bledsoe/benner, critical care paramedic © 2006 by pearson education, inc. upper saddle river, nj...

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



Specific parameters measured– CO– Right arterial pressure– Right ventricular pressure– Pulmonary artery pressure– Pulmonary artery wedge pressure (PAWP)

PAP



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


Waveform Interpretation

Pressure changes during systole and diastole Waveforms classified as:

– Right atrial– Right ventricular– Pulmonary artery pressure– Pulmonary artery wedge pressure

PAP


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


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


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


Insertion of PA Catheter (2 of 2)


Right Atrial Pressure

Mean right atrial pressure– 8 mmHg

Right Atrial Pressure


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


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


Pulmonary Artery Pressure (2 of 4)

Systolic– 15–30 mmHg– Equal to right ventricular systolic pressure

PAP


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


Pulmonary Artery Wedge Pressure (PAWP)

Measures left-atrial and ventricular end-diastolic pressure– More accurate than estimate from pulmonary artery diastolic pressure

PAWP


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


Complications of PA Catheterization

Pulmonary injury– During needle puncture

Dysrhythmias Infection Pulmonary artery rupture

PAWP


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


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


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



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)


Intra-Aortic Balloon Pump (IABP) (2 of 3)

IABP


Indications for IABP Therapy

Cardiogenic shock Left ventricular failure Drug-induced cardiovascular failure Septic shock Cardiac surgery preparation

IABP


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



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



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



Ensure proper IABP functioning, including:– Correct timing– Consistent triggering– Appropriate troubleshooting of all alarm situations– Safe operation



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


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


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


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


Shock


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


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


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


Compensatory Mechanisms

Counter effects of shock state Inability to correct insult may lead to death


Cell Physiology


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.


TCA Cycle



Pathophysiology


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



Metabolic requirement for oxygen (MRO2)– Rate at which oxygen is metabolized to water in the mitochondria– Water is byproduct of the TCA (Krebs) cycle



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



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



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)


Precursors to Shock

Inadequate CO Inadequate Hb concentration or oxygen-carrying

capacity Inadequate arterial oxygen saturation


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


Sodium/Potassium (Na/K) Pump (2 of 2)



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


Organ Systems in Shock When cell lysis

involves many cells, organ function is compromised

Shock develops


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



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)


Symptoms of Shock


Neurohumoral Agents and Effects


Hormonal and Nervous Factors Influencing Blood Pressure


Norepinepherine Vasoconstriction Increased myocardial contractility

Compensation


Epinephrine

Increased heart rate Increased myocardial contractility

Compensation


Angiotensin II Vasoconstriction Promotes secretion of

antidiuretic hormone

Compensation


Antidiuretic Hormone(ADH)

Increases water retention in kidneys


Aldosterone

Promotes Na and water retention in kidneys

Compensation


Cortisol

Suppresses immune and inflammatory response Promotes protein catabolism Increases blood glucose

Compensation


Stages of Shock


Compensated Shock

Body able to detect decrease in CO– Baroreceptors– Chemoreceptors

Stages of Shock


Baroreceptor Reflex



Chemoreceptor Reflex



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


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


Decompensated Shock

Cellular death– Can occur suddenly or over days

Prognosis poor

Stages of Shock


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


Initial Assessment and Management

Same as any other critically ill patient Goal is to identify and treat any potentially life-

threatening injuries


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


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


Circulation(1 of 2)

Assessment– Blood pressure– Pulse rate and quality– Skin color/temperature– Capillary refill time


Circulation(2 of 2)

Management– BLS maneuvers

Raise legs

– IV cannulation Fluid administration Vasopressors

Dopamine Dobutamine Epinephrine Norepinephrine


Disability, Neurologic Deficit

Assessment– AVPU– GCS– Level of consciousness– Motor, sensation– If altered, rule out:

Trauma Substance abuse


Examine/Exposure

Remove all clothing to fully expose patient Cover with blankets to preserve heat once exam

is complete


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


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


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


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


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


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


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


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


Volume Expanders(1 of 3)

Hypertonic saline– Showed potential initially– Recent evidence suggests it is no more effective

than standard isotonic crystalloids



Colloids– Popular outside the United States

Australia

– No more or less effective than crystalloids



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


Pharmacological Agents

For shock unresponsive to fluid bolus administration– Dopamine– Dobutamine– Epinephrine– Norepinepherine


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


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


Arterial Blood Gas: Normal Values(2 of 2)


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


Imaging Tests

CT Ultrasound X-rays Echocardiogram


Classifications of Shock

Hypovolemic Obstructive Distributive Cardiogenic


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


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


Management of Hypovolemic Shock

Volume resuscitation– Crystalloids– Colloids– Vasopressors only after volume resuscitation


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


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


Management of Obstructive Shock

Specific to etiology


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


Septic Shock

Occurs secondary to systemic infection Predisposing factors

– Immunoinsufficiency– Nosocomial infection

Release of endotoxins by infecting organism– Vasodilation– Increased cell membrane permeability


Signs and Symptoms ofSeptic Shock

Fever Chills, diaphoresis Petechial rash Pulmonary edema


Management of Septic Shock

Identification and removal of infection source Fluid therapy Vasopressors


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


Signs and Symptoms of Anaphylactic Shock

Dyspnea Bronchospasm Dysphagia Rashes, flushing


Management of Anaphylactic Shock

Epinephrine Antihistamine


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


Signs and Symptoms of Neurogenic Shock

Bradycardia– If insult below T6

Hypotension Warm, flushed skin


Management of Neurogenic Shock

Fluid administration Vasopressors


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


Signs and Symptoms of Cardiogenic Shock

Vary with etiology


Management of Cardiogenic Shock

Volume replacement Vasopressors IABP placement Ventricular assist devices Pacemaker CABG


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

bledsoe/benner, critical care paramedic © 2006 by pearson education, inc. upper saddle river, nj...

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