SLOs for Shock and DIC

shock and its underlying pathophysiology

drop in blood flow and oxygen to vital organs, perfusion stops and cells become hypoxic → organs die

cells switch from aerobic to anaerobic metabolism (without oxygen) → lactic acid production as liver is unable to process → cells cease and swells/leaky

1. septic: type of distrubutive

2. hypovolemic: low blood volume, could be blood loss, low perfusion, and/or fluid loss (like burns)

3. cardiogenic: impaired cardiac output due to heart not pumping appropriately

4. anaphylactic: type of distributive

5. neurogenic: type of distributive

compare signs/symptoms of compensatory, progressive, and irreversible stages of shock along with treatment for each stage

inital: decreased CO, decreased BP, patient becomes acidotic, elevated lactate level (normal: 0.5-1)

→ treat underlying cause, lab work, IV fluids, and oxygen

compensatory: stimulation of sympathetic nervous system, epi/norepinephrine released, increase in HR/RR/CO/perfusion, blood is shunted away from kidneys/GI system (decreased urine output, Na/water retention, oliguria, increased BUN/Cr), cool/pale extremities, changes in mental status, tachypnea and hypoxia, blood pressure is normal

→ address underlying issue

progressive: damage to vessels cause micro clots to form (if runs out causes DIC), complete drop in CO → MODS, dysrrhythmias and MI, increased ammonia and bilirubin, massive edema, ARDS, lethargic

→ oxygen, IV fluids, vasopressors

refractory: irreversible damage, MODS occured → respiratory failure/ARDS, cardiovascular instability, hypermetabolic state, liver/renal dysfunction, hematologic dysfunction, coma

→ ventilation, IV fluids, vasoconstrictive agents, dialysis, bleeding precautions, end of life care, pallative care

vasoactive agent used in treatment of shock and nursing implications associated with their use

1. inotropic agents (dobutamine, dopamine, epinephrine, milrinone) → improves contractility, increases stroke volume/cardiac output (however increases oxygen demand of the heart)

2. vasodilators (nitroglycerin, nitroprusside) → reduces preload/afterload, reducing oxygen demand of the heart (can cause hypotension)

3. vasopressor agents (norepinephrine, dopamine, phenylephrine, vasopressin, epinephrine, angiotensin II) → increases blood presure by vasoconstriction (increases afterload, cardiac workload, compromise perfusion to skin/kidneys/lungs/GI tract)

similarities and differences between the types of shock

1. cardiogenic → heart unable to circulate blood

tx: ECG 12 lead, trend troponins/CKMB, diuretics, intra-aortic balloon pump

2. hypovolemic → low fluid volume, cool/clammy skin in compensatory stage

tx: IV fluids of NS or LR, blood transfusion

3. septic → release of inflammatory cytokines, causing vasodilation and hypovolemia

tx: blood cultures, IV antibiotics, inotropes, steroids (decrease inflammation)

4. neurogenic → sympathetic nervous system loses ability to stimulate nerve impulses that causes massive vasodilation

tx: atropine (increases HR), c-spine precautions, warming device, foley catheter placement, DVT prophylaxis with sequential compression devices and SQ heparin)

5. anaphylactic → body releases histamines due to allergen either anaphylactic or anaphylactoid, cool/clammy in compensatory stage

tx: avoid allergen, epinephrine, monitor airway, albuterol/nebulizer (open airways), antihistamines (benadryl), corticosteroids (decrease inflammation)

describe multiple organ dysfunction syndrome (MODS) and its relation to shock

dysfunction of 2 or more organs, body is no longer able to compensate that leads to drop in cardiac output → organ shut down

- lungs → respiratory failure/ARDS

- cardiovascular instability

- hypermetabolic state → hyperglycemia and hyper lactic acidemia

- renal and liver dysfunction

- hematologic dysfunction → risk of bleeding

- neuro response → coma

understand the pathophysiology of disseminated intravascular coagulation (DIC)

widespread platelet aggregation causing obstruction of blood flow and bruising seen in tissues that is followed by massive bleeding, resulting in consumption of all clotting factors leading to hemorrhaging

lab values common with DIC

1. INR or PT prolongation → no clotting factors present

2. fibrinogen

3. D-dimer → protien fragment produced when blood clot forms

4. platelets

identify clinical manifestations and nursing interventions to treat DIC

s/s:

- bleeding around wounds/surgical sites/blood draws

- bleeding from gingiva, rectum, vagina, and catheters

- ecchymosis, hematomas, petechiae

- oliguria, anuria, hematuria

- dyspnea, cyanosis, hemoptysis (from pulmonary hemorrhage or embolism)

- mental status changes

- hypovolemia, hypotension, decreased CO, tachycardia

interventions:

- platelets, plasma, and prothrombin transfusions

- administer heparin or low molecular weight heparin

- draw lab work Q6hrs to check on clotting factors

- treat underlying cause (ex: infection if caused by sepsis)