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Transcript of Bledsoe/Benner, Critical Care Paramedic © 2006 by Pearson Education, Inc. Upper Saddle River, NJ...
![Page 1: Bledsoe/Benner, Critical Care Paramedic © 2006 by Pearson Education, Inc. Upper Saddle River, NJ Pulmonary Artery Pressure Monitoring (1 of 3) Central.](https://reader031.fdocuments.net/reader031/viewer/2022012923/5a4d1b617f8b9ab0599ad9d8/html5/thumbnails/1.jpg)
Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Pulmonary Artery Pressure Monitoring (1 of 3)
Central venous catheter passed through right atrium, right ventricle, past tricuspid valve, and into pulmonary artery
Allows monitoring of:– Right ventricular function– Pulmonary vascular status– Left ventricular function (indirectly)
PAP
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Pulmonary Artery Pressure Monitoring (2 of 3)
Specific parameters measured– CO– Right arterial pressure– Right ventricular pressure– Pulmonary artery pressure– Pulmonary artery wedge pressure (PAWP)
PAP
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Pulmonary Artery Pressure Monitoring (3 of 3)
Catheter– Flow-directed, balloon-tipped pulmonary artery
catheter Swan-Ganz catheter Dual lumen
Distal port Proximal port
Balloon inflated to: “Float” catheter into position Measure pulmonary wedge
pressures
PAP
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Waveform Interpretation
Pressure changes during systole and diastole Waveforms classified as:
– Right atrial– Right ventricular– Pulmonary artery pressure– Pulmonary artery wedge pressure
PAP
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Indications of PA Catheter Placement (1 of 2)
Diagnosis of shock states and shock types Diagnosis of high-pressure versus low-pressure
pulmonary edema Assessment of vascular tone Assessment of myocardial contractility, including
determination of cardiac output Assessment of intravascular fluid balance
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Indications of PA Catheter Placement (2 of 2)
Analysis of mixed venous oxygen saturation Monitoring and management of complicated AMI Assessment of hemodynamic response to
therapies Management of hemodynamic instability after
cardiac surgery
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Insertion of PA Catheter(1 of 2)
Catheter placed in vein Catheter fed into vein until distal tip in right
atrium Distal balloon inflated with 1.5 cc of air Distal tip “floated” through tricuspid, into right
ventricle, through pulmonic valve, and into pulmonary artery
Balloon allowed to “wedge” itself in branch of pulmonary artery
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Insertion of PA Catheter (2 of 2)
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Right Atrial Pressure
Mean right atrial pressure– 8 mmHg
Right Atrial Pressure
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Right Ventricular Pressure(1 of 2)
Right-atrial end-diastolic pressure– 0–8 mmHg– Equal to right atrial pressure when tricuspid valve
opens
Right Ventricular Pressure
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Right Ventricular Pressure(2 of 2)
Right-atrial systolic pressure– 15–30 mmHg– Opens pulmonic valve
Propels blood into pulmonary artery
– Higher-pressure chamber
Right Ventricular Pressure
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Pulmonary Artery Pressure (2 of 4)
Systolic– 15–30 mmHg– Equal to right ventricular systolic pressure
PAP
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Pulmonary Artery Pressure (3 of 4)
Diastolic– 8–15 mmHg– Reflects resistance of pulmonary vascular bed
Left-ventricular end-diastolic pressure also PA diastolic pressure is indirect measurement of left
ventricular pressure
PAP
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Pulmonary Artery Wedge Pressure (PAWP)
Measures left-atrial and ventricular end-diastolic pressure– More accurate than estimate from pulmonary artery diastolic pressure
PAWP
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
PAWP 8–12 mmHg Catheter tip placed in
pulmonary artery– In-place pulmonary
artery catheter used– Balloon on distal tip
inflated
PAWP
– Balloon advanced until it lodges in branch of pulmonary artery Forward blood flow stopped Static column of blood created
Branch of artery Pulmonary capillaries Pulmonary vein Left atrium Open mitral valve
During diastole Left ventricle
Balloon deflated after measurements completed
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Complications of PA Catheterization
Pulmonary injury– During needle puncture
Dysrhythmias Infection Pulmonary artery rupture
PAWP
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Preparation for Hemodynamic Monitoring
Prime the flush system Connect the transducer to the monitor Leveling the transducer Zero the pressure system to atmospheric
pressure Calibrate the pressure system
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Intra-aortic Balloon Pump (IABP) (1 of 6)
Augments weakened heart’s cardiac output Percutanous placement of balloon catheter in aorta
