| what are the semilunar valves? | o Pulmonary,
o Aortic |
| allow blood to be pumped from the right ventricle to the lungs (through the pulmonary artery) where it will receive oxygen. | pulmonary valve |
| allows blood to leave the heart from the left ventricle through the aorta and the body. | aortic valve |
| generates an electrical signal that causes the upper heart chambers (atria) to contract. | SA node |
| path of blood flow through the heart starting at the vena cava: | • Blood travels from the superior and inferior vena cava,
• right atrium,
• tricuspid valve,
• right ventricle,
• pulmonary valve,
• pulmonary trunk,
• pulmonary arteries,
• lungs,
• pulmonary veins,
• left atrium,
• mitral (bicuspid) valve,
• left ventricle, aortic valve,
• aorta. |
| contraction phase | systole |
| refilling phase | diastole |
| heart sound: closure of bicuspid and tricuspid valves; beginning of systole. | lub |
| heart sound: closure of aortic and pulmonary valves; end of systole. | dub |
| heart sound: the lub beat | S1 |
| heart sound: the dub beat | S2 |
| heart sound: abnormal ventricular “gallop”. Heard after S2. A heart murmur. | S3 |
| heart sound: abnormal atrial “gallop”. Heard before S1. A heart murmur. | S4 |
| amount of blood that is ejected from the ventricles per minute | Cardiac output (CO) |
| takes the CO and compares to body surface area. | Cardiac Input (CI) |
| percentage of total blood volume actually ejected from the ventricle. Never 100%, always some reserved. | Ejection fraction (EF) |
| average pressure in the arteries over time. | Mean Arterial Pressure (MAP) |
| normal value for CO? | normal: 4-6 L/min. |
| normal value for CI? | Normal: 2.5-3.5 L/min/meter2 |
| normal value for EF? | Normal rate: 55-75%. |
| normal value for MAP? | Normal: >60 mmHg. |
| how to calculate a pt’s CO based on the given heart rate and stroke volume: | = HR x SV |
| how to calculate a healthy pt's max HR: | = 220 – age of pt |
| how to calculate a healthy pt's target HR: | = desired percentage x MHR |
| decrease in BP upon change in position from supine to sit to stand. | Orthostatic hypotension |
| Clinical signs of orthostatic hypotension: | patient will report light-headedness or faintness upon head elevation. |
| Preventative measures for orthostatic hypotension: | meds, TED hose (Thrombo Embolic Deterrent), abdominal binder, circulation exercises. |
| what is the range for normal BP? | 120/80 |
| what is the range for pre-HTN? | 120-130/80-89 |
| what is the range for Stage 1 HTN? | 130-140/90-100 |
| what is the range for Stage 2 HTN? | 140-160/100-110 |
| what is the range for Stage 3 HTN? | >160/>110 |
| decreased diameter of lumen of coronary arteries, usually from atherosclerosis. | Coronary Artery Disease (CAD) |
| risk factors for coronary artery disease: | o smoking,
o hypercholesterolemia,
o genetics,
o hypertension,
o diabetes,
o emotional stress,
o obesity,
o sedentary lifestyle. |
| 4 types of Congestive Heart Failure (CHF): | • 1. Biventricular
• 2. LV systolic
• 3. LV diastolic
• 4. RV failure |
| CHF type that affects both ventricles | Biventricular |
| CHF type with inadequate CO with decreased perfusion, contractility, and EF. Common type | LV systolic |
| CHF type with elevated filling pressures, decreased ventricular capacity. | LV diastolic |
| CHF type that causes cor pulmonale; heart failure from increased arterial pressure in pulmonary artery; from COPD. Common type | RV failure |
| Clinical Manifestations of CHF: | o Increased HR,
o Dyspnea,
o Increased fatigue,
o Increased water and sodium reabsorption resulting in edema/weight gain.
