Medical Emergencies.Anuradha Perera (B.Sc.N)special

Respiratory failure

Definitionsacute respiratory failure occurs when:pulmonary system is no longer able to meet the metabolic demands of the bodyhypoxaemic respiratory failure:PaO2 50 mm Hg when breathing room airhypercapnic respiratory failure:PaCO2 50 mm Hg.

Oxygen inDepends onPAO2Diffusing capacityPerfusionVentilation-perfusion matching

Carbon dioxideWater vapourOxygenNitrogen

Chart2

14.74

5

1.26

79

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Oxygen14.74

Carbon dioxide5

Water vapour1.26

Nitrogen79

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Pathophysiology

Perfusion without ventilation (Shunting)Intra-cardiacAny cause of right to left shunteg Fallots, EisenmengerIntra-pulmonaryPneumoniaPulmonary oedemaAtelectasisCollapsePulmonary haemorrhage or contusion

Perfusion without ventilation (shunting)Intra-pulmonarySmall airways occluded ( e.g asthma, chronic bronchitis)

Alveoli are filled with fluid ( e.g pulm edema, pneumonia)

Alveolar collapse ( e.g atelectasis)

BrainstemSpinal cordNerve rootAirwayNerveNeuromuscular junctionRespiratory muscleLungPleuraChest wallSites at which disease may cause ventilatory disturbance

Respiratory FailureSymptomsCNS:HeadacheVisual DisturbancesAnxietyConfusionMemory LossWeaknessDecreased Functional Performance

Respiratory FailureSymptomsPulmonary:CoughChest painsSputum productionStridorDyspnea

Respiratory FailureSymptomsCardiac:OrthopneaPeripheral edemaChest pain

Other:Fever, Abdominal pain, Anemia, Bleeding

ClinicalRespiratory compensationSympathetic stimulationTissue hypoxiaHaemoglobin desaturation

ClinicalRespiratory compensationTachypnoea RR > 35 Breath /minAccessory musclesRecesssionNasal flaringSympathetic stimulationTissue hypoxiaHaemoglobin desaturation

ClinicalRespiratory compensationSympathetic stimulationHRBPsweatingTissue hypoxiaHaemoglobin desaturation

ClinicalRespiratory compensationSympathetic stimulationTissue hypoxiaAltered mental stateHR and BP (late)Haemoglobin desaturation

ClinicalAltered mental statePaO2 +PaCO2 acidosis dilatation of cerebral resistance vesseles ICP

DisorientationHeadachecomapersonality changes

ClinicalRespiratory compensationSympathetic stimulationTissue hypoxiaHaemoglobin desaturationcyanosis

Respiratory FailureLaboratory TestingArterial blood gasPaO2PaCO2PHChest imagingChest x-rayCT sacnUltrasoundVentilationperfusion scan

Respiratory FailureLaboratory TestingRespiratory mechanicsSpirometry (FVC, FEV1, Peak flow)

Respiratory muscle pressuresMIP ( maximum inspiratory pressure)MEP ( maximum expiratory pressure)

Respiratory FailureLaboratory TestingOther testsHemoglobinElectrolytes, blood urea nitrogen, creatinineCreatinine phosphokinase, aldolaseEKG, echocardiogramElectromyography (EMG)Nerve conduction study

True or FalseDiffusion abnormality is considered the most common cause of hypoxia.

True or FalseDead space ventilation decreases when blood flow is reduced

True or FalseShunt occurs when areas of lung are perfused but not ventilated

True or FalseIn myasthenia gravis mechanism of hypoxia may be due to alveoli being perfused but not ventilated

True or FalseArterial hypoxemia may be caused by alveolar hypoventilation alone

True or FalseThe distinction between ventilation/perfusion mismatch and intrapulmonary shunting can be made by measuring the response to the administration of 100% oxygen

True or FalseThere is a good relationship between dyspnea and arterial hypoxemia but a poor relationship between dyspnea and arterial carbon dioxide retention

Which of the following statements regarding the physical examination for patients with acute respiratory failure are true or false?

Central nervous examination is importantBreath sounds are commonly diminishedSupraclavicular and intercostal space muscle retractions do not correlate with increased work of breathing

QUESTIONS

Pulse oximetry

Cardiac failure

Heart AttackAcute myocardial infarction (AMI)Pain signals death of cells.Opening the coronary artery within the first hour can prevent damage.Immediate transport is essential.

Signs and SymptomsSudden onset of weakness, nausea, sweating without obvious causeChest pain/discomfortOften crushing or squeezingDoes not change with each breathPain in lower jaw, arms, back, abdomen, or neckSudden arrhythmia with syncopeShortness of breath or dyspneaPulmonary edemaSudden death

Pain of Heart AttackMay or may not be caused by exertionDoes not resolve in a few minutesCan last from 30 minutes to several hoursMay not be relieved by rest or nitroglycerin

Sudden Death40% of AMI patients do not reach the hospital.Heart may be twitching.