– Insertion site: Femoral– Balloon placed about 2 cm distal to aortic arch
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Intra-Aortic Balloon Pump (IABP)(1 of 3)
Provides mechanical circulatory support for failing heart Catheter
– 30-cm balloon on distal end Balloons sized according to height
– Placed in aorta distal to left of subclavian artery – Inserted in femoral artery– During operation, rapidly inflated and deflated with 35–40 ml
of helium
IABP
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Intra-aortic Balloon Pump (IABP) (2 of 6)
Balloon inflated during ventricular diastole– Displaces blood forward and backward
Forward Increases systemic blood flow Increases CO by 10 to 20 percent
Backward Increases coronary artery filling Increases myocardial perfusion
Balloon deflated during onset of ventricular systole– Decreases afterload– Improves ejection fraction (EF)
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Intra-Aortic Balloon Pump (IABP) (2 of 3)
IABP
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Indications for IABP Therapy
Cardiogenic shock Left ventricular failure Drug-induced cardiovascular failure Septic shock Cardiac surgery preparation
IABP
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Intra-Aortic Balloon Pump (IABP) (3 of 3)
IABP pump– Rate adjustable
1:1, 1:2, 1:8– Inflation volume adjustable
IABP©Craig Jackson/In the Dark Photography
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Intra-aortic Balloon Pump (IABP) (3 of 6)
Transport management of patient on IABP includes:– Evaluating patient response to treatment in terms of:
Hemodynamic status Dysrhythmia control Systemic perfusion Relief of symptoms of cardiac ischemia
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Intra-aortic Balloon Pump (IABP) (4 of 6)
Transport management of patient on IABP includes:– Observing such early signs of complications from IABP
therapy as: Limb ischemia Bleeding Infection Thrombus formation Displacement of balloon catheter Arterial damage
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Intra-aortic Balloon Pump (IABP) (5 of 6)
Ensure proper IABP functioning, including:– Correct timing– Consistent triggering– Appropriate troubleshooting of all alarm situations– Safe operation
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Intra-aortic Balloon Pump (IABP) (6 of 6)
Air medical transport considerations Hypobaric environment can impeded IABP functioning
– Volume decreases on ascent– Volume decreases on descent
IABP must be reprimed– During ascent– At altitude– During descent
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
IABP Contraindications
Gross aortic insufficiency Peripheral vascular disease with poor femorals Irreversible brain damage Chronic end state heart disease Dissecting aortic or thoracic aneurysms Peripheral vascular disease
IABP
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Side Effects and Complications Limb ischemia Bleeding at insertion site Thrombocytopenia Immobility of balloon catheter Balloon leak or rupture
– Helium embolization– Thrombus formation
Infection Aortic dissection Compartment syndrome
IABP
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Summary Critical care paramedics will most likely not be
required to establish/insert hemodynamic monitoring catheters– Must be familiar with insertion technique, however
Must be prepared to:– Interpret data– Use data in differential diagnosis and treatment
decisions Manage complications of devices
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Shock
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Introduction to Shock(1 of 2)
Shock is often unrecognized in early stages– Clinical signs and symptoms can vary– Clinical signs and symptoms can be subtle– Many different presentations
Shock is not a primary diagnosis– Physiologic adaptation to an insult– Body is attempting to preserve vital functions
Shock is a “rude unhinging of the machinery of life” Samuel Gross, 1862
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Introduction to Shock(2 of 2)
Shock results from changes in:– Circulating volume– Cardiac function– Peripheral vascular resistance
Shock can cause changes in organ systems– Cardiovascular– Respiratory– Renal– Gastrointestinal
Classified in stages– Compensatory– Progressive– Irreversible
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Shock Defined
Local or systemic hypoperfusion resulting in an inability to meet cellular demands– Can affect tissue, organs, or organ systems– Can result from insult to:
Heart Lungs Blood vessels Blood Nervous system
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Compensatory Mechanisms
Counter effects of shock state Inability to correct insult may lead to death
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Cell Physiology
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Glycolysis
From Essentials of Anatomy & Physiology, 2nd ed., by Frederick H. Martini, Ph.D. and Edwin F. Bartholomew, M.S. Copyright © 2000 by Frederic H. Martini, Inc. Published by Pearson Education, Inc.
