Shock

Priority actions for first hour of diagnosis of sepsis

measure lactate level
obtain blood cultures before administering antibiotics
administer broad-spectrum antibiotics within the first hour while you are waiting for culture results
begin rapid administration of 30 ml/kg crystalloid for hypotension or lactate >4 mmol/L
apply vasopressors if hypotensive during or after fluid resuscitation to maintain a map > 65

Priority interventions for various shocks (incl. meds)

Kinds of shock: cardiogenic, hypovolemic, obstructive, & distributive (septic, neurogenic, & anaphylactic)

-add in distributive shock-

Hypovolemic Shock:

Non-surgical: fluid, meds, oxygen, IABP etc.
- Oxygen therapy is used at any stage of shock
- IV fluids is the primary intervention for hypovolemic shock
- Crystalloid and colloids are often used
- Crystalloid solutions contain minerals, salts, sugars; help to maintain F&E balance (LR and NS)
- Colloid solutions contain large molecules or protein or starches (PRBCs, plasma)
- Drug therapy is used in addition to fluid therapy when volume loss is severe and the patient does not respond sufficiently to fluid replacement and blood products
- Vasoconstrictors (epi/NE) - improve MAP
- Inotropes (dobutamine, epi, NE) - improve cardiac contractility
- Sodium Nitroprusside - improve myocardial perfusion
- Monitoring vitals and LOC is a major nursing action
- Can only be done by RN for shock patients, not UAP or LPN!
- Assess every 15 minutes until shock is controlled and patient’s condition has improved
- Hemodynamic monitoring can be used in critical care settings (IAPB)
Surgical
- May be needed in addition to nonsurgical management to correct the cause of shock
- Vascular repair
- Surgical hemostasis of major wounds
- Closure of bleeding ulcers
- Chemical scarring of varicosities
- CHECK THEIR PULSE OFTEN → NOTICE THE QUALITY OF THE PULSE → TELL TALE SIGN OF POSSIBLE SHOCK

Septic Shock

Interventions for septic shock focus on identifying the problem as early as possible, correcting the conditions causing it, and preventing complications
SHOCK SIGNS AND SYMPTOMS HAVE TO DO WITH THE BODY'S COMPENSATORY MECHANISMS TO CORRECT THE SHOCK
Sepsis resuscitation bundle
- Within first 3 hours of suspecting severe sepsis:
- Measure serum lactate levels
- Obtain blood cultures before administering antibiotics
- Administer broad spectrum antibiotics
- Administer 30 mL/kg crystalloids intravenously for hypotension or lactate ≥4 mmol/L
- Within 6 hours of initial indications of suspected septic shock:
- Administer prescribed vasopressors for hypotension that does not respond to fluid resuscitation measures to maintain MAP ≥65 mmHg
- If arterial hypotension persists despite initial fluid resuscitation or lactate remains ≥4 mmol/L, reassess volume status and tissue perfusion and document findings
- Remeasure lactate level
- Document reassessment of volume status and tissue perfusion with either
- Repeat focused examination including VS, cardiopulmonary, cap refill, pulse, and skin findings
- OR two of the following:
  - Measure CVP
  - Measure Central venous O2 sat
  - Beside cardiovascular ultrasound
  - Dynamic assessment of fluid responsiveness with passive leg raise or fluid challenge
Oxygen therapy is useful whenever poor tissue perfusion and poor gas exchange are present
Drug therapy to
enhance CO and restore vascular volume are the same as those used in hypovolemic shock
Drug therapy to combat sepsis, adrenal insufficiency, hyperglycemia, and clotting problems is also needed
Gram-negative bacteria are the most common agents, NPSGs require that antibiotics that are active against gram-negative bacteria are given before organisms are identified, preferable within 1 hour of sepsis diagnosis
Adrenal insufficiency may be caused by the severe stress sepsis causes, low dose corticosteroids may be needed - IV hydrocortisone and oral fludrocortisone
Patients typically have elevated blood glucose, which is associated with a poor outcome, insulin therapy is needed to keep levels between 110-150
Microvascular abnormalities and the formation of small clots occur, give heparin to limit inappropriate clotting
Blood replacement therapy is used when clotting with hemorrhage occurs and may include clotting factors, platelets, FFP, or PBRCs