o Peripheral vascular vasoconstriction,
o Ventricular remodeling,
o Pulmonary edema |
| part of the ECG strip that causes atrial contraction (depolarization). | P wave |
| part of the ECG strip that is the filling time for ventricles | PR segment |
| part of the ECG strip that causes ventricular contraction | QRS complex |
| part of the ECG strip that is the return to baseline | ST segment |
| part of. the ECG strip that causes ventricular relaxation (repolarization) | T wave |
| clutching of chest over sternum. | Levine sign |
| predictable, recurring bouts of pain resulting from ischemia. Occurs with activity, not at rest. Relieved with rest and meds. *Warning signs for infarctions. Should be followed closely by doctor. | Stable angina |
| no precipitating factors. Occurs at rest. No predictable pattern. *Seek immediate attention! | Unstable angina |
| temporary decrease in oxygen supply; reversible condition. | ischemia |
| death of cells occurs as a result of complete ischemia. Not reversible. | infarction |
| EKG will show ST segment elevation infarction, along with cardiac enzyme elevation.
o Intervention – administer anticoagulants.
o Clinical manifestations – chest pain or pain that radiates to jaw, neck, back, arms, or abdomen, shortness of breath, nausea, or vomiting. | STEMI – ST Segment Elevation and MI |
| less severe than STEMI. No change in EKG but will have elevated enzymes. May not have symptoms.
o Intervention – DO NOT give anticoagulants, could cause hemorrhage.
o Clinical manifestations – pressure-like substernal pain, occurring at rest or with minimal exertion. | NSTEMI – Non-ST Segment Elevation MI |
| uses ultrasound technology to produce a picture of the heart at rest. | Echocardiogram |
| radioactive isotope (thallium) injected during stress test to “light up” areas of good blood supply. Can detect CAD (coronary artery dissection). | Cardiolite |
| uses ultrasound tech to produce picture of heart during stress. | Doppler ultrasound |
| graded stress (max to diagnose, submax if know CAD) added to pt until pt fatigues or symptoms onset. Monitor ECG, BP, O2. Induced pharmalogically. | Pharmalogical-induced stress test |
| exploratory procedure. Catheter bulb inserted through main artery in leg or arm into ventricles. Measures EF and uses angiogram to check for arterial occlusions. | Cardiac catheterization |
| if cardiac cath detects an area of blockage, can utilize insertion of balloon and stent to keep artery open, if considered viable. | Angioplasty |
| Surgical harvesting of a peripheral vein or artery and reattaching in place of faulty coronary artery. | CABG – Coronary Artery Bypass Graft |
| effects of ACE inhibitors: | o dry cough,
o hyperkalemia,
o extreme tiredness or dizziness from hypotension,
o headaches,
o loss of taste. |
| effect of Alpha blockers: | o dizziness,
o headache,
o asthenia,
o postural hypotension,
o rhinitis,
o sexual dysfunction. |
| effects of Antiarrhythmics: | o constipation,
o dizziness,
o excessive thirst,
o skin changes,
o headaches,
o nausea,
o tinnitus,
o sun sensitivity. |
| effects of Anticoagulants: | o bleeding gums,
o diarrhea,
o rash,
o hair loss,
o dizziness,
o headache,
o chest pain,
o nausea,
o bruising. |
| effects of Antihypertensives: | o cough,
o diarrhea/constipation,
o dizziness,
o ED,
o anxiety,
o fatigue,
o headache,
o nausea or vomiting. |
| effects of beta blockers: | o fatigue,
o dizziness,
o hypotension |
| effects of calcium channel blockers: | o constipation,
o dizziness,
o tachycardia,
o extreme tiredness,
o headache,
o nausea,
o swelling in LEs. |
| effects of digitalis compounds: | o confusion,
o irregular pulse,
o loss of appetite,
o nausea or vomiting,
o diarrhea,
o tachycardia,
o vision changes. |
| effects of nitrates: | o headaches,
o dizziness,
o fainting,
o hypotension,
o arrhythmia. |
| PT interventions after a CABG: | Primary concern is return of mobility.
o Pre/post assessments: monitor BP, O2, SATS, HR, pain level. Get permission from nurse to see pt.
o Education: use of exertion scale, warm up/cool down exercises, physiological need for increased mobility, exercise techniques, breathing techniques, reinforce post-op precautions (no reaching, lifting, or stretching with arms).
