IM Shortness of Breath

Shortness of Breath

• DDX:
  • CHF, Arrhythmia, MI
  • Resp alk or metabolic acidosis, respiratory failure
    
  • PNA, PTX, Pl effusion, PNX, PE, ARDS, DAH, Asthma, COPD/Exacerbation
    
• Dx:
  • EKG, ABG, CXR include all except PE

Heart Failure

• Etiology:
  • When CO is inadequate for bodily demand
• Prognosis:
  • 25-30% mortality in the first 5 years after diagnosis
• Classification of HF:
  • 1) SYSTOLIC FAILURE
    
  • 2) DIASTOLIC FAILURE
    
  • NB SYSTOLIC and DIASTOLIC USUALLY CO-EXIST.
    
  • A) Left-sided
    
  • B) Right-sided
• Normal EF:
  • 55-70%
• Normal Ventricular volume:
  • 100ml
• Systolic Failure:
  • Inability of the Ventricle to contract effectively -> CO decreased. LV Ejection Fraction <40%
  • Causes:
    • MI, Cardiomyopathy, IHD
• Diastolic Failure:
  • Failure of the Ventricles to relax and fill properly -> Increased filling pressure. EF>50% but the CO is still low
  • Causes:
    • Restrictive pericarditis, Cardiac Tamponade, Restrictive cardiomyopathy, HTN
• CHF:
  • when LVF and RVF occur together
• LVF:
  
  • Presentation:
    • Dyspnoea, poor exercise tolerance, fatigue
      
    • orthopnoea, paroxysmal nocturnal dyspnoea (PND)
      
    • nocturnal cough, wheeze (cardiac ‘asthma’),
      
    • nocturia, cold peripheries
      
    • weight loss, muscle wasting.
    • Significance Orthopnea: Signifies cardiac cause
    • Specific symptom of cough in LVF: Pink Frothy Sputum
  • Causes LVF in a normal heart:
    • Running a fluid infusion too fast -> Fluid overload
• RVF
  • Causes:
    • LVF, pulmonary stenosis, lung disease (anything that increases afterload of RV)
  • Presentation:
    • Peripheral oedema (up to thighs, sacrum, abdominal wall), ascites, facial engorgement
    • nausea, anorexia
    • pulsation in neck and face (tricuspid regurgitation),
    • epistaxis.
• Overview Left heart failure + symptoms:
  • 1) Whether Syst. or Diast. The CO of LV is reduced
    
  • 2) Blood builds up in lungs
    
  • 3) Pulm oedema (pink frothy sputum cough)
    
  • -> reduced gas exchange -> SOB, Exercise intolerence, Cyanosis, Wheeze (cardiac asthma) Weight loss
    
  • +PND, Orthopnea
• Overview R heart Failure:
  • Usually caused by LVF.
    
  • 1) Increased after load in pulmonary circulation leads to RV can’t pump blood into effectively
    
  • 2) blood regurg through tricuspid into systemic circ
    
  • 3) systemic oedema
    • organs most affected by oedema in RHF:
      • Lower limbs
        
      • Ascites
        
      • Sacral
        
      • Hepatic
  • Good measure of severity of RHF: JVP
• Exacerbating HF factors:
  • VERAPAMIL (-ve ionotrope)
    
  • NSAIDS (fluid retention)
• Acute Heart Failure:
  • Acute heart failure is often used exclusively to mean new onset or acute decompensation of chronic heart failure
• Chronic HF:
  • Slowly progresses.
    
  • Venous oedema but Arterial pressures maintained until late on.
• Low output Vs. High output HF:
  • Low output – most common
    
    • Where output is low and does not increase to meet demands upon exertion.
      
    • Causes:
      • Pump failure: MI, Cardiomyopathy etc.
        
