5.1 Intro to Shock Flashcards
Shock
- State characterized by decreased tissue perfusion and impaired cellular metabolism.
- Oxygen supply and demand imbalance and systemic response
CV System Fails Due To Alterations in
- Blood volume
- Myocardial Contractility
- Change in PVR or Tone
- WHEN ONE COMPONENT FAILS THE OTHER SYSTEMS COMPENSATE
Denominators of Shock
- Inadequate tissue perfusion causes reduction of nutritional blood flow through microcirculation
- This causes cells to swell and become more permeable which also causes electrolytes to seep in and out of the cell
- Mitochondria and lysosomes become damaged in the cell and the cell dies
What Does Shock Do?
- It affects all body systems
- Can develop slow or rapidly
- Any patient with any disease is at risk for it
- Regardless of how it happened all shock is hypoperfusion to the cells, hypermetabolism, and activation of inflammatory response
Signs of Shock
Early Signs
- Mean arterial pressure decreases by 10 mmHg from baseline
- Increased HR
- Effective compensation
- O2 shunted to vital organs
Compensatory Signs (Non-Progressive)
- Mean Arterial Pressure decreases by 10-15 mmHg from baseline
- Decreased pulse pressure
- Decreased pH
- Increased Renin, ADH, Heart Rate
- Vasoconstriction
- Restless, Apprehensive
Progressive Signs (Intermediate)
- Mean Arterial Pressure Decreased by 20 mmHg from baseline
- Decreased urine (Oliguria)
- Decreased pH
- Tissue/Organ hypoxia
- Weak Rapid Pulse
- Sensory neural changes
Refractory Signs (Irreversible)
- Excessive cell/organ damage
- Multi-system organ failure
- Decreased pH
Initial Stage of Shock
- Cellular response to low oxygen
- USUALLY NOT CLINICALLY APPARENT
- No visible changes
- HIGH INDEX OF SUSPICION
- Impaired oxygen perfusion
- Impaired cellular metabolism and oxygen/glucose use
- NA moves into cell and K moves out which alters nervous, CV, and muscular cell function
- Change in circulating volume, cardiac function, and post-void residual (PVR)
Compensatory Stage of Shock
- Body attempts to increase cardiac output and restore perfusion/oxygenation.
Compensation for water drawn into cells
- Water is drawn from vascular space
Compensation for low BP
- Vasoconstriction, renin system activated
- GI system is shut off
- Shunting of blood to vital organs
- Blood shunted from lungs causes increased respiration rate, depth and decrease in SPO2
Shift from aerobic to anaerobic metabolism causes lactic acid buildup and metabolic acidosis. This causes cellular damage and altered glucose metabolism
CNS System
- Baroreceptors sense low bp and stimulate catecholamine release
- Increased HR, CO, BP means increased myocardial oxygen demand
- Decreased urinary output
Clinical Manifestations of Shock
Neurological
- Altered mental status
- Irritability
- Seizure/Coma
Pulmonary
- Increased RR
- Crackles from fluid shift
- Decreased O2 sat despite increase in o2 administration
Cardiovascular
- Increased HR
- Dysrhythmias
- Decreased/absent peripheral pulses
GI
- N/V
- Absent bowel sounds
Genitourinary
- Decreased urinary output
- Increased specific gravity
Integumentary
- Cool clammy skin
- Mottling
- Cyanosis
- Development of pressure injuries
Musculoskeletal
- Generalized Weakness
- Wasting
- Inability to wean from ventilator due to wasting
Progressive Stage of Shock
- Compensatory mechanisms begin to fade
- If oxygen debt is not corrected permanent damage will start to occur
- Eventually compensation will fail
Fluid Movement
- Altered capillary permeability leads to interstitial edema which affect organs and peripheral tissue
- Further decrease in vascular volume
