Hfd Respiratory Emergencies

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SNORING

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PARTIAL UPPER AIRWAY OBSTRUCTION, USUALY CAUSED BY TONGUE

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STRIDOR

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HARSH INSPIRATORY SQUEAL, PARTIAL UPPER AIRWAY OBSTRUCTION

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WHEEZING

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LOWER AIRWAY, WHISTLING SOUND CAUSED BY NARROWING OF SMALL AIRWAY, HEARD PRIMARILY ON EXPIRATION

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RONCHI

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RATTLING SOUND IN LARGER AIRWAYS, MUCUS OR FLUID BUILD UP

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RALES

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CRACKLES, MOIST CRACKLING SOUND, FLUID OR MUCUS IN ALVEOLI, ATELECTASIS-WHEN ALVEOLI ARE REINFLATED

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FRICTION RUB

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DRY, GRATING, LEATHERYSOUND HEARD ON OSCULATION, DUE TO INFLAMED PLUREA, CAUSES CHEST PAIN ON INSPIRATION

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PULSUS PARADOXUS

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DECREASE IN SYSTOLIC PRESSURE (10mmHg) OR LOSS OF PERIPHERAL PULSE DURRING INSPIRATION

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WHAT ARE SOME CAUSES OF PULSUS PARADOXUS

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COPD, ASTHMA, TENSION, TAMPONADE

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EUPNEA

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STEADY EVEN BREATHS, 12-20 MIN.

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TACHYPNEA

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RAPID, RATE OVER 20

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BRADYPNEA

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COMONLY DUE TO NEURO DISTURBANCES, RATE LESS THAN 12

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CHEYNE-STOKES

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PROGRESSIVE INCREASE IN TITAL VOLUME, FOLLOWED BY DECLINING VOLUME, SEPERATED WITH PERIODS OF APNEA

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WHAT DOES SIGHING LEAD TO

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HYPERINFLATION OF LUNGS, REINFLATION OF ALVEOLI, DECREASES ATELECTASIS

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KUSSMAUL

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ABNORMALY DEEP VERRY RAPID SIGHING RESPIRATION, CAUSED BY KETOACIDOSIS OR OTHER METABOLIC ACIDOSIS

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BIOTS

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IRREGULAR GASPING RESPIRATIONS VARYING IN DEPTH AND INTERUPTED BY APNEA, SEEN IN PATIENTS WITH INCREASING INTERCRANIAL PRESSURE

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WHAT IS NORMAL O2 SAT.

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95-100 NORMAL, 91-94 MILD HYPOXEMIA, 86-90 MODERATE HYPOXEMIA, <85 SEVERE HYPOXEMIA

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HOW IS PEAK FLOW MEASURED

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WRIGHT METER ON EXPIRATION, NORMAL-MALE-555-650, FEMALE-400-500,

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WHAT ARE CAUSES OF UPPER AIRWAY OBSTRUCTION

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TONGUE, TEETH, FOOD, EDEMA, TRAUMA, CROUP, EPIGLOTTITIS

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WHAT SHOULD BE ASSESSED ON RESPIRATORY PATIENT

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LOC, SPEAK-BREATH-COUGH, ANAPHYLAXIS OR BURNS, ANGEONEUROTIC EDEMA CAUSING LUMP IN THROAT FEELING

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WHAT SHOULD BE DONE IF THERE IS OBSTRUCTION

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IF PATIENT IS MOVING AIR LEAVE IT ALONE, SWEEP SUCTION REMOVE, HEIMLICH, OR MAGILL FORCEPS&LARYNGOSCOPE

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ADULT RESPIRATORY DISTRESS SYNDROME

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NON-CARDIOGENIC PULMONARY EDEMA, CAUSED BY INJURY OR ILNESS, PROTINE RICH FLUID LEAKS INTO ALVEOLI, LEADS TO RESPIRATORY FAILURE, ARRHYTHMIAS, BARO TRAUMA, CHF, RENAL FAILUREMANAGED BY PEEP OR CPAP

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POSITIVE END EXPIRATORY PRESSURE

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INTUBATED PATIENT EXHALES AGAINST METAL, HELPS ALVEOLI STAY INFLATED DURRING EXPIRATION

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CONTINUOUS POSITIVE AIRWAY PRESSURE

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DELIVERED THROUGH MASK CANULA OR CANNULA ATTACHED TO MACHINE THAT DELIVERS 4-25 CM OF CO2 CONTINUOUSE PRESSURE

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HOW IS ARDS MANAGED

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IV, BETA ANTAGONISTS, CORTICOSTEROIDS, DIURETICS, ANTIBIOTICS, ANTI-INFLAMITORY MEDS

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HOW IS EMPHYSEMA CAUSED

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SMOKING #1, POLLUTION, CHEMICALS, CHRONIC ASTHMA, 50% MORTALITY RATE WITH IN 10 YEARS, INCREASED MUCOUS ALLOWS AIR IN BUT NOT OUT , AIR TRAPING OCCURS

