Do we always treat a wheeze?
Apr 27th, 2010 by
RH-111
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The other night while on ALS rotations I came across the following patient.
Dispatch info: Elderly Male AMS. Diabetic history.
On arrival find an 84 year old male sitting at table in no apparent distress. Wife states that he been sleeping a lot and just woke up after a 20 hour sleep. Patient is AxOx3 denies any pain or distress and states that his wife was nervous because he wasn’t answering properly. Glucose stick reads 119. Hx of HTN, NIDDM and Asthma.
Airway is patent, breathing is eupneic and color and temp are normal. Lungs reveal an end expiratory wheeze in upper left lobe and nearly absent lung sounds in all other fields. SpO2 is 79% on room air. EKG is NSR as is 12 lead. No edema noted.
Turns out patient is taking a strong narcotic based cough medicine for a persistent productive cough x 4 days, possibly the cause of his lethargy (the narcs that is).
My treatment plan was hi-con O2 and transport. (15 lpm had brought his sat up to 98%). My preceptor wanted to treat the wheeze with albuterol and ipratropium which I thought was unnecessary. She got her way and a treatment did nothing for his slight wheeze and sat was already at 98%.
A while later when I returned to the ER I confirmed that his CXR showed a bilateral pneumonia just as I had suspected.
Question; do we really need to treat every wheeze? If o2 corrected the saturation problem do we need to throw a drug in too?
Funny Video
Mar 3rd, 2010 by
RH-111
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You may have seen this already…funny but sadly all too true (sorry about the language)
Mnemonic for treatment of Pulmonary Edema
Nov 13th, 2009 by
RH-111
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Our remake of an old mnemonic (Not performed in this order)
MOIST N DAMP
M orphine
O xygen
I ntubation
S it-up
T welve lead
N itrates
D angle legs
A tivan (lorazepam)
M onitor Q 3-5
P ulmonary Congestion (CPAP)
Your comments are welcome!
STEMI Imposters
Jun 15th, 2009 by
RH-111
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Updated in this post – See here http://www.rhmedicclass.com/index.php/12-lead-ekg-in-acs/
(From Tim Phalen’s lecture)
LVH – Primary cause is HTN
increased QRS amplitude – variety of formulas exist – read the interpretation – machine does the math. (Or – look at v1 – from baseline to most negative deflection – count mm – then look at v5 and v6 and count the tallest. add depth of v1 to highest of v5 or v6 – if over 35 you have LVH (if under age 35 use 53mm)
BBB – Primary cause is aging process
Widens the QRS complex – QRS Dur. >0.12 sec (120ms)
Ventricular Rhythms including paced
Widens the QRS complex – QRS Dur. >0.12 sec (120ms)
Benign Early Repolarization (BER)
ST elevations often in lateral leads and lead II
Tall peaked T waves – and tall QRS
Fishhook ST segment
Young healthy male (20-40 years, +African Americans)
does not typically produce reciprocal changes
Pericarditis (epicardium may be inflamed too)
May be in all leads
May be in leads not grouped anatomically
sharp pain
localize with a finger
positional – prefer leaning forward
radiates to base of neck or shoulder blade
might hear friction rub on auscultation
does not typically produce reciprocal changes
Pediatrics 3
Mar 29th, 2009 by
RH-111
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March 29, 2009, Dr Cooper
Pediatric Circulatory Emergencies
PAT
Is he in shock? Volume or Cardiogenic, assess vitals, mentation, etc, (BP last indicator)
Peds, who present with dysrhythmias, present like they are in shock. They won’t tell you that they have palpitations, etc, do not presume that if a child is in shock you always give fluid…must rule out cardiogenic causes.
