CRITICAL CARE BOOT CAMP CLASS #1
Lian Santiago RN, CPN
Clinical Educator
Pediatric Intensive Care Unit
CHEST TUBE 101 Critical Care Boot Camp Class 1
NORMAL BREATHING
Inhalation - the diaphragm contracts, the ribs move up and out, the sternum moves out, and the lungs expand
Exhalation - the diaphragm relaxes, the ribs move down and in, the sternum returns to normal position, and the lung volume decreases
This process occurs automatically, as regulated by the central nervous system via the respiratory centers in the pons and medulla
Negative intra-pleural pressure keeps the lungs against the chest wall. Loss or disruption of this pressure leads to lung collapse.
A & P BASICS
Visceral/Pulmonary pleura - a thin membrane covering the lungs
Parietal pleura - a thin membrane lining the rib cage
Pleural space - the space between the parietal and visceral pleura
Pleural fluid - a thin layer of lubricating fluid in the pleural space that allows the two membranes to slide across one another when the lungs expand and contract
INDICATIONS FOR CHEST TUBE INSERTION
Pneumothorax- Collection of air in the pleural space
Hemothorax- Collection of blood in space between chest wall and the lung .
Hemopneumothorax- Combination of both conditions
Tension pneumothorax- collection of air in the pleural space that results in tracheal and mediastinal shifts (Opposite Side)
Empyema- Collection of pus in the pleural cavity
Chylothorax- Lymphatic Fluid in the Pleural Space
Pleural Effusion- Excess Fluid build up
Post-Operative cardio-thoracic surgery
VISUALS
ChylothoraxEmpyema
HOW TO CHEST TUBES WORK?
A = Suction Control Chamber
B = Water Seal Chamber
C = Air Leak Monitor
D = Collection
System Set-up
CARE AND ASSESSMENT OF PATIENT WITH A CHEST TUBE
Physical assessment of the patient
Special consideration given to the patient’s respiratory status
Check the chest tube site/dressing for leakage
Reinforce the dressing, if necessary, to ensure the tube’s safety
Starting from the patient, work your way down to the collection chamber, checking for kinks in the tubing
Make sure the connections are secure, paying close attention to the connection between the chest tube/pigtail and the drainage tubing
Assess for any blood or tissue clots in the chest tube, as these may prevent adequate drainage
ASSESSMENT
Check the drainage systemCollection chamber
Note the date/time of the last recorded volume
Drainage rate > 10 mL/kg/hour should be reported to the physician
Water seal chamber
Disconnect system from suction and assess for water level fluctuation with respirations
Note the presence of bubbling, as this will indicate an air leak
Suction control chamber
The water in this chamber should bubble gently when suction is applied. If the bubbling is vigorous, the amount of suction needs to be decreased
IMPORTANT POINTS!
IF THE CHEST TUBE FALLS OUT: Quickly cover and seal the insertion site with a sterile petroleum gauze dressing to prevent air from entering into the pleural cavity. Notify the physician immediately!!!
SAFETY SACK: there should ALWAYS be an emergency chest tube kit at the bedside. The kit should contain:
sterile petroleum gauze dressing
2 x 2 or 4 x 4 gauze
transparent dressing
hemostats
a small bottle of sterile water
REMOVAL OF A CHEST TUBE
An order must be obtained and the chest tube is always removed by a physician!
Administer pain medication prior to chest tube removal
Obtain a suture removal kit
Have your emergency kit supplies open and ready
The MD/NP/PA will remove the chest tube:
Ask the patient to take a deep breath or wait for the infant/small child to inspire
The tube is removed during inspiration
Sterile dressing is applied: Petroleum gauze to seal the insertion site
2 x 2 or 4 x 4 covering the petroleum gauze
Cover with a transparent dressing
INTERVENTIONS POST CHEST TUBE REMOVAL
Incentive spirometry, coughing, and deep breathing exercises are very important after chest tube removal
These activities should be reinforced with all patients who are able to participate
CARING FOR THE CHILD IN SHOCK Critical Care Boot camp Class 1
WHAT IS SHOCK?
oA sustained, progressive circulatory dysfunction resulting in inadequate cardiac output and delivery of oxygen to meet metabolic demand, along with compromised tissue utilization of available oxygen
HUH?!
What does that mean?
