡️ chemotaxis
➡️ phagocytosis
➡️ foreign cell lysis - activated components destroy pathogens directly
➡️ increases bacterial aggregation, which increases suspectibility to phagocytosis
-
complement cascade
activation after antigen-antibody reaction
Adaptive immunity
- attacks specific microbes ( antigens )
- develops after exposure to specific antigen
humoral immunity
antibodies produced from B lymphocyte cells * antibodies are secreted into the circulation & mucosal fluid & neutralize or eliminate microbes *
cell-mediated immunity
t cells ( protect against viruses )
cytokines
soluble proteins secreted by cells of both the innate & adaptive immunity
chemokines
cytokines that stimulate the migration & activation of immune & inflammatory cells
colony-stimulating factors
stimulate the growth & differentiation of bone marrow progenitors of immune cells
Two types of immune cells
regulatory cells: assist in orchestrating & controlling the immune response
effector cells: accomplish the final stages of the immune response with the elimination of the antigen
➡️ activated t lymphocytes, mononuclear phagocytes, & other leukocytes function as effector cells in different immune responses
antigens
substances foreign to the host that can stimulate an immune response
antibodies
recognize antigens ( receptors on immune cells; secreted proteins )
types of antigens
bacteria, fungi, viruses, protozoa, parasites, antimicrobial agents
Antigen Presentation
- macrophages & dendritic cells process & present antigen peptides to CD4+ helper t cells
- capture antigens & then enable their recognition by t cells
- initation of adaptive immunity
what immunity are b cells?
humoral immunity, memory
what immunity are t cells?
cell-mediated immunity, memory
functions of t lymphocytes
- activation of t cells & b cells
- control of intracellular viral infections
- rejection of foreign tissue grafts
- delayed hypersensitivity reactions
IgG
displays antiviral, antitoxin, & antibacterial properties, responsible for protection of newborn; activates complement, & binds to macrophages
IgA
predominant Ig in body secretions; protects mucous membranes
IgM
forms natural antibodies; prominent in early immune responses, activates complement
IgD
found on b lymphocytes, needed for maturation of B cells
IgE
binds to mast cells & basophils; involved in parasitic infections, allergic & hypersensitivity
Elderly Immune System
- declining ability to adapt to environmental stresses
➡️ decline in immune responsiveness
➡️ decrease in size of the thymus glands
➡️ biological block in t cells
➡️ altered responses of the immune cells to antigen stimulation
People who have chronic high blood pressure have disruptions in homeostasis related the activation of?
renin-angiotensin-aldosterone system
Steps in renin-angiotensin-aldosterone system
- renin is released to the bloodstream by the kidneys
- angiotensin to angiotensin I
- angiotensin I to angiotensin II
- vasconstriction occurs in the lungs due to angiotensin II
- arteriolar constriction
- angiotensin II causes arteriolar constriction in adrenal glands
- aldosterone is secreted by adrenal glands
- aldosterone causes sodium & water retention
- retained sodium & water leads to increased volume
- arteriolar constriction increases peripheral vascular resistance
Steps in arterial blood flow development in hypertension
- non-modifiable & modifiable risk factors
- alternating dilation & constriction
- intra-arterial pressure is increased
- angiotensin constricts endothelial wall
- plasma leaks from endothelium
- macrophages migrate to the damaged area
- necrosis due to plasma deposits
- plaque formation
- atherosclerosis
- increased peripheral resistance
What are specific umbrella terms to describe CV disease?
- heart & blood vessel disease
- heart attack ( MI )
- stroke ( CVA )
- R & L heart failure
- arrhythmia ( disrhythmia )
- heart valve disorders
Stage 1 Hypertension
systolic rate: 130-139
diastolic rate: 80-89
Stage 2 Hypertension
systolic rate: 140 or higher
diastolic rate: 90 or higher
Hypertensive Crisis
systolic rate: higher than 180
diastolic rate: higher than 120
What causes hypertension?
- increased cardiac output ( ⬆️ SV & ⬆️ HR )
- increased peripheral resistance
Non-modifiable risk factors
age, sex, race/ethnicity, family history, genetics
Modifiable risk factors
diet ( dyslipidemia & obesity ), physical activity, tobacco, metabolic considerations, obstructive sleep apnea
What is primary hypertension?
a possible genetic deficit; no causative clinical condition
What is secondary hypertension?
related to another clinical condition
- illicit drugs: stimulants
- sympathomimetic amines: drugs that speed up HR; also causes HTN
- kidney disease
- adrenal disease
- oral contraceptive agents
What are hypertension consequences in certain target organ diseases?
