Shock Flashcards
What is shock
- decreased tissue perfusion and impaired cellular metabolism
- tissue perfusion does not meet the cellular 02 requirements
- imbalance between supply and demand for 02 and nutrients
Shock is a problem with….
- pump: cariogenic
- volume: hypovolemic
- vessels: distributive and obstructive
TRUE OR FALSE: shock is defined by low blood
false
CO
SV X HR and is where perfusion comes from
CO is..
-amount of blood ejected by the heart in one minute (N= 4-8)
SV is …
-amount of blood ejected with each beat (N= 60-150)
SV is altered by…
- preload
- contractility
- afterload
how to assess preload
- weight
- I/O
- UO
- VS
- edema
- indicator of volume
How to assess afterload
- vasoconstriction (cold and clammy)
- vasodilation (red and sweating)
- BP
- Skin assessment
- peripheral pulse (weak or bounding?)
how to assess Contractility
- Echo
what happens to vitals when preload goes down
- increased HR and decreased BP
what is CO used to evaluate
- contractility but hard to pinpoint actual cause of low CO
Things that can affect CO
- decreased contractility from direct myocardial insult (from cardiogenic shock)
- inadequate myocardial stretch from preload being too low (from hypovolemic shock)
- overstretched myocardium from preload being too high
- low afterload (vasodilation from neurogenic or spetic shock)
- high afterload (vasoconstriction)
why do we use pressure as a measurement
- because its difficult to measure volume in the ventricles so we use pressure to estimate volume
- pressure indicates stretch and volume
what measures preload
- CVP
- PAWP
what measures afterload
-SVR/PVR
How is perfusion measured
-by MAP and BP
organ perfusion measures
- RN orders to titrate
- MAP > 65 OR greater (MAP > 60 needed to perfuse and sustain vital organs)
- SBP > 90 (kidneys wont produce urine below 60)
pulse pressure
- difference between systolic and diastolic
- provides info on what peripheral vessels are doing to maintain BP
- N= 40
- <40= vasoconstriction
- > 40= vasodilation
a narrowed pulse pressure and increased heart rate indicates
hypovolemia
types of shock
- Cardiogenic: pump failure
- Hypovolemic: decrease intravascular volume
- Distributive: misdistribution of circulating blood volume
- Neurogenic shock: loss of sympathetic tone
- Anaphylactic shock: massive hypersensitivity response
- Septic shock: overwhelming inflammatory response - Obstructive: physical blockage of blood flow
cardiogenic shock
- Pump failure
- Systolic or diastolic dysfunction→ decreased stroke volume→ reduced CO
causes of cardiogenic shock
- MI (systolic dysfunction)
- Cardiac tamponade or cardiomyopathy (diastolic)
- Structural issue (valvular disorder)
- Dysrhythmia
cardiogenic shock mani
- Similar to decompensated heart failure
- Tachycardia, hypotension, narrow pulse pressure
- ↑SVR
- Increase in pulmonary wedge pressure
- Tachypnea
- Crackles
- Signs of peripheral hypoperfusion (Cyanosis, pallor, diaphoresis, weak peripheral pulses, cold/clammy skin)
- ↓urine output
- Anxiety, confusion, agitation
Hypovolemic shock
- After a loss of intravascular fluid volume, inadequate circulating volume
- Fluid deficit
Absolute hypovolemia
-loss of fluid d/t hemorrhage, GI, DI, diuresis
relative hypovolemia
-fluid out of vascular into extravascular (third spacing) d/t increased capillary permeability like in burns
patho behind hypovolemic shock
-↓intravascular ↓venous return ↓decrease preload ↓SV ↓CO
when in hypovolemic shock how much of fluid loss can the body compensate for
- 15 % (750 ml fluid loss)
*15-30% RESULTS IN SNS response: ↑HR, CO, RR
↓SV, CVP, PAP
Clinical mani: anxious and decreased UO
Class one hemorrhagic shock
-(up to 15%) ≤ 750ml, S/S-normal BP/RR/UO, HR≥100, minimal to no change, anxious
class two hemorrhagic shock
- (15-30%) 750-1500ml, ↑SNS-mediated response: S/S-Increase CO, HR 100-120, ↓PP, RR: 20-25, ↓CVP, PA pressure, U/O: 20-30ml/hr, restless
class three hemorrhagic shock
- (30-40%) 1500-2000ml, significant ↓BP, HR >120, RR: 25-30, U/O 5-15ml/hr
class four hemorrhagic shock
- (≥40%) >2000ml, S/S-DECREASED BP (SBP <90), HR>120, ↓PP, RR 30-40, U/O: minimal to no U/O, Confused, lethargy, loss of autoregulation in microcirculation and irreversible tissue destruction.