o Transfers/gait: be cautious of excessive pressure on sternum, explain use of pillow on chest for pain. Work toward independence with transfer/gait. |
| 4 types of peripheral artery disease (PVD) | • Inflammatory,
• Arterial occlusive disease,
• Deep vein thrombosis,
• Vasomotor disorders |
| inflammation of blood vessels of any type. Can affect any organ or system. Acute or chronic.
o Etiology: thickened vascular walls occlusions ischemia nerve/vessel damage neuropathy. | inflammatory PVD |
| ex: atherosclerosis, thrombus, embolus.
o Clinical manifestations: intermittent claudication, increased pallor with limb elevation, delayed venous filling after elevated position, dependent rubor, peripheral necrosis. | Arterial occlusive disease |
| blood clot
symptoms: localized rubor, positive homan | Deep vein thrombosis |
| symptoms: hot flashes, night sweats, heart palpitations, changes in BP. | vasomotor disorders |
| sudden cardiac arrest in young athletes. Genetic thickening of cardiac ventricular walls, needs to be identified early. 1/500 persons.
o Clinical manifestations: arrhythmias, abnormal BP response to exercise, fainting, evidence of thickened heart walls via diagnostic tests. | Hypertrophic cardiomyopathy |
| causes tearing of artery wall, which restricts blood flow and can lead to acute MI.
o Healthy women with no signs of arteriosclerosis, men after extreme exertion.
o No warning signs
o Stents can cause further damage to arteries; medication typical treatment.
o High risk for reoccurrence
o Prescribed reduced activity, monitor BP, monitor dietary intake. | Spontaneous Coronary Artery Dissection (SCAD) |
| sudden onset of neurologic signs and symptoms resulting from a disturbance of blood supply to brain with lasting effects greater than 24 hrs.
o Symptoms: changes in level of consciousness, sensory, motor, language, perceptual, and cognitive functions. | Cardiovascular Accident (CVA) “stroke” |
| Signs of stroke: | Face,
Arm,
Speech,
Time |
| 2 types of stroke: | - ischemic,
- hemorrhagic |
| Classifications of stroke: | - major,
- deteriorating,
- young |
| A classification of stroke that is stable, yet severe. | major |
| a classification of stroke where the neurological status declined after hospital. | deteriorating |
| a classification of stroke when it occurred at an age of less than 45 years old. | young |
| risk factors of stroke: | smoking,
inactivity,
diabetes,
high BP,
obesity,
high cholesterol. |
| what is the prevalence of stroke? | - 3rd leading cause of death,
- 795,000 strokes per yr in US,
- 500,000 were preventable,
- 137,000 mortality rate per yr |
| Stage of cardiac rehab:
o Begins one day post-op CABG
o Obtain permission from nurse
o Stress increased mobility, protect sternum, appropriate ther ex with warm up/cool down.
o Transfers protect sternum. Logroll and assist as able.
o Be cautious of lines and tubes.
o Monitor vitals
o Start with rwx and gait belt. | phase 1 |
| stage of cardiac rehab:
o Outpatient rehab
o Pt on monitor entire time
o Pt given ETT, ther ex prescribed based on results
o CO and EF most important determinants
o One on one guided exercise | phase 2 |
| stage of cardiac rehab:
o Can now begin strength training, overall strengthening to enhance return to ADLs.
o Can be a personal trainer or PT
o Pt not on heart monitor, just BP/HR | phase 3 |
| interventions for phase 1 of cardiac rehab: | o Pursed lip breathing,
o Ambulation with RWX at first, then cane.
o Always use gait belt, take rest breaks when needed,
o Stair training if allowed and needed for home. |
| interventions for phase 2 of cardiac rehab: | o 3 mins on stationary bike (legs only), heart beats monitored,
o Repeat 3-4x,
o Progress 1 min each visit,
o Progress to airdyne (bike for arms and legs). |
| interventions for stage 3 of cardiac rehab: | o Strengthening exs, not till 8 weeks post CABG and at least 3 weeks of completed cardiac rehab.
