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Acute 4526 > week 11/12 > Flashcards

week 11/12 Flashcards

1
Q

What are three things that lead to shock/inability of circulatory system to supply adequate oxygen/nutrients to tissues

A
  1. ineffective cardiac pump
  2. ineffective circulatory system
  3. inadequate blood volume
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2
Q

What is the key/staple that happens in all types of shock

A

All shocks lead to inabiltiy of circulatry system to supply adequate oxygen and nutrients to tissues - causes cellular death
LACTATE - anaerobic metabolism - acidotic
Demand for oygen is not met by oygen delivery

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3
Q

What are the consequences of reduced O2 supply

A
  • cellular oxygen deprivation
  • changes to cell membranes causes fluid shifts
  • Na-Kpump fails
  • if vital organs dont recieve O2- they will shut down - more then 3 vital organs shut down - HIGH mortality rate
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4
Q

What is SIRS & symptoms

A

systemic inflammatory response syndrome
* nonspecifc and can be caused by ischemia, inflmmation, trauma, infection, or combination of severe insults
* not always related to infection

Symptoms
* meidator excess
* widespread epithelial injury & dysfunction
* vasodialtion & increased capilliary permeability
* tissue edema
* neutrophil entrapment in microcirculation

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5
Q

what is MODS

A

multi-organ dysfunction syndrome – failure of more than one orgna in an acutely ill clinet in which homesatsis can bot be maintained without intervention - very high mortality rate

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6
Q

What are the 4 stages of shock

A

initial, compensatory, progressive, decompensated or irreversible

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7
Q

What happens/S&S in the inital stage of shock & major treatment

A
  • no outward signs
  • imbalance of oxxygen supply & cellular demand
  • aeorbic - anaerobic metabloism
  • lactic acid builds up - acidosis - cells swell/permeabiity increases - less ATP
  • OXYGEN - non-rebreahter 15L
  • systemic venous oxygen important bc it tells you how much oxygen is being used by the tissues- good to check if interventions are working
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8
Q

What happens in the compensatory stage of shock S/S - why

A
  • specific to each type of shock
  • priority is to treat underlying disorder
  • relies upon mehcnaisms of homeostasis
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9
Q

what happens in the progressive stage in shock

A
  • compensatory mechanism begin to fall
  • organ perfusion grossly inadeqaute (resp, cardiac, renal, GI, liver, hematological sys.)
  • first system to display dysfunction respritary - decreased blood flow & SNS stimulation, pulomary arterioles contrict, capiliary leakage - tachypnea, crackles, WOB
  • CO falls - BP falls - hypoperfusion to kidneys (BUN, CR - met. acidosis) - GI development ischemia, liver failure (jaundice) - DIC (dissemnitaed intravascular coagulation - bleeding)
  • progresses to multisystem failure
  • aggressive interventions
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10
Q

what happens in the refractory/irreversible stage of shock

A
  • death is imminent
  • profound hypotension & hypoxia
  • failure of liver, lungs, kidneys (accumulation of lactate, ammonia, urea CO2)
  • failure of one organ leads to failure of several others
  • respiraotry and caridac arrest are inevitable
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11
Q

What is hypovolemic shock - Causes & problems

A
  • loss of fluid or blood form body, third spacing of fluid or blood – loss of intravascular fluid volume
  • survival mechanism - increase HR, vasoconstriction
  • RAAS - increase Na, vasoconstriction, & ADH inrease H2O
  • NEED FLUID REPLACMENT BEFORE VASOPRESSORS
  • 3 ways - fluid move out of blood vessles into body spaces (hemothorax), fluid can move interstitial spaces (sepsis, bruns) loss of fluid from the body (diarrhea/vomiting, diuresis)
  • symptoms apparent after 1/5 loss in adult (750ml) or 1/3 in children
  • Abosulte – fluid leaves body. Relative - fluid moves extravascular space (third spacing)

human has 5L of blood in body ISH

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12
Q

Patho of hypovolemia

A
  • ↓ circulating volume
  • ↓venous return
  • ↓ stroke volume
  • ↓CO
  • ↓ cellular O2 supply
  • ↓ tissue perfusion
  • impared cellular metabolism

increase HR & vasocontriction - SNS, catecholamines (adrenaline/nor)
kidney compensate - RAAS - angiotensin, ACE, ADH - aldosterone - sodium reasorbtion - increase BP

