Advanced Medical Life Support

Chapter 4

Hypoperfusion (Shock)

Introduction
Hypoperfusion is shock -inadequate distribution of oxygen and other nutrients to the bodys cells. It is the physical mechanism by which we all eventually die.

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Topics
Defining Hypoperfusion and Shock
Anatomy and Physiology of Perfusion

Differential Diagnosis
Assessment Priorities

Management Priorities
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C ASE S TUDY
Situation
Call to private residence regarding a syncopal event 65 yo male supine on floor. Seems oriented, coherent, flushed & anxious. Breathing obviously labored. Large dressing noted on foot. C/o vague discomfort, like Im jumping out of my skin. Patient describes no pain, but pants noticeably after speaking. Feels better with head & shoulders raised.

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C ASE S TUDY
Situation
History & Findings
Patient released from hospital yesterday where he had a bunion removed from his foot. Had been watching TV when he became nauseated. Tried to get up but became dizzy & passed out, was helped to floor. Meds: Vasotec for hypotension, Motrin for pain (both regularly). Sedentary lifestyle; denies other history.
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Anatomy & Physiology of Perfusion

Arteries Arteriole Precapillary sphincters Vein

Venule

Capillaries

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Components of Perfusion
Breathable gases A clear airway Adequate lung tissue Healthy blood Sufficient fluid volume A competent pump Intact vessels A functioning nervous system
Failure of one means Failure of all!

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Changes That Affect Perfusion

cardiac output CNS function

vasomotor tone

AIRWAY!

oxygenation & ventilation

permeability blood chemistry emboli blood volume bleeding
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I. Normal Cell II. Hypoxia & cellular ischemia. Anaerobic metabolism begins; increased lactic acidosis leads to metabolic acidosis. Sodium pump fails. III. Ion shift. Sodium moves into cell, bringing water. IV. Cellular swelling occurs. V. Mitochondrial swelling. Energy production fails.

Death of a Cell

VI. Intracellular disruption occurs. Lysosomes released; plasma membrane begins to break down.

VII. Cell destruction begins.

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Indications Are...
Blood pressure Mentation Cardiac output Perfusion

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Autonomic Response to Shock

Example: Response to Bleeding

Any change in intra-aortic pressure results in stimulation of baroreceptors in the aortic arch, which transmit impulses to the medulla.

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Autonomic Response to Shock

Example: Response to Bleeding

The stimulus is then relayed to the adrenal cortex of the kidney, via the ganglia of the sympathetic nervous system.

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Autonomic Response to Shock

Example: Response to Bleeding
The adrenal cortex responds by secreting epinephrine & norepinephrine, thus triggering beta and alpha adrenergic responses by organs throughout the body.
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Autonomic Control of Perfusion

Dynamic Process; Constantly Responds to Demand
Alpha

(Norepinephrine)

Beta

(Epinephrine)

vasomotor tone PVR preload stroke volume cardiac output diaphoresis

C (contractility) A (automaticity) R (rate) D (dilation of coronary arteries) I (irritability) O (oxygen demand) Also: bronchodilation, respiratory drive
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3 Stages of Shock
1 2
Compensated
(Quickly correctible, possibly without help)

Progressive
(Increased acidosis, risk of damage)

Irreversible
(Permanent damage; death is likely to result)
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Compensated Shock
Reversible by Natural Means

Body detects fall in perfusion

(alert & anxious)

Sympathetic nervous system secretes norepinephrine (alpha effects) & epinephrine (beta effects) Patient may exhibit signs of shock
(anxiety, pulse & respirations, and pale, clammy skin)
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Progressive Shock
Classic Signs of Shock -- More Serious

Changes in mentation
(drowsiness, lethargy & combativeness)

Skin changes
(pallor/cyanosis, diaphoresis & cooling)

Tachycardia/tachypnea Hypotension Patient appears gravely ill

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Irreversible Shock
Onset of Death

Acidosis produces widespread cell death, tissue damage, organ failure Skin becomes gray, mottled, cold Patient becomes unresponsive Pulse & BP disappear Respirations become agonal & cease
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Differential Diagnosis
Any factor that impedes cardiac function, vascular integrity, or intravascular fluid volume can cause shock. Diagnosis is based on

organs/systems affected.
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Types of Shock
Hypovolemic (many causes; e.g., hemorrhagic) Obstructive (e.g., pulmonary embolus, cardiac
tamponade, tension pneumothorax)

Distributive (e.g., neurogenic, anaphylactic,

septic)

Cardiogenic (pump failure)

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Types of Shock
Hypovolemic

Insufficient fluid volume If related to blood loss, referred to as hemorrhagic shock (most common)

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Classic Hemorrhagic Shock

Compensated (Early) Stage
Mentation Skin
Alert or slightly anxious

BP Pulse Resp. Other

Norm. to fast

Becoming Norm. Norm. cool, to fast pale.

