Alterations in Hemodynamic Stability: Shock

Shock

Life-threatening

- syndrome caused by alteration in tissue perfusion and impaired cellular metabolism

- results in imbalance between supply of & demand of O2 + nutrients

4 Main Categories of Shock

Cardiogenic

Hypovolemic

Distributive

Obstructive

Hypovolemic Shock

Occurs from inadequate fluid volume in the intravascular space

- most common type of shock

How does hypovolemic shock occur?

Loss of blood (most common)

- traumatic bleeding

Fluid losses

- severe burns

- severe diarrhea &/vomiting

- renal losses

- third spacing

Absolute Hypovolemic Shock

Fluid lost through:

- Hemorrhage

- Gastrointestinal (GI) loss (e.g., vomiting, diarrhea)

- Fistula drainage

- Diabetes insipidus

- Diuresis

Relative Hypovolemic Shock

Occurs when fluid volume moves out of the vascular space into the extravascular space

- aka third spacing

- bowel obstruction

- internal bleeding

- ascites

Pt's response to Acute Volume Loss

Depends on several factors:

- extent of injury

- age

- general state of health

Up to 15% of Total Blood Volume Loss (750 mL)

Pt can compensate

Up to 15%-30% Blood Loss

Results in SNS mediated response

- increase in HR, CO, RR and depth

- decrease in SV, CVP & PAWP

> 30% Volume Loss

Compensatory mechanism may fail

- immediate replacement with blood products should be started

> 40% Volume Loss

Loss of autoregulation in microcirculation & irreversible tissue destruction

Early S&S of Hypovolemic Shock

Irritability

Tachycardia

Slight Tachypnea

Pink to Pale Skin change

Dry mucous membranes

Compensation of Early Hypovolemic Shock

Decrease Preload, PAP, PAWP, CO

- increased SVR & afterload --> due to vasoconstriction of vessels

Acid-Base Imbalance --> respiratory alkalosis & metabolic acidosis

Later S&S of Hypovolemic Shock

- Altered mental status

- HypoTN (more profound)

- Rapid, weak, thready pulse & bradycardic

- Cool, clammy skin

- Rapid + shallow respirations

- Hypothermia

- Cold + mottled skin (esp. extremities)

- Anxiety & restlessness

- Oliguria to anuria

Decompensation of Later Hypovolemic Shock

Decreased Preload (CVP)

PAP

PAWP

CO

SVR

Afterload

What is always include in tx plan, no matter the type of shock?

Supplemental O2

Tx of Hypovolemic Shock: Hemorrhagic

1. Supplemental O2

2. Rapid fluid resuscitation

3. Hypertonic - 3% & 6% NaCL

- given via central line

4. Crystalloids (Sodium Chloride [0.9%] or LR)

5. Colloids (will depend on pt)

6. Plasma and albumin

- albumin is hypertonic

7. Polysaccharide (Dextran), Polygeline & hetastarch (Hespan) - synthetic blood products

8. Blood Replacements

9. Repair of the problem

Tx of Hypovolemic Shock: Non-Hemorrhagic

1. Supplemental oxygen

2. Isotonic IV Fluids / Hypertonic Fluids

3. PRBC'S

4. Vasopressin

- will help promote/bring up BP

5. Antiemetics

6. Antidiarrheals

Resuscitation Fluid Requirements for Adults

1-2L isotonic IV fluids as initial bolus

Warm blood & fluids (if appropriate)

Why are cold IV Bags bad?

Can cause vasospasms and drop in BP & body temp

Metabolic Acidosis

Occurs in long standing or severe shock

- do not routinely use sodium bicarb to see if it corrects acidosis

What does a correction of Metabolic Acidosis result as?