- increased perfusion pressure
- vascular endothelial damage
- cardiac hypertrophy
- ischemic heart disease
- CV accident ( stroke )
- end-stage renal disease
- dementia
- cognitive impairment
- visual impairment
What two neural mechanisms monitor & regulate blood pressure?
baroreceptors & chemoreceptors
Baroreceptors
- monitors BP through changes in pressure
- signals sent to medulla oblongata or vagus nerve
- sympathetic & parasympathetic nervous system
Chemoreceptors
- monitors chemicals
- changes in low oxygen, high carbon dioxide, acidosis
- sympathetic stimulation of arterioles & veins
- located in carotid sinus & aortic arch
What is an antidiuretic hormone that involves a short term effect with being a vasoconstrictor?
vasopressin
What is a specific vasoconstrictor that causes increased amount of activity in the heart?
- epinephrine/norepinephrine
➡️ increased SNS activity
➡️ increased vasoconstriction
➡️ increased HR
➡️ increased cardiac contractility
Diseases of the arterial system
dyslipidemia & atherosclerosis
Dyslipidemia
imbalance of lipids
➡️ imbalanced amount of triglycerides: >150
➡️ imbalanced amount of lipoproteins: >130
➡️ imbalanced amount of HDL: <45
➡️ imbalanced amount of cholesterol: >200
Primary dyslipidemia
- familial hypercholesterolemia
➡️ deficient LDL receptor
➡️ high cholesterol
➡️ xanthomas: yellow deposits of cholesterol in tendons & soft tissues
➡️ atherosclerosis in childhood
Secondary dyslipidemia
➡️ poor diet ( high fat, low fiber )
➡️ obesity ( high trig, high LDL, low HDL )
➡️ metabolic disease
What are thin, yellow intimal discolorations that progressively enlarge over time & stick to the lumen vessels?
fatty streaks
What is the accumulation of intracellular & extracellular lipids, proliferation of vascular smooth muscle cells, & formation of scar tissue?
fibrous atheromatous plaque
What is hemorrhaging, ulceration, & scar tissue that develops?
complicated lesions
Atherosclerosis
build up of fats, cholesterol, & other substances in & out of the artery walls
Major Risk Factors for Atherosclerosis
- hypercholesterolemia
- HDL cholesterol < 40mg/dL
- cigarette smoking
- hypertension
- family history of premature CVD in a first degree relative
- age: men over 45 years & women over 55 years
- CRP levels
- homocysteine levels
Major Complications for Atherosclerosis
- ischemic heart disease
- stroke
- peripheral vascular disease
- signs & symptoms:
➡️ narrowing of the vessel & resulting ischemia
➡️ vessel obstruction due to plaque hemorrhage or rupture
➡️ aneurysm formation
Which vessels have the important complications of thrombus formation & weakening of the vessel wall?
large vessels
In which arteries are ischemia & infraction due to vessel occlusion is more common in?
medium-sized arteries
Ischemia plays a role in?
atherosclerosis & microvascular dysfunction
Coronary Heart Disease
occurs when the coronary arteries that supply blood to the heart get blocked by layers of fatty streaks building up
Two classifications for CAD
chronic ischemic heart disease & acute coronary syndrome
Basis techniques for diagnosis
- pain severity & presenting symptoms
- hemodynamic stability
- ECG ( EKG ) findings
- serum cardiac markers
angina
chest pain, discomfort, or tightness that occurs when an area of the heart muscle is not receiving enough blood oxygen
Stable angina
- fixed coronary obstruction
- disparity between coronary blood flow & myocardial metabolic demands
- initial manifestation of ischemic heart disease
Unstable angina
- more persistent & severe course
➡️ occurs at rest
➡️ > 20 minutes
➡️ severe
➡️ new onset
➡️ more severe, longer duration or more frequent than most previous
Causes of unstable angina
- atherosclerotic plaque disruption
- platelet aggregation
- secondary cardiomyopathy
Cardiomyopathy
disease of the heart muscle that makes it harder for the heart to pump blood to the rest of the body which causes the heart muscle to be enlarged, thick or rigid
➡️ can lead to valve disorders, arrhythmias, or heart failure
Disorders of the heart valves include?
