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41 Cards in this Set
- Front
- Back
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5 types of shock....
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Distributive: neurogenic, septic, anaphylactic
Hypovolemic Cardiogenic Obstructive |
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Describe Distributive Shock...
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A.K.A. vasogenic shock
- changes that occur in blood vessel tone that increase in size w/o increase in circulating volume |
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Describe Neurogenic shock...
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A Distributive Shock
Def: from massive vasodilation, precipitating factors are: •SCI, •problem w/ spinal cord block, •vasomotor center depression (drugs, OD, hypoglycemia, severe pain) S/S: hypotension, bradycardia, warm/dry extremities, decreased CO TX: elevate extremities, vasopressors (dopamine, dubamine, adrenaline, noradrenaline, atropine) |
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Describe Septic Shock....
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A Distrubitive Shock
Def: results when bacteria releases endotoxins that cause systemic inflammation and causes vasodilatation Precipitating Factors: bacterial infection S/S: fever, can be fast (bile story) or slow onset, tachycardia, hyperventilation, HYPER stuff, ↓ urine output TX: antibiotics, broad spectrum, fluids, vasopressors for VS, positioning, Xigris medicine FDA approved. (acts as blood thinner and only for sepsis clients) infused over 2 – 3 days •bleeding precautions – no blood cultures, no sticking, only manual BP, monitor urine, occult blood in stool |
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What is Xigris.....
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Xigris medicine FDA approved. (acts as blood thinner and only for sepsis clients) infused over 2 – 3 days
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What is Anaphylactic Shock..
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A distributive shock type.
Def: body reacts to foreign protein and reacts w/ massive vasodilation, increase permeability, intra- goes to extra- so edema, very rapid, severe brincospasm, laryngeal edema, facial edema Cause: foods, bee stings, animal bites, latex, meds, environmental, blood transfusion, vaccines, contrast medium S/S: depends on what caused it, hives, stridor, SOB, swelling, large welts, itching, chest pain, hypotension, weak rapid pulse, more exposed to it the faster the reaction will happen and will get worse TX: Solumedrol, epi pen #1, Benedryl, intubation to protect airway if reaction is very bad |
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Blood transfusion reaction....?
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Blood transfusion reaction:
*itching, *temperature of 1 degree increase, * SOB, * rash on chest and arms – STOP IMMEDITAELY and save blood and draw blood for bank |
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Describe hypovolemic shock...
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Can happen via hemorrhage or membranes become very permeable and leaks out (third spacing)
- body can compensate up to 750 ml then it goes into shock Cause: GI bleed, trauma, burns, loss of other body fluids (urine) such as over dose of Lasix (dehydration), nausea, diarrhea, ascities, compartment syndrome S/S: hypotension, altered mental status, rapid/weak pulse ↓ CO, thirst, dry mucous membranes, Cutis Marmorata – mottled skin Goals/TX: restore volume, control bleeding, find source of hypovolemia * raise legs but keeping core flat w/ head on pillow * IV large bore of 20, O2, fluids of NS initially, third spacing so increase albumin • colloids and are large molecules so are harder to loose = albumin of 5% or 25% • Hespan that is a rapid volume expander (a starch so is large molecules) • blood to replace (can put in 5-6 U then worry about DIC d/t banked blood does not have clotting factors), • FFP will add the clotting factors and will also add platelets |
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What is the concern w/ blood bank blood?
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No clotting factors
So may have concern w/ DIC Can + FFP for clotting |
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Tx for hypovolemia?
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* raise legs but keeping core flat w/ head on pillow
* IV large bore of 20, O2, fluids of NS initially, third spacing so increase albumin •colloids and are large molecules so are harder to loose = albumin of 5% or 25% •Hespan that is a rapid volume expander (a starch so is large molecules) •blood to replace (can put in 5-6 U then worry about DIC d/t banked blood does not have clotting factors), •FFP will add the clotting factors and will also add platelets |
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What is cardiogenic shock?