Sweating
(begins w/ face)

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Classic Hemorrhagic Shock

Progressive (Middle) Stage
Mentation Skin
Drowsy, lethargic, combative Cool/ cold, pale, cyanotic, mottled
(delayed cap. refill)

BP Pulse Resp. Other

& shallow urine

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Classic Hemorrhagic Shock

Irreversible (Advanced) Stage
Mentation Skin
Becoming unresponsive Gray, mottled, cyanotic, waxen Sweating ceases
(skin moisture depends on rate of evaporation)
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BP Pulse Resp. Other

Findings diminish & cease; death ensues Cardiac irritability arrest

Non-Hemorrhagic Hypovolemic Shock

Distinctions From Classic Hemorrhagic Shock
Mentation Skin
sweating urine turgor

BP Pulse Resp. Other

thirst
(except in elderly w/ impaired thirst mech.)

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Types of Shock
Obstructive

Occurs when a physical obstruction prevents return of blood to heart

Cardiac tamponade Pulmonary embolism Tension pneumothorax

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Pulmonary Embolus
Distinctions From Classic Hemorrhagic Shock
Mentation Skin
Anxious Sense of doom

BP Pulse Resp. Other

(?) chest pain (?) clear LS (?) syncope (?) cardiac dysrhyth. &/or arrest
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Pale or cyanotic, esp. around mouth & nose

Cardiac Tamponade
Distinctions From Classic Hemorrhagic Shock
Mentation Skin BP Pulse Resp. Other
paradoxical; narrowing pulse pressure Clear LS Distended neck & hand veins; cyanotic, esp. around mouth & nose at first

Distant HS (hard to detect in field)

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Tension Pneumothorax
Distinctions From Classic Hemorrhagic Shock
Mentation Skin BP Pulse Resp. Other
paradoxical; Sudden, sharp ch. pain narrowing & SOB pulse in COPD pressure pt. w/ ruptured bleb; Clear LS
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cyanotic, esp. around mouth & nose at first

Distended neck & hand veins;

Unequal LS
(key difference vs. cardiac tamponade)

Types of Shock
Distributive

Abnormal blood distribution, either through extreme vasodilation or abnormal vascular permeability (or both)
Neurogenic Anaphylactic Septic
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Neurogenic Shock (non-trauma)

Distinctions From Classic Hemorrhagic Shock
Mentation Skin
At first: Warm, pink, dry;

BP Pulse Resp. Other

Depends on toxin Depends Expect on toxin; hypothermia; May be slow, Anticipate shallow Pulmonary irregular; edema w/ poisoning May cease

Later: pale, cyanotic w/mottling in dependent areas

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Anaphylactic Shock
Distinctions From Classic Hemorrhagic Shock
Mentation Skin
Hives Itching

BP Pulse Resp. Other

Rapid, shallow (?) SOB Swelling of mucous membranes;

(?) Petechiae
(?) Flushing (?) Pallor/ cyanosis

(?) pulm. (?) stridor, edema wheezing, crackles

(?) arrest
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Septic Shock
Distinctions From Classic Hemorrhagic Shock
Mentation Skin
Pink (w/ fever) to pale & cyanotic

BP Pulse Resp. Other

Early: Late: Dyspnea (?) fever w/change (except in some in LS
elderly & very young)

(?) petechiae

(?) purpura
(?) peeling

Late: frank pulmonary edema

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Types of Shock
Cardiogenic

Pump failure, most commonly caused by destruction of left ventricle after myocardial infarction

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Cardiogenic Shock
Distinctions From Classic Hemorrhagic Shock
Mentation Skin
cyanotic

BP Pulse Resp. Other

varies LS Pulmonary wheezing, edema crackles; (key finding)

Note! It is essential to distinguish cardiogenic shock from hemorrhagic shock. The correct therapy in one case is deadly in the other.

