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Older Adults Part 3 > 5.1 Intro to Shock > Flashcards

5.1 Intro to Shock Flashcards

1
Q

Shock

A
  • 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
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2
Q

Denominators of Shock

A
  • 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
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3
Q

What Does Shock Do?

A
  • 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
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4
Q

Signs of Shock

A
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5
Q

Early Signs

A
  • Mean arterial pressure decreases by 10 mmHg from baseline
  • Increased HR
  • Effective compensation
  • O2 shunted to vital organs
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6
Q

Compensatory Signs (Non-Progressive)

A
  • Mean Arterial Pressure decreases by 10-15 mmHg from baseline
  • Decreased pulse pressure
  • Decreased pH
  • Increased Renin, ADH, Heart Rate
  • Vasoconstriction
  • Restless, Apprehensive
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7
Q

Progressive Signs (Intermediate)

A
  • Mean Arterial Pressure Decreased by 20 mmHg from baseline
  • Decreased urine (Oliguria)
  • Decreased pH
  • Tissue/Organ hypoxia
  • Weak Rapid Pulse
  • Sensory neural changes
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8
Q

Refractory Signs (Irreversible)

A
  • Excessive cell/organ damage
  • Multi-system organ failure
  • Decreased pH
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9
Q

Initial Stage of Shock

A
  • 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)
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10
Q

Compensatory Stage of Shock

A
  • 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

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11
Q

Clinical Manifestations of Shock

A

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

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12
Q

Progressive Stage of Shock

A
  • 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
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13
Q

Final Stage - Refractory Shock

A
  • 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
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14
Q

Hypovolemic Shock

A
  • 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

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15
Q

Absolute Hypovolemia

A
  • 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

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16
Q

Relative Hypovolemia

A
  • Fluid moves out of vascular spaces into extravascular space (interstitial or intracavitary spaces)
  • “Third Spacing”
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17
Q

Clinical Manifestations of Hypovolemic Shock

A
  • Anxiety/LOC changes
  • Tachypnea
  • Increased HR
  • Cool Clammy Skin
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18
Q

Care/Management of Hypovolemic Shock

A

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

19
Q

Cardiogenic Shock

A
  • 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

20
Q

Cardiogenic Shock Manifestations

A
  • 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
21
Q

Cardiogenic Shock Care

A
  • 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
22
Q

Obstructive Shock

A
  • 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
23
Q

Care/Management for Obstructive Shock

A
  • Early determination of cause is crucial
  • Oxygen and Ventilation
  • Volume resuscitation
  • Inotropic medication
  • Treat underlying cause
24
Q

Treating underlying causes

A

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)

25
Q

Distributive Shock

A

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

26
Q

Anaphylactic Shock

A
  • 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

27
Q

Anaphylactic Shock Treatment

A

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)
28
Q

Neurogenic Shock

A
  • 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)

29
Q

Neurogenic Shock Treatment

A
  • 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
30
Q

Septic Shock

A
  • 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

31
Q

Sepsis guidelines

A
  1. Initial Resuscitation
    - 30 mL/kg fluid within 3 hours
    - Norepinephrine for vasoconstriction. Goal is MAP >65 mmHg
  2. Identify source of infection ASAP and obtain 2 blood cultures before starting antibiotics.
  3. Antibiotics should be broad spectrum ASAP then assess for deescalated antibiotics
  4. Limit RBC transfusion for patients with <7 g/dL hemoglobin (unless MI, hypoxemia, acute hemorrhage)
  5. Mechanical ventilation (lower tidal volume strategy). If they are in acute respiratory distress syndrome (ARDS) then higher end expiratory pressure (PEEP)
  6. Glucose control to <180 mg/dL
  7. Enteral nutrition (tube feeding) preferred
  8. Proton Pump Inhibitors or H2 Blockers to lower risk of GI bleed
  9. Low molecular heparin for thromboembolism prophylaxis
  10. Communication with family
32
Q

SIRS (Systemic Inflammatory Response Syndrome)

A

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
33
Q

Septic Shock

A

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

34
Q

Manifestations of Septic Shock

A
  • 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)
35
Q

Septic Shock Management

A
  • ABCs
  • Fluid Resuscitation
  • Cultures
  • Antimicrobials
  • Epinephrine (vasopressor)
  • Corticosteroids
36
Q

SHOCK IN GENERAL

A

LABS
- Elevated lactate
- Lower pH increased CO2
- Decreased Hgb and Hct in Hypovolemic shock

37
Q

Care Management of Shock

A
  • 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
38
Q

Septic, Hypovolemic, Anaphylactic Shock

A
  • Cornerstone of therapy is volume expansion
  • Isotonic solution for initial treatment and if they don’t respond, blood transfusions
  • Albumin for blood expansion
39
Q

Drug Therapy

A
  • 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
40
Q

Vasodilator Therapy

A

Cardiogenic Shock - Nitroglycerin
Non-Cardiogenic Shock - Nitroprusside

41
Q

Assessment of Shock

A
  • ABCs
  • VS
  • Peripheral Pulses
  • LOC
  • Capillary Refill
  • Skin (temperature, color, moisture)
  • Urine Output
42
Q

Nursing Interventions

A
  • 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

43
Q

Nutrition

A
  • 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

Older Adults Part 3 (54 decks)

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