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Definition: results in adequate pumping action of the heart d/t MI, ventricular/valvular and structural problems
S/S: cyanosis, cool/clammy skin, change in mental status, ↓ CO, ↓ organ perfusion (change in LOC), ↓ cap refill TX: no position necessary as don’t know what side it is, * drugs to sustain cardiac - positive inotropes > Increased contractility = digoxin, doputamine, dopamine, milrenone - negative inotropes > decrease contractility = beta blockers, calcium channel blockers * caution fluid replacement depending on side, * may put on balloon pump, * ventricular assist device (external) |
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What is a positive inotrope?
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Increased contractility = digoxin, doputamine,
dopamine, milrenone |
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What is a negative inotrope?
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Decrease contractility = beta blockers, calcium
channel blockers |
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Describe obstructive shock
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- occurs w/ sudden obstruction of blood flow d/t cardiac tamponade
* pulsus paradoxus = pulse weaker w/ inspiration and stronger w/ expiration all due to room - tension pneumothorax (air gets into pleural cavity and displacement of lungs and pressing on heart) and pulmonary embolism - Cardiac tamponade: pericardial window to drain it - Tension pneumothorax = chest tube - pulmonary embolism = blood thinners |
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What is pulsus paradoxus
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pulse weaker w/ inspiration and stronger w/ expiration all due to room
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Describe the stages of shock
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1. Initial: aerobic → anaerobic → lactic acid → metabolic acidosis
- changes occur only on cellular level so wont present s/s - O2 depleted then metabolism goes from aerobic to anaerobic - not enough O2 = lactic acid is produced and flushed thru liver * the acid becomes acidosis 2. Compensatory: worsening acidosis -Release of adrenaline (vasoconstriction) and noradrenaline - it is trying to remain homeostasis - s/s of distress: hyperventilation d/t acidosis - barrow receptors release adrenaline and noradrenaline (vasoconstriction of pressure and HR increase) d/t hypoBP 3. Progressive: massive cell hypoxia Third spacing - acidosis increased, cap become more permeable = third spacing 4. Refractory: Organ failure d/t hypotension |
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Define shock
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tissue perfusion is insufficient to meet the
demand of oxygen and nutrients thus hypo-perfusion of tissue and organs. Massive vasodilatation and increased permeability of vascular membranes |
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What is SIRS
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Systemic inflammatory response syndrome
Over and above of normal inflame system w/ systemic effects Normally the inflammation stays local but SIRS goes systemic |
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SIRS characteristics..
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Cause: ischemia, trauma, burns, surgery complications, infection, snake bites, bowel, many causes
DX w/ HR >90, T = < 36 or > 38, hyperventilation, WBC > 12K Tx: -anti-infectives, -maintenance of tissue perfusion and O2 (mechanical vent), -nutrition support (TPN), -immunomodulation of Xigris medication SIRS and proof of infection = sepsis Starts as SIRS then when have proof of infection becomes sepsis |
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What happens in DIC
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In DIC = liver gets tricked by something that makes the liver think that there is bleeding so will dump lots of fibrinogen and it will find thrombin to make the fibrin. Now lots of fibrin that looks for platelets – they produce a fibrin clot throughout the body. Lots of clots in the blood stream – they obstruct micro-circulation of systemic including organs.