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HOW IS COPD CAUSED

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SMOKING CAUSES INFLAMITORY REACTION, PROMOTES INFLUX OF LEUKOCYTES THAT RELEASE CHEMICAL MEDIATORS THAT DIALATE VESSELS AND MAKE THEM PERMIABLE, AND BREAK DOWN ELASTIN, LEADS TO EMPHYSEMA

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POLYCYTHEMIA

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ELEVATED HEMATOCRIT, INCREASED RBC TO HELP O2 TRANSPORT, THIS THICKENS BLOOD, INCREASED WORKLOAD OF HEART

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COR PULMONALE

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RIGHT VENTRICULAR HYPERTROPHY, LEADS TO RIGHT VENTRICULAR HEART FAILURE

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THORACIC HYPER-EXPANSION

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BARREL CHEST, RESULTS FROM AIR TRAPED FROM LOSS OF ELASTIC RECOIL, EXPIRATION BECOMES AN ACTIVE PROCESS

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CHRONIC BRONCHITIS

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MUCOUS PRODUCING COUGH, RESULTS FROM EXPOSURE TO IRRITANTS AND EXCESSIVE MUCOUS SECRETIONS

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BRONCHIECTASIS

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ABNORMAL DILATION OF BRONCHI DUE TO PUS-PRODUCING INFECTIONS OF THE WALL

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WHAT MAKES COPD BREATHING EASIER

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SITTING WITH ELBOWS RESTING ON THIGHS OR TABLE, BREATHING THROUGH PURSED LIPS

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HOW DO YOU TELL IF COPD IS EMPHYSEMA OR BRONCHITIS

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USE OF ACCESSORY MUSCLES WITH EMPHYSEMA-EXPIRATION, BRONCHITIS-INSPIRATION/EXPIRATION

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PINK PUFFER

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EMPHYSEMA

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BLUE BLOATER

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CHRONIC BRONCHITIS

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WHAT ARE SOME FINDINGS OF COPD'ER

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WHEEZING, RONCHI, RALES, REDUCED BREATH AND HEART SOUNDS DUE TO REDUCED AIR EXCHANGE, INCREASED THORACIC CAVITY

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WHAT ARE LATE SIGNS OF COPD'ER

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PERIPHERAL CYANOSIS, CLUBBING OF FINGERS, RIGHT SIDED HEART FAILURE SIGNS, CARDIAC DISRHYTHMIAS

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WHAT IS TREATMENT OF COPD

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O2, IV-TKO, CARDIAC MONITOR, PULSE OX, ENCOURAGE COUGH IF PRODUCTIVE

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COPD MEDICATIONS

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B2 ANTAGONIST BRONCHODILATORS(IPRATROPIUM,NEBULIZED ATROPINE,TERBUTALINE,ALBUTEROL,METAPROTERENOL), XANTHINE BRONCHODILATORS(AMINOPHYLLINE), CORTICOSTEROIDS

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WHEN DO MOST ASTHMA DEATHS OCCUR

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OVER 45, 50% OCCUR BEFORE REACHING ER

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EXTRINSIC ASTHMA

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CHILDHOOD ONSET, GENETICALLY PREDISPOSED, 50% DEVOLOPE PRIOR TO AGE TEN, USUALY RESOLVES WITH AGE, CAUSED BY RELEASE OF IgE

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ATOPY

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IF ONE PARENT IS SENSITIZED 40% OF OFFSPRING WILL HAVE ALLERGIES, IF BOTH PARENTS 80% WILL HAVE ALLERGIES

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INSTRINSIC ASTHMA

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STARTS IN ALDLT WITHOUT STRONG HISTORY, 33& PRIOR TO AGE 30, USUALY PERSISTANT, CAUSED BY SNS-PNS RESPONSE ACh

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ASTHMA DEVELOPMENT

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HYPOXIA, BRONCHIOL MUSCLES CONTRACT, HYPERSECRETION OF MUCUS,INFLAMATION OF BRONCHIAL WALLS

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ASTHMA PHASE 1

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BRONCHOCONSTRICTION, EDEMA, DECREASED EXPIRATORY AIR FLOW, MUCUS PLUGGING, INFLAMMATION OF BRONCHIAL WALLS, USUALLY RESOLVES IN 1-2 HOURS OR WITH BETA2 DRUGS

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ASTHMA PHASE 2

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INCREASE IN EDEMA, BRONCHIAL CONSTRICTION, DECREASSE IN EXPIRATORY FLOW, OCCURS WITHIN6-8 HOURS AFTER PHASE 1 ATTACK, DOES NOT RESPOND TO BETA 2 DRUGS, STEROIDS ARE NEEDED