      • Low heart rate: B-Blockers, Heart block, Post MI
        
      • Excessive Pre-load: Mitral regurg, fluid overload
  • High output- Rare
    
    • Where output is normal or increased in the face of increased need.
    • Causes:
      • Anaemia, pregnancy, hyperthyroidism, Paget’s disease, arteriovenous malformation, beri beri
• Diagnosis:
  • Symptoms of Failure + Cardiac dysfunction @ rest
• Congestive Cardiac Failure Criteria:
  
  • FRAMINGHAM CRITERIA
• Tests:
  • 1. ECG and B-type Natriuretic Peptide (BNP)
    
    • ECG:
      • May indicate cause
        
      • look Prev MI or ventricular hypertrophy
  • 2. If either abnormal ECHO (= KEY)
    
  • N.B IF ECG and BNP normal, HF unlikely. look for another diagnosis
  • 3. CXR
    • CXR: cardiomegaly (cardiothoracic ratio >50%)
    • prominent upper lobe veins (UPPER LOBE DIVERSION)
    • peribronchial cuffing
    • diffuse interstitial or alveolar shadowing,
    • classical perihilar ‘bat’s wing’ shadowing,
    • fluid in the fissures,
    • pleural effusions,
    • septal (formerly called ‘Kerley B’) lines (variously attributed to interstitial oedema and engorged
    • peripheral lymphatics).
    • LVF (ABCDE):
      
      • Alveolar oedema (bat’s wings)
      • Kerley B lines
      • Cardiomeg
      • Diversion upper lobe
      • Pulm Effusion
  • 4. Endomyocardial biopsy – rarely needed
• Managment:
  • Diuretics to use in HF:
    • 1) LOOP – Furosemide or Bumetanide increase dose as necissary
  • S/E LOOP DIUTETICS:
    • HYPOK, Renal impairment
      
    • Monitor U/Es, if K falls too low add K sparing diuretic (Spironolactone)
  • Interaction Loop diuretics and digoxin:
    • Loops cause hypoK
      
    • hypoK increases chance Digoxin toxicity.
  • Refractory Edema in Loop diuretic HF management:
    • Add THIAZIDE
• Management Chronic HF:
  • Stop smoking. Eat less salt. Optimize weight & nutrition.
    
  • Treat the cause (eg if dysrhythmias; valve disease).
    
  • Treat exacerbating factors (anaemia, thyroid disease, infection, BP).
    
  • Avoid exacerbating factors, eg NSAIDS (fluid retention) and verapamil (-ve inotrope).
• Drugs in HF:
  • For Everyone:
    • 1) DIURETICS – Loop, if k low add spiro. if refractory oedema add thiazide
      
    • 2) ACE-i (if LV diatolic) (ARB if cough)
      
      • if intollerent – vasodilators (hydralazine/isosorbide dinitrate)
        
      • ARB ex: Candesartan
  • Add if still symptomatic:
    
    • 3) B-Blocker
      
    • 4) SPIRONOLACTONE
      
    • 5) Digoxin
• Intratible HF management:
  • 1) Furosemide to Bunetamide
    
  • 2) Strict bed rest + Na and Fluid restriction
    
  • 3) DVT prophylaxis
    
  • 4) U+E beware hypoK
    
  • 5) Opiates and IV nitrates amy relieve symtpoms
    
  • 6) If extreme try IV IONOTROPES
    
  • 7) Cardiac resynch, LV assist device, Transplant
• Avoid IV ionotropes:
  • bc it can be difficult to wean patients off of them
• Palliative care in HF:
  • 1) Treat/prevent comorbidities (eg flu vaccination).
    
  • 2) Good nutrition (allow alcohol!).
    
  • 3) Involve GP: continuity of care and discussion of prognosis is much appreciated.
    
  • 4) Dyspnoea, pain (from liver capsule stretching), nausea, constipation, and low mood all need tackling.
    
  • 5) Opiates help pain and dyspnoea. O2 may help.
• BNP:
  • Use of BNP:
    • Most reliable way to distinguish HF from other causes of dyspnoea
      
    • ANP also good but not best
  • Rapid rise BNP:
    • Associated with sudden death
  • Systemic effects of ANP and BNP:
    • DECREASE PRELOAD:
      
    • ANP and BNP both increase GFR and decrease renal Na+ resorption
      
    • they also decrease preload by relaxing smooth muscle.
      
    • ANP partly blocks secretion of renin and aldosterone.

