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Cardiognic Pulmonary Edema

This document discusses pulmonary edema, pleural effusion, and asthma. It covers the causes, pathophysiology, clinical presentation, investigations, and management of cardiogenic pulmonary edema. It also discusses the differences between cardiogenic and non-cardiogenic pulmonary edema. For pleural effusion, it describes the criteria for exudates vs transudates. For asthma, it outlines how to assess severity and provides guidelines for treatment and admission criteria.

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Deepak Benjamin
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0% found this document useful (0 votes)
42 views41 pages

Cardiognic Pulmonary Edema

This document discusses pulmonary edema, pleural effusion, and asthma. It covers the causes, pathophysiology, clinical presentation, investigations, and management of cardiogenic pulmonary edema. It also discusses the differences between cardiogenic and non-cardiogenic pulmonary edema. For pleural effusion, it describes the criteria for exudates vs transudates. For asthma, it outlines how to assess severity and provides guidelines for treatment and admission criteria.

Uploaded by

Deepak Benjamin
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
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PULMONARY

EDEMA, PLEURAL
EFFUSION, ASTHMA
CARDIOGENIC PULMONARY
EDEMA
• CAUSES:
 Acute complication of MI & IHD.
 Exacerbation of pre-existing cardiac problems- HTN,
aortic/mitral valve disease.
 Arrhythmias.
 Failure of prosthetic valves.
 Ventricular septal defect.
 Cardiomyopathy.
 ß-Blockers.
 Acute myocarditis. Left Atrial myxoma.
 Pericardial disease.
• PATHOPHYSIOLOGY:

 Left heart failure results in ↑LV end-diastolic pressure causing


↑pulmonary capillary hydrostatic pressure → fluid collection
in the extravascular pulmonary tissues faster than the
lymphatics could clear it.

• HISTORY:

 Dyspnoea & distress.


 Time of onset & any associated chest pain.
 Check for current medications.
GRADES OF DYSPNEA
• Grade I – Minimal Dyspnea. Dyspnea on
running or on doing more than ordinary effort.

• Grade II – On doing ordinary effort.

• Grade III – Considerable Dyspnea. On doing


less than ordinary effort.

• Grade IV – Dyspnea at rest.


EXAMINATION:
• Tachypnoeic, tachycardic & anxious.

• Cyanosed, coughing out pink frothy sputum & unable to talk-


severe cases.

• Look for ↑JVP.

• Inspiratory crepitations.

• Wheeze may be more prominent.

• Cardiogenic pulmonary edema is associated with evidence of


decreased CO.
INVESTIGATIONS:
• ECG- Arrhythmias, LVH, LBBB, recent or evolving MI.
• Blood- U&E, glucose, FBC, Troponin.
• ABG if saturations are very low.
• CXR- Features in cardiogenic pulmonary edema:
 Upper lobe diversion- Distension of upper pulmonary veins.
 Cardiomegaly.
 Kerley A,B & C septal lines.
 Fluid in interlobar fissures.
 Peribronchial & perivascular cuffing.
 Pleural effusion.
 Bat’s wing Hilar Shadows.
TREATMENT
• Raise the head-end to sitting position.
• High flow O2 with tight fitting face mask.
• If SBP>90mmHg, give S/L Sorbitrate & then start
NTG.
• IV Furosemide 50-60mg. Higher doses for the once
already on Furosemide.
• Monitor urine output.
• Treat underlying cause.
• Non-Invasive ventilation- CPAP should be started.
• Invasive ventilation when CPAP doesn’t improve or
cardiovascular collapse takes place.
PROSTHETIC VALVE FAILURE
• Acute failure results in dramatic acute onset pulmonary
edema with loud murmurs.

• Resuscitation should be carried out as per protocol.

• Urgent help- ICU Team, Cardiologist & CT Surgeon.

• Confirmation- Transthoracic or transesophageal ECHO.

• Immediate valve replacement is the treatment of choice.


NON-CARDIOGENIC PULMONARY OEDEMA
• This can occur in the absence of ↑ pulmonary venous pressure.
• Mechanisms:
 ↑ Capillary permeability.
 ↓ Plasma oncotic pressure.
 ↑ Lymphatic pressure.

• Causes:
 ARDS.
 IC Bleed.
 IVF overload.
 Hypoalbuminaemia.
 Drugs/Poisons/Chemical inhalation.
 Lymphangitis carcinoma.
 Smoke inhalation.
 Near drowning incidents.
 High altitude moutain sickness.
APPROACH
• To distinguish it from cardiogenic cause.

• Treatment should be initiated as per the


underlying cause.

• Primary management should be as per the


cardiogenic pulmonary edema protocol.
PLEURAL EFFUSION
• Normal- 20ml in each pleural cavity.

• Exudate- If Pleural Fluid : Serum Protein >0.5

Pleural Fluid : Serum LDH >0.6

Fluid LDH >2/3 the upper limits of normal


serum LDH value.
EXUDATES TRANSUDATES
• Pneumonia. • Cardiac failure.

• Malignancy.
• Nephrotic syndrome.
• TB.
• Hepatic failure.
• PE with pulmonary infarction.
• Ovarian hyper stimulation.
• Collagen vascular disease.

• Subphrenic abscess. • Ovarian fibroma.

• Amoebic liver abscess. • Peritoneal dialysis.