Cardiogenic Shock

Class IV Heart failure
Necrosis of more than 40% of the LV
Monitor, report, and document manifestations of cardiogenic shock immediately:
- Tachycardia
- Hypotension
- SBP less than 90 mm Hg or 30 mm Hg less than baseline
- Urine output less than 0.5-1 mL/kg/hr
- Cold, clammy skin with poor peripheral pulses
- Agitation, restlessness, or confusion
- Pulmonary congestion
- Tachypnea
- Continuous chest discomfort
Early detection is essential due to the high mortality rate
Interventions aim to relieve pain and decrease myocardial oxygen demand
IV morphine to decrease pulmonary congestion and relieve pain
O2 is administered, intubation and mechanical ventilation may be necessary
Immediate reperfusion is an invasive intervention that shows some promise for managing cardiogenic shock (immediate left-sided cardiac cath)
- If the occlusion(s) are treatable, PCI or CABG is performed ASAP

Dobutamine!!!

WHAT ARE SOME INTERVENTIONS AND PRIORITIES THAT ARE DIFFERENT BETWEEN THE DIFFERENT TYPES OF SHOCK? → Oxygen is always first

WHAT IS THE RECOMMENDED FLUID VOLUME TO GIVE FOR SEPTIC SHOCK WITHIN THE FIRST THREE HOURS? HOW MUCH WOULD THAT BE FOR A 75KG MAN?

Give 30 mL/kg of crystalloids
75 x 30 = 2,250 mL

RECOGNIZE MODS AND DIC

MODS

Multiple organ dysfunction syndrome
Vicious cycle, dead cells open and release metabolites
Microthrombi form, which block tissue perfusion and damage more cells, continuing the cycle
Liver, heart, brain, and kidney functions are lost first
- Most profound change is to cardiac muscle
Signs are rapid loss of consciousness, shallow respirations, unmeasurable O2 sat
Therapy, including fluid replacement, is not effective in saving the patient’s life, even if the cause of shock is corrected and MAP temporarily returns to normal

Recognize hypovolemic shock

Hypovolemic Shock

Overall cause: total body fluid decreased
Risk factors/causes:

HemorrhageTraumaGI ulcerSurgeryInadequate clottingHemophiliaLiver diseaseCancer therapy	Anticoagulation therapy DehydrationVomitingDiarrheaHeavy diaphoresisDiureticsNG suctionDI (diabetes insipidus)

Recognize stages of the various shocks

Initial stage

baseline MAP is decreased by less than 10. Compensatory mechanisms are effective at returning systolic pressure to normal at this stage; oxygen perfusion to vital organs is maintained.
there is increased anaerobic metabolism in some tissues with production of lactic acid but overall metabolism is still aerobic
AKA → no visible changes in client parameters; only changes on the cellular level
1. Compensatory stage

MAP decreases by 10-15 from baseline
kidney and hormonal compensatory mechanisms are activated because cardiovascular responses alone are not enough to maintain MAP and supply oxygen to vital organs
Decrease in MAP causes release of renin, ADH, aldosterone, epinephrine, and norepinephrine to start kidney compensation - Urine decreases, sodium reabsorption increases, blood vessel constriction occurs
tissue hypoxia occurs in less vital organs (skin, GI) and kidney - increase metabolites from anaerobic metabolism causes acidosis and increased K+

1. s/s from poor perfusion - increased thirst and anxiety, restless, tachy, fast respirs, decreased output, decreased pulse pressure, increase diastolic, decreased systolic, decreased oxygen sat