- trauma
- ischemic damage
- degenerative changes
- inflammation
- congenital defects ( in new borns )
stenosis
narrowing of the valve opening
➡️ flaps can be stiff or thick
➡️ does not open properly
➡️ decreased blood flow
mitral & aortic valve stenosis
causes a reduce of blood flow with narrow opening
mitral valve prolapse
valve flaps bulge ( prolapse ) into upper left atrium during each heartbeat
➡️ can cause blood to leak backwards ( regurgitation )
mitral & aortic valve regurgitation
valves do not close properly
➡️ backflow of blood in the left ventricle
Definition of aortic valve disorders
- valve between left ventricle & aorta narrows
- cannot open fully
- reduces or blocks blood flow to the aorta & the rest of the body
Potential Complications of Aortic Valve Disorders
- heart failure
- stroke
- blood clots
- heart rhythm abnormalities
- death
dilated cardiomyopathy
enlarged ventricles
hypertrophic cardiomyopathy
enlarged stiff septum; enlarged myocardium
➡️ causes the heart chambers to become smaller
restrictive cardiomyopathy
walls of the ventricles become stiff
primary cardiomyopathy
genetic & mixed cardiomyopathy
secondary cardiomyopathy
caused by a systemic disease
When determining the extent of infract, always remember…
- 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
- heart rate, blood pressure, cardiac rhythm
Who are at risk for myocardial infractions?
- people who are asymptomatic without other evidence of CAD
- people who have a history of previous MI & continued episodes of silent ischemia
- people who have angina & who also have silent ischemia
Signs & Symptoms of MI
➡️ radiation to other areas: left arm or both arms, shoulders, neck, jaw, lower back or abdomen
➡️ angina ( stable or unstable )
➡️ heart palpatations ( racing or skipping )
➡️ shortness of breath
➡️ anxiety
➡️ sweating
➡️ nausea
➡️ stomach discomfort
➡️ feeling lightheaded, dizzy, or fainting
➡️ weakness ( r/o hypotension )
vasculitis
- inflammation of the blood vessel wall resulting in vascular injury & necrosis
➡️ the inflammatory process may be initiated by direct injury, infectious agents or immune processes
Signs & Symptoms of vasculitis
fever, myalgia, arthralgia, malaise
atherosclerotic occulsive disease
sudden event that interrupts arterial flow to the affected tissues or organs
➡️ fatty deposits, like in atherosclerosis
➡️ narrowed arteries reduce blood flow to the arms or legs
thromboangiitis obliterans
inflammatory arterial disorder that causes thrombus formation
raynaud disease & phenomenon
- intense vasospasm of the arteries & arterioles in the fingers, less often, the toes
➡️ risk factors: women more than men, colder climates
➡️ signs & symptoms: cold fingers or toes, color change in skin in response to cold or stress numbness or stinging pain upon warming or stress relief
seven “ p’s “ of acute arterial embolism
- pistol shot ( acute onset )
- pallor
- polar ( cold )
- pulselessness
- pain
- paresthesia ( numbness )
- paralysis
thrombus
stationary blood clot
emboli
a blood clot that moves freely in the arteries
berry aneurysm
most often found in the circle of willis in the brain circulation, containing a small, spherical vessel dilation
fusiform & saccular aneurysm
most often found in the thoracic & abdominal aorta
aortic dissection ( dissecting aneurysm )
acute, life-threatening condition that involves the hemorrhaging into the vessel wall with longitudinal leaking of the vessel wall to form a blood-filled channel
venous circulation
- one way valves in large veins
- limited contractility
- decreased driving pressure
- thin-walled vessel
Disorders of the venous circulation
- produce congestion of the affected tissues
- predispose to clot formation because of stagnation of flow & activation of the clotting system
➡️ primary & secondary varicose veins
thrombophlebitis
- causes a blood clot to form in the veins of the legs
- signs & symptoms: warmth, tenderness & pain, redness, swelling
Virchow’s Triad associated with venous thrombosis
stasis of blood, increased blood coagulability, & vessel wall injury
Risk factors for venous stasis
bed rest & immobility
deep vein thrombosis ( DVT )
causes deformity of the valves leaflets
valvular incompetence
loss of unidirectional blood flow
stasis dermatitis
chronic inflammation state in the legs due to poor circulation; itchy
venous ulcers
pooling of blood causing increased pressure in veins
primary function of the respiratory system
- gas exchange
- moves oxygen into blood
- removes carbon dioxide
