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