Shock - failure of circulation to meet the metabolic demands of the tissues (energy)
Hypoperfusion – inability of circulation to deliver blood to tissues, results in hypoxia
Hypotension – not enough pressure to deliver blood to core organs
Compensated shock – inability to meet needs of peripheral tissues
Decompensated shock – inability to meet metabolic demands of core organs
Cardiopulmonary failure – moribund state resulting in from total respiratory and/or circulatory collapse
Preload – tension in ventricle wall at end diastole – corresponds with RAP /LAP (potential amount of force that can be generated by the ventricle based upon the amount of stretching by the muscle fibers – determined by end diastolic volume
Afterload - tension in ventricular wall at end systole (covaries with PVR peripheral vascular resistance) (pressure head against which the heart has to squeeze)
Contractility – force developed by the ventricular wall during systole
Pediatric Hemodynamic changes
Blood Loss Heart rate immediately increases and only drops at around 45% loss
BP maintains until about 30% loss and then drops severely (soft arteries can constrict much better than adults)
CO starts dropping immediately and also drops severely of at 30% loss
Shock – A Hydraulic Solution
Pump Failure (cardiogenic)
Electrical dysrhythmias (defib cardiovert)
Mechanical – cardiomyopathy (inotrope, vasopressor)
Pipe Failure
Distributive –(anaphylaxis, neurogenic – decreased vascular tone) (volume resuscitation MAST, Epi, contain the spread)
Obstructive (Pneumothorax, Tamponade) (decompress tension pneumo)
Prime Failure
Hypovolmic dehydration, hemorrhage, GI
Dissociative –CO poisoning (o2 specific antidote)
Kids have proportionally larger blood volume but absolute volume is smaller
Softer more compliant vessels – capable of intense vasoconstriction
Smaller heart ventricles less compliant – less stretch per Starling’s Law – cannot really increase contractility – more dependent on rate to increase CO
Pulse higher than 150 – (5x age in years) is tachycardia, BP <70 +2 x age is lowest BP
Hypovolemic shock most common is peds, then septic, then cardiogenic
Hypovolemic – mostly dehydration, then hemorrhagic, GI
Septic –more common endotoxin vs extotoxin – (results in inability for cells to extract o2)
Cardiogenic – usually electrical (SVT VFIB)
Kids don’t usually get clammy unless cardiogenic, mottled in Hypovolemic
Simultaneous palpation of proximal and distal pulses (eg. femoral vs Pedal) big diff indicates compensated shock
Fluid Doses 20ml/kg of NS or LR – does it help? See study…Bottom line – maybe not be effective in short transport times. Focus on maintaining airway.
2 attempts or 90 sec, AC or saphenous at ankle. Then try IO. IO must be injected under pressure, gravity drip will not work
Pediatric Trauma
Immature anatomy
Different mechanisms
Long term sequela
Age specific equipment
Normoventilate(30) for resp failure, decomp shock, traumatic coma
Hyperventilate (35)– single dilated pupil, fixed dilated, apneic spells
SCIWORA Syndrome: (Spinal Cord Injury w/o Radiologic Abnormality)
Head Trauma – ….
Neck Trauma ……
Chest Trauma – soft bone structure –
Abdominal Trauma – upper organs are lower, lower organs are higher (liver not well protected), thinner walled, abdominal viscera less protected
MSK Trauma , lose less blood, growth plate involvement, incomplete fractures, vascular injury common
ABCDEF – Airway Breathing Circulation Disability (pupils and GCS), E exposure, (but keep warm) F (focused physical on stable patient)
El Physiocontrol Lifepak 12, así como muchos otros tipos de equipos médicos usados se pueden comprar en línea por mucho más barato que comprar nuevos.
Pediatrics 2
Mar 25th, 2009 by
RH-111
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3/25/09 Dr Cooper
Pediatric Airway Management
Bag and drag, get control of lungs and heart will follow – get control of airway and move
Start with PAT – Appearance – example, seesaw respirations – upper airway obstruction. Snoring; soft tissue, gurgling; secretions, stridor; croup FBAO, epiglottis. Hoarseness; laryngeal trauma
Mandibular block, needs to be moved forward– use OPA or Jaw thrust
Larynx, higher and more forward in the throat, airway is funnel shaped, particulate matter can get wedged below cords but above cricoid ring.