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13
Q

Clinical manifestations of hypovolemic shock

A
  • reasonable BP with up to 15% loss
  • increase RR - correct aciodsis (lactic acid)
  • greater then 750ml loss - S/S
  • pallor, cool/clammy, delayed cap refil, HR increase, oliguria, nausea, absent bowel sounds, increased RR (acidosis), altered LOC, lyte changes, decrease hct
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14
Q

Collab care for hypovolemic shock

A
  • oxygen
  • find cause, volume replacement, warmed fluids
  • increase CO - adrenaline, noaradrenaline, dopamine (inortopes, pressors)
  • hemodynamic monitrong - pulmonary arterial pressure line, pulmonary capilliary wedge pressure
  • blood transfusion (possibly)
  • In & Out, crystalloids initally (dextorse, RL, volume lose up to 1500ml) - isotonic (RL, NS - more long term, can ccontirbute to acidosis)
  • if BP remain low after fluid - then pressors
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15
Q

What is cardiogenic shock & causes

A

results from heart failure, 80% mortality, the normal compensaotry mechanisms lead to heart damage
most common cause MI - tamponade, arrhythmias, valve disease, pericarditis, drug toxicity

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15
Q

compensatory mechanisms in cardiogenic shock

A
  • Decreased CO – SNS maintain BP - counterproductive due to cardaic workload (SNS - increases peripheral resistance and increase HR, increase cardiac contractility (stroke volume) - pump failure, shock, impared cellular metabolism
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16
Q

Manifestations of cardiogenic shock

A
  • falling BP, cold, clammy skin, dyspnea (pulmonary edema), increase cardiac markers,
  • increase Na, H2O retention, oliguria, anxiety, confusion, agitation, N/V, decrease bowel sounds, chest pain, arrythmias, increase blood glucose, increase BUN
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17
Q

Care for cardiogenic shock

A
  • OXYGEN
  • dilate cornary arteries, improve contractility, reduce preload, redcue afterload, reduce heart rate
  • dilation - nitro,
  • contractility - inotropic, pressors (dobutmaine, dopamie, epi)
  • afterload - ACE, b-blocker, vasodilators,
  • calcium channel blockers
  • morphine - pain, treat arrythmias, cricualotry assist
  • PCI or CABG

FIRST RELAX HEART DECREASE WORKLOAD

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18
Q

What are the three types of distributive shock

A

neurogenic
anaphylactic
septic
loss of blood vessel tone, enlargement of the vascular compartment & displacement of vascular volume away from heart - skin feels warm - vasodilation

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19
Q

what is neurogenic shock - causes

A
  • factors that stimulate PSNS or inhibit SNS
  • trauma to spinal cord, spinal anaesthesia
  • vasomotor centre depression, severe pain, drugs, hypoglycemia, injury
  • rarest form of shock
  • vasodilation leads to pooling of blood -
  • decrease venous return - decreased CO - hypoxia
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20
Q

Manifestations of Neurogenic shock

A

**bradycardia **
* hypotension, hypothermia cool or warm DRY skin
* flaccid paralysis, loss of reflex acitvity, bowel / bladder fundtion -
* increase ICP– vomiting, headache, changes in behaviour, progressive decrease consciousness, lethargy, neuro deficits, seizures

21
Q

care for neurogenic shock

A
  • oxygen
  • treat underlying cause
  • careful neuro observations - GCS
  • monitor temp (vasodilation)
  • DVT from pooling
  • watch for increased ICP - reverse anaesthetic if appropriate
22
Q

what is anaphylactic shock & anaphylactic pathway

A

systemic allergic reaction to antigen - occurs on second exposrue to allergen (first exposure created antibodies, second allergen provoked defence reaction)
anaphylactic pathway
* body prodcues IgE antibodies, subsequent exposure - IgE binds to mast/basophils - cascade - vasodilation, increase permability, bronchocontriction, increased mucous, increase inflammaotry mediators - swelling, angioedema,
* third sapcing of fluids - ascities

