Shock

Presenter :Dr . Mostafa Shokati

Post Doctoral (PDF) in cardiac critical care

What is shock?

Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism

Imbalance in supply/demand for O2 and nutrients

Inadequate cellular oxygenation ◦ Oxygen delivery equation

◦ DO2 = CaO2 x Q

◦ CaO2 = (1.34 x Hgb x SaO2) + (0.003 x PaO2)

◦ Q = HR x SV

Pathophysiology of Shock

Classification of shock

◦Low blood flow

◦Cardiogenic

◦Hypovolemic

◦Maldistribution of blood flow

◦Septic

◦Anaphylactic

◦Neurogenic

Low Blood FlowCardiogenic Shock

Definition

◦ Systolic or diastolic dysfunction

◦ Compromised cardiac output (CO)

Precipitating causes

◦ Myocardial infarction

◦ Cardiomyopathy

◦ Blunt cardiac injury

◦ Severe systemic or pulmonary hypertension

◦ Cardiac tamponade (Obstructive)

◦ Myocardial depression from metabolic problems

Early manifestations

◦ Tachycardia

◦ Hypotension

◦ Narrowed pulse pressure

◦ ↑ Myocardial O2 consumption

Physical examination

◦ Tachypnea, pulmonary congestion

◦ Pallor; cool, clammy skin

◦ Decreased capillary refill time

◦ Anxiety, confusion, agitation

↑ in pulmonary artery wedge pressure

Decreased renal perfusion and UO

Hypovolemic Shock

Absolute hypovolemia: Loss of intravascular fluid volume

◦ Hemorrhage

◦ GI loss (e.g., vomiting, diarrhea)

◦ Fistula drainage

◦ Diabetes insipidus

◦ Hyperglycemia

◦ Diuresis

Relative hypovolemia

◦ Results when fluid volume moves out of the vascular

space into extravascular space

◦ Termed third spacing

Hypovolemic Shock (Cont’d))

Clinical manifestations

Anxiety

Tachypnea

Increase in CO, heart rate

Decrease in stroke volume, PAWP, UO

If loss is >30%, blood volume is replaced

Maldistribution of Blood FlowNeurogenic Shock

Hemodynamic phenomenon that can occur

within 30 minutes of a spinal cord injury

at the fifth thoracic (T5) vertebra or above

and

can last up to 6 weeks

Results in massive vasodilation leading to

pooling of blood in vessels

Neurogenic Shock (Cont’d)

Clinical manifestations

◦ Hypotension

◦ Bradycardia

◦ Temperature dysregulation (resulting in heat loss)

◦ Dry skin

◦ Poikilothermia (taking on the temperature of the

environment)

Anaphylactic Shock

Acute, life-threatening hypersensitivity

reaction

◦Massive vasodilation

◦Release of mediators

◦ ↑ Capillary permeability

Anaphylactic Shock (Cont’d)Clinical manifestations

◦ Anxiety, confusion, dizziness

◦ Tachycardia, tachypnea, hypotension

◦ Wheezing, stridor

◦ Sense of impending doom

◦ Chest pain

◦ Swelling of the lips and tongue, angioedema

◦ Wheezing, stridor

◦ Flushing, pruritus, urticaria

◦ Respiratory distress and circulatory failure

Septic Shock

Sepsis: Systemic inflammatory response to documented or suspected infection

Severe sepsis = Sepsis + Organ dysfunction

Septic shock = Presence of sepsis with hypotension despite fluid resuscitation + Presence of

tissue perfusion abnormalities

Mortality rates as high as 50%

Primary causative organisms

◦ Gram-negative and gram-positive bacteria

◦ Endotoxin stimulates inflammatory response

◦ Septic shock = Presence of sepsis with hypotension despite fluid resuscitation + Presence of tissue perfusion abnormalities

Pathophysiology of Septic Shock

Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

Clinical manifestations◦ ↑ Coagulation and inflammation

◦ ↓ Fibrinolysis

◦ Formation of microthrombi

◦ Obstruction of microvasculature

◦ Hyperdynamic state: Increased CO and decreased SVR

◦ Tachypnea/hyperventilation

◦ Temperature dysregulation

◦ ↓ Urine output

◦ Altered neurologic status

◦ GI dysfunction

◦ Respiratory failure is common

Stages of ShockInitial Stage

Usually not clinically apparent

Metabolism changes from aerobic to anaerobic

◦Lactic acid accumulates and must be removed by blood and

broken down by liver

◦Process requires unavailable O2

Compensatory Stage (Nonprogressive)