TX of class 1 and 2 hemorrhagic shock
- crystalloid fluid replacement
TX of class 3 and 4 hemorrhagic shock
- crystalloid fluid and/OR blood replacement
Distributive shock
- Misdistribution of blood flow and volume
- 3 subcategories
1. Neurogenic Shock
2. Anaphylactic Shock
3. Septic Shock
distributive neurogenic shock
- Occurs within 30 minutes of spinal cord injury and can last up to 6 weeks
- Loss of SNS vasoconstrictor with massive vasodilation (hypoperfusion)
causes of distributive neurogenic shock
- T6 or above**
- Epidural anesthesia
- Drugs (opioids/benzos)
Distributive: Neurogenic ShockClinical manifestations
- Hypotension
- Bradycardia
- Unable to regulate body temperature
- warm dry skin from pooling of blood in extremeties
Distributive: Anaphylactic Shock
- sudden Hypersensitivity reaction to a sensitizing substance
- Massive vasodilation → ↑capillary permeability→ edema→ bronchospasm
- Major increase in capillary permeability= relative hypovolemic state
causes of Distributive: Anaphylactic Shock
- Drug, chemical, vaccine, food, insect venom
- Contact, inhalation, ingestion, or injection
manifestations of Distributive: Anaphylactic Shock
- Dizziness
- Chest pain
- INC
- Swelling of lips & tongue
- Wheezing
- Stridor
- Bronchospasm
- Flushing
- angioedema
Distributive: Septic Shock
- Systemic inflammatory to a suspected infection
- Hypotension despite adequate fluid resuscitation
- Inadequate tissue perfusion
- Microorganism enters body→ normal immune response →immune response exaggerated → ↑inflammation & coagulation → microthrombi
causes of Distributive: Septic Shock
- Unknown organism 50%
- Gram-negative and gram-positive bacteria*
- Parasites, fungi, virus
manifestations of Distributive: Septic Shock
- Vasodilation
- Misdistribution of blood flow
- Myocardial depression
- May be euvolemic but d/t vasodilation become hypovolemic and hypotensive
- EF decreased first few days →ventricles dilate →maintain stroke volume
- Initially hyperventilates →respiratory alkalosis →uncompensated turns to respiratory acidosis (eventually respiratory failure)
obstructive shock
Physical obstruction to blood flow with a decrease CO
causes of obstructive shock
- Impaired ventricular filling or emptying
- Cardiac tamponade, tension pneumothorax, abdominal compartment syndrome, stenotic aortic valve, PE, right ventricular thrombi
manifestations of obstructive shock
-Decreased CO, increased afterload, jugular distension, pulsus paradoxus
pulseless paradoxus
- abnormally large drop in SBP greater than 10 with inspiration
stages of shock
- Initial stage: no clinical mani but cellular level: anerobic to aerobic met= lactic acid buildup
- Compensatory
- Progressive
- refractory
compensatory stage
Body attempts to regulate with neural, hormonal, biochemical, compensatory
how is the compensatory stage a multisystem response
- ↓CO → ↓ BP and narrow pulse pressure →activate SNS →stimulates vasoconstriction → ↑HR, contractility, BP → dilate coronary vessels because the heart is working extra hard
- ↓ BP activate SNS → angiotensin II → H2O and NA reabsorption, K excretion
- Cold and clammy skin* (except with septic shock- warm and flushed)
- Cause of shock not correct patient enters progressive stage
how long can stay in compensatory stage
- If compensatory mechanisms are supported patient can stay in this stage for hours without sustaining permanent damage
- might only see: slight increase in HR, RR, anxiety, LOC chnages
which pt have hard time tolerating compensatory mechanisms
- HTN, Elders, kids, cardiovascular disease, DM with vascular issues
- The word compensated does not mean ideal or good. It means you are holding your own, but you can get better or worse if the underlying problem does not get reversed
progressive stage
-As compensatory mechanisms fail
-Life-threatening emergency
-Massive SNS response
(Profound vasoconstriction)
-Frequently this is when patients receive interventions to prevent MODS
hallmark signs of progressive stage
-↓BP ↑RR, ↑HR, LOC listless, agitated
if there is complete deterioration of cadio system in progressive stage what signs will you have?