- Pulmonary edema, bronchoconstriction, decreased surfactant, tachypnea, crackles, increased workload of breathing (WOB)
CO Failure
- Decreased peripheral perfusion, hypotension, weak pulses and ischemia
- Vasoconstriction causes further injury
Renal System Impaired
- UO decreases, kidneys may not be able to detox body from anaerobic metabolism (lactic acid)
- Acute tubular necrosis and acute renal failure
GI system shuts down
- Risk of ileus, ulcers, bleeding, translocation of bacteria
- Liver failure - Risk of DIC and bleeding
- Muscle breaks down into amino acids causing muscle wasting
- Brain requires the most glucose/oxygen from the body so neurological issues
- Acute lung injury
- Further myocardial dysfunction
- Multiple Organ Dysfunction Syndrome (MODS)
- TIME IS VERY IMPORTANT HERE, IF NOT CORRECTED WITHIN HOURS PATIENT WILL DIE
Final Stage - Refractory Shock
- Irreversible shock - Total Body Failure
- Too much cell death and tissue damage where organs are overwhelmed
- Exacerbation of anaerobic metabolism causing accumulation of lactic acid
- Profound hypoxemia and hypotension
- Decreased coronary blood flow
- Cerebral ischemia
- Failure of one organ system leads to failure of others
- Recovery unlikely
Hypovolemic Shock
- Loss of blood volume in vascular spaces causes decrease in MAP (5-10 below baseline) and loss of oxygen carrying capacity due to loss of circulating RBC’s
- Needs to reversed within 1-2 hours of onset
STEPS
- Decreased intravascular volume
- Decreased venous return
- Decreased stroke volume
- Decreased cardiac output
- Decreased tissue perfusion
Absolute Hypovolemia
- Loss of intravascular fluid volume
- Decreased MAP slows tissue perfusion which causes lactic acidosis
Causes
- Hemorrhage
- Trauma injury/burns
- Fistula drainage, vomiting, diarrhea
- Diabetes insipidus
- Diabetic Ketoacidosis
- Diuresis
Relative Hypovolemia
- Fluid moves out of vascular spaces into extravascular space (interstitial or intracavitary spaces)
- “Third Spacing”
Clinical Manifestations of Hypovolemic Shock
- Anxiety/LOC changes
- Tachypnea
- Increased HR
- Cool Clammy Skin
Care/Management of Hypovolemic Shock
FOCUSED ON
- Stopping fluid loss
- Restoring circulating volume
- Generally can be corrected with crystalloid fluid in early stages
INTERVENTIONS
- Oxygenation
- Rapid fluid replacement (2 IVs until CVP is 15 mmHg or PAWP (pulmonary arterial wedge pressure) is 10-12 mmHg
- Fluid Replacement 3:1 rule 3 mL isotonic crystalloid for every 1 mL of estimated blood loss.
- MOST COMMON SOLUTION IS 5% ALBUMIN
- If blood loss >30% blood volume is replaced
- USE WARMED FLUIDS
Cardiogenic Shock
- The actual heart muscle is impaired, pumping is directly impaired causing decreased CO. Can be systolic or diastolic dysfunction
CAUSES
- MI is the most common cause
- Cardiomyopathy
- Blunt cardiac injury
- Severe hypertension
- Cardiac tamponade
- Myocardial depression from metabolic problems
Cardiogenic Shock Manifestations
- Tachycardia
- Hypotension (less than 90 mmHg or 30 mmHg below baseline)
- Narrowed pulse pressure
- Increased myocardial o2 consumption
- UO <30 mL/Hr
- Restlessness
- Pulmonary Congestion
- Tachypnea
- Continued Chest Pain
Cardiogenic Shock Care
- Restore blood flow to myocardium by restoring O2 supply and demand
- PRIMARY GOAL IS OXYGENATION NEEDS NOT LIMITING MYOCARDIAL DAMAGE
- Thrombolytics, angioplasty with stenting, revascularization (emergency)
- Valve replacement
- Hemodynamic monitoring
- Diuretics to reduce preload
- Oxygenation
- Correct EKG changes
Obstructive Shock
- Physical obstruction of circulation to or from the heart.