23
Q

manifestations of anaphylactic shock

A
  • chest pain from 3rd spacing
  • swelling of lips/tongue
  • SOB, wheezing, rhinitis, stridor, edema of larynx & epiglottis
  • flushed skin, puritis, urticaria (rash, hives), angioedema, anxiety, impending doom, decreased LOC, metalic taste
  • abdominal pain, cramping, N/V, diarrhea
24
Q

care for anaphylactic shock

A
  • **epineprhine **- 1/10,000, 0.5ml SQ/IV every 20 min depending on severity
  • withdraw antigen
  • Oxygen - non-rebreather
  • bronchodialtors (salbutamol), antihistamines (diphenhydramine, IM or IV ), corticosteriods (predisome)
  • fluids - colloids (albumin)
  • airway - intubation
  • Pay attention to rebound infection
25
Q

what is septic shock - who is at risk

A

bacteremia leads to chemcial cascade and inflammatory response
* most common form of distributive shock - morbidity/mortlaity higher in gram neg - can trigger DIC
Risk
* elderly, neonate, critically ill, malnourished, immunocompromised
* majority gram neg

26
Q

manifestations of septic shock early & late

A

early
* vasodilation, pink warm flushed skin, tachycardia, bounding pulse, tachypnea, decreased SVR, elevated CO, crackles

Late
* vasocontrtction, skin pale & cool, tachycardia, hypotension, changes in LOC, increased SVR, decreased CO, clotting dysfunction, met & resp. acidosis

Note - initally respiraory alkalosis bc hyperventilating - then lactic acid effect lumg

27
Q

Progression of septic shock

A
  • SIRS - temp >38 or <36, HR >90, RR>20, PaCO@ <32, WBC >12000 or <4000
  • sepsis - SIRS & infection
  • severe sepsis - sepsis & end organ damage
  • septic shock - severe sepsis & refractory hypotension
  • MODS - usually death
28
Q

hour 1 bundle - initial resuscitation for sepsis & septic shock

A
  1. lactate level (elevated >2)
  2. obtain blood cultures
  3. adminster broad specturm antibiotics
  4. Begin rapid adminstration of crystalloid for hypotension or lactate >4 (30ml/kg)
  5. vasopressors if hypotensive during or after fluid resusctiation to maintain mean arterial pressure >65mm Hg
29
Q

collab care for septic shock

A
  • idenity cause - OXYGEN, cultures, antibiotic, IV fluids
  • +/- inotropes - norepinephrine
  • correct acidosis
  • strict precautions
  • cardiovascular system often need inotropic therpay bc ineffectivness of simple fluid resuscitation - norepi
30
Q

blood pressure, CO, SVR in hypovolemic, cardiogenic & septic shock

A
31
Q

Progression of code blue in hospital

A
  • CPR, O2, attach defib.
  • shockable rhythm - yes shock, CPR 2 min, IV/IO access - again yes shock, CPR 2 min epi, advanced airway, - yes CPR 2 min shock amnio
  • shockable rhythm no - CPR 2 min epi q3-5 min, IV/IO, advanced airway - CPR 2min,
  • treat reversible causes - 5 Hs and 5 Ts
  • Hypoxia, Hypovolemia, Hydrogen (acid), Hypothermia, Tension pheumothroax, Tamponade, Toxins, Thrombosis (PE), thrombosis (ACS)
32
Q

what is considered high quality CPR

A

2-2.4 inches deep
100-120 bpm
complete chest recoil
avoid excessive ventilations (10/min)
change compressors q 2min
monitor end-tidal CO2

33
Q

What is parses preparation for death

A

person live out their experience on the basis of valued choices - no standards of normality
quality of life

34
Q

what is important in end of life care

A

comfort & support, imporve quality, ensure dignified death

35
Q

what is “good death”

A
  • not prolonged, stregnthed relationships, relive burden of loved ones, adequate pain & symptom managment, sense of control

CONTROL - advanced directives - POA, Will

36
Q

what is definition of death

A

irreversible cessation of circulaotry and respiratory function
OR
irreversible cessation of all functions of the entire brain, including the brainstem

37
Q

Sensory manifestations of death

A
  • hearing last sense to disappear
  • decrease touch senstation, pain, taste & smell decreased
  • vision blurry - glazing of eyes, absent blink reflex, eyelids half open
38
Q

integumentary manifestations of death

A

mottling, cool/clammy, cyanosis
cyanosis nail beds, & knees, wax-like skin very close to death