Respiratory Failure

• Type I Respiratory Failure:
  • HYPOXIC + low or normal CO2
  • Hypoxia: <8kPa O2
  • Causes:
    • V/Q mismatch:
      
    • Pneumonia
      
    • Pulmonary oedema
      
    • PE
      
    • Asthma
      
    • Emphysema
      
    • Pulmonary fibrosis
      
    • ARDS
      
    • -anything that interferes with gas exchange etc.
• Type II Resp failure:
  • HYPOXIA + HYPERCAPNIA
  • Hypercapnia: >6kPa
  • Causes:
    • Alveolar HYPOVENTILATION +/- VQmismatch
    • 1) RESPIRATORY DISEASE
      
    • 2)REDUCED RESPIRATORY DRIVE:
      
      • Iatro/drugs, CNS tumour, CNS trauma
        
    • 3)NEUROMUSCULAR DISEASE:
      
      • cervical cord lesion, diaphragmatic paralysis, poliomyelitis, myasthenia gravis, Guillain-Barré syndrome
        
    • 4) THORACIC WALL DISEASE:
      
      • flail chest, kyphoscoliosis
• Presentation of Acute Hypoxia:
  
  • Dyspnoea;
  • restlessness;
  • agitation;
  • confusion;
  • central cyanosis.
• Longterm effects hypoxia:
  • Polycythaemia, Pulmonary HTN, COR PULMONALE
• Presentation of Hypercapnia:
  • Headache;
  • peripheral vasodilatation;
  • tachycardia;
  • bounding pulse;
  • tremor/flap;
  • papilloedema;
  • confusion;
  • drowsiness;
  • coma.
• Tests/Imaging:
  • Blood tests: FBC, U&E, CRP, ABG.
    
  • Radiology: CXR.
    
  • Microbiology: sputum and blood cultures (if febrile).
    
  • Spirometry (COPD, neuromuscular disease, Guillain-Barré syndrome)
• Type I Resp failure management:
  • 1) Tx underlying cause
    
  • 2) O2 therapy
  • If kPa<8 despite 60% O2 -> use assisted ventilation in T1 Resp failure
• Type II Resp failure management:
  • 1) Tx underlying cause
  • 2) Controlled oxygen therapy: start at 24% O2.
    
    • Recheck ABG after 20min. If PaCO2 is steady or lower, increase O2 concentration to 28%.
    • If PaCO2 has risen >1.5kPa and the patient is still hypoxic, consider assisted ventilation (NIPPV)
  • 3) Rarely add a respiratory Stimulant DOXAPRAM
  • 4) Ventilation and Intubation
• Nasal Canula flow rate and O2%:
  • 1-4L/min
    
  • 24-40% O2
• Simple face mask:
  • Flow rate – 15L/min
    
  • Dont use <5L/min as Rx CO2 accum
    
  • C/I in T2 Resp failure as NOT PRECISE
• Venturi mask:
  • Use in T2 Resp failure
• O2% venturis:
  • BLUE 24%
    
  • WHITE 28%
    
  • YELLOW 35%
    
  • RED 40%
    
  • GREEN 60%
• Venturi use in COPD to start:
  • Blue or White (24-28%)
• Consider ABG measurement:
  • Any unexpected deterioration in an ill patient.
  • Anyone with an acute exacerbation of a chronic chest condition.
  • Anyone with impaired consciousness or impaired respiratory effort.
  • Signs of CO2 retention, eg bounding pulse, drowsy, tremor (flapping), headache.
  • Cyanosis, confusion, visual hallucinations (signs of low PaO2; SAO2 is an alternative)
  • To validate measurements from transcutaneous pulse oximetry.
• V/Q mismatch imaging:
  • V/Q mismatch scintogram:
    
  • Inhaled Xenon-133 or technetium plus injected macro-aggregates, which lodge in lung capillaries.
    
  • Normal perfusion ex- cludes PE but ventilation component requires a normal CXR for comparison

COPD Exacerbation

• Etiology:
  • A common medical emergency especially in winter. May be triggered by viral or bacterial infections.
• Tests:
  • Arterial blood gases
    
  • CXR to exclude pneumothorax and infection.
    
  • FBC; U&E; CRP.
    
  • Theophylline level if the patient is on therapy at home.
    
  • ECG.
    
  • Send sputum for culture if purulent.
    