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TCA Cycle
From Essentials of Anatomy & Physiology, 2nd ed., by Frederick H. Martini, Ph.D. and Edwin F. Bartholomew, M.S. Copyright © 2000 by Frederic H. Martini, Inc. Published by Pearson Education, Inc.
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Pathophysiology
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
The Cell in Shock (1 of 7)
Peripheral tissues cannot store oxygen– Rely on constant perfusion – Deliver oxygen– Remove metabolic waste
Oxygen uptake (VO2, oxygen consumption)– The amount of oxygen taken up by the
mitochondria in the body– The amount of oxygen consumed
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
The Cell in Shock (2 of 7)
Metabolic requirement for oxygen (MRO2)– Rate at which oxygen is metabolized to water in the mitochondria– Water is byproduct of the TCA (Krebs) cycle
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
The Cell in Shock (3 of 7)
VO2 must match or exceed MRO2 for aerobic respiration to occur– VO2 MRO2 Normal metabolism
Aerobic respiration Complete oxidation of one molecule of glucose results in production of:
36 molecules of ATP Water
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The Cell in Shock (4 of 7)
When VO2 falls below MRO2, anaerobic metabolism occurs– Oxygen uptake fails to meet metabolic demand for oxygen– VO2 MRO2 anaerobic metabolism
Anaerobic respiration results in production of: Two molecules of ATP Pyruvic acid
Pyruvic acid converted to lactic acid
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The Cell in Shock (7 of 7)
Oxygen-carrying capacity of hemoglobin – (1.34 mL/g of Hb)
Normal VO2 100–160 mL/min/m2
V02 Cardiac Output (CO) 13.4 Hb (Sa02 Sv02)
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Precursors to Shock
Inadequate CO Inadequate Hb concentration or oxygen-carrying
capacity Inadequate arterial oxygen saturation
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Sodium/Potassium (Na/K) Pump (1 of 2)
Most energy produced by cell drives sodium/potassium pump
Maintains ionic gradient across cell membrane– Intracellular environment
Sodium: 10 mEq/L Potassium: 140 mEq/L
– Extracellular environment Sodium: 140 mEq/L Potassium: 4 mEq/L
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Sodium/Potassium (Na/K) Pump (2 of 2)
From Essentials of Anatomy & Physiology, 2nd ed., by Frederick H. Martini, Ph.D. and Edwin F. Bartholomew, M.S. Copyright © 2000 by Frederic H. Martini, Inc. Published by Pearson Education, Inc.