- the clots then just lyse they release fibrin degradation product (has anti coagulation in it) and D-dimer. |
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DIC description
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Cause of DIC
Acute = infection, blood txfusion b/c blood has not clotting factors, shock, Chronic = cancer patients, lung cancer, liver dx, DVT, aortic aneurisms. DX studies: - PT = elevated - PTT = measures clotting ability = elevated - Fibrinogen = elevated - Platelets = used up on clot formation = decreased - Fibrin split (degradation product)= increased - D-Dimer = increased Collaborative care: - Tx underlying cause is #1 to stop DIC - Monitor for signs of bleeding, bleed precaution - Replace blood loss w/ PRBC - FFP, cryoprecipitate (replaces factors 8 and fibrinogen), platelets - Adding “fuel to the fire” b/c adding clotting factors (fibrinogen) - Can put on Heparin to help them w/ the clots in the microcirculation - VS manually - No invasive procedures |
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Factors that influence ICP
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- arterial pressure
- venous pressure - intra-abdominal and intra thoracic pressure - posture - temperature - CO2 level |
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Compensatory Mechanisms for ICP
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-compliance = ability of brain to adjust to ICP by displacement CSF into spinal canal
-reduction = blood flow and blood volume is reduced -displacement = brain tissue is being displaced down into spinal canal |
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Munro-Kellie Hypothesis
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- if one part of the total brain increases in size then something else is going to shrink or the pressure is going to rise
- Volume intracranial (constant) = v. brain/v. CSF/V. blood/V. mass lesion |
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ICP ranges...
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- 0-15 mm Hg = normal
- > 20 bad - > 40 super bad |
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Increased ICP = ????
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Decreased CPP (cerebral perfusion pressure
- normal CPP to allow proper O2 and glucose to the brain is 70-100 mm Hg |
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Causes of ICP
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-head trauma based on the following:
Concussion – disruption of neural activity lasting less than 5 min., retrograde amnesia, no break in skull, no change in CAT or MRI Contusion- major brain injury, bruising of brain tissue • Coup-counter coup closed head injury = whiplash • Hitting brain on same and opposite side of skull Lacerations – major or minor, scalp = minor, scalp wounds bleed a lot as it is very vascular, Cerebral laceration = tearing of brain tissue and is major injury Skull fracture: • visual signs: Battle’s sign = bruising behind ear @ base of skull; raccoon eyes = purple bruised edematous area around eyes so injury @ base of skull • Have CSF leakage visible as clear nasal drip as otorrhea or rhinorrhea • Care = test the CSF for glucose or drop on paper w/ red center and yellow halo around • Cerebral hematoma Epidural hematoma = b/t skull and duramatter, arterial bleeding d/t rupture of menegial artery • s/s are quick: change of mental status, LOC, confusion, vomiting, fixed dilated pupil on side of impact w/ contralateral weakness (anisocoria = blown pupil) Subdural hematoma = collection of blood in subdural space d/t tearing of bridging b/t duramatter and arachnoid, venous in origin so slow onset of s/s: slow dev. neuro deficit intracerebral hematoma= bleed into brain tissue, hemorrhagic stroke (hemorrhagic stroke) Brain tumors Hydrocephalus = inc. CSF in ventricles so put in shunt into abdomen. Inflammatory condition of the brain (meningitis) Penetrating injury: •Never remove the object |
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Clinical manifestations of ICP:
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- change of mental status, change in orientation, dec. level of attention, no response to voice-touch-sternal rub
- change in pupil reflexes - no swallow/cough reflex - ocular signs – double vision, sluggish response to light, anisocoria, dialtion of pupils, - Dec. in motor function on contralateral side Projectile vomiting w/ ICP HA that is abnormal Frightening fever = Coning fever = temperatue goes to 106 + so it displaces into base of skull and takes on shape of cone Change in VS – is later w/ ICP = BP becomes widening pulse pressure b/w - bradycardia, irregular respiratory pattern and all d/t pressure on hypothalamus - Cushing’s Triad: damage is already happened and ischemia is occurring • Widening pulse pressure • Bradycardia • Irregular respiratory pattern and change in body temp Seizures |
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Posturing during ICP
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-Decoriticate response – results of interruption of voluntary motor tracts = flexion of upper arms and bringing up to chest
•Can be a reaction to a stimulus so need to stop! Decerebrate response – more serous damage to brain stem and mid brain; in clients extending all extremities and plantar flexion of palms up w/ stimulus Decorticate on Rt. And decerebrate on Lt – combination |
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Coning Fever??