o Exercise large muscle groups first,
o Avoid Valsalva and prolonged gripping,
o Slow/controlled movements |
| Upper respiratory tract: | o Nose,
o Sinuses,
o Nasopharynx,
o Larynx (vocal cords),
o Trachea |
| Lower respiratory tract: | o Right/left bronchi,
o Secondary bronchi,
o Bronchioles,
o Alveolar ducts,
o Alveoli |
| outer layer, attaches to the chest wall | Parietal pleura |
| fluid filled space that surrounds the lungs. | Pleural cavity |
| inner layer, covers the lungs, blood vessels, nerves, and bronchi. | Visceral pleura |
| 5 lobes of the lungs: | right upper, middle, and lower; left upper and lower. |
| left and right main bronchi in the upper portion of the lungs. | bronchi |
| the middle of your lungs. | secondary bronchi |
| smaller branches that divide into the bronchi. | bronchioles |
| tiny air sacs in the lungs | alveoli |
| references only the physical movement of air through the pathways. | Ventilation |
| incorporates an exchange of gas between body tissues. | Respiration |
| takes place at the capillary level, between the capillaries and the surrounding tissues. | Internal respiration |
| occurs between atmospheric air and the pulmonary capillaries/alveoli. | External respiration |
| atmospheric pressure > internal lung pressure. intake of air | Inspiration |
| atmospheric pressure < internal lung pressure. expelling of air | expiration |
| muscles involved in inspiration: | scalenes,
SCM,
pec minor,
serratus anterior,
UT. |
| muscles involved in expiration: | abdominals and intercostals. |
| the amount of air inspired and expired during normal resting ventilation. | Tidal Volume (TV) |
| the room “left over” that was not yet occupied by the tidal volume. The volume of air that can be inspired when needed but is usually kept on reserve. | Inspiratory Reserve Volume (IRV) |
| the amount of “left over” air that could be exhaled beyond TV exhalation. | Expiratory Reserve Volume (ERV) |
| lungs are never totally cleared of air even after ERV has been exhaled. There is still a residual volume. The “absolute leftovers” | Residual volume (RV) |
| TV + IRV + ERV + RV; the sun of all lung volumes. | Total lung capacity (TLC) |
| TV + IRV; the amount of air that can be inspired beginning after a tidal exhalation. | Inspiratory capacity (IC) |
| RV + ERV; the volume of air that remains in the lungs after a tidal expiration. | Functional residual capacity (FRC) |
| IRV + TV + ERV; the total amount of air in the lungs that is under voluntary control. | Vital capacity (VC) |
| forced expiratory volume; in the first second of FVC exhalation. Used to reflect the status of the airways in the lungs. | FEV1 |
| normal reading for FEV1: | Normal reading: 70% |
| collapsed lung | Atelectasis |
| punctured lung | Pneumothorax |
| excessive fluid in pleural cavity | Pleural effusion |
| excessive fluid in alveoli interstitial space. | Pulmonary edema |
| blood clot that obstructs the pulmonary artery. | Pulmonary embolus |
| foreign material into lungs and blocks airflow or causes infection. | Aspiration |
| lung auscultation: normal soft, rustling sounds. | vesicular |
| lung auscultation: louder, more hollow and echoing sound. | bronchial |
| lung auscultation: very quiet and barely audible. | decreased |
| lung auscultation: rustling sound superimposed over lung auscultations. | crackle/rales |
| lung auscultation: whistling sound superimposed over lung auscultations. | wheezing |
| clear, thin, frothy.
o Disease indications: asthma, chronic bronchitis, emphysema, lung cancer, mycoplasma pneumonia, pulmonary edema, viral pneumonia. | mucoid |
| yellow or green, thick, viscid, offensive odor (pus).
o Disease indications: bronchiectasis, lung abcess, pneumococcal/pseudomonas/staphylococcal pneumonia, TB | purulent |
| both mucoid and purulent.
o Disease indications: asthma, chronic bronchitis, cystic fibrosis, emphysema, lung abcess, lung cancer, pneumococcal pneumonia, TB. | mucopurulent |
| bright red, frothy blood.
o Disease indications: bronchiectasis, lung cancer, neoplasm, pulmonary infarct, TB. | hemoptysis |
| blood clots.
