Pt w/ SOB Flashcards
Acute asthma attack presentation?
What are precipitants of asthma attack?
Acute asthma attack
- Acute SOB
- Wheeze
- Cough
- Cyanosis (if extreme)
PRECIPITANTS in hx: cold, exercise, allergens, smoke, infection
***the patient might not know they have asthma or they might come in with a dx and having tried to manage their own asthma at home and failed
**for the patient who does not know wheeze is an important sign
Grading of severity for acute asthma (moderate, severe, life threatening) -think about the nemonics
At what point would you think this is near FATAL?
MODERATE = PEFR 50-75% with none of below features
SEVERE = 50STaR
- 33%-50% PEFR
- Sentences-Inability to complete full sentences
- Tachycardia >110/min
- RR >25/mi
LIFE-THREATENING = 33 92, NO CHEST
- <33% PEFR
- 92% Sats
- Normal CO2 (4.6-6kPa)
- Oxygen (<8kPa)
- Cyanosis
- Hypotensive
- Exhaustion/confusion
- Silent chest
- Tachycardia (can get arrhythmia)
Near FATAL: ↑PaCO2> 6kpa ± requiring mechanical intervention
Investigations in acute asthma
Bedside
- O2 sats
- Resp rate
- ECG (look for arrhythmias)
- Peak flow (PEFR)
Bloods
- ABG (increased Co2 concerning, high bicarbonate suggests poorly controlled asthma over several days)
- FBC (infection)
- CRP
- Us and Es
Imaging
-CXR
How many puffs of inhaler is maximum before going to hospital?
Management of acute asthma in hospital?
GO TO A AND E IF NO IMPROVEMENT AFTER 10 PUFFS
Management of acute asthma:
• ABCDE
• Oxygen -15L/min via non-rebreathe mask(maintain sats of 94-98%)
• Salbutamol 5mg NEB with oxygen (back to back-THREE IN A ROW)
• If severe or life threatening (PEFR<50%) add ipatropium bromide 0.5mg NEB
• Early treatment with Oral Pred (40mg) or IV hydrocortisone 100mg if can’t tolerate
Reassess every 15 mins
• If still <75% repeat salbutamol nebs every 15-30 mins
CALL SENIOR - Magnesium sulphate (with cardiac monitoring), theophylline, or IV salbutamol
(in reality you would just get nurses to mix ipratropium bromide and salbutamol for nebs-takes longer to run through but its good to get both going)
Monitoring response to treatment
What is an important side effect of treatment used in acute asthma?
When should you refer to ICU?
Monitoring response to treatment
- PEFRs regularly
- Repeat ABGs 1-2hrly (consider arterial line)
Side effect
-Monitor serum K+ (hypokalaemia as a result of β2-agonists) (also cardiac monitoring for mag sulphate)
***if poor response or life threatening (33% PEFR) arrange admission to ICU
Acute COPD presentation
COPD
- SOB
- Wheeze
- Cough (productive, infective if infective exacerbation)
- Fever
- Tachypnoeic
- Accessory muscle use
Acute COPD examination findings
Examination
- hyperinflation
- hyper-resonant
- wheeze
- cyanosis
- right sided heart failure (cor pulmonale)
- signs of hypercapnia (flap, bounding pulse, vasodilatoin)
Causes of acute COPD
Can either be infective or non-infective
INFECTIVE = H. influenzas or S. pneumonia
Hx factors will help determine (productive sputum, fever, malaise, anorexia)
Investigations for acute COPD, what would they show?