39
Q

respiratory manifestations in death

A

increase RR, cheyne-stokes ( apnea & hyperventilation), death rattle (inability to cough, clear) , terminal gasps, irregular breathing

40
Q

Urinary & bowel manifestations in death

A

gradual decrease, incontinence, anuria, accumulation of gas, distension & nausea,
BM may occur when death is imminent or at time of death

41
Q

MSK manifestations in death

A

loss of ability to move, sagging jaw (loss of facial muslce tone), difficulty speaking, swallowing, difficulty maintaining posture, loss of gag refle
myoclonus jerkings (seen with opiods)

42
Q

cardiovascular manifestations in death

A

increase HR, later slowing & weak, irrgular rhythm, decreased BP, delayed absoprtion of drugs given IM/SC

43
Q

Physical care in death

A
  • PAIN - minimize irritation, regular schedule, reasses
  • delirium - quiet, well lit room, reorient, reassure, touch, family, benzo, sedative, antipsychotics
  • scopolamine, sidelying, anticholinergic, semiprone - for secretions
  • support aids for positiong
  • fluids, enemas, laxatives, suppositories, high fibre for bowel
  • absorbent pads, catheter - urine
  • small frequent meals/snacks, give antiemetic right before meals
44
Q

general S/S in death

A
  • pain, delirium, restlesness
  • dysphagia, dehydration, dyspnea
  • pooling of secretions, weakness & fatigue
  • myclonus, skin breakdown, constipation urinary incontince, anorexia, N/V
45
Q

Psychological concerns in death

A
  • anxiety depression (encourage, support)
  • fear
  • communication - therapeutic communication, listen
  • greif – client expression of feelings, without judgment, privacy, anger is normal, hoplessness & powerlesness need to encurage with realistic hopes, allow family and client to have control over what they can
  • encourage saying good-bye, verbalization of sadness loss, forgivenss, touch, hugs & tears

provide cultural/spiritual support, consistency in care, symptom managment, emotional support

46
Q

5 themes relfected by family caregivers at death

A

non-abandonement, respect of client, care of family, facilitation of family process, follow up with family after death

47
Q

what is the formula for cardiac output

A

CO = HR x Stroke volume
stroke volume - preload, afterload, contractility
Preload - tension in muscle fibres prior to next contraction
Afterload - pressure heart has to overcome to pump (vasodilatoin/constriction) - vascular resistance
Contractility - how hard heart contracts (calcium, weight, aciodosis, hyperkalemia - CCblocker will decrease, norepi will increase)

48
Q

what are the four components of hemodynamic monitoring

A

bedside monitor
invasive catheter & high pressure tubing
transducer
flush system

49
Q

what does an arterial line do what is important nursing care

A

continuous artreial pressure monitoring via percutaneous introdcution of a catheter into the radial, brachial or femoral artery (MAP)
nursing care
* assess system q1-4hr - pressure bag 300mmHg, fluid level, patency
* monitor for complications (infection, haemorrhage, thrombus, neurovascular compromise)
* neurovascular status - 5ps (pain, pulse, pallor, paresthesia & paralysis), CSM, cap refil

50
Q

What is a pulmonary artery catheter & nursing care

A

It is introduced through the jugular into right atrium, into right ventrical and sits in the pulmonary artery
- measures pressure - inflates ballon then measure the back pressure (pressure related to lungs) - wedge pressure (PAOP)
- PAP - 4-12,, Hg, PAOP - 6-12 mm Hg
- can be used for transvenous pacing
- can measure blood temp, give med/fluid

Nursing care
* monitor for complications
* assess q 1-4 hr (pressure bag 300 mm Hg, fluid levle, patency)
* patient position, respiration variation (take reading after expiration so intrahtoracic pressure is neutral)
* PEEP

51
Q

what can affect PA measurment

A
  • if transducer is placed at level of phebostatic axis, HOB 0-60 degree will not affect
  • if change position of client, wait 5-15 minutes before doing a reading
  • if doing PAOP - breathing impacts reading, read at end-expiration as it is the most stable point, when intrapleural pressure is close to zero

Acute 4526 (4 decks)

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