ArrhythmiasBradycardiaVentricular Tachycardia

Cardiogenic ShockHeart lacks power to force blood through the circulatory system.Onset may be immediate or not apparent for 24 hours after AMI.

Congestive Heart FailureCHF occurs when ventricles are damaged.Heart tries to compensate.Increased heart rateEnlarged left ventricleFluid backs up into lungs or body as heart fails to pump.

You are the Provider (continued)You obtain a brief history while taking the patients blood pressure.Your partner retrieves the nitroglycerin and obtains permission from medical control.Your partner administers the nitroglycerin.What else can you do at this time?

Focused History and Physical Exam

Medications are important! Medications often prescribed for CHF:FurosemideDigoxinAmiodarone

Focused Physical ExamCardiac and respiratory systemsLook for skin changes.Lung soundsBaseline vital signsBOTH systolic and diastolic BP readings

CommunicationRelay history, vital signs, changes, medications,and treatments.

AspirinAdminister according to local protocol.Prevents clots from becoming biggerNormal dosage is from 162 to 324 mg.

NitroglycerinFormsPill, spray, skin patchEffectsRelaxes blood vessel wallsDilates coronary arteriesReduces workload of heart

Nitroglycerin ContraindicationsSystolic blood pressure of less than 100 mm HgHead injuryMaximum dose taken in past hour

Nitroglycerin PotencyNitroglycerin loses potency over time.Especially if exposed to lightWhen nitroglycerin tablets lose potency:May not feel the fizzing sensationMay not experience the burning sensation and headacheFizzing only occurs with a potent tablet, not in the spray form.

Assisting With Nitroglycerin (1 of 4)Obtain order from medical direction.Take patients blood pressure.

Assisting With Nitroglycerin (2 of 4)Check that you have right medication, patient, and delivery route.Check expiration date.Find out last dose taken and effects.Be prepared to lay the patient down.

Assisting With Nitroglycerin (3 of 4)Administer tablet or spray under tongue.Have patient keep mouth closed until tablet dissolves or is absorbed.

Assisting With Nitroglycerin (4 of 4)Recheck blood pressure.Record each activity and time of application.Reevaluate and note response.May repeat dose in 3 to 5 minutes.

Ongoing AssessmentRepeat initial assessment. Reassess vital signs every 5 minutes.Monitor closely.If cardiac arrest occurs, begin defibrillation or CPR immediately.Record interventions, instructions from medical control, patients response. Obtain medical control physicians signature.

Heart Surgeries and PacemakersCoronary artery bypass graft (CABG) AngioplastyCardiac pacemaker

Automatic Implantable Cardiac Defibrillators (1 of 2)Maintains a regular heart rhythm and rateDo not place AED patches over pacemaker.

Automatic Implantable Cardiac Defibrillators (2 of 2)Monitor heart rhythm and deliver shocks as needed.Low electricity will not affect rescuers.

Cardiac ArrestThe complete cessation of cardiac activity, either electrical, mechanical, or both.

Automated External Defibrillator (AED)AEDs come in various models.Some operator interaction required.A specialized computer recognizes heart rhythms that require defibrillation.

Potential AED ProblemsBattery is dead.Patient is moving.Patient is responsive and has a rapid pulse.

AED AdvantagesALS providers do not need to be on scene.Remote, adhesive defibrillator pads are used.Efficient transmission of electricity

Non-Shockable RhythmsAsystolePulseless electrical activity

Rationale for Early DefibrillationEarly defibrillation is the third link in the chain of survival.A patient in ventricular fibrillation needs to be defibrillated within 2 minutes.

AED MaintenanceRead operators manual.Check AED and battery at beginning of each shift.Get a checklist from the manufacturer.Report any failures to the manufacturer and the FDA.

Medical DirectionShould approve protocolsShould review AED usageShould review speed of defibrillationShould provide review of skills every 3 to 6 months

PreparationMake sure the electricity injures no one.Do not defibrillate a patient lying in pooled water.Dry a soaking wet patients chest first.Do not defibrillate a patient who is touching metal.Remove nitroglycerin patches.Shave a hairy patients chest if needed.

Using an AED (1 of 8)Assess responsiveness.Stop CPR if in progress.Check breathing and pulse.If patient is unresponsive and not breathing adequately, give two slow ventilations.

Using an AED (2 of 8)If there is a delay in obtaining an AED, have your partner start or resume CPR.If an AED is close at hand, prepare the AED pads.Turn on the machine.

Using an AED (3 of 8)Remove clothing from the patients chest area. Apply pads to the chest.Stop CPR.State aloud, Clear the patient.