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temperatue goes to 106 + so it displaces into base of skull and takes on shape of cone
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Dx for ICP
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Dry CT w/o contrast
MRI EEG Cerebral angiography = cerebral blood flow catheter and is similar to cardiac ICP measurement No LP (lumbar puncture) b/c when make hole it will come out w/ ICP |
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Goals for ICP clients
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Maintain cerebral oxygenation by giving O2 via intubation
Maintain normal perfusion via ICP monitoring device (ventriculostomy) that is placed into ventricle but has transducer for continuous reading of ICP - closed system - has drainage bag that is regulated w/ stopcock that can be opened to drain extra CSF to lower pressure - make sure HOB remains constant Decrease ICP Maintain patient airway Maintain neurologic function HOB above 30 degree Antipyretics Balance fluids Cooling blanket on hands Permissive hypercapnia (therapeutic hyperventilation) - Co2 accumulation = vasodialtion of cerebral perfusion - Blow it off = vasoconstriction of cerebral perfusion so hyperventilation induced |
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What is permissive hypercapnia
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(therapeutic yperventilation)
- Co2 accumulation = vasodialtion of cerebral perfusion - Blow it off = vasoconstriction of cerebral perfusion so hyperventilation induced |
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Drugs for ICP?
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-diuretics to decrease volume to decrease pressure
-Manatol specific for head trauma to increase osmotic pressure of glomular filtrate to inhibit absorption of water/electrolytes • Administered as PRN depending on serum osmolarity • Serum osmolarity = number of particles in a solution/like concentration If keep slightly elevated will bring fluid from cells out High serum os = cell dehydration Low serum os = cell swelling • Barbituates: placed in barbiturate induced coma to keep calm and will provide body w/ nutrites and O2 for consumption to decreased ICP • Neuromuscular drugs (paralyzing drugs) • Anti seizure meds (Mannitol) and prophylactic and steroids |
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Nsg Assessment for ICP
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-Glascow coma scale but is not conducive for head trauma
-Some are coming up w/ their own scales (Mayo Clinic) for ICP to include eye response, motor responses, brain stem reflexes, respiration quality but not 100% -Assessment q 30 minutes for neuro trauma -Respiratory assessment q hr. in beginning then q 4 per protocol -ABG w/ any change and as needed for respiratory status -VS is to keep BP to maintain adequate CPP -Monitor for Cushing’s Triad and -Document any minor changes |
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What is Cushings Triad?
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Damage is already happened and ischemia is occurring
• Widening pulse pressure • Bradycardia • Irregular respiratory pattern and change in body temp |
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Examples of Urgency 1 triage
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o 1 = life, limb, eye
ice pick in eye, eye trauma, acute eye pain (retinal detachment), chemical splash to eye, accidental-traumatic amputation of limb, absence of pedal pulses, cardiac/acute respiratory arrest (asthma, pneumothorax), acute neuro. changes/change in mental status, life threatening trauma, fracture (but depends on kind) |
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Examples of Urgency 2 triage
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o 2 = need tx w/in 20 minutes to 2 hrs
abd. Pain, fever, dehydration, kidney stones, asthma (sometimes), fracture (but depends on kind), laceration |
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Examples of Urgency 3 triage
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o 3 = wait for hrs or days
sprain, muscle pain, flu/cold, rashes, simple HA (migraine) |
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Primary survey in triage
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These are the priority and once one needs attention, it must be dealt w/ first.
A = airway - anything that causes airway obstruction (pneumo, rib fx, active seizures, near drowning B = breathing - inadequate ventilation (asthma, P Emboli, SOB, hypoxia, cyanosis) C = circulation - of blood thru body (so measure HR, evaluate for adequate blood volume, BP, peripheral circulation, degree of disability that measures the neurological/LOC of client) D = Disability |
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Secondary survey in triage
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E = exposure to env. Control
- undress client, IV fluids, blankets, secure/safe environment F = full set of VS (HR, Temp, BP in both arms, RR, O2 sat, pulse rate), pull full blood work up, determine if any family present G = give comfort measures - alleviate pain/anxiety H = history and head-to-toe assessment - patient hx |