CAUSES
Prevents blood from entering right heart during diastole
- Tension pneumothorax
- Pericardial Tamponade
Prevents blood from ejecting
- Pulmonary embolism
- Left ventricular outflow obstruction
- Critical Aortic Stenosis or coarctation of the aorta
Care/Management for Obstructive Shock
- Early determination of cause is crucial
- Oxygen and Ventilation
- Volume resuscitation
- Inotropic medication
- Treat underlying cause
Treating underlying causes
Tension Pneumothorax
- Oxygen and needle decompression or chest tube
Pericardial Tamponade
- Pericardiocentesis
Pulmonary Embolism
- Anticoagulation (thrombolytics)
Left Ventricle Outflow Obstruction
- Can be treated with medication but usually definitive treatment is surgery (such as replacement of stenotic aortic valve)
Distributive Shock
STEPS
- Event
- Vasodilation
- Activation of inflammatory process
- Maldistribution of intravascular volume
- Decreased venous return
- Decreased cardiac output
- Decreased tissue Perfusion
3 Types
- Anaphylactic Shock
- Neurogenic Shock
- Septic Shock
Anaphylactic Shock
- Type 1 hypersensitivity to an allergen which occurs in seconds to minutes
- Massive vasodilation, release of mediators, increased capillary permeability and bronchoconstriction causing respiratory distress
Causes
- Parenteral route more often than oral or topical
Manifestations
- Anxiety, confusion, dizziness
- Sense of impending doom
- Chest pain
- Incontinence
- SWELLING OF LIPS AND TONGUE
- WHEEZING/STRIDOR
- FLUSHING, PRURITIS, URTICARIA (hives)
- Respiratory distress from laryngeal edema or severe bronchoconstriction
- Circulatory failure from severe vasodilation
Anaphylactic Shock Treatment
MAINTAIN AIRWAY
- Nebulized bronchodilators
- Endotracheal tube
- Epinephrine, Diphenhydramine
- Aggressive fluid replacement
- IV corticosteroids for significant hypotension after 1-2 hours of aggressive therapy
- Adrenalin, Benadryl, Corticosteroids
- H2 Blocker (Ranitidine and Famotidine)
- PPI (Omeprazole)
Neurogenic Shock
- Usually caused within 30 minutes of spinal cord injury leading to loss of sympathetic nervous system signals
- Vasodilation which causes hypoperfusion and damage to cellular metabolism
- Can also be caused by spinal anesthesia
- MASSIVE HYPOTENSION
Clinical Manifestations
- Hypotension due to vasodilation
- Bradycardia due to unopposed parasympathetic stimulation
- Temperature drop due to heat loss
- Dry Skin (NOT CLAMMY)
- Poikilothermia (Taking temperature of the environment)
Neurogenic Shock Treatment
- ABC’s
- Immobilization
- Cautious Fluid Replacement
- Vasopressors or Atropine (administered for bradycardia)
- IV corticosteroids
INITIAL MANAGEMENT IS FLUID RESUSCITATION AND VASOPRESSORS
- BLOOD PRESSURE GOALS ARE DIFFERENT THAN SEPTIC SHOCK
- Target MAP of 85-90 mmHg greater
- Fluid replacement should be monitored closely because fluid overload can cause more damage to spinal cord swelling
- Phenylephrine avoid due to reflex bradycardia
- Dopamine and epinephrine is choice of drug
- Pacemaker may be required if heart block occurs
Septic Shock
- Most commonly caused by respiratory tract infections (pneumonia) and have the highest mortality rate.
- Mortality rates increase by 7% for every hour antibiotics are delayed.
SEPSIS SCREENING
- Systemic Inflammatory Response Syndrome (SIRS)
- Infection
- Organ Dysfunction
Sepsis guidelines
- Initial Resuscitation
- 30 mL/kg fluid within 3 hours
- Norepinephrine for vasoconstriction. Goal is MAP >65 mmHg - Identify source of infection ASAP and obtain 2 blood cultures before starting antibiotics.