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Sodium/Potassium Pump Dysfunction
Lack of ATP production in anaerobic metabolism results in failure of the Na/K pump– Sodium moves to the intracellular environment
Osmotic shift of water into cell
– Swelling– Lysis
Clinically significant organ damage may occur
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Organ Systems in Shock When cell lysis
involves many cells, organ function is compromised
Shock develops
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Neurohumoral Responses in Shock (1 of 3)
Overall effects termed compensatory mechanisms– Increased heart rate– Increased myocardial contractility– Increased peripheral vasoconstriction– Renal retention of salt and water to maintain plasma
volume– Assembling of metabolic fuels
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Neurohumoral Responses in Shock (2 of 3)
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Neurohumoral Responses in Shock (3 of 3)
Compensatory mechanisms can only be tolerated for a short period due to:– Myocardial stress– Decreased blood flow to nonvital organs
Ischemia Lactic-acid production and accumulation (metabolic
acidosis)
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Symptoms of Shock
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Neurohumoral Agents and Effects
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Hormonal and Nervous Factors Influencing Blood Pressure
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Norepinepherine Vasoconstriction Increased myocardial contractility
Compensation
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Epinephrine
Increased heart rate Increased myocardial contractility
Compensation
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Angiotensin II Vasoconstriction Promotes secretion of
antidiuretic hormone
Compensation
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Antidiuretic Hormone(ADH)
Increases water retention in kidneys
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Aldosterone
Promotes Na and water retention in kidneys
Compensation
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Cortisol
Suppresses immune and inflammatory response Promotes protein catabolism Increases blood glucose
Compensation
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Stages of Shock
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Compensated Shock
Body able to detect decrease in CO– Baroreceptors– Chemoreceptors
Stages of Shock
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Baroreceptor Reflex
From Essentials of Anatomy & Physiology, 2nd ed., by Frederick H. Martini, Ph.D. and Edwin F. Bartholomew, M.S. Copyright © 2000 by Frederic H. Martini, Inc. Published by Pearson Education, Inc.
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Chemoreceptor Reflex
From Essentials of Anatomy & Physiology, 2nd ed., by Frederick H. Martini, Ph.D. and Edwin F. Bartholomew, M.S. Copyright © 2000 by Frederic H. Martini, Inc. Published by Pearson Education, Inc.
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Compensated Shock
Body able to compensate for decrease in CO– Compensatory mechanisms activated
Increased peripheral vasoconstriction Increased heart rate Increased myocardial contractility
– Maintenance of blood pressure– If insult not recognized and corrected, will proceed to
progressive stage of shock
Stages of Shock
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Progressive Shock
Anaerobic metabolism, tissue hypoxia appreciated
Additional compensatory mechanisms activated– Water retention in kidney– Profound vasoconstriction– Increased heart rate– Increased myocardial contractility
Stages of Shock
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Decompensated Shock
Cellular death– Can occur suddenly or over days
Prognosis poor
Stages of Shock
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General Management of Shock Correct the underlying problem Provide supportive care while attempting to identify the insult
– Airway Ensure patency
– Breathing Adequate ventilation, oxygenation
– Circulation Ensure adequate tissue perfusion
Volume resuscitation Vasoactive medications
– Correct acid-base abnormalities– Conserve body temperature
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Initial Assessment and Management
Same as any other critically ill patient Goal is to identify and treat any potentially life-
threatening injuries
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Airway First priority Assessed immediately Controlled with:
– Chin lift– Jaw thrust– Insertion of BLS airway adjunct
OPA/NPA– Endotracheal intubation
Assure cervical spine stabilization when warranted
Source: Courtesy of Mark C. Ide
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Breathing and Ventilation Assessment
– Verify presence of bilateral breath sounds on auscultation– Assess rate and depth of respirations– Expose chest and inspect for signs of trauma
Anterior, lateral, and posterior
Management – Administer 100 percent oxygen via appropriate method– Assess ventilatory status with capnography