• Pancreatitis.
CLINICAL PRESENTATION
SYMPTOMS SIGNS
 Not apparent until >500ml
A mild dull ache & of fluid present.
dyspnea may be present  Dyspnoea.
in large effusion.  Stony dullness to
percussion.
Absent breath sounds.
H/O of vomiting
 ↓ Breath sounds.
followed by chest pain
Bronchial breathing.
→ ruptured esophagus.
Large unilateral Effusion→
Mediastinal Shift.
• INVESTIGATIONS:
 CXR- Only if ≥ 250mL.

• TREATMENT:
 Provide O2 if required.
 Emergency therapeutic pleural aspiration if severe respiratory
distress.
 Involve medical team.

BLUNTING OF
COSTOPHRENIC ANGLE
ACUTE ASTHMA: ASSESSMENT
• Peak expiratory flow rate should be measured and be compared with
the expected rate!!

• MODERATE EXACERBATIOB OF ASTHMA:


 Increasing symptoms.
 Peak flow 50-75%.
 No features of acute severe asthma.

• ACUTE SEVERE ASTHMA:


 Inability to complete sentences in 1 breath.
 RR >25/min
 HR >110/min
 Peak flow 33-50%.
• LIFE-THREATENING ASTHMA:
 Cyanosis.
 Exhaustion, confusion, coma.
 Feeble respiratory effort.
 SpO2 <92%.
 Silent chest.
 Bradycardia, arrhythmia, hypotension.
 pO2 <60mmHg.
 Normal pCO2.
 Peak flow <33%.

• NEAR FATAL ASTHMA:


 ↑ pCO2 and may require mechanical ventilation.
• CLINICAL FEATURES THAT INCREASE
THE PROBABILITY OF ASTHMA:

 Diurnal variation in symptom severity.

 Symptoms in response to exercise, allergen exposure &


cold air.

 Px or family h/o atopic disorders.

 Peripheral blood eosinophilia.

 H/O improvement with treatment.


• INVESTIGATIONS:
 Peak expiratory flow rate.

 ABG if SpO2 <92% or Life threatening asthma.

 CXR if the following conditions are suspected.


 Suspected pneumomediastinum or pneumothorax.
 Suspected consolidation.
 Life-threatening asthma.
 Failure to respond to treatment as expected.
 Requirement for ventilation.
ACUTE ASTHMA: MANAGEMENT
• High flow O2 to maintain saturations at 94-98%.
• Patient in sitting position.
• Check trachea & chest signs for pneumothorax.
• Salbutamol 5mg nebulization- consider continues nebulizations.
• Inj. Hydrocortisone 100mg IV.
• Add Ipratropium Bromide 500mcg to salbutamol nebulization.
• Inj. Magnesium Sulphate 1.2-2gm IV over 20min.
• Inj. Aminophylline 5mg/kg over 20min if never used before. If on
aminophylline, blood levels should be sent and then infusion @ 0.5-
0.7mg/kg/hr.
• Inj. Salbutamol 5mg in 500mL 5% Dextrose.
• Proper hydration.
• Avoid antibiotics.
• Repeat ABG within an hour.
• Watch out for Hypokalaemia.
• CRITERIA FOR ADMISSION:

 A life-threatening or near-fatal attack.


 Severe attack persisting after initial treatment.

• INTENSIVE CARE REFERRAL:

 Drowsiness, confusion.
 Exhaustion, feeble respiration.
 Coma or Respiratory arrest.
 Persisting or worsening hypoxia.
 Hypercapnoea.
 ABG showing ↓ pH.
 Deteriorating peak flow.
DISCHARGE CRITERIA &
MANAGEMENT
• Consider discharge if peak flow is >75% or predicted 1hr
after initial treatment.

• Tab. Prednisolone 40-50mg for 5days if initial peak


inspiratory flow rate <50%.

• Adequate supply of Inhalers.

• Inhaler technique and PEFR monitoring should be reviewed.

• GP follow-up within 2 days.


CARDIAC ARREST IN ACUTE
ASTHMA
• Underlying rhythm is usually PEA.

• This may be because of prolonged severe hypoxia,


hypoxia-related arrhythmias or tension pneumothorax.

• ACLS Protocol to be followed.

• Tension pneumothorax to be relieved if present.

• Intubation early during resuscitation.


SOME ISSUES TO BE CONSIDERED
• Handover book to be completed daily.
• All procedures to be entered into the computer. Lately no one
is doing it!!!!
• 2DECHO to be done for all P1 cases from our side!!!
• Provisional diagnosis should be meaningful and sensible!!!
• You all should know the difference between comorbids n
provisional diagnosis.
• Please don’t act as duty doctors!!!
• Do not go away from our protocols.
• Px history to be taken properly and entered properly into the
initial assessments.
• Past medical treatment should be taken in detail n present
history to be correlated properly!!!
• Know your ATLS protocol properly and follow it!!!
• Log roll to be done for all P1 trauma cases without fail.
• When resuscitating a patient, follow your ACLS protocol
strictly!! Do not give bicarb, heparin and other nonsense!!!
• In Hypovolemic shock, always consider blood!!!
• If you don’t know or understand something, call me or the
registrar posted in the center!!!
• In respiratory distressed Px, always have NIV option on the
back of your mind!!
• Know our Sepsis Protocol thoroughly!!!
• Read your OHEM properly.
• Last but not least, you all r residents and you all have to learn a
lot. Please don’t forget that and concentrate on your work!!
Don’t get distracted with other stuff!!!

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