Clinically apparent

◦ Neural

◦ Hormonal

◦ Biochemical compensatory mechanisms

Attempts are aimed at overcoming consequences of anaerobic metabolism and

maintaining homeostasis

If deficit not corrected, patient enters progressive stage

Baroreceptors in carotid and aortic bodies activate SNS in response to ↓ BP

◦ Vasoconstriction while blood to vital organs maintained

↓ Blood to kidneys activates renin–angiotensin system

◦ ↑ Venous return to heart, CO, BP

If perfusion deficit corrected, patient recovers with no residual sequelae

Progressive Stage (intermediate)

Begins when compensatory mechanisms fail

Aggressive interventions to prevent multiple organ dysfunction syndrome

Hallmarks of ↓ cellular perfusion and altered capillary permeability:

◦ Leakage of protein into interstitial space

◦ ↑ Systemic interstitial edema

Anasarca (severe generalized edema)

◦ Fluid leakage affects solid organs and peripheral tissues

◦ ↓ Blood flow to pulmonary capillaries

Movement of fluid from pulmonary vasculature to interstitium

◦ Pulmonary edema

◦ Bronchoconstriction

◦ ↓ Residual capacity

Progressive Stage Cont’d)

Fluid moves into alveoli

◦ Edema

◦ Decreased surfactant

◦ Worsening V/Q mismatch

◦ Tachypnea

◦ Crackles

◦ Increased work of breathing

CO begins to fall

◦ Decreased peripheral perfusion

◦ Hypotension

◦ Weak peripheral pulses

◦ Ischemia of distal extremities

Progressive Stage (Cont’d)

Myocardial dysfunction results in

◦ Dysrhythmias

◦ Ischemia

◦ Myocardial infarction

◦ End result: Complete deterioration of cardiovascular system

Mucosal barrier of GI system becomes ischemic

◦ Ulcers

◦ Bleeding

◦ Risk of translocation of bacteria

◦ Decreased ability to absorb nutrients

◦ Acute tubular necrosis/acute renal failure

Progressive Stage Cont’d)

Liver fails to metabolize drugs and wastes

◦ Jaundice

◦Elevated enzymes

◦Loss of immune function

◦Risk for DIC and significant bleeding

Progressive (intermediate)Stage of Shock

Copyright © 2010, 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved.

Refractory Stage (Irreversible)

Exacerbation of anaerobic metabolism

Accumulation of lactic acid

↑ Capillary permeability

Profound hypotension and hypoxemia

Tachycardia worsens

Decreased coronary blood flow

Cerebral ischemia

Failure of one organ system affects others Recovery unlikely

Diagnostic Studies

Thorough history and physical examination

No single study to determine shock

◦ Blood studies

◦ Elevation of lactate

◦ Base deficit

◦ 12-lead ECG

◦ Chest x-ray

◦ Hemodynamic monitoring

treatment

Overall goal:

1.increase O2 delivery

2.decrease demand

Collaborative CareSuccessful management includes :

◦ Identification of patients at risk for shock

◦ Integration of the patient’s history, physical examination, and clinical findings to establish a diagnosis

◦ Interventions to control or eliminate the cause of the decreased perfusion

◦ Protection of target and distal organs from dysfunction

◦ Provision of multisystem supportive care

General management strategies

◦ Ensure patent airway

◦ Maximize oxygen delivery

Cornerstone of therapy for septic, hypovolemic, and anaphylactic shock = volume expansion

◦ Isotonic crystalloids (e.g., normal saline) for initial resuscitation of shock

Collaborative Care (Cont’d)

Volume expansion

◦ If the patient does not respond to 2 to 3 L of crystalloids, blood administration and

central venous monitoring may be instituted

◦ Complications of fluid resuscitation

◦ Hypothermia

◦ Coagulopathy

Primary goal of drug therapy = correction of decreased tissue perfusion

◦ Vasopressor drugs (epinephrine)

◦ Achieve/maintain MAP >60 to 65 mm Hg

◦ Reserved for patients unresponsive to other therapies

Collaborative Care (Cont’d)

Nutrition is vital to decreasing morbidity from shock

◦ Initiate enteral nutrition within the first 24 hours

◦ Initiate parenteral nutrition if enteral feedings contraindicated or

fail to meet at least 80% of the caloric requirements

◦Monitor protein, nitrogen balance, BUN, glucose, electrolytes

Other treatment

1. correction of acid- bace balance

2.steroids- Hydrocortisone

3.Antibiotics

4.Nasal O2/Ventilatory support

5.CVP line

6.Control of pain

7.ICU-Critical care management

Collaborative CareCardiogenic Shock

Restore blood flow to the myocardium by restoring the balance between O2 supply

and demand

Thrombolytic therapy

Angioplasty with stenting

Emergency revascularization

Valve replacement

Hemodynamic monitoring

Drug therapy (diuretics to reduce preload)