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ASTHMA TREATMENT

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IF FATIGUED PREPARE TO VENTILATE, ADMINISTER BRONCHODILATORS, STEROIDS(METHYLPREDNISONE/HYDROCORTISON) MAY TAKE 2-6 HOURS, MAGNESIUM SULFATE (PHASE 2 OR STATUS) TO LOWER ACh RELEASE, THE LONGER TIME BEFORE TREATMENT THE LESS LIKELY BETA2 WILL WORK

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STATUS ASTHMATICUS

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PHASE 2 PRECIPITATED BY VIRAL INFECTION, CAN NOT BE BROKEN WITH BETA 2,NEEDS ANTICHOLINERGIC, CORTICO STEROIDS, MAGNESIUM, ANTIBIOTICS

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OTHER ASTHMA MEDS

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ANTICHOLINERGIC AGENTS, CORTICO STEROIDS, MAGNESIUM, ANTIBIOTICS, KATAMINE, HELI-OX-HELIUM,

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PNEUMONIA

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INFLAMMATION OF RESPIRATORY BRONCHIOLS, ALVEOLI, 5TH MOST COMMON CAUSE OF INFECTIOUS DISEASE DEATHS

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LUNG CANCER

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NEOPLASM-NEW GROETH OR TUMOR, MOST OCCUR BETWEEN 55-65, #1 CAUSE IS SMOKING, #2 CAUSE IS RADON GAS,

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LIST FOUR TYPES OF LUNG CANCER

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ADENOCARCENOMA-MOST COMMON, SMALL CELL CARCINOMA, EPIDERMOID CARCINOMA, LARGE CELL CARCINOMA

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CAUTION

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CHANGE IN BOWELOR BLADDER, A SORE THAT DONT HEAL, UNUSUALY BLEEDING OR WEIGHT LOSS, THICKENING OR LUMP, INDEGESTION, OBVIOUS CHANGE IN WART OR MOLE, NAGGING COUGH OR HOARSENESS

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CARBON MONOXIDE

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COLORLESS, ODORLESS, TASTLESS GAS, COMBINES WITH HEMOGLOBIN 200-250 TIMES TIGHTER THAN O2

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SIGNS/SYMPTOMS OF CO POISON

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<10%- NONE, 20%- HEADACHE, NAUSEA, VOMITING, FATIGUE, 30%-ALTERED CNS, DIZZINESS, VISION, 40-60%- COMA, HALF LIFE IS 4 HR IN ROOM AIR, 30-40 MIN IN 100% 02

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PULMONARY EMBOLUS

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BLOCKAGE OF PULMONARY ARTERY, 90% ARISE FROM LEGS, 11% OF DEATHS WITHIN ONE HOUR, 38% IN 2ND HOUR,

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WHAT FACTORS CAUSE PE

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VENOSTASIS-TRAVEL,OBESITY, VENOUS INJURY, INCREASED COAGULATION, PREGNANCY, DISEASE, MULTIPLE TRAUMA

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TUBERCULOSIS

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TRANSMITTED BY SMALL DROPLETS FROM COUGH OR SNEEZE, PROTECTED BY STRONG COATING THAT HELPS IT SURVIVE, SIGNS ARE FEVER, NIGHT SWEATS, MALAISE, WEIGHT LOSS, COUGH WITH GREEN OR YELLOW SPUTUM

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AMYOTROPHIC LATERAL SCLEROSIS

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LOU GEHRIGS, PROGRESSIVE DEGENERATION OF CNS NERVES, 80% BETWEEN 40-70, 50%DIE IN 3 YRS, SET AIRWAY, VENT, O2, IV TKO

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GUILLIAN-BARRE

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ILNESS AFTER INFECTION, EXPOSURE TO TOXINS, CERTAIN VACCINES, 50% FOLLOW MILD UPPER RESPIRATORY OR UPPER GI INFECTION, RESOLVES ITSELF IN A FEW WEEKS OR MONTHS, DAMAGED MYLIN COVERING, HOSPITALIZE, GIVE FLUIDS

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MYAESTHENIA GRAVIS

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PRONOUNCED MUSCLE WEAKNESS, CIRCULATING ANTIBODIES BLOCK ACH RECEPTORS THAT AFFECT POSTSYNAPTIC ACH RECEPTORS, NERVE IMPULSES DONT CAUSE MUSCLE CONTRACTIONS

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MANAGEMENT OF MG

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AIRWAY SUPPORT, DRUGS-ANTICHOLINEESTERASE, STEROIDS, IMUNOSUPPRESSANTS, PLASMA EXCHANGE, SURGERY- THYMECTOMY TO REMOVE TUMOR

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CARPOPEDAL SPASMS

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HYPERVENTILATION LEADS TO INCREASED AMOUNT OF BOUND CALCIUM LEADING TO SPASMS IN FINGERS AND TOES

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POLIO

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VIRUS THAT LIVES IN DIRT, ONCE IN STOMACH IT GOES TO CNS, PTS ARE PLACED ON IRON LUNG