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Circulation(1 of 2)
Assessment– Blood pressure– Pulse rate and quality– Skin color/temperature– Capillary refill time
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Circulation(2 of 2)
Management– BLS maneuvers
Raise legs
– IV cannulation Fluid administration Vasopressors
Dopamine Dobutamine Epinephrine Norepinephrine
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Disability, Neurologic Deficit
Assessment– AVPU– GCS– Level of consciousness– Motor, sensation– If altered, rule out:
Trauma Substance abuse
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Examine/Exposure
Remove all clothing to fully expose patient Cover with blankets to preserve heat once exam
is complete
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Detailed Exam/History
Re-evaluation of initial assessment followed by complete head-to-toe exam
Necessary to ensure that all acute and chronic insults/disease is identified and considered
Allows for trend identification Review of studies
– Imaging– Laboratory
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Patient History Understand the circumstances surrounding the
injury/illness– Mechanism of injury (MOI)– History of present illness (HPI)
Medical history important to identify comorbidities– Pre-existing disease– Medications/alcohol/illicit drugs– Allergies– Tetanus immunization history
AMPLE
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Performing the Detailed Exam Head-to-toe exam
– Head/face– Neck/cervical spine– Chest
Anterior, lateral, posterior– Abdomen– Perineum/genitalia– Back/spine– Extremities– Vascular– Neurological
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Management and Further Evaluation
Management is same as for any critically ill patient
ABCDE method for prioritizing the management of life threats
Specific management for shock can occur after management of potential life threats– Management of potential life threat may help
manage shock as well
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General Treatment Considerations
Airway management and ventilation key– Begin aggressive airway management early– Endotracheal intubation when necessary
Use of NMBAs when necessary Confirm placement with ETCO2 detection
ETCO2 monitoring
Mechanical ventilation Must be familiar with patient needs, available vent settings
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Fluid Resuscitation(1 of 2)
IV access– Peripheral IV access
Two large-bore IV lines
– Central venous cannulation if: Peripheral IV access cannot be obtained Administration of large volumes of fluid are anticipated Hemodynamic monitoring is required
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Fluid Resuscitation(2 of 2)
Goal is to achieve no more than 75 percent of preinjury blood pressure– Permissive hypotension
Prevents: Excessive bleeding Loss of coagulation factors 200 mL fluid boluses
Re-evaluate, repeat as needed
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Hemoglobin-Based, Oxygen-Carrying Solutions (HBOCs)
Major development in emergency and critical care medicine Differ from traditional IV volume expanders
– Can transport oxygen– Contain polymerized hemoglobin
Obtained from human, bovine blood Removed from red blood cells Isolated
No infectious agents, antigenic proteins, other blood constituents Hemoglobin molecules joined into large chains
Polymerization Compatible with all blood types
Does not require: Typing Testing Cross-matching
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Volume Expanders(1 of 3)
Hypertonic saline– Showed potential initially– Recent evidence suggests it is no more effective
than standard isotonic crystalloids
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Volume Expanders(2 of 3)
Colloids– Popular outside the United States
Australia
– No more or less effective than crystalloids
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Volume Expanders(3 of 3)
Blood and blood products– O negative used if time for typing and cross-
matching does not exist Typed and cross-matched products preferred
– Whole blood versus packed red blood cells
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Pharmacological Agents
For shock unresponsive to fluid bolus administration– Dopamine– Dobutamine– Epinephrine– Norepinepherine
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Hemodynamic Monitoring
Noninvasive means initially– Heart rate– Heart rhythm – Blood pressure
Invasive monitoring: Normal values– Urine output: 0.5–1.0 mL/hr
Via foley
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Arterial Blood Gas: Normal Values(1 of 2)
pH: 7.35–7.45 PaO2: 80–100 mmHg Oxygen saturation: 96 to 98 percent PaCO2: 35–45
HCO3: 22–26 mEq/L Base/excess: 3 mEq/L
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Arterial Blood Gas: Normal Values(2 of 2)
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Additional Assessment and Management
Complete blood cell count and differential
Platelet count Complete serum chemistry
profile (includes electrolytes) Prothrombin and activated