Results of improved perfusion and tissue oxygenation

Cardiogenic Shock

Occurs when either systolic or diastolic dysfunction of the heart's pumping action causes:

- reduced CO, SV and BP

- often called "pump failure"

- compromised CO

Systolic Dysfunction

The heart's inability to pump blood forward

Diastolic Dysfunction

↓ filling of the heart resulting in ↓ stroke volume

Causes of Cardiogenic Shock

MI (most common)

HF

Cardiomyopathy

Dysrhythmias

Severe systemic or pulmonary HTN

Pericardial tamponade

Tension pneumothorax

PE

Myocardial depression from metabolic problems

Systolic Dysfunction Pathophysiology

Ineffective forward movement of blood → ↓ SV, ↓ CO → ↓ Cellular O2 supply → ↓ Tissue perfusion → Impaired Cellular metabolism

Diastolic Dysfunction Pathophysiology

Ineffective filling → ↑ Pulmonary pressure → Pulmonary edema → ↓ Oxygenation → ↓ Cellular O2 supply → ↓ Tissue perfusion → Impaired cellular metabolism

Early Manifestations of Cardiogenic Shock

Tachycardia

HypoTN

↑ Myocardial O2 consumption

- ↑ in SVR

Narrowed pulse pressure

Signs and Symptoms of Cardiogenic Shock

- Tachypnea

- Crackles on breath sounds

- ↑ in PAWP, SVV, PVR

- Signs of peripheral hypoperfusion

- Decreased renal blood flow

- Impaired cerebral perfusion

Signs of Peripheral Hypoperfusion

Cyanosis

Pallor

Weak peripheral pulses

Cool and clammy skin

Delayed capillary refill

Decreased Renal Blood Flow

Results in:

- Sodium and water retention

- Decreased urine output

Causes of Impaired Cerebral Perfusion

Anxiety

Confusion

Agitation

Compensation for Cardiogenic Shock

Low BP + HR = Low CO

- so SNS kicks in and creates vasoconstriction

- CVP & wedge pressure will be high

Additional S&S w/ Cardiogenic Shock

Chest Pain

SOB

JVD (due to backup of blood)

Weak/absent pulse

Dysrhythmias

Increased Preload (CVP), PAP, PAWP, SVR + afterload

Decreased CO

Tx for Cardiogenic Shock

Supplemental O2

Inotropic drugs

Vasodilators

Diuretics

Thrombolytic therapy

IABP (balloon pump)

VAD

Heart transplant

Tx for Cardiogenic Shock: Labs

H&H

Electrolytes

BUN

Creatinine

Tx for Cardiogenic: Inotropic Drugs

Dopamine & Dobutamine

Tx for Cardiogenic: Vasodilators

NTG (nitroglycerin)

- vasodilates

- will help decrease backup of blood

Tx for Cardiogenic Shock: Diuretics

Not only decrease blood volume, also decreases workload on heart

- the heart can pump more blood forward & less volume to shift into lungs (no pulmonary edema)

Tx for Cardiogenic Shock: IABP (balloon pump)

- In cardiogenic shock --> no afterload & increased SVR (due to vasoconstriction)

- W/ tx of balloon pump --> decreased SVR due to increased movement of blood

NSG Interventions for Cardiogenic Shock: Limit Myocardial Oxygen Demand & Consumption

- Administer analgesics and sedatives.

- Position the patient in position of comfort.

- can open their lung & be comfortable

- Limit activities.

- Reduce anxiety; calm, quiet environment.

- stress & anxiety increased SNS response

NSG Interventions for Cardiogenic Shock: Enhance Myocardial Oxygen Supply

- Administer oxygen.

- Monitor respiratory status.

- Administer medications as prescribed.

NSG Intervention for Cardiogenic Shock

- Monitor pt's response to tx

- Tx the cause

Anaphylactic Shock

Acute, life-threatening hypersensitivity (allergic) reaction to a sensitizing substance

- drug

- chemical

- vaccine

- food

- insect venom

What does Anaphylactic Shock cause?

Quickly causes:

- massive vasodilation

- release of vasoactive mediators

- increase in capillary permeability (fluid leaking to vascular space)

What can Anaphylactic Shock Lead to?