  • Blood cultures if pyrexial.
• O2 Therapy in COPD:
  • Is often required – a most common cause of death in COPD
  • HOWEVER, some rely on Hypoxic drive to breathe – if there is evidence of hypercapnia, prescribe O2 WITH CAUTION
  • Start with 24-28% O2 in such patients.
  • Whenever you initiate or change oxygen therapy, do an ABG within the next hour or sooner if the patient is deteriorating.
  • Max O2 in COPD: 40%
• Management:
  • 1) Nebulised Bronchodilators – SALBUTAMOL and IPRATROPIUM
    
  • 2) AIM O2 88-92% – start at 24-28% O2, adjust accordingly – aim PaO2>8, PaCO2 rise<1.5
    
  • 3) STEROIDS 1-2wks IV HYDROCORTISONE and ORAL PREDNISOLONE
    
  • 4) ABx if Signs infection (Amoxicillin or clarithromycin or doxycycline)
    
  • 5)Physio to aid sputum expulsion
• NO RESPONSE STEROIDS etc. in Acute COPD:
  • 1) AMINOPHYLINE IV
    
    • No improvement -> Go to next step
      
  • 2) (pH low, Respiratory high, PaO2 low) Non-Invasive PPV
    
    • No improvement -> Go to next step
  • 3) VENTILATION USING INTUBATION
    
    • No improvement -> Go to next step
  • 4) Respiratory stimulant: DOXAPRAM
    • S/E Doxapram: Agitation, confusion, tachycardia, nausea
• Overall medical steps in COPD:
  • 1) O2 88-92%
    
  • 2) Neb Salb + Ipratropium
    
  • 3) Steroids: IV hydrocort, Oral Pred (1-2wk)
    
  • 4)Non inv- PPV
    
  • 5) Intubate
    
  • 6) DOXAPRAM resp stim

Pleural Effusion

• Etiology:
  • Fluid in the pleural space
• Classification of Pleural effusions:
  • 1) Transudates <25g/L protein
    
  • 2) Exudates >35g/L protein – EXTRA PROTEIN IN EXudate
• Terms:
  • Haemothorax: Blood in pleural space
  • Empyema: Pus in pleural space
  • Chlyotho: Fat and lymph in pleural space
  • Haemopneumothorax: Blood and air in pleural space
• TRANSUDATES caused by:
  • Transudates may be due to increased venous pressure (1) or Hypoproteinaemia (2)
    
  • 1) cardiac failure, constrictive pericarditis, fluid overload
    
  • 2) cirrhosis, nephrotic syndrome, malabsorption
• EXUDATES caused by:
  • LEAKINESS of Pleural Capillaries due to INFECTION, INFLAMMATION or MALIGNANCY
    
  • Pneumonia; TB; pulmonary infarction; rheumatoid arthritis; SLE; bronchogenic carcinoma; malignant metastases; lymphoma; mesothelioma; lymphangitis carcinomatosis
• Presentation:
  • Asymptomatic—or dyspnoea, pleuritic chest pain.
  • Decreased expansion
    
  • stony dull percussion note
    
  • diminished breath sounds occur on the affected side
    
  • Bronchial breathing above effusion
    
  • if severe trachea dev. away from eff.
• Imaging/Tests:
  • CXR of Pleural effusion:
    • Small: Blunted CP angles
      
    • Large: Shadowing with Miniscus sign
  • USS in Pleural effusion:
    • Helps identify where fluid is and guide aspiration
  • Aspiration:
    • Insert 1-2 intercostal spaces below where the upper border is (wary of going into the abdomen) JUST ABOVE upper border of rib – avoids neurovascular bundle
    • Draw off 10-30mL of pleural fluid and send it to the lab for clinical chemistry (protein, glucose, pH, LDH, amylase), bacteriology (microscopy and culture, auramine stain, TB culture), cytology and, if indicated, immunology (rheumatoid factor, ANA, complement)
    • if aspirate testing is inconclusive, then go to next step
  • Pleural Biopsy
• Management Pleural effusion:
  • 1) Drain – repeatedly if req. ? Chest drain rather than just single tap each time
    
  • 2) Tx underlying cause
    
  • 3) Pleurodesis
• Pleurodesis:
  • Artificial obliteration of the pleura to cause adhesion of the lung parenchyma -> no future Pulmonary effusions in this area.
    