Using an AED (4 of 8)Push the analyze button, if there is one.Wait for the computer.If shock is not needed, start CPR. If shock is advised, make sure that no one is touching the patient. Push the shock button.

Using an AED (5 of 8)After the shock is delivered, begin 5 cycles of CPR, beginning with chest compressions.After 5 cycles, reanalyze patients rhythm.If the machine advises a shock, clear the patient and push shock button.If no shock advised, check for pulse.

Using an AED (6 of 8)If the patient has a pulse, check breathing.If the patient is breathing adequately, provide oxygen via nonrebreathing mask and transport.

Using an AED (7 of 8)If the patient is not breathing adequately, use necessary airway adjuncts and proper positioning to open airway. Provide artificial ventilations with high-concentration oxygen.Transport.

Using an AED (8 of 8)If the patient has no pulse, perform 2 minutes of CPR.Gather additional information on the arrest event.After 2 minutes of CPR, make sure no one is touching the patient.Push the analyze button again (as applicable).If necessary, repeat alternating CPR/Analyze/Shock until ALS arrives.Transport and check with medical control.Continue to support the patient as needed.

After AED ShocksCheck pulse.No pulse, no shock advisedNo pulse, shock advisedIf a patient is breathing independently:Administer oxygen.Check pulse.If a patient has a pulse but breathing is inadequate, assist ventilations.

Transport ConsiderationsTransport:When patient regains pulseAfter delivering six to nine shocksAfter receiving three consecutive no shock advised messagesKeep AED attached.Check pulse frequently.Stop ambulance to use an AED.

Cardiac Arrest During Transport (1 of 2)Check unconscious patients pulse every 30 seconds.If pulse is not present:Stop the vehicle.Perform CPR until AED is available.Analyze rhythm.Deliver shock(s).Continue resuscitation according to local protocol.

Cardiac Arrest During Transport (2 of 2)If patient becomes unconscious during transport:Check pulse.Stop the vehicle.Perform CPR until AED is available.Analyze rhythm.Deliver up to three shocks.Continue resuscitation according to local protocol.

Acute respiratory failure can defined as a state in which the pulmonary system is no longer able to meet the metabolic demands of the body. It can be divided into hypoxaemic respiratory failure and hypercapnic respiratory failure. Hypoxaemic respiratory failure is defined as an arterial partial pressure of oxygen of less than or equal to 6.7 kPa when breathing room air and hypercapnic respiratory failure is defined as an arterial partial pressure of carbon dioxide of more than or equal to 6.7 kPaGetting oxygen into the body depends on the partial pressure of oxygen in the alveoli, the diffusing capacity of the alveolar membrane, ventilation, perfusion and the relationship between the two.The partial pressure of each gas in a mixture of a gases is directly related to the proportions in which they are present. The sum of the partial pressures is equal to the total pressure inside the container. Thus the partial pressure of a particular gas can be increased by increasing the total pressure or by increasing the proportion of that gas in the mixture. Therefore increasing the alveolar pressure or the proportion of the alveolar gas that consists of oxygen increasing will increase alveolar PO2Increasing the inspired concentration of oxygen increases the proportion of alveolar gas that is oxygen while reducing the proportion that consists of nitrogen.The proportion of alveolar gas that is water vapour remains constant and therefore water vapour has no effect on changes in alveolar PO2. On the other hand the proportion of alveolar gas that is CO2 does change and so alveolar PCO2 does affect alveolar PO2Finally as oxygen diffuses out of the alveolus and carbon dioxide diffuses in the alveolar PO2 falls and PCO2 rises. Ventilation with fresh gas is necessary to restore these to their initial values

Shunting can also occur at an intra-cardiac level but this is an unusual cause of hypoxaemia in the ICU. Causes of intrapulmonary shunting include pneumonia, pulmonary oedema, atelectasis, collapse and pulmonary haemorrhage or contusionHypoventilation can be caused by disease at any of the anatomical sites involved in ventilation. Brainstem injury or disease may result in impaired functioning of the respiratory centre, which may also be suppressed by depressant drugsClinical signs of respiratory failure can be divided into signs of respiratory compensationSuch as tachypnoea, use of accessory muscles, recession and nasal flaringSigns of sympathetic stimulation such as tachycardia, hypertension and sweatingSigns of tissue hypoxia such as altered mental status and at a very late stage bradycardia and hypotensionAnd signs of haemoglobin desaturationThe pulse oximeter is an extremely useful monitor which estimates arterial saturationthe relationship between saturation and PaO2 is described by the oxyhaemoglobin dissociation curvea saturation ~90% is a critical threshold because below this level a small fall in PaO2 produces a sharp fall in SpO2 .Conversely a rise in arterial PO2 has little effect on saturation and therefore little effect on oxygen delivery to tissues******** Photos.com******************