Can lead to:

- Respiratory distress due to laryngeal edema or severe bronchospasm

- Circulatory failure from the massive vasodilation

2 Major Issues w/ Anaphylactic Shock

Major drop in BP

Fluid vascular shift

Patho of Anaphylactic Shock

Anaphylactic Shock S&S: Skin Changes

Skin eruptions and hives

Flushing of skin

Pruritus

Urticaria

Angioedema

Anaphylactic Shock S&S: Other S&S

Dizziness

Chest pain

Incontinence

Swelling of lips & tongue

Wheezing

Stridor

Weak & rapid pulse

Localized edema (esp. around face)

Breathlessness & cough (due to bronchoconstriction)

Anaphylactic Shock S&S: Hemodynamic

Decreased:

- preload (CVP)

- PAP

- PAWP

- CO

- SVR

- afterload

Tx for Anaphylaxis Shock

1. Airway management & supplemental O2

2. Administer Catecholamines (Epi), Antihistamines (Benadryl), Bronchodilators, Corticosteroids

Use of Catecholamines (Epinephrine) for Anaphylaxis Shock

Will be an increase in HR and vasoconstriction

- make sure to teach pts this is a normal response

Sepsis

Severe illness in which the bloodstream is overwhelmed by bacteria

Common Sepsis Sites

- Bowel (peritonitis)

- Kidneys (UUTI or pyelonephritis)

- Lining of brain (meningitis)

- Lungs (bacterial pneumonia)

- Skin (cellulitis)

- Bone (osteomyelitis)

- Any opening in barrier of skin

Stages of Sepsis

1. Infection (fever)

2. System inflammatory response syndrome (SIRS)

3. Sepsis (SIRS + infection on culture)

4. Severe sepsis/Septic Shock (organ dys, hypoTN or hypoperfusion)

Septic Shock

An overwhelming systemic infection

- 70% of septic chock causes are due to HAI (prevention is key)

- characterized by persistent hypoTN and inadequate tissue perfusion that results in tissue hypoxia

Organisms causing septic shock

- Gram negative bacteria (ex: E. coli, Proteus species, Klebsiella coli, etc.)

- Some Gram positive bacteria (strep or pneumococcal)

- Also can be caused by yeasts, fungi, parasites, protozoa, mycobacteria, rickettsia

3 Pathophysiologic Effects of Septic Shock

Vasodilation --> leads to hypoTN

Maldistribution of blood flow

Myocardial depression

- decreased EF

- ventricular dilation

Phases of Septic Shock: Hyperdynamic Phase

Increased CO

Decreased SVR

Moderate tachycardia + normal BP

Widened pulse pressure

Pyrexia (fever)

Warm, dry, flushed skin

Moderate alteration in sensorium (early sign)

Normal cap refill

Tachypnea (early indicator)

Phases of Septic Shock: Hypodynamic Phase

S&S are similar to uncompensated and irreversible shock

- Significant tachycardia changing to bradycardia

- Dysrhythmias

- Profound hypotension

- Decreased pulse pressure

- Decreased SVP, PAP, PAWP, CO, SVR + afterload

CMs of Septic Shock

- Tachypnea/hyperventilation

- results in respir. alkalosis

- occurs due to backup in blood

- ↓ Urine output

- Altered neurologic status

- GI dysfunction, GI bleeding, paralytic ileus

- not getting blood flow to gut

Tx for Septic Shock

1. Supplemental O2

2. Fluids (for vasodilation)

3. Antibiotics (start within 1st hr of dx)

4. Inotropic drugs

5. Vasopressor drugs

Antibiotics Tx for Septic Shock

Culture pt first before starting antibiotics

- will culture the sputum, blood, urine

Stages of Shock: Initial Stage

Occurs at a cellular level

- usually not clinically apparent

- metabolism changes from aerobic to anaerobic = lactic acid buildup

What is lactic acid?

Waste product that is removed by liver

- process requires O2 --> which is unavailable due to decrease tissue perfusion in shock pts

Stage of Shock: Compensatory Non-Progressive Stage (1st Part)

1. Body activates neural, hormonal and biochemical compensation to try to maintain homeostasis

- respiratory alkalosis

- baroreceptors in arteries detect hypoTN

- catecholamines are released

- RAAS is activated

- Vasopressin (ADH)

Release of Catecholamines in Compensatory Non-Progressive Stage

Norepinephrine

- causes predominately vasoconstriction w/ mild increase in HR

Epinephrine

- predominately causes an increase in HR w/ small effect on vascular tone --> results in increase in BP

Release of Vasopressin (ADH) in Compensatory Non-Progressive Stage

Conserves fluids via kidney & GI tract

- causes vasoconstriction of kidneys, GI tract, and other organs → divert blood to heart, lungs and brain