- barrier defense between external & internal environment *
➡️ regulates vasoconstricting substances: bradykinin, angiotensin II, heparin
ventilation
movement of air into & out of the lungs
perfusion
movement of blood through the lungs
respiration
diffusion of gases between the lungs & the blood
purpose of conducting airways
warms & humidifies air & traps inhaled particles
type I alveolar cells
flat squamous epithelial for gas exchange
type II alveolar cells
produces surfactant, a lipoprotein that decreases the surface tension in the alveoli & allows ease for lung inflation
pulmonary circulation
starts at the pulmonary artery ( gas exchange function of the lungs )
bronchial circulation
starts at the thoracic aorta * circulatory system of the lungs *
- supplies at the lungs & lung structures with oxygen
- distributes blood to the conducting airways
- warms & humidifies incoming air
phrenic nerve
specifically in the diaphragm ( controls the dilation & constriction )
Automatic regulation of ventilation
chemoreceptors: monitors blood levels of oxygen, carbon dioxide & adjust ventilation to meet the changing metabolic needs
lung receptors: monitor breathing patterns & lung function
Voluntary regulation of ventilation
- integrates breathing with voluntary acts such as speaking, blowing & singing
- causes a temporary suspension of automatic breathing
inspiration
air is drawn into the lungs as the respiratory muscles expand the chest activity
expiration
air moves out of the lungs as the chest muscle recoil, & the chest cavity becomes smaller
Ventilation factors
➡️ pulmonary ventilation: total exchange of gasses between the atmosphere & lungs
➡️ alveolar: ventilation in the gas exchange portion of the lungs
➡️ distribution: varies with lung volume & body position
➡️ dead air space: air that is moved with each breath but does not participate in gas exchange
Perfusion factors
➡️ distribution of blood flow: affected by body position & gravity
➡️ hypoxia: induced vasoconstriction
➡️ shunt: blood that moves from the right to the left side of circulation without being oxygenated
lung compliance
how easily lungs can be inflated depends on:
- elastic & collagen factors
- water content
- surface tension
- decreases with conditions that reduce natural lung elasticity or block the bronchi or smaller airways
signs of dry cough
- asthma
- cold
- GERD
- sleep apnea
- vocal cord dysfunction
- allergies
- COVID
signs of wet cough
- cold
- flu
- lung infection
- cystic fibrosos
- acute bronchitis
- bronchiectasis
Cheyne-Stokes
abnormal pattern of breathing
➡️ oscillation of ventilation between apnea & hyperpnea
➡️ compensate for changing pressures ( can also occur if there is some serious diseases in the lungs )
What are the diffusion disorders of the respiratory system?
hypoxemia & hypercapnia
Hypoxemia
abnormally low blood oxygen levels
➡️ causes: inadequate oxygen in the air, respiratory system disease, neurological system dysfunction, changes in circulatory function, mismatching of ventilation & perfusion
➡️ signs & symptoms: hypoventilation, impaired gas diffusion, inadequate pulmonary capillary circulation
Hypercapnia
elevation in the arterial carbon dioxide
➡️ causes: decreased or shallow respiration, low level of consciousness, high muscle contraction, low nerve firing, high respiration
➡️ signs & symptoms: vasodilation, headache, conjunctival hyperemia, warm flushed skin
Types of Hypoxemia
- mild hypoxemia:
➡️ increased HR
➡️ peripheral vasoconstriction
➡️ diaphoresis
➡️ increase in BP
➡️ slight mental performance impairment - chronic hypoxemia:
➡️ insidious onset
➡️ can attributed to other causes
➡️ high ventilation
➡️ pulmonary vasoconstriction
➡️ high production of red blood cells
➡️ cyanosis
pleural effusion
abnormal accumulation of fluid in the pleural cavity
hemothorax
blood in the pleural cavity
pneumothorax
accumulation of air in the pleural cavity that causes partial or complete collapse of the lungs
pleuritis
inflammation of the pleura * pain common symptom *
Atelectasis
incomplete expansion of the lung or the portion of the lung
➡️ causes: airway obstruction, lung compression, increased recoil of lung
➡️ signs & symptoms: tachypnea, tachycardia, dyspnea, cyanosis, decreased & absent breath sounds
Asthma
chronic disorders of airways
➡️ causes of diffuse airway inflammation: bronchoconstriction, edema & swelling, airway hyperreactivity, airway remodeling
➡️ causes: genetics, IgE response to allergens, family history, smoking, pollution, environmental toxins, reflux disease