partial thromboplastin times (PT and PTT)
Serum lactate Urinalysis Serum amylase
Arterial blood gases 12-lead EKG Pregnancy test for all
females of child-bearing age Blood, sputum, and urine
gram stains and cultures Blood products
– Packed red blood cells– Fresh frozen plasma
Drug toxicity screening, if indicated
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Imaging Tests
CT Ultrasound X-rays Echocardiogram
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Classifications of Shock
Hypovolemic Obstructive Distributive Cardiogenic
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Hypovolemic Shock Secondary to decrease in circulating blood volume
– Etiologies include: Hemorrhage
Trauma GI bleeding
Other methods of fluid loss Dehydration Excess diuretic use GI loss Sweating Burns
Fluid shift Sepsis
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Signs/Symptoms ofHypovolemic Shock
Altered mental status Diaphoresis Tachycardia, tachypnea Pallor, mottling Thirst Collapsed veins, increased skin turgor Decreased urine output, oliguria, concentrated urine Hypotension
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Management of Hypovolemic Shock
Volume resuscitation– Crystalloids– Colloids– Vasopressors only after volume resuscitation
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Obstructive Shock
Secondary to impedance of normal blood flow– Etiologies
Cardiac tamponade Tension pneumothorax Pericarditis Compression of great vessels
Supine hypotension syndrome Pulmonary embolism Aortic dissection
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Signs and Symptoms of Obstructive Shock
Mirror those of hypovolemic and cardiogenic shock– Signs and symptoms specific to etiology
Tension pneumothorax Cardiac tamponade Pulmonary embolism Aortic dissection
Management Specific to etiology
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Management of Obstructive Shock
Specific to etiology
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Distributive Shock
Characterized by:– Decrease in vascular resistance or– Increased venous capacity secondary to vasomotor
dysfunction Can be further classified as:
– Septic shock– Anaphylactic shock– Neurogenic shock
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Septic Shock
Occurs secondary to systemic infection Predisposing factors
– Immunoinsufficiency– Nosocomial infection
Release of endotoxins by infecting organism– Vasodilation– Increased cell membrane permeability
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Signs and Symptoms ofSeptic Shock
Fever Chills, diaphoresis Petechial rash Pulmonary edema
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Management of Septic Shock
Identification and removal of infection source Fluid therapy Vasopressors
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Anaphylactic Shock Exaggerated, systemic response to an allergen
– Profound vasodilation– Third spacing of fluid– Bronchospasm
Etiologies– Food, drug allergies– Administration of blood products– Envenomation
Speed and severity of symptoms vary– Can occur over minutes or days
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Signs and Symptoms of Anaphylactic Shock
Dyspnea Bronchospasm Dysphagia Rashes, flushing
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Management of Anaphylactic Shock
Epinephrine Antihistamine
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Neurogenic Shock Results from disruption of sympathetic nervous system
secondary to cervical or thoracic spinal injury– Can also occur secondary to:
Severe head injury Migration of spinal anesthesia
– Reduction in peripheral vascular resistance Widespread vasodilation below level of insult
– If insult below level of T6, bradycardia develops Secondary to unopposed vagal tone Prevents compensatory tachycardia
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Signs and Symptoms of Neurogenic Shock
Bradycardia– If insult below T6
Hypotension Warm, flushed skin
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Management of Neurogenic Shock
Fluid administration Vasopressors
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Cardiogenic Shock Results from hearts inability to maintain sufficient CO Often result of myocardial insult
– Ischemia secondary to: AMI Trauma
Myocardial contusion
– Dysrhythmia– Vascular insufficiency
Left ventricular failure results in pulmonary hypertension and edema
Treatment goal is to restore cardiac output
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Signs and Symptoms of Cardiogenic Shock
Vary with etiology
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Management of Cardiogenic Shock
Volume replacement Vasopressors IABP placement Ventricular assist devices Pacemaker CABG
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Bledsoe/Benner, Critical Care Paramedic© 2006 by Pearson Education, Inc. Upper Saddle River, NJ
Summary
Early identification of shock and aggressive management are important
Clinical trends guide continued treatment Appreciation of resources and proficiency with
pharmacology and equipment important