Circulatory assist devices (e.g., intra-aortic balloon pump, ventricular assist device)

Collaborative CareHypovolemic Shock

Management focuses on :

stopping the loss of fluid and restoring the circulating volume

Fluid replacement is calculated using a 3:1 rule (3 ml of isotonic crystalloid for

every 1 ml of estimated blood loss)

Collaborative CareSeptic Shock

Fluid replacement (e.g., 6 to 10 L of isotonic crystalloids and 2 to 4 L of colloids) to restore perfusion

◦ Hemodynamic monitoring

Vasopressor drug therapy; vasopressin for patients refractory to vasopressor therapy

Intravenous corticosteroids for patients who require vasopressor therapy, despite fluid resuscitation, to

maintain adequate BP

Antibiotics after obtaining cultures (blood, wound exudate, urine, stool, sputum)

Drotrecogin alfa (Xigris)

◦ Major side effect: Bleeding

Glucose levels <10 mg/dl

Stress ulcer prophylaxis with histamine (H2)-receptor blockers

Deep vein thrombosis prophylaxis with low-dose unfractionated heparin or low-molecular-weight heparin

Collaborative CareNeurogenic Shock

In spinal cord injury: Spinal stability

◦Treatment of the hypotension and bradycardia with vasopressors

and atropine

◦Fluids used cautiously as hypotension is generally not related to

fluid loss

◦Monitor for hypothermia

Collaborative CareAnaphylactic Shock

Epinephrine, diphenhydramine

Maintaining a patent airway

◦ Nebulized bronchodilators

◦ Endotracheal intubation or cricothyroidotomy may be necessary

Aggressive fluid replacement

Intravenous corticosteroids if significant hypotension persists after 1 to 2 hours

of aggressive therapy

Nursing Assessment

ABCs: Airway, breathing, and circulation

Focused assessment of tissue perfusion

◦ Vital signs

◦ Peripheral pulses

◦ Level of consciousness

◦ Capillary refill

◦ Skin (e.g., temperature, color, moisture)

◦ Urine output

Brief history

◦Events leading to shock

◦Onset and duration of symptoms

Details of care received before hospitalization

Allergies

Vaccinations

Nursing Diagnoses

Ineffective tissue perfusion: Renal, cerebral,

cardiopulmonary, gastrointestinal, hepatic, and peripheral

Fear

Potential complication: Organ ischemia/dysfunction

Planning

Goals for patient

◦Assurance of adequate tissue perfusion

◦Restoration of normal or baseline BP

◦Return/recovery of organ function

◦Avoidance of complications from prolonged states of

hypoperfusion

Nursing Implementation

Health Promotion

◦ Identify patients at risk (elderly patients, those with debilitating illnesses or

who are immunocompromised, surgical or accidental trauma patients)

◦ Planning to prevent shock

(monitoring fluid balance to prevent hypovolemic shock, maintenance of

handwashing to prevent spread of infection)

Nursing Implementation (Cont’d)

Acute Interventions

◦ Monitor the patient’s ongoing physical and emotional status to detect subtle

changes in the patient’s condition

◦ Plan and implement nursing interventions and therapy

◦ Evaluate the patient’s response to therapy

◦ Provide emotional support to the patient and family

◦ Collaborate with other members of the health team when warranted

Nursing Implementation (Cont’d)

Neurologic status: Orientation and level of consciousness

Cardiac status

◦Continuous ECG

◦VS, capillary refill

◦Hemodynamic parameters: central venous pressure, PA pressures,

CO, PAWP

◦Heart sounds: Murmurs, S3, S4

◦

Nursing Implementation (Cont’d)

Respiratory status

◦Respiratory rate and rhythm

◦Breath sounds

◦Continuous pulse oximetry

◦Arterial blood gases

◦Most patients will be intubated and mechanically ventilated

Nursing Implementation (Cont’d)

Urine output

Tympanic or pulmonary arterial temperature

Skin: Temperature, pallor, flushing, cyanosis, diaphoresis,

piloerection

Bowel sounds

Nursing Implementation (Cont’d)

Nasogastric drainage/stools for occult blood

I&O, fluid and electrolyte balance

Oral care/hygiene based on O2 requirements

Passive/active range of motion

Nursing Implementation (Cont’d)

Assess level of anxiety and fear

◦Medication PRN

◦Talk to patient

◦Visit from clergy

◦Family involvement

◦Comfort measures

◦Privacy

◦Call light within reach

Evaluation

Normal or baseline, ECG, BP, CVP, and PAWP

Normal temperature

Warm, dry skin

Urinary output >0.5 ml/kg/hr

Normal RR and SaO2 ≥90%

Verbalization of fears, anxiety

Thanks for your attention