- decreased CO and BP
- altered CAP permeability = anasarca (diffuse profound edema)
progressive stage first system to display dysfunction
- pulmonary
- Pulmonary arteries constrict = increase PA pressure = ventilation-perfusion mismatch
- Fluid from pulmonary vasculature = interstitial space = interstitial edema = fluid to alveoli = alveoli edema and decreased surfactant production
progressive stage: cardiac
- CO drops=poor perfusion
- altered capillary permeability =fluid to interstitial space, Anasarca (diffuse profound edema)
- Weak peripheral pulses
- Dysrhythmias, MI
signs of pulmonary dysfunction in progressive stage
- tachypnea
- crackles
- poor perfusion
- increased effort with breathing
GI GUT) affects in the progressive stage -
- Prolonged decreased tissue perfusion=mucosal barrier becomes ischemic, inability to absorb nutrients
- ischemia, bleeds, ulcers, kidneys have tubular ischemia with decreased UP
GI (liver) affects in the progressive stage
- Unable to metabolize drugs/waste products, increased bilirubin, unable to remove bacteria from GI tract
- cant metabolize drugs and waste products
GU (kidneys) in progressive stage
-Renal tubular ischemia =ATN, decreased UO, metabolic acidosis
Hematologic in the progressive stage
risk for DIC
refractory stage
- decreased perfusion from peripheral vasoconstriction and decreased CO
- Lactic acid increases and fluid is leaving the vascular space causing hypotension and tachycardia.
- Profound hypotension and hypoxemia
- Failure of many organs leads to increase waste products: Lactate, urea, ammonia, carbon dioxide
can you recover from the refractory stage
-unlikely
signs of the refractory phase
-unconscious, unresponsive, BP is falling with diastolic at zero, arrythmias, resp failure, ischemia: to renal, GI, brain, cyanosis
Systemic inflammatory response syndrome (SIRS)
- Presents like sepsis but can’t isolate infectious cause
- Generalized inflammation, not necessarily at initial site
- Treatment is the same: antibiotics AND FLUIDS
Multiple organ dysfunction syndrome
- Failure of 2 or more organ systems
- Cannot maintain homeostasis
- Poor prognosis 70-80% mortality with 3+ system failures
MODS: NEURO
non responsive; coma, Glasgow coma scale
MODS: CV
vasoactive support, hypotension
MODS: HEME
platelet count decreasing
MODS: Pulmonary
mechanical ventilator
MODS: renal
CRRT, serum creatinine (increased-should be less than one), UO
MODS: Liver
coagulopathies(liver is where clotting factors are made) hypoalbuminemia, serum bilirubin
MODS: GI
not tolerate TF
MODS: skin
mottling
care for MODS
-prevent and treat infection (if present), maintain tissue oxygenation, nutritional and metabolic support, and support the individual failing organs.
