week 11/12 Flashcards
What are three things that lead to shock/inability of circulatory system to supply adequate oxygen/nutrients to tissues
- ineffective cardiac pump
- ineffective circulatory system
- inadequate blood volume
What is the key/staple that happens in all types of shock
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
What are the consequences of reduced O2 supply
- 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
What is SIRS & symptoms
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
what is MODS
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
What are the 4 stages of shock
initial, compensatory, progressive, decompensated or irreversible
What happens/S&S in the inital stage of shock & major treatment
- 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
What happens in the compensatory stage of shock S/S - why
- specific to each type of shock
- priority is to treat underlying disorder
- relies upon mehcnaisms of homeostasis
what happens in the progressive stage in shock
- 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
what happens in the refractory/irreversible stage of shock
- 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
What is hypovolemic shock - Causes & problems
- 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
Patho of hypovolemia
- ↓ 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
Clinical manifestations of hypovolemic shock
- 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
Collab care for hypovolemic shock
- 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
What is cardiogenic shock & causes
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
compensatory mechanisms in cardiogenic shock
- 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
Manifestations of cardiogenic shock
- 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
Care for cardiogenic shock
- 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
What are the three types of distributive shock
neurogenic
anaphylactic
septic
loss of blood vessel tone, enlargement of the vascular compartment & displacement of vascular volume away from heart - skin feels warm - vasodilation
what is neurogenic shock - causes
- 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
Manifestations of Neurogenic shock
**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
care for neurogenic shock
- oxygen
- treat underlying cause
- careful neuro observations - GCS
- monitor temp (vasodilation)
- DVT from pooling
- watch for increased ICP - reverse anaesthetic if appropriate
what is anaphylactic shock & anaphylactic pathway
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
manifestations of anaphylactic shock
- 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
care for anaphylactic shock
- **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
what is septic shock - who is at risk
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
manifestations of septic shock early & late
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
Progression of septic shock
- 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
hour 1 bundle - initial resuscitation for sepsis & septic shock
- lactate level (elevated >2)
- obtain blood cultures
- adminster broad specturm antibiotics
- Begin rapid adminstration of crystalloid for hypotension or lactate >4 (30ml/kg)
- vasopressors if hypotensive during or after fluid resusctiation to maintain mean arterial pressure >65mm Hg
collab care for septic shock
- 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
blood pressure, CO, SVR in hypovolemic, cardiogenic & septic shock
Progression of code blue in hospital
- 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)
what is considered high quality CPR
2-2.4 inches deep
100-120 bpm
complete chest recoil
avoid excessive ventilations (10/min)
change compressors q 2min
monitor end-tidal CO2
What is parses preparation for death
person live out their experience on the basis of valued choices - no standards of normality
quality of life
what is important in end of life care
comfort & support, imporve quality, ensure dignified death
what is “good death”
- not prolonged, stregnthed relationships, relive burden of loved ones, adequate pain & symptom managment, sense of control
CONTROL - advanced directives - POA, Will
what is definition of death
irreversible cessation of circulaotry and respiratory function
OR
irreversible cessation of all functions of the entire brain, including the brainstem
Sensory manifestations of death
- hearing last sense to disappear
- decrease touch senstation, pain, taste & smell decreased
- vision blurry - glazing of eyes, absent blink reflex, eyelids half open
integumentary manifestations of death
mottling, cool/clammy, cyanosis
cyanosis nail beds, & knees, wax-like skin very close to death
respiratory manifestations in death
increase RR, cheyne-stokes ( apnea & hyperventilation), death rattle (inability to cough, clear) , terminal gasps, irregular breathing
Urinary & bowel manifestations in death
gradual decrease, incontinence, anuria, accumulation of gas, distension & nausea,
BM may occur when death is imminent or at time of death
MSK manifestations in death
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)
cardiovascular manifestations in death
increase HR, later slowing & weak, irrgular rhythm, decreased BP, delayed absoprtion of drugs given IM/SC
Physical care in death
- 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
general S/S in death
- pain, delirium, restlesness
- dysphagia, dehydration, dyspnea
- pooling of secretions, weakness & fatigue
- myclonus, skin breakdown, constipation urinary incontince, anorexia, N/V
Psychological concerns in death
- 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
5 themes relfected by family caregivers at death
non-abandonement, respect of client, care of family, facilitation of family process, follow up with family after death
what is the formula for cardiac output
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)
what are the four components of hemodynamic monitoring
bedside monitor
invasive catheter & high pressure tubing
transducer
flush system
what does an arterial line do what is important nursing care
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
What is a pulmonary artery catheter & nursing care
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
what can affect PA measurment
- 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