o Disease indications: neoplasm, klebsiella pneumonia | currant jelly |
| mucopurulent with red tinge.
o Disease indications: Bronchiectasis, neoplasm, pneumococcal pneumonia. | rusty |
| dark brown, mucopurulent, offensive odor.
o Disease indications: Klebsiella and pneumococcal pneumonia | prune juice |
| type of sputum: Disease indications - pneumococcal and pseudomonas pneumonia. | Blood streaked |
| type of sputum: Disease indications - Pulmonary edema | pink, frothy |
| infant acute respiratory distress syndrome.
o Pathology/etiology: lack of surfactant; high alveolar surface tension. Premature infants, <28 weeks. Hyaline-type membrane formation on alveoli, atelectasis.
o Clinical manifestations: rapid, shallow breaths, inward chest movement upon inspiration, cyanosis, flared nostrils, swollen limbs, grunting exhales.
o Treatment: surfactant replacement therapy | Hyaline Membrane Disease |
| • Pathology/etiology: asbestos exposure; the toxic asbestos fibers become trapped in the spaces between the mesothelial cells.
o Asbestos fibers cause cancerous cells to divide abnormally, resulting in the thickening of the pleural membrane, and typically creating pleural effusion.
o The fluid begins to place pressure on the lungs and the respiratory system in general, causing dyspnea and hypoxia.
• Clinical manifestations: persistent dry or raspy cough, hemoptysis, dysphagia, dyspnea, persistent pain in the chest or rib area, night sweats or fever.
• Treatment: chemotherapy or radiation | mesothelioma |
| 3 types of COPD: | - asthma,
- emphysema,
- chronic bronchitis |
| periods of reversible airway narrowing in the presence of aeroallergens, irritants, or exercise.
o Pathophysiology: an external trigger causes bronchial spasms, an inflammation response, and increased airway secretions.
o Clinical presentation: chest is expanded, accessory muscles are used to help breathe, wheezing, crackling, decreased breath sounds due to poor air movement. FEV1 will be decreased but is reversible through use of recovery drugs. | asthma |
| progressive destruction of alveolar walls, which leads to chronic hyperinflation and expansion. “pink puffers”. Can result from genetic abnormalities in the alpha-antitripsin.
o Destruction of alveoli walls leads too: decreased surface area of respiration, destruction of pulmonary capillaries; ischemia, destruction of elastic properties, destruction of surrounding structures; bronchioles, fibrosis and hypertrophy of bronchial walls; decreased capacity to remove secretions, restricted airways, decreased efficiency of expiration, flattened diaphragm, chronic CO2 retention, dyspnea, increased use of accessory muscles; increased fatigue, cor pulmonae.
o Clinical manifestations: forward flexed posture, high anxiety, SOA, clubbed fingers, barrel chest shape, chronic cough; usually dry, wheezing/crackles, cyanosis. | emphysema |
| caused by cigarette smoke or prolonged exposure to environmental pollutants.
o Leads to: inflamed mucosa, chronic irritation and secretions; bronchial fibrosis; labored productive cough, decreased cilia; risk of infection, cyanosis, cor pulmonae.
• Interventions for COPD – postural drainage techniques, incentive spirometry devices, positive expiratory pressure devices, oral airway oscillation devices, supplemental oxygen if prescribed. | chronic bronchitis |
| increases resistance to expiratory airflow to promote mucus clearance by preventing airway closure and increasing collateral ventilation. | PEP (positive expiratory pressure) device |
| combines the benefits of PEP therapy and airway vibrations to mobilize pulmonary secretions. | Acapella |
| a technique that involves laying/sitting in certain positions to drain secretions from airways using gravity. | postural drainage |
| drugs taken every day to prevent symptoms. | Maintenance drugs |
| drugs taken as needed when your symptoms become worse. | Rescue drugs |
| appropriate patient position and location of percussion for draining each section of the lungs: | • Percussion is applied over uppermost area of lower right rib to drain right side; same for left.