DEFINITION IN PLAIN ENGLISH
oA drop in cardiac output = decreased blood flow to the tissues
oDecreased blood flow = not enough oxygen reaching the tissues (decreased perfusion)
oLack of perfusion leads to multi-system failure
oIf not treated, the body’s response to inadequate perfusion is death
PERFUSION
oDependent Variables:
oBlood Volume
oCardiac Pump
oVascular Tone
oAdequate Oxygenatio n
oCellular Function
oWhen one variable fails, the other must compensate
TYPES OF SHOCK
o Cardiogenic
o Obstructive
o Hypovolemic
o Distributive
o Anaphylactic
o Neurogenic
o Septic
CARDIOGENIC SHOCK
o The result of myocardial dysfunction
o Structural: congenital heart defects
o Non-structural: inflammatory heart disease,
metabolic/electrolyte imbalances, drug toxicities, cardiac
tamponade, dysrhythmias
o The heart is unable to pump enough blood out to meet the body’s
needs, resulting in pulmonary congestion and inadequate tissue
perfusion
o TREATMENT: increase cardiac output by restoring myocardial
function
HYPOVOLEMIC SHOCK
oThe most common type of shock in infants and children
oResults from inadequate intravascular volume
oCaused by blood loss, dehydration, fluid shifts related to capillary leak
oLack of volume = decreased blood flow to tissues and organs
oTREATMENT: fluid resuscitation and treatment of the underlying cause
DISTRIBUTIVE SHOCK
oDecreased blood flow due to decreased systemic vascular resistance
oCommon causes
oEarly septic shock, anaphylaxis, toxic ingestions, spinal or epidural anesthesia, spinal cord injuries
oAssessment details
oFlushed skin, warm extremities, bounding pulses, tachycardia (except SCI), wide pulse pressure, brisk capillary refill
oTREATMENT: reversal of underlying etiology, rapid volume expansion, vasoactive medications
ANAPHYLACTIC SHOCK
oInitiated by an overwhelming response to an allergen
oComplete vasodilation and increased capillary permiability
oThird-spacing results in intravascular hypovolemia
oTREATMENT: removal of allergen, when possible, and symptom management (antihistamines, subcutaneous epinephrine, and steroids)
NEUROGENIC SHOCK
oOccurs following insult to the spinal cord or nervous system (spinal cord injury, spinal anesthesia, nervous system injury)
oCauses loss of sympathetic tone, which leads to arterial and venous vasodilation
oTREATMENT: stabilize spinal cord injury and minimize additional trauma, elevate lower extremities and apply anti-embolic stockings and/or compression devices to encourage venous return
SEPTIC SHOCK
oRelated to a severe infection, usually caused by gram-negative bacteremia
o“Sepsis” = the body’s systemic response to infection
oDefinition: sepsis with hypotension, despite adequate fluid resuscitation, along with perfusion abnormalities
oTREATMENT: treat the infection and support circulation/perfusion. Antibiotics must be given as soon as possible after blood cultures are obtained
SEPSIS
oThe body’s systemic response to infection
oA systemic inflammatory response syndrome (SIRS) that alters capillary permiability, impairing vasoregulation
oInflammatory cells and mediators cause endothelial injury, tissue hypoxia, and microthrombi formation
oLeads to organ dysfunction/failure, and can cause death
LEVELS OF SEPSIS
o Sepsis – the presence of SIRS accompanied by an infection
o Severe Sepsis – sepsis plus end-organ dysfunction resulting from lack of
perfusion
o Septic Shock – severe sepsis with persistent hypotension and decreased
tissue perfusion, despite fluid resuscitation
o Multiple Organ Dysfunction Syndrome (MODS) – Presence of altered
organ function in an acutely ill patient, such that homeostasis cannot be
maintained without interventions
CLASSIFICATION OF SHOCK
• Compensated– Blood pressure remains NORMAL
– Compensatory mechanisms are able to redistribute blood flow or maintain vascular tone
• Decompensated– Blood pressure is LOW
– Compensatory mechanisms are no longer able to support blood flow or vascular tone
• Irreversible– Decompensated shock where cardio-pulmonary arrest is imminent
CLINICAL ASSESSMENT
o The most successful treatment of shock is EARLY RECOGNITION
o Tissue perfusion is assessed by monitoring:
o Oxygenation
o Vital signs
o Circulation
CLINICAL ASSESSMENT CONT.
o Neurological Status
o Irritability
o Lack of desire to play
o Altered LOC
o Poor feeding
o Compensatory mechanisms
o Tachycardia
o Tachypnea
o Systemic Perfusion
o Capillary Refill
o Quality of Peripheral Pulses
o Urine Output
CLINICAL ASSESSMENT CONT.
“Warm” Shock – Early- Compensated
oAbnormal temperature regulation
oFlushed skin
oWide pulse pressure
oNormal to brisk capillary refill
oTachycardia
oTachypnea
oNormal Blood Pressure
“Cold” Shock- Late- Decompensated
oTachycardia
oCold extremities
oNarrow pulse pressure
oProlonged capillary refill
oRapid, shallow respirations
oAltered LOC
oCyanosis R/T V-Q mismatch
oOliguria
oHypotension LATE SIGN of shock
CLINICAL ASSESSMENT CONT. Hypovolemic & Cardiogenic Shock
Tachycardia
Hypotension
Peripheral vasoconstriction Pale, mottled skin
Cool extremities
Prolonged capillary refill
Weak peripheral pulse
*Wide pulse pressure = Hypovolemic
*Narrow pulse pressure = Cardiogenic
CLINICAL ASSESSMENT CONT.