➡️ signs & symptoms: dyspnea, chest tightness, cough & audible wheezing, tachypnea, tachycardia, shortness of breath
triggers of asthma
- environmental or occupation allergens
- cold, dry air
- infections
- exercise
- inhaled irritants
- stress
- aspirin & other nonsteroidal anti-inflammatory agents ( NSAIDS )
- gastroesophageal reflux disease ( GERD )
COPD
airflow limitation caused by inflammatory response to inhaled toxins, often cigarette smoke
➡️ other causes in non-smokers: alpha-1 antitrypsin deficiency & occupational exposure
➡️ signs & symptoms: productive cough & dyspnea that develops over years, decreased breath sounds, prolonged expiratory phase of respiration, coughing & wheezing; barrel-like chest, fatigue, chest tightness; phelgm
➡️ in severe cases: weight loss, pneumothroax, frequent acute decompensation episodes, right heart failure, and/or respiratory failure ( acute or onset )
emphysema
- destruction of lung parenchyma
- loss of elastic recoil
- loss of alveolar shape & structure
- high tendency for airway collapse
- complications: lung hyperinflation, airflow limitation, & air trapping
- airspaces enlarge & may eventually develop blebs or bullae
chronic bronchitis
- productive cough on most days of the week for at least 3 months total duration in 2 successive years ( periods of excerbations with increased thick mucus often result in viral & bacterial infections )
- chronic productive cough, wheezing, & partially reversible airflow obstruction
- more common in smokers with history of asthma
bronchiectasis
permanent dilation of the bronchi & bronchioles secondary to persisting infection or obstruction
➡️ signs & symptoms: atelectasis, obstruction of smaller airways, diffuse bronchitis, recurrent bronchopulmonary infection, cough, copious amounts of foul-smelling & purulent sputum, hemoptysis * weight loss & anemia are common *
cystic fibrosis
an autosomal recessive disorder involving fluid secretion in the exocrine glands & the epithelial lining of the respiratory, gastrointestinal, & reproductive tracts
➡️ causes: genetic inherit disorder
pulmonary embolism
substance from bloodstream lodges in branch of pulmonary artery & obstructs blood flow
➡️ thrombus: blood clot
➡️ air: blood clot from IV
➡️ fat: blood clot from fracture
➡️ anmiotic fluid
➡️ causes: conditions that impair venous return, i.e. DVT; conditions that cause endothelial injury or dysfunction, i.e. dyslipidemia, & blood clotting disorders
➡️ signs & symptoms: dyspnea, pleuritic chest pain, lightheadedness, tachypnea, tachycardia, syncope, hypotension or cardiorespiratory arrest
pulmonary hypertension
- increased pressure in the pulmonary circulation
➡️ increased pulmonary vascular resistance
➡️ increased pulmonary venous pressure
➡️ increased pulmonary venous flow due to congenital heart disease - pulmonary vessels become constricted, shriveled, lost, and/or obstructed * if severe ➡️ leads to R ventricular overload & failure *
➡️ signs & symptoms: exertional dyspnea, fatigue, chest discomfort, & lightheadedness or syncope
➡️ most common caused by: left HF, diastolic dysfunction or chronic hypoxia
cor pulmonale
right-sided heart failure secondary to respiratory disease:
➡️ decreased lung ventilation
➡️ pulmonary vasoconstriction
➡️ increased workload on the right heart
➡️ decreased oxygenation
➡️ kidney releases ➡️ erythropoietin ➡️ more red blood cells made ( renin system )
➡️ polycythemia makes blood more viscous
➡️ increased workload of heart
manifestations of cor pulmonale
signs & symptoms of primary lung disease & signs of right-sided heart failure
acute respiratory distress syndrome
- more severe form of acute lung injury
- severe hypoxemia ( PaO2 < 60 mmHg ) without hypercapnia
➡️ pathologic lung changes: diffuse epithelial cell injury with increased permeability of the alveolar ( capillary membrane )
➡️ causes: pneumonia, sepsis, drowing, fat embolism, burns, severe COVID-19
➡️ signs & symptoms: dyspnea, restlessness, anxiety, confusion or alternation of consciousness, cyanosis, tachypnea, tachycardia, & diaphoresis ( sweating ) * cardiac arrhythmias & coma can result *
acute respiratory failure
- life-threatening
- impairment of oxygenation, carbon dioxide elimination or both
- may result from impaired gas exchange, decreased ventilation, or both
➡️ signs & symptoms: dyspnea, use of accessory muscles of respiration, tachypnea, tachycardia, diaphoresis, cyanosis, altered consciousness, & eventually obtundation, respiratory arrest & death