SHOCK quick intervention
- Specific numbers less important than the trends
- Sooner you recognize better survival
shock: o2 and ventilation care
- Increase CO by fluid replacement
- Increase hemoglobin by whole or PRBC
- Supplemental oxygen:High flow typically or Mechanical ventilation
*want to optimize 02 delivery by making sure thye have the appropriate levels of HgB, arterial 02 sat, and CO
shock care: fluid resuscitation
-Septic, hypovolemic & anaphylactic
-Large bore IV or central venous catheter (femoral, subclavian, jugular)- 14 or 16 g
-Fluids: Crystalloids (NS or hypertonic solutions), Colloids (albumin), Blood products for
Hemoglobin <7-8
-Fresh frozen plasma (FFP) increase coagulation factors by 20%
shock care: improve perfusion
-Give drugs after adequate fluid resuscitation or for those who don’t respond to fluid (need volume to have vasoactive drugs work)
shock care: sympathomimetic drugs
- Cause peripheral vasoconstriction= increase SVR by activating catecholamines (Norepinephrine, dopamine, phenylephrine, vasopressin)
- Increase SVR can harm patient in cardiogenic shock
- Goal MAP > 65mm HG
shock care: vasodilators
- cause
- For cardiogenic shock to decrease afterload
- Nitroglycerin, nitroprusside,
- Prevention the harmful widespread vasoconstriction
- Goal MAP >65 mmHG
inotropic drugs
- increase or decrease the force of muscular contraction
Positive inotropes
- improve contractility = increases SV and myocardial 02 demand
- Epinephrine
- Norepinephrine
- Isoproterenol
- Dopamine
- Dobutamine
- Digitalis
- Calcium
negative inotropes
- reduce contractility
- Calcium channel blockers
- B-adrenergic blockers
- Clinical conditions (acidosis)
vasoactice drugs administration
- FLUIDS FIRST: otherwise just clamping down on a vessel that doesnt help perfusion
- Norepinephrine (Levophed)
- Dopamine (Intropin)
- Phenylephrine (Neo-Synephrine)
- Vasopressin (Pitressin)
What happens when you administer vasoactive agents?
- agents increase the after load (increases BP)which means the heart will need to work harder to push blood out.
- Remember you need to be careful using them on patients in cardiogenic shock.
Shock care: nutrition
- High protein High caloric
- Enteral nutrition with 24 hours (Parenteral if unable to meet at least 80% caloric requirements enterally, Slow continuous drip)
- Insulin drips in ICU to regulate blood sugar
- Insulin drips used to keep BS below 180
DX of shock
- There is not one diagnostic test to confirm shock
- Accumulation and trending values
Hemodynamic monitoring in shock
- measurement of pressure, flow and oxygenation within the cardiovascular system.
- assesses heart function, fluid balance, and effects of interventions (fluids/meds) on CO
- Both invasive and noninvasive devices can be used to assess hemodynamic status.
Hemodynamic monitoring: PAWP
-measures left ventricular end diastolic pressures if that number is high we worry about left ventricular failure
Hemodynamic monitoring: CVP
- through a triple lumen catheter and it is a measurement of preload or volume.
- A high level means volume overload
- low level means hypovolemia.
Hemodynamic monitoring: SVR
- Afterload is measured by SVR.
- pressure against left ventricle
hemodynamic monitoring: PVR
- measures afterload
- pressure against right ventricle
SCVO2
- Central venous oxygen saturation
- Derived from central venous pressure with oximetric capability
- N=70-80% indicating a stable oxygen balance
perfusion indicators: continous monitoring of venous 02 sat
indicated for the critically ill patient who has the potential to develop an imbalance between oxygen supply and metabolic tissue demand like with sepsis, ARDS, or high-risk cardiac surgery
-subtract 30 from sao2 to get SV02
SVO2
- mixed venous oxygen saturation
- derived from the pulmonary arterial catheter
- N=60-80%
Svo2/Scvo2
- If Svo2 or Scvo2 changes by more than 10% and is maintained for more than 10 minutes, then think about these four factors:
1. Arterial oxygen saturation
2. Cardiac output
3. Hemoglobin: low
4. Oxygen consumption
care for cardiogenic shock: cardiac cath (initial)
- restores BF to myocardium
- Angioplasty with stenting
- Valve replacement
- Vascular bypass
care for cardiogenic shock: most effective treatment
coronary artery reperfusion
care for cardiogenic shock: circulatory assist device
- used to decrease workload of the heart through mechanical support.