  • Talc, Tetracyclin, Bleomycin, surgical

Pneumonia

• Etiology:
  • Infection of the lung parenchyma.
    
  • Mortality = 14% of hospital admissions
• Causative organisms:
  • Streptococcus Pneumoniae – commonest 60-75%
    
  • Haemophilus Influenzae – Commonest in COPD
    
  • Mycoplasma Pneumoniae
    
  • Staph Aureus – Commonest on ITU
    
  • Legionella species and Chlamydia Psittaci
    
  • Viruses including influenza – 15%
• Presentation:
  • Fever, rigors, malaise, anorexia, dyspnoea, cough, purulent sputum (classically ‘rusty’ with pneumococcus), hemoptysis, and pleuritic chest pain.
    
  • Fever, cyanosis, herpes labialis (pneumococcus), confusion, tachypnoea, tachycardia, hypotension, signs of consolidation, and a pleural rub.
• Signs of Consolidation (4):
  • Diminished expansion
    
  • Dull percussion note
    
  • Bronchial breathing
    
  • Increased vocal fremitus/resonance
• ABG:
  • SpO2 <92% or Severe pneumonia
• Tests:
  • CXR
    
  • ABG
    
  • FBC, U&E, LFT, CRP, atypical serology
    
  • Urine pneumococcal (and legionella) antigen.
    
  • Viral throat swabs if appropriate.
    
  • Blood cultures if pyrexial.
    
  • Pleural fluid may be aspirated for culture.
    
  • Bronchoscopy and bronchoalveolar lavage -> if the patient is immunocompromised or in ICU.
• Measurement of Pneumonia Severity:
  • Calculate the core adverse features
    
  • ‘CURB-65’ score:
    
    • Confusion (abbreviated mental test ≤8)
      
    • Urea >7mmol/L
      
    • Respiratory rate ≥30/min
      
    • BP <90/60mmHg
      
    • Age≥65
  • 0-1 HOME Tx
    
  • 2= Hospital Tx
    
  • >3 = ITU admission – SEVERE PNEUMONIA
• Management:
  • 1) A-E approach – O2
    
  • 2) If in hypotension/shock – manage – IV FLUIDS
    
  • 3) Analgesia e.g. ibuprofen if pleuritic chest pain
    
  • 4) Ix
    
  • 5) ABx if Bacterial
    
  • 6) if no improvement:
    
  • Cyanotic still – CPAP/intubation
    
  • ICU admission
• Severe Pneumonia Tx:
  • Co-Amoxiclav +Clarithromycin
• Pneumonia Tx pen allergy:
  • CEPHALOSPORIN instead of co-amoxiclav
• Legionella pneumonia Tx:
  • levofloxacin + rifampicin
• HAP or Neutropenic Pneumonia Tx:
  • aminoglycoside IV (eg gentamicin) + antipseudomonal penicillin (eg ticarcillin)

Pneumothorax

• Etiology:
  • air in the pleural space
• Causes:
  • Spontaneous (especially in young thin men) due to rupture of a SUBPLEURAL BULLA
    
  • CHRONIC LUNG DISEASE: asthma; COPD; cystic fibrosis; lung fibrosis; sarcoidosis
    
  • INFECTION: TB; pneumonia; lung abscess
    
  • TRAUMATIC: including iatrogenic (CVP line insertion, pleural aspiration or biopsy, percutaneous liver biopsy, positive pressure ventilation).
    
  • Carcinoma
    
  • Connective tissue disorders: Marfan’s syndrome, Ehlers-Danlos syndrome
• Presentation:
  • May be Asymptomatic
    
  • Sudden onset of dyspnoea and/or pleuritic chest pain.
    
  • If on ventilation, Sats may drop or Ventilation pressure may suddenly rise
    
  • Reduced expansion, hyper-resonance to percussion, and diminished breath sounds on the affected side.
• Management:
  • DEPENDS IF PRIMARY OR SECONDARY (due to an underlying pathology)
• Management Primary Pneumothorax:
  • 1) SOB and/or >2cm air space on CXR
    
    • – no: discharge
      
    • – yes: step 2
      
  • 2)Aspirate – successful?
    