AKA → measures to increase CO to restore tissue perfusion and oxygenation
1. Progressive stage

sustained decrease in MAP of more than 20
compensatory mechanisms are functioning but no longer deliver sufficient oxygen even to vital organs
vital organs become hypoxic and non vital are anoxic (no o2) and ischemic
s/s - impending doom feeling, confusion, increased thirst, rapid weak pulse, low bp, pallor to cyanosis of oral mucosa and nail beds, cool moist skin, anuria, 5-10% o2 decrease, low pH, rising lactic and potassium
AKA → compensatory mechanisms begin to fail
1. Refractory stage

too much cell death and tissue damage resulting from too little oxygen reaching tissues - vital organs have too much damage and don’t respond effectively to interventions, so the damage continues
cell damage caused by massive release of toxic metabolites and enzymes is termed multiple organ dysfunction syndrome (MODS)
As more cells get damaged, more metabolites are released which trigger small clots to form which block tissue perfusion and damage more cells – this is a continuing cycle. Liver heart, brain, and kidney functions are lost first - most damage to heart
s/s rapid loss of consciousness, nonpalpable pulse, cold, dusky extremities, slow shallow respirs, unmeasurable o2 sat (fluid replacement is not effective)
AKA → irreversible shock & total body failure
keep giving blood, fluids, vasopressors

Expected findings with DIC (Disseminated intravascular coagulation)

Widespread microthrombi formation, which consumes many of the available platelets and clotting factors faster than they are able to be reproduced → eventually leads to poor clotting ability
Amplified Systemic Inflammatory Response Syndrome (SIRS) and cytokine release increase capillary leakiness, cause cell injury, and increase cellular metabolism
Continued stress response triggers continued release of glucose from the liver → hyperglycemia
Damage to endothelial cells reduce anti-clotting actions and triggers the formation of even more microthrombi, increasing DIC
Excessive clotting in DIC causes the formation of microthrombi in the liver, kidney, brain, spleen, and heart → widespread hypoxia and ischemia
Poor clotting abilities occur in the septic shock stage
- Hemorrhage + continuous capillary leak → hypovolemia, decreased CO, decreased BP, decreased pulse pressure
- Petechiae and ecchymoses
- Low H&H, fibrinogen, platelets counts
- Blood may ooze from gums and other mucous membranes as well as IV sites

Know sepsis

extreme response to infection that can cause tissue damage, organ failure, and death if not treated
normal infection - local inflammation to confine and eliminate the organism and prevent the infection from becoming worse or widespread
- wbc secrete cytokines to trigger local inflammation and bring more wbcs to kill invading organisms - this constricts small veins and dilate the arterioles in the area which increases perfusion to locally infected tissues
- capillary leak occurs, allowing plasma to leak into tissues causing edema - inflammation normally subsides within a few days when infection has been managed - no fever, tachy, decreased o2 or reduced output with this
sepsis occurs when infectious organism enters blood stream and causes infection
- as infection spreads, there's widespread inflammation aka systemic inflammatory response syndrome (SIRS) - with the organisms and toxins in the bloodstream and spreading, inflammation becomes an enemy leading to extensive hormonal, tissue, and vascular changes and oxidative stress that further impairs gas exchange and tissue perfusion
- s/s mild hypotension, low urine output, increased respirs - result in a hypodynamic state with decreased cardiac output - body temp varies based on duration and wbc function
- inappropriate clotting with microthrombi form in organ capillaries causes hypoxia and reduce organ function (reversible if sepsis caught at this stage)
- this creates a constant cycle of poor perfusion and gas exchange
- as sepsis continues many tissues and organs become hypoxic and microthrombi are forming everywhere using up the platelets and clotting factors aka disseminated intravascular coagulation (DIC)
- anaerobic metabolism continues and cell uptake of oxygen is poor - stress response is triggered and glucose is released from the liver and causes hyperglycemia
- at early stage - fast heart rate, higher systolic, poor o2, WBC may be low (prolonged infection, cannot produce more), rapid respirs, decreased output