Continuous observation
Bloods FBC, U+E, CRP, ESR, gas
CXR (hyperinflation, flattened diagphrams,?consolidation)
ECG
• AF
• RVH increase in p wave amplitude
• Right axis deviation
• RBBB
ABG (type 2 resp failure, high bicarb-met compensation)
Septic screen (blood cultures, CXR, sputum culture)
Initial management of acute COPD
Initial COPD management- COSICARRR
- Controlled Oxygen 88-92% targets
- Salbutamol (5mg) NEB
- Ipatropium bromide (0.5mg) NEB
- Corticosteroid- oral prednisolone 30mg or IV hydrocortisone
- Antibiotics if infective (amoxicillin/clarithromycin/ doxycycline)
- Aminophylline if SEVER
- Radiography - CXR
- Respiratory support - BiPAP
- Refer
Criteria for NIV in acute COPD
CPAP or BiPAP
- Persisting respiratory acidosis after 1hr of medical management: (O2, salbutamol, ipratropium, prednisolone, and abx when indicated)
- Bipap is for T2RF
Pneumonia presentation (symptoms and on examination)
PNEUMONIA
• Shortness of breath
• Cough
- Productive in adults - purulent sputum
- Often dry in infants/elderly or atypical pneumonia
- Sometimes haemoptysis
• Pleuritic chest pain - most painful on inspiration
• Fever, rigors, sweats
• Nausea
O/E
Tachycardia, tachypnoea, crackles, hypotensive, febrile, confused
What are the most common organisms to cause a CAP?
name some atypical causes?
CAP
- Streptococcus pneumoniae 50%
- Haemophilus influenzae (COPD)
- Moraxella catarrhalis
Atypical
- Mycoplasma pneumoniae
- Legionella
- Chlamydia pneumoniae
- Define HAP
- What are the common organisms?
HAP
-Pneumonia 48 hours after admission (or 5+ days depending on trust) OR 4-6 WEEKS post admission
- different profile of organism
1. Gram negative enterobacteria
2. Staphylococcus aureus
3. Pseudomonas
4. Klebsiella pneumoniae
Investigations for pneumonia
BEDSIDE
- regular observations (HR, RR, BP, temp,ECG)
- sputum culture if not improving or atypical suspicion
- urinalysis (pneumococcal and legionella antigen)
BLOODS
- ABG
- Cultures
- FBC
- CRP
- Glucose
- Us and Es (urea prognostic)
- LFTS (can affect liver + also side effect of antibacterials)
IMAGING
-CXR
SPECIAL
-CURB 65 score
Score for CAP severity? Explain it
Whats the managment for each score?
CURB-65 should be worked out for all
- Confusion - present as symptom (AMTS ≤ 8)
- Urea >7mmol/L
- Resp rate ≥ 30
- Blood pressure Systolic < 90 mmHg or Diastolic ≤ 60
- 65yo +
***influences anti-microbial management
Initial management of pneumonia
O2 - 15L NRBM aim for sats 94-98% (less for COPD patients)
IV fluids
Obtain blood cultures and sputum cultures
VTE prophylaxis
IV abx
Anitmicrobial management for CAP (depending on CURB65 score)
Antimicrobial treatment for HAP?
CAP
- Mild (score 0-1) = amoxicillin OR clarithromycin
- HOME MONITORING
- Moderate (score 2) = amoxicillin AND clarithromycin (or tetracycline)
- ADMIT or CLOSE OUTPATIENT MONITORING
- Severe (score 3+) IV antibiotics (e.g. co-amoxiclav)
- DEFFO ADMIT (switch to oral when improving 5-7 days)
HAP
- IV aminoglycoside e.g. gentamicin (gram neg cover) and IV piperacillin Tazocin
Explain the pathophysiology of pulmonary oedema (caused by cardiac)
Give examples of what may cause this
Explain the pathophysiology of pulmonary oedema (caused by non cardiac)
Give examples of what may cause this
CARDIOGENIC
-LVF leads to increased pulmonary capillary pressure so fluid collects in extravascular pulmonary tissues faster than lymphatics clear it
E.g. arrhythmias, failure of prosthetic valve, VSD, cardiomyopathy, negative inotropic drugs (beta blockers), hypertension/acute complication of MI/IHD/myocarditis
NON CARDIOGENIC
-increased capillary permeability, decreased plasma oncotic pressure (so water leaves vessels), increased lymphatic pressure
-E.g.
•ARDS
• IV fluid overload
• Smoke inhalation
• Near drowning incident (water drawn out of vessels into interstitium)
Symptoms of acute pulmonary oedema presentation
SEVERE DYSPNOEA (main sx)
- Coughing up frothy pink sputum, unable to talk
- Orthopnea- sitting up and tripod helps breathlessness
- Breathlessness wakes at night (PND)
- Reduced exercise tolerance
- Sweaty, peripherally cool (incr CRT) and clammy (these all point towards a cardiogenic cause)