- Antibiotics should be broad spectrum ASAP then assess for deescalated antibiotics
- Limit RBC transfusion for patients with <7 g/dL hemoglobin (unless MI, hypoxemia, acute hemorrhage)
- Mechanical ventilation (lower tidal volume strategy). If they are in acute respiratory distress syndrome (ARDS) then higher end expiratory pressure (PEEP)
- Glucose control to <180 mg/dL
- Enteral nutrition (tube feeding) preferred
- Proton Pump Inhibitors or H2 Blockers to lower risk of GI bleed
- Low molecular heparin for thromboembolism prophylaxis
- Communication with family
SIRS (Systemic Inflammatory Response Syndrome)
2 or more variables
- Temp greater than 100.4 or less than 96.8
- HR greater than 90
- Respiratory rate >20
- WBC >12,000 or <4,000
- Immature neutrophil bands (>10%)
Does the patient have a documented infection, being treated for an infection, pneumonia. Is WBC found in normally sterile fluid, does the patient have a perforated hollow organ (bowel)
Acute Organ Dysfunction Criteria
Cardiovascular - Hypotension
Respiratory - Increasing O2 requirements
Renal - Decreasing Urine Output
Hematologic - Coagulopathies
Metabolic - Lactate >4
Hepatic - Elevated LFT (liver function tests)
CNS - Change in mental status
- MUST BE A NEW DYSFUNCTION FOR PATIENT NOT PATIENTS WITH EXISTING DEFICITS SUCH AS CHRONIC DIALYSIS, DEMENTIA, HOME OXYGEN DEPENDANT
Septic Shock
Sepsis - Systemic inflammation response due to infection
- Severe Sepsis - Sepsis with organ dysfunction
- Septic Shock - Sepsis, hypotension despite fluid resuscitation, tissue perfusion abnormalities.
Septic Shock
- Exaggerated response to infection resulting in coagulation, inflammation, and decrease in fibrinolysis
- PREVENTION IS BEST MANAGEMENT
Manifestations of Septic Shock
- Increased coagulation and inflammation
- Decreased fibrinolysis (thrombi formation, obstructed microvasculature)
Hyperdynamic State - Increased CO and Decreased SVR
- Tachypnea and hyperventilation (which can lead to respiratory alkalosis, once respiratory system fails can lead to acidosis)
Septic Shock Management
- ABCs
- Fluid Resuscitation
- Cultures
- Antimicrobials
- Epinephrine (vasopressor)
- Corticosteroids
SHOCK IN GENERAL
LABS
- Elevated lactate
- Lower pH increased CO2
- Decreased Hgb and Hct in Hypovolemic shock
Care Management of Shock
- Identify patients in shock
- Establish early diagnosis and move quickly
- Eliminate cause of decreased perfusion
- Protection of organs from dysfunction
- CALL RAPID RESPONSE TEAM EARLY
Septic, Hypovolemic, Anaphylactic Shock
- Cornerstone of therapy is volume expansion
- Isotonic solution for initial treatment and if they don’t respond, blood transfusions
- Albumin for blood expansion
Drug Therapy
- Reach MAP of 60-65 mmHg
- Vasopressors
- Vasoactive medication if fluid therapy alone does not maintain MAP
- Check VS every 15 minutes
- Medication should be given through central line if possible due to risk of extravasation causing damage
Vasodilator Therapy
Cardiogenic Shock - Nitroglycerin
Non-Cardiogenic Shock - Nitroprusside
Assessment of Shock
- ABCs
- VS
- Peripheral Pulses
- LOC
- Capillary Refill
- Skin (temperature, color, moisture)
- Urine Output
Nursing Interventions
- Respiratory status
- Neurologic Status (LOC)
- Cardiac Status (ECG, VS, Heart Sounds, MAP via arterial line, Pulmonary Artery Catheter)
Hemodynamic Monitoring
- Invasive measurements of systemic, pulmonary arterial, and venous pressures
- MAP of 70 mmHg is reasonable target
Nutrition
- Vital to decrease morbidity of shock
- Enteral nutrition for the first 24 hours
- Parental nutrition if failure to meet 80% of caloric requirements
- Early feedings maintain perfusion to GI tract to maintain GI mucosa integrity
- Nutrition to prevent further catabolism due to depleted glycogen