- lack of blood to renal system → causes characteristic low urine production

Stages of Shock: Compensatory Non-Progressive Stage (2nd Part)

2. SNS stimulation increases myocardial O2 demands

3. Shunting blood from lungs increases physiologic dead space, causing:

- V/Q mismatch

- decreased arterial O2 levels

- increase in rate/depth

4. Impaired GI motility

- causing slowed peristalsis & risk for paralytic ileus

5. Decreased blood flow to skin

- pt feels cold & clammy

Is the body able to compensate during the Compensatory Stage of Shock?

Yes, the body is able to compensate for changes in tissue perfusion

- if correct --> pt recovers w/ little or no effects

- if not corrected --> pt enters progressive stage

Stages of Shock: Progressive (Decompensating)

Begins as compensatory mechanisms fail

- Na+ builds up as K+ leaks out

- Anaerobic metabolism continues = worsening metabolic acidosis

Stages of Shock: Progressive - Cardiovascular System

CO begins to fall

- decrease in BP, coronary artery, cerebral and peripheral perfusion

Altered capillary permeability occurs

- fluids & proteins leak into interstitial space causing anasarca (profound edema)

Myocardial dysfunction = dysrhythmias, MIs

Pt is at higher risk for DIC

- consumption of PLTs and clotting factors = increased bleeding

Stages of Shock: Progressive - Pulmonary System

WILL SHOW CRITICAL DYS FIRST!!

Results in:

- impaired gas exchange

- decreased compliance

- worsening ventilation-perfusion mismatch

Blood flow to lungs is reduced

Fluid moves from pulmonary area into interstitial space

- causing edema and bronchoconstriction

Fluid moving into alveoli = alveolar edema & decrease in surfactant products (ARDS!)

What would the pt have CLINICALLY in the progressive stage of shock (pulmonary system)?

Tachypnea

Crackles

Increased WOB

Stages of Shock: Progressive - GI System

Affected by prolonged decreased tissue perfusion

Mucosal barrier becomes ischemic

- increases risk of ulcers and GI bleeding and bacteria migration

- decreased ability to absorb nutrients

Stages of Shock: Progressive - Liver

Los of liver function leads to failure to metabolize drugs and waste products (ex. lactate, ammonia)

1. Jaundice results from increased bilirubin

2. As liver cells die = increased liver enzymes

3. No more immune function

- cannot destroy bacteria from GI tract = increased risk of bacteremia

Stages of Shock: Progressive - Kidneys

Causes renal tubular ischemia & leads to an AKI

- can be worsened by nephrotoxic drugs

- metabolic acidosis occurs from decreases ability to excrete acids and reabsorb bicarbonate

What can be seen CLINCIALLY in a pt who is in the progressive stage of shock (kidneys)?

Decreased urine output

Increased BUN & serum creatinine

Stages of Shock: Refractory (Irreversible)

Decreased perfusion worsens anaerobic metabolism

- caused by peripheral vasoconstriction and decreased CO

- vital organs have FAILED

What will be seen in a pt in the refractory stage of shock?

- Profound acidosis

- Profound hypoTN & hypoxemia

- Tachycardia worsen (decreased O2 to heart)

- Brain damage and cell death occurred

- Organ systems are in failure

RECOVERY IS UNLIKELY

Obstructive Shock

Develops when physical obstruction to blood flow occurs with decreased CO

- associated w/ obstruction of the big vessels or the heart

What is Obstructive Shock caused by?

1. Restricted diastolic filling of right ventricle from compression

2. Abd. compartment syndrome

- abd. pressure compressing IVC

3. PE and right vent. thrombi

- causes decreased blood flow to lungs & blood return to LA

Forms of Obstructive Shock

PE

Tension pneumothorax

Cardiac tamponade

Symptoms of Obstructive Shock

Rapid assessment and immediate tx = important!!!

- Decreased CO

- Increased Afterload

- Variable LV filling pressure

- JVD

- Pulsus paradoxus (abn. decrease in BP during inspiration)

Interprofessional Care for Obstructive Shock

Having early recgnitina tx

- echa ial therapy

- yjt