• Pt will lie on the right side, leaning forward with hips and legs elevated with pillows. |
| What is the prevalence of burns injuries? | - 486,000 burn injuries receive medical treatment per year,
- 40,000 hospitalized per year,
- 30,000 admitted to special burn centers |
| What's the mortality rate of burn injuries? | - 3,275 fire/smoke inhalation deaths per year,
- 2,745 deaths from residential fires,
- 310 from MVA,
- 220 from other sources,
- 1 civilian fire death occurs every 2 hrs and 41 mins |
| what's the survival rate of burn injuries? | 96.8% |
| what are gender trends for burn injuries? | 68% male and 32% female |
| what are ethnicity trends for burn injuries? | - 59% caucasian,
- 20% african american,
- 14% hispanic,
- 7% other |
| what are the etiology trends for burn injuries? | - 43% fire/flame,
- 34% scald,
- 9% hot object contact,
- 4% electrical,
- 3% chemical,
- 7% other |
| what percentage of places do fires occur at? | - 73% home,
- 5% street/highway,
- 8% occupational,
- 5 % recreational/sport,
- 9% other |
| what are the 5 layers of epidermis from most superficial to most deep? | - stratum corneum,
- stratum lucidum,
- stratum granulosum,
- stratum spinosum,
- stratum basale |
| pigment producing cells, reside in stratum basale layer. | melanocytes |
| primary cell in epidermis, produce keratin which waterproofs skin. | keratinocytes |
| increase strength of skin | Merkel cells |
| nonspecific immune protection from invading microorganisms. Reside in stratum spinosum layer. | Langerhans cells |
| located in basement membrane. Interdigitations of basale layer of epidermis and papillary dermis that hold together. Hills and valleys that increase surface area and resist shearing forces | rete pegs |
| extends fingerlike projections into basement membrane | papillary dermis |
| collagen-dense layer; dermal elements of hair follicles, sebaceous glands, sweat glands, and vascular and nervous supply seeded here. | reticular dermis |
| primary cell of dermis. Produces proteins collagen and elastin. | fibroblasts |
| provide nonspecific immune protection | macrophages |
| 7 functions of the skin: | - protection,
- electrolyte balance,
- neurosensory,
- metabolism,
- immunological,
- thermoregulation,
- social interaction |
| direct contact to a heat source or currents of air used to carry heat.
ex: flash, scald, contact | thermal burn |
| acidic or alkaline
o Acids neutralized by skin and cause coagulation, necrosis of soft tissue and bone limiting extent of tissue injury.
o Produces a dry eschar
o Alkali burns are more severe and denature proteins in skin, causing liquefication necrosis, deeper tissue penetration.
‘soupy’ wound appearance
Ex: household cleaners, wet cement | chemical burns |
| brief high-dose radiation to skin
o Industrial accidents
o Radiation therapy
o Junk yard
o Fallout – mishandling
o Damage to epidermis and dermis, loss of tissue, deep ulceration, pain, prolonged clinical course, healing very slow. | radiation burns |
| injury incurred depends on type of current, pathway of flow, local tissue resistance, duration of contact.
o Low voltage: 120-240 volts
o High voltage: >1000 volts
o Takes path of least resistance
o Contact pts: can be small, charred areas, widely injured areas, or areas without visible damage. | electrical burns |
| low resistance tissues: | - nerve,
- blood vessels,
- wet skin |
| high resistance tissues: | - muscle,
- dry skin,
- tendon,
- fat,
- bone |
| most common cause of burn related deaths. Occurs from burns in enclosed environments and chemical injuries. Burn to trachea and lungs leading to increased edema in airway. | inhalation injury |
| 3 types of inhalation injury: | Carbon monoxide poisoning,
Injury above glottis,
Injury below glottis |
| occurs when fluids in tissues and cellular spaces freeze and crystallize causing damage to blood vessels.
o Causes: exposure to cold temp, high altitude, humidity, and wind chill.