    • – yes: discharge
      
    • – No: repeat
      
  • 3) Aspirate – successful?
    
    • – yes: discharge
      
    • – No: chest drain
• Management Secondary Pneumothorax:
  • 1) SOB and/or >2cm air space on CXR
    
    • – No: Aspirate and admit for 24 hrs
      
    • – Yes: Chest Drain (or if Aspirate not succ.)

Tension Pneumothorax

• Etiology:
  • Air drawn into the pleural space with each inspiration has no route of escape during expiration.
  • The mediastinum is pushed over into the contra-lateral hemithorax, kinking and compressing the great veins.
  • Unless the air is rapidly removed, a cardiorespiratory arrest will occur.
• Presentation:
  • Same as pneumothorax + TRACHEA DEVIATED AWAY FROM PNEUMOTHORAX
  • Respiratory distress,
  • tachycardia,
  • hypotension,
  • distended neck veins,
  • trachea deviated away from the side of the pneumothorax.
  • Increased percussion note, reduced air entry/breath sounds on the affected side.
• Management:
  • IF TENSION DO NOT WASTE TIME TESTING – JUST Tx
    
  • If NOT tension – CXR
  • 1) To remove the air, insert a large-bore (14-16G) needle with a syringe, partially filled with 0.9% saline, into the 2nd intercostal interspace in the midclavicular line on the side of the suspected pneumothorax.
    • Remove plunger to allow the trapped air to bubble through the syringe (with saline as a water seal)
  • 2) until a chest tube can be placed.
  • Alternatively, insert a large-bore Venflon in the same location.

Pulmonary Edema

• Causes:
  • – Cardiovascular, usually left ventricular failure (post-MI or ischaemic heart disease). Also valvular heart disease, arrhythmias, and malignant hypertension.
  • – ARDS from any cause, eg trauma, malaria, drugs. Then look for predisposing factors, eg trauma, post-op, sepsis. Is aspirin overdose or glue-sniffing/drug abuse likely? Ask friends/relatives.
  • – Fluid overload.
  • – Neurogenic e.g. head injury
• Presentation:
  • Dyspnoea,
  • orthopnoea (eg paroxysmal),
  • pink frothy sputum
• Auscultation in Pulmonary Edema:
  • fine lung crackles,
  • triple/gallop rhythm,
  • wheeze
• Tests:
  • CXR, look signs HF
    
  • ECG: again look signs HF
    
  • U&E, troponin, ABG, Plasma BNP
    
  • Consider Echo.
• DDX:
  • Asthma/COPD, pneumonia, and pulmonary edema are often hard to distinguish, especially in the elderly, where they may co-exist.
    
• Management:
  • If the patient is extremely unwell and you are not sure, consider treating all three (eg with salbu- tamol nebulizer, furosemide IV, diamorphine, amoxicillin
  • IF LVEF<40%:
    • use ACEi/ARB/B-blocker in pulmonary edema
• Management of Pulmonary Edema:
  • BEGIN Tx BEFORE Imaging/Tests
  • 1) O2 + IV access
  • 2) Tx underlying arrhythmias – e.g. AF (Warfarin + Digoxin)
  • 3) DIAMORPHINE
  • 4) Deal with fluid overload – Weigh daily and aim 0.5kg loss/day
    
    • – LOOP diuretics: Furosemide/bumetanide
    • – K+ sparing if low – Spironolactone
    • – If rebound edema/on large doses loop consider THIAZIDE
  • 5) if Tx does not respond:
    • ACE-i/ARB
    • B-Blocker
  • 6) GTN spray !! only if Systolic BP>90!!
  • 7) IV NITRATE
  • 8) CPAP – drives fluid back into vascular and recruits alveoli
• Diamorphine Caution:
  • 1) COPD, LIVER Failure
• Impact of renal failure on the dose of furosemide:
  • LARGER DOSES REQUIRED
• If GTN spray used and still systolic BP>100:
  • IV NITRATE INFUSION
• Have done everything but Pulmonary Edema still worsening:
  • 1) INCREASE IV NITRATE if BP staying>100
    
  • 2) Treat as cardiogenic shock and admit to ITU