- Intra-aortic balloon pumping (IABP)
- VAD for people awaiting heart transplant
care for cardiogenic shock: Cardiogenicintra-aortic balloon pump (IABP)
- Balloon on a catheter is positioned in descending thoracic aorta.
- Inflate during diastole to increase coronary perfusion
- Deflates immediately before systole to decrease afterload
- Assist with O2 delivery to heart and increase contractility
what can cardiogenic shock lead to
- heart failure which can can be treated with a left ventricular assist device.
- People with severe heart failure have a choice they can either be put on palliative care-hospice care, get a heart transplant, or an LVAD.
cardiac pain care for cardiogenic shock
- Morphine to reduce sympathetic stimulation caused by pain/anxiety
- which decrease cardiac workload and risk associated with catecholamines
care for cardiogenic shock: decrease o2 consumption
- Sedation agents, address pain, calm environment,
- reduce fever
- Give blood, more oxygen, improve CO
cardiogenic shock: goal of drugs
- Dilating coronary arteries
1. IV nitrates (dilate coronary arteries)
2. Diuretics: ↓Preload: (lasix)
3. Vasodilators: ↓afterload: (nipride, nitroglycerin)
4. Betablockers: reduce rate, contractility
5. Inotropic agents: contractility: Doba, Epi, Milrinone
fluids with cardiogenic shock
- restrict IV fluids
- requires careful attention to the stress being placed on the heart so fluids are restricted
care for hypovolemic shock
- Stop fluid loss: bleeding
- Fluid resuscitation is a 3:1 rule (3ml if crystalloid fluids for every 1 ml of blood loss
- Blood products:
PRBCs, FFP, or platelets - 2 large bore peripheral IVs- central access if able
- May give calcium: blood loss you will also have a los of calcium which is important for the clotting cascade so Ca will also be given
- Vasoactive drugs
*FLUIDS GIVEN FIRST
septic shock care
- Large amounts of fluid replacement: 30-50ml/kg with target CVP 8-12
- Vasopressors added
- Corticosteroids if not responding to fluids and vasopressors
- Obtain blood culture, antibiotics started early
- Frequent monitoring of blood glucose (<180 mg/dL)
- Stress ulcers
*measure lactate, give fluid, get blood cultures, give antibiotics, and then give vasopressors
QSOFA
- looking at the outcome or prognosis if someone has sepsis
- BAT: blood pressure (100), altered mental status, tachypnea >22
- HAT: hypotension, altered mental status, tachypnea
care neurogenic shock
- Stabilize spine*
- Vasopressors (phenylephrine)
- Atropine (bradycardia)
- Monitor for hypothermia
care for anaphylactic shock
- First step is to prevention do a thorough history
- IM Epinephrine is 1st drug of choice: Causes peripheral vasoconstriction and bronchodilation and opposes histamine
- Adjunct Diphenhydramine and ranitidine
- Block the massive release of histamine
- Patent airway (Bronchodilators, aerosolized epinephrine to treat laryngeal edema, Endotracheal intubation or cricothyroidotomy)
care for obstructive shock
- Mechanical decompression
- Pericardial tamponade
- Tension pneumothorax
- Hemopneumothorax - PE
- Thrombolytic therapy - Abdominal
- Decompressive laparotomy: compartment syndrome
summary
- Outcome of shock are the same despite different causes (decreased tissue perfusion and altered cellular metabolism)
- Treat the cause of shock
- Fluids and drugs EXCEPT with cardiogenic shock
summary with regard to BP
arterial blood pressure is considered the gold standard.
point of BP
serves as a warning that hemodynamics may be threatened, use this parameter in addition to YOUR assessment of the patient for S/S of poor tissue perfusion
contractility: with less resistance to flow
- vasodilation
- the myocardium is less stimulated to contract and ejects with less force; BP drops and perfusion declines.
contractility: with greater resistance
- vasoconstriction
- the heart contracts with more force (using more O2 and increasing workload). Vasoconstriction helps with BP, however, a critical point is reached in which too much vasoconstriction occurs and the heart cannot overcome this resistance, and CO falls.
contractility is about
finding the perfect balance