Size of Infant airway= drinking straw. Adult=Garden hose
Management
Non- rebreather Pulse Oximeter of 90-95%, GCS 14, AVPU of V , compensated shcok – SBP 70-90 + 2x age
BVM ,
Spo2 <90%, SBP <70 + 2x age (decompensated shock), Traumatic Coma, AVPU P or U, GCS 8 or less – disable pop-off valve, watch the chest
just rise,
Size the mask, completely cover nose and mouth, face mask cannot press against eye, causes profound vagal response in baby
EC Clamp
OPA – teeth to angle of mandible
NPA – nares to tip of earlobe
Positioning
Medical – Sniffing plus
Trauma – Neutral airway position
Squeeze – relax, 20 times per minute
Do not hyperextend neck in either case
Infant – pad entire body (or use a backboard with a hole for head). Head is too high and padding aligns plane of face to be parallel with stretcher. Disproportion ends around 8 years of age. Older child may need a shoulder roll.
Steeles rule of three, spinal cord is only one third of spinal canal. Hard to add further injury as long as you keep some degree of caution, a little movement won’t injure,
May have to remove C collar in order to intubate
Technique for high pressure ventilation- Sniff plus, jaw thrust up into mask, two thumbs on side of mask
ETT – respiratory failure decompensated shock, traumatic coma
ETT vs BVM – No significant mortality differences, true for medical and trauma patients.
BVM the single most important skill to master
(TUBE TOOLS – CD Rom)
The Physiocontrol Lifepak 12 as well as many other types of used medical equipment can be purchased online for much cheaper than buying new.
___________________
Respiratory Problems
Respiratory distress – increased effort but enough to compensate for tissue hypoxia – due to mild hypoxemia (days)
Respiratory failure increased or decreased effort not enough to compensate for tissue hypoxia – due to sever hypoxemia (hours)
Respiratory arrest – if uncorrected leads to cardiopulmonary arrest (2 minutes)
Upper airway obstruction – extrathoracic
Lower airway disease – intrathoracic
Grunting = PEEPing
Peripheral mottling – circulatory problem; central mottling- respiratory problem
Sniffing and tripod – severe distress, head bobbing or grunting – respiratory failure
Oxyhemoglobin dissociation curve – kid won’t turn blue until o2 is dangerously low
Pediatric Respiratory volumes -Kids have smaller oxygen cushion than adults, will deteriorate more quickly. Higher o2 requiements
Upper Airway Obstructions
Lower Airway
Asthma –reactive airway disease
Bronchiolitis – caused by RSV
Pneumonia – lung tissue disease
FB – small FB lodged in lower airway – generally caused resorbtion atelectasis
Pediatric Airway Assessment – determine degree of problem – altered mental status very worrying sign, indicates respiratory failure – BVM – if the baby accepts the mask he needs the mask.
Treatment – o2 always primary – everything else is adjunct
Pediatrics 1
Mar 23rd, 2009 by
RH-111
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Pediatric Assessment, Dr Cooper
3/23/09
See www.cpem.org
Planning: Triage & transport – Needs vs. resources – enroute, review and plan
Arrival: General Impression: Pediatric Assessment Triangle (PAT) – Hands off assessment – ABC Appearance, Work of Breathing, Circulation to skin
Initial Assessment: Rapid cardiopulmonary assessment – Hands on
Focused History: pertinent negatives, relevant findings
Pediatric Assessment Triangle
Appearance
Work of Breathing
Chest rise
Rocking motions
Retractions
Nasal flailing
Head bobbing
Grunting
Snoring
Stridor
(C)Circulation
Initial Assessment: Rapid cardiopulmonary assessment – Hands on
Airway –clear? Maintainable?, stable?
Breathing – ventilation, oxygenating, stable? In peds rates and effort are not necessarily related like adults, effort much more important!