Anaphylactic, Neurogenic & Septic Shock
oTachycardia
oWide pulse pressure
oOverwhelming vasodilation
o Flushing
o Warm extremities
o Brisk capillary refill
o Bounding peripheral pulses
CLINICAL ASSESSMENT CONT. Compensated Shock
oApprehension
oIrritability
oUnexplained Tachycardia
oNormal Blood Pressure
oPulse Pressure Changes
oThirst
oPallor
oDecreased Urine Output
oDecreased Extremity Perfusion
CLINICAL ASSESSMENT CONT.
oConfusion
oSomnolence
oTachypnea
oOliguria
oCool, Pale Extremities
oDecreased Skin Turgor
oProlonged Capillary Refill
CLINICAL ASSESSMENT CONT.
Irreversable shock o Weak, Thready Pulses
o Hypotension
o Apnea
o Bradycardia
o Anuria
o Stupor/Coma
CARDIO-PULMONARY ARREST IS IMMINENT!
WHAT DO WE DO?! CLINICAL INTERVENTIONS
o The management goals for shock focus on maximizing cardiac
output and oxygen delivery, while minimizing the body’s oxygen
demand
o Remember your ABC’s
o Provide supplemental oxygen
o IV access is a MUST (the more, the merrier!)
WHAT DO WE DO?! CLINICAL INTERVENTIONS
o Just add “water”o Isotonic fluid bolus
o Administer 10-20 mL/kg rapidlyo Colloids (Albumin)
o 5% Albumin for volume expansiono 25% Albumin for low albumin levels
o Blood productso Administer 10-15 mL/kg
o *Cardiogenic shock: be cautious with fluid administration, as it may lead to systemic and/or pulmonary edema
o **If poor tissue perfusion persists, vasoactive and/or inotropic infusions may be required
WHAT DO WE DO?! CLINICAL INTERVENTIONS
o Minimize oxygen demand by keeping the patient calm &
comfortable
o Decrease anxiety
o Adequate pain management
o Allow the parents to remain at the bedside
o Offer distractions
PULMONARY HYPERTENSION Critical Care Boot Camp Class
#1
PULMONARY HYPERTENSION
♥An elevation of the pulmonary artery pressure above 25 mmHg while at rest
♥Primary (PPHN) or Secondary
♥Anticipatory management♥PREVENT acute exacerbations
FETAL CIRCULATION
♥Patent ductus venosus
♥Bypass the liver
♥Liver not needed for primary fetal metabolism
♥Patent ductus arteriosus
♥Bypass the lungs
♥Lungs not needed for primary fetal respiratory function
PERSISTENT PULMONARY HYPERTENSION OF THE NEWBORN (PPHN)
♥Failure to change over from fetal to normal newborn circulation
♥MAP ½ of mean systemic pressure
♥Fall in PVR
♥Decreased PA pressure
♥Decreased RVEDP
♥Failure to drop pressures leads to elevated PA pressures
♥Pulmonary vasoconstriction
PPHN CONT.
Blood unable to get to the lungs Hypoxia
Usually develops within 72 hours of birth
Risk factors: meconium aspiration, infection, low body temp, congenital heart disease, underdeveloped lungs
Signs & Symptoms
Treatment: improve blood oxygen levels, relax pulmonary blood vessels, maintain normal blood pressure Oxygen therapy
Medications
ECMO
SECONDARY PULMONARY HYPERTENSIONoRelated to a pre-existing disease process that causes increased pulmonary congestion or blood flow
oBlood unable to get to the lungsoHypoxia
oVasoconstriction
oRisk factors: congenital heart disease, left ventricular failure
oSigns & Symptoms
oTreatment: manage precipitating condition, improve blood oxygen levels, relax pulmonary blood vessels, maintain normal blood pressureoOxygen therapy
oMedications
oECMO
CLINICAL MANIFESTATIONS
♥Dyspnea
♥Most common symptom
♥Caused by impaired oxygen delivery
♥Chest pain
♥Results from coronary ischemia in the right ventricle
♥Syncope
♥Secondary to decreased cardiac output
♥Right-sided heart dysfunction
♥Progressive detail – indicates poor prognosis
♥Venous congestion
♥Edema
PPHN THERAPIES
♥No known cure
♥Treatment is supportive, aimed at improving quality of life
♥Current available therapies
♥Supplemental oxygen
♥Anti-coagulant therapy
♥Vasodilators
♥PO: Sildenafil, Bosentan
♥IV: Prostacycline (Flolan, Remodulin), Milrinone
♥PO Calcium Channel blockers
♥Bilateral lung transplantation
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