Patient c/o SOB;

Coughing, prod. white/ pink sputum.
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Severity of Shock Depends on:

Type of shock Age of patient Pre-existing disorders Speed of onset Effects of drugs & other substances

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Assessment Priorities
Initial Assessment Focused History & Physical Exam

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Initial Assessment
Sx of shock can be recognized almost instantly, during initial assessment of mentation, ABCs, and baseline vitals.
React quickly! Protect airway Position for shock
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Focused History & Physical

A thorough history & physical exam are necessary to differentiate between appropriate treatments.
(Treatments for some kinds of shock are contraindicated for other kinds.)

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Keys to History
Patients age Previous medical history

History of this event (OPQRST)

Consider treating for shock while gathering history.
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Keys to Physical Assessment

Skin vitals (color, temp, moisture)

Mentation (also note history of changes)

Vital signs (pulse, respirations, BP, pulse-ox)

Lung sounds
Postural hypotension (key early sign)
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Management Priorities
General

Open the airway. Administer high-flow O2 /ventilate. Establish IV access (crystalloids). Apply a cardiac monitor.
Type-Specific

Treat the mechanism

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Treatment Pathway for Shock

Scene Size-up Initial Assessment Suspect shock? Airway, O2, ventilations if necessary. Shock position (Fowlers for pulm. edema). Keep warm. Focused History & Physical Exam General supportive measures; adjust O2. IV, ECG, pulse oximetry

Hypovolemic? IV of NS or RL to replace fluids

Obstructive? Tension Pneumo: O2 via NRB mask; needle decompression

Distributive? Neurogenic: monitor, support hemodynamics Drug-induced: consult poison control Fluid challenge if LS clear P. edema w/ hypotension: dopamine

Cardiogenic? General: High-flow O2: IV of NS, TKO

Monitor heart rate, ECG

(continued)
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Treatment Pathway for Shock (continued)

Obstructive? Cardiac Tamponade: Notify receiving hosp. & consider fluid bolus Pulmonary Emboli: High-flow O2, monitor ECG Distributive? Anaphylaxis: bronchodilator for wheezes epinephrine for hives, severe airway/cardiovascular effects Next consider Benadryl or dopamine as necessary Fluid boluses as necessary Cardiogenic? Atropine for S. Bradycardia. For other bradycardias: ext. pacer, adenosine, lidocaine. For tachycardias (awake): sedation & cardioversion. For non-rate-related cardiogenic shock, titrate dopamine to systolic pressure that supports perfusion.

Sepsis: high-flow O2 w/ intubation as needed

Crystalloid boluses first, then dopamine.

Monitor ECG; manage PVCs w/O2

Possible dehydration/ patient on diuretics: crystalloid fluid challenge; monitor respiratory effects
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C A S E S T U D Y F O L L O W-U P
Situation
Call to private residence regarding a syncopal event. Patient supine on floor. Seems oriented, coherent, flushed & anxious, but denies pain. Breathing obviously labored. Feels better in semi-sitting position. Large dressing noted on foot. C/o vague discomfort, like Im jumping out of my skin.

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C A S E S T U D Y F O L L O W-U P
Situation
History
Patient released from hospital yesterday where he had a bunion removed from his foot. Had been watching TV when he became nauseated. Tried to get up but became dizzy & passed out, helped to floor. Meds: Vasotec for hypotension (last dose 30 min. ago) & Motrin for pain (12 hours). Sedentary lifestyle; denies allergies or other history.
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C A S E S T U D Y F O L L O W-U P
Findings & Treatment
Vitals: P=140 (carotid only), R=28, BP=60/palp. ECG reveals sinus tach. High-flow O2 via NRB mask, IV of NS/300cc fluid challenge administered, along w/ Alupent breathing treatment. LS remain clear, 2nd BP is 76/52. 0.5 mg Epi 1:1,000 administered sub cu.

Within minutes, patient says he feels better. New vitals reveal P=120, R=20, BP=88/64. Skin color nearly normal, respirations more relaxed.
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C A S E S T U D Y F O L L O W-U P
Findings & Treatment
Response to Care
On arrival at the ED, vitals are unchanged. Patient receives additional 500 ml of IV fluids & 50 mg of Benadryl IM. Patient admitted for acute anaphylaxis.

Patient instructed to avoid taking Vasotec in the future; alternate medication prescribed instead.

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