Circulation: Shock? Cardiogenic?, stable? Shock: inability of blood to meet metabolic needs of the tissues- Mental status, pulse rate and character; distal vs. proximal, skin color, BP. Cardiogenic shock: Dysrhythmias, other , compensated, decompensated, cardiopulmonary failure (cardiogenic shock not initially treated with fluid)
Focused History : pertinent negatives, relevant findings
Why peds don’t have heart attacks: no CAD, atherosclerosis, etc –congenital heart diseases are rare. Adults drop dead, kids droop dead (secondary to respiratory arrest, etc)
Anatomic & Physiologic differences
Child airway – funnel shaped, narrowest part is at crichoid ring- adult s cylinder, narrowest at glottis
Small jaw, large tongue, prone t soft tissue obstruction – reposition
Immature immune system. lack of specific antibodies, protective mucus layer
Infants are nasal breathers, keep clear
Floppy omega shaped epiglottis
Narrow subglottic area
Remember if suspected C spine injury, stabilize c spine before/while maintaining airway
Breathing anatomy
Adult – diagonal ribs, stiff cartilage, stronger muscles
Ped – horizontal ribs, soft cartilage, weaker muscles – diaphragmatic breathers, much less alveoli – faster o2 depletion. Susceptible to barotraumas, high risk of Pneumothorax, bag until chest rise, no more. (head bobbing grunting – near end resp failure)young tissue – high elastin content– shift mediastinum -easily
Breathing assessment requires an open Airway! – ASSESS A, THEN FIX A! THEN GO ON TO B!
Is ventilation adequate – inspect chest rise – capability
Auscultation – air entry
(Missed slide)
Always consider hypoxia first as cause for AMS
Auscultate in armpits, small chest, sounds travel
ETT only of BVM ineffective
Consider NG/OG if abdominal distention
Circulation
Adults, big hearts large chambers and thin walls, Starlings Law (like a spring, recoil helps CO)
peds – small chambers thick walls – can’t vary CO well with heart walls, CO depends only on HR
Adults – stiff vessels – vigorous response to hypovolemia and hypothermia
Peds – soft vessels – more compliant vessels
Smaller blood volume, lose lager percentage compared to adult
Smaller fat mass – larger relative blood volume
Bleeding control – direct pressure – retain systemic o2
Shock assessment – cause assessment – cardiogenic etc – Simultaneous palpation of central and peripheral pulses – strong central weak peripheral – compensated – everything weak; decompensated shock
Tachycardia = 150 – 5x age in year
Kids get mottled – not clammy
Cap refill – use warm extremities
Minimum systolic BP: 80 + 2x age
Adrenaline makes you stupid – use a Broselow Tape
Study Topics
Jan 11th, 2009 by
RH-111
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Random topics of interest, not in lectures yet
1/11/09
ACE inhibitor (ACEI) blocks conversion of angiotensin I to angiotensin 2 – results in lowering of BP, used to treat HTN & CHF. (Mechanism of Action : inhibits angiotensin converting enzyme, interfering w/ conversion of angiotensin I to angiotensin II) RAAS
Vasopressin
Calcium Channel Blocker (CCB) Most calcium channel blockers decrease the force of contraction of the myocardium (muscle of the heart). This is known as the negative inotropic effect of calcium channel blockers.
Pituitary
Krebs cycle
Diuretic
Fremitus
Uremia is a term used to loosely describe the illness accompanying
kidney failure (also called renal failure), in particular the nitrogenous waste products associated with the failure of this organ.
In kidney failure, urea and other waste products, which are normally excreted into the urine, are retained in the blood. Early symptoms include anorexia and lethargy, and late symptoms can include decreased mental acuity and coma. It is usually diagnosed in kidney dialysis patients when the glomerular filtration rate , a measure of kidney function, is below 50% of normal.[2]
Tetany – is a medical sign, the involuntary contraction of muscles , caused by diseases and other conditions that increase the action potential frequency. The muscle cramps caused by the disease tetanus are not classified as tetany; rather, they are due to a blocking of the inhibition to the neurons that supply muscles.
Motor_end_plate
Cushing’s Triad
Pnuemonia
Pulmonary embolism (PE)