o Wearing wet clothes and shoes
o History of ingestion of alcohol and other drugs with vasoconstrictive effects
o History of malnutrition or exhaustion | cold injury |
| current is more, where resistance is less. So tissues with low resistance burn more. | path of least resistance |
| acute complications of electrical burn: | - tetanic muscle contractions,
- concomitant fractures and dislocations,
- cardiac dysfunction,
- neurologic changes,
- cataract formation,
- single and multi-organ system dysfunction,
- amputation |
| What percentage of high volt injuries require amputation? | 80% |
| initial treatment for chemical burns: | irrigate burn to get chemical off skin |
| why do radiation burns take longer to heal? | radiation obliterates vessels that bring blood flow to area |
| what are some safety and preventions for thermal burns? | - over mitts,
- sunglasses/sunscreen,
- watch water heater temp |
| what is the safe temp of a water heater? | no greater than 120 degrees |
| first degree; involves epidermis only,
pink or bright red in color,
blanches with pressure,
possible small blisters,
painful,
heals within 3-7 days,
no scarring. | superficial burn |
| 2nd degree; involves epidermis and extends into papillary dermis,
bright red and edema,
most surface with blister formation,
extremely painful due to exposed nerve endings,
blanches with pressure,
sensation to touch and pain intact,
heals within 10-14 days,
no scarring,
dry with pigment changes. | superficial partial thickness burn |
| involves epidermis and extends into papillary and reticular dermis,
pale with red capillary appendages,
may be painful or have areas of insensitivity,
sensation to pressure still intact with diminished pinprick sensation,
edematous,
blanching present but diminished,
blisters possible,
dry and itchy,
requires > 21 days to heal,
will likely result in hypertrophic scarring,
fragile epithelium,
pigment changes,
contracture development unless debrided and grafted | deep partial thickness burn |
| 3rd degree; involves the epidermis, papillary and reticular dermis and may extend to sebaceous tissue, muscle, or bone.
tissue charred, paled, mottled, waxy, yellow/brown, or nonblanching red appearance.
dry, leathery, firm to the touch.
insensible to pain, pressure, or temp.
can still be painful due to varying depths of burns.
hair follicles, sweat glands, sebaceous glands, and epidermal elements destroyed and do not regenerate.
blanching absent
requires surgical debridement or excision and grafting or surgical closure.
hypertrophic scarring will occur and at risk for contracture. | full thickness burns |
| 4th degree; areas of destruction: deep soft tissue damage to fat, muscle, bone, blood vessels thrombosed, nerves.
charred or mummified appearance.
dry with minimal edema
may have exposed tendons, muscle, fascia, cartilage, capsule, and bone.
sensation and blanching absent.
requires surgical excision and graft or flap.
may require fasciotomy and/or escharotomy due to compartment syndrome.
may require amputation
may have muscle paralysis due to permanent nerve damage. | sub-dermal burns |
| determinants of burn severity: | - time exposed,
- length in high temp |
| area of greatest destruction
destruction of all levels of protein architecture leading to coagulation.
region suffered irreparable damage.
coagulation, ischemia, necrosis.
in full thickness - area white, leathery, insensate
in partial thickness - area red, blistered, painful. | zone of coagulation |
| zone of lesser injury lying deep and adjacent to and underneath zone of coagulation.
temporarily lacks blood supply, not avascular.
necrosis may follow and may convert zone to dead eschar.
may be reversed with cell recovery within a week.
dehydration, pressure, hypovolemia, over-resuscitation, infection, further trauma, and hyponatremia may lead to necrosis. | zone of stasis |
| 2 areas zone of stasis is divided into: | - superficial zone,
- delayed zone |
| area of zone of stasis where injury is most severe; ischemia occurs within 2 hrs or less. | superficial zone |
| area of zone of stasis where injury is less severe; more deeply located, ischemia occurs between 4-24 hrs post burn. | delayed zone |
| located furthest from injury.
peripheral to zone of stasis.
minimal cell injury with vasodilation.
vascular integrity maintained and blanches with pressure.
complete cellular recovery occurs if no complications. | zone of hyperemia |
| 2 methods of healing: | - re-epithelialization,
- scar formation |
| when an injury heals on it own, with minimal to no scar.
method of healing for deep partial and full thickness burns | re-epithelialization |
| when granulation tissue is involved a scar forms.
method of healing for superficial, superficial partial, and partial thickness burns | scar formation |
