Hilman K, (1992) Acute cardiogenic pulmonary edema. In: Vincent JL (ed) Year-book of intensive care and emergency medicine 1992. Springer, Berlin, pp 185–193Google Scholar
Takayama Y, Iwasaka T, Sidiura T, Sumimotot T, Takeuchi M, Tsuji H, Takashima H, Taniguchi H, Inada M (1991) Increased extravascular lung water in patient with low pulmonary artery occlusion pressure after acute myocardial infarction. Crit Care Med 19:21–25Google Scholar
Toyofuku T, Kobayashi T, Kubo K, Koyama S, Kusama S (1988) Effects of coronary ischemia on lung fluid balance in conscious sheep. J Appl Physiol 65:617–624Google Scholar
Raijmakers PGHM, Groeneveld ABJ, Schneider AJ, Van Lingen A, Teule GJJ, Eijsman L, Thijs LG (1993) Transvascular transport of67Ga after cardiopulmonary bypass surgery. Chest 104:1825–1832Google Scholar
Brody W, Criley JM (1970) Intermittent severe mitral regurgitation. Hemodynamic studies in a patient with recurrent acute left-sided heart failure. N Engl J Med 283:673–676Google Scholar
Matthay MA, Wiener-Kronish JP (1990) Intact epithelial barrier function is critical for the resolution of alveolar edema in humans. Am J Respir Crit Care Med 142:1250–1257Google Scholar
by Alan Batt. Last modified: 11/04/14
Patient & Apparent Chief Complaint
An 83 year old female presents to ambulance crew after an episode of sudden weakness. A GP is on scene and has assessed the patient, deciding on hospital admission by ambulance as a matter of urgency.
Patient became very weak and was put to bed by NOK. Her breathing became very laboured and the NOK called for the local GP out-of-hours service to attend. The doctor was on scene within 15 minutes, and upon assessing the patient requested an ambulance transfer to the ED.
Initial Clinical Findings
- Airway – clear & patent
- C Spine – not indicated (MOI/NOI: episode of weakness)
- Breathing – tachypnoeic
- Circulation – Pulse present, irregular, tachycardic; skin colour normal, cap refill normal
- Disability – No LOC before ambulance arrival, patient responding to verbal stimuli
- ? Exacerbation of CHF
- ? CVA
- ? Post-seizure
- A – Allergic to penicillin
- M – Currently taking Warfarin, Furosemide
- P – History of CVA x 1 year, CHF
- L – Last oral intake 7pm the evening previous
- E – Son stated patient became very weak before going to bed
- Pulse rate 110bpm
- Pulse rhythm Irregular
- ECG rate 116
- ECG rhythm A Fib
- Resp rate 24 per minute, regular, shallow
- Resp quality Bibasal consolidation & rales on auscultation
- SpO2% 89% @ room air
- Cap Refill <2secs
- BP 178/112
- Pupils PEARRL, size 4
- GCS 11/15 (E4, V2, M5)
- BGL 14.4.0mmol/l
Pre-hospital care & management
GTN 800mcg given SL & Furosemide 40mg administered IV as patient was dyspnoeic with audible crackles bi-basally. O2 @15lpm commenced via non-rebreather mask. 12 Lead ECG showed AFib, no obvious acute pathological changes. En-route to hospital patient’s SpO2% decreased to 85% on 15lpm via non-rebreather mask. Ventilations assisted as RR>30 per minute. Resuscitation equipment prepared as patient’s GCS remained at 11/15. SpO2% increased to 99% with assisted ventilations.
In-hospital care & management
Patient triaged as Category 1 (Life-Threatening Condition) with ? CHF Exacerbation. CPAP therapy initiated. Blood tests taken. Urinary catheter inserted.
Exacerbation of CHF, hypoxia secondary to same. Unresponsive to medication therapy.
Patient’s condition deteriorated, intubated. Patient on ventilator in ICU department. Poor prognosis, same discussed with family by medical team.
Identification of all interventions initiated and rationale
- Pulse oximetry – to monitor oxygen saturation levels in the blood
- Vital signs (HR, RR, SpO2, BM) – to gain a baseline set of vital signs for reference
- Furosemide IV – loop-osmotic diuretic, to decrease pulmonary oedema, allowing for improved respiratory effort
- Pulse oximetry – to monitor oxygen saturation levels in the blood
- Supplemental oxygen – to re-oxygenate patient
- Assisted ventilations – to provide adequate oxygenation to patient’s tissues as RR >30
- 3 Lead ECG – to identify any life-threatening arrhythmias
- 12 Lead ECG – to identify any life-threatening arrhythmias or ECG changes indicative of myocardial damage (secondary to hypoxia etc.)
- CXR – to identify aspiration, pleural effusion etc. that may increase morbidity
- Blood tests – to identify any electrolyte imbalances etc.
- Urinary catheter – to monitor urinary output to ensure adequate renal function
- CPAP Therapy – to provide assistance with ventilation at a safe, controlled, effective pressure, combating fatigue and improving respiratory gas exchange
Continuous Positive Airway Pressure
Continuous Positive Airway Pressure (CPAP) is a form of non-invasive positive pressure ventilation (NIPPV) that is commonly used in the treatment of pulmonary oedema associated with congestive heart failure. CPAP improves the ability of the alveoli to diffuse oxygen to the red blood cells, by using pressure to drive gas into the alveoli and open alveoli that are filled with fluid, collapsed or unused. It also increases the resistance of gas flow during exhalation providing resistance to the exiting airflow of gas from the lungs.
CPAP can relieve the level of dyspnoea experienced by a patient by improving cardiac output and increasing pulmonary compliance (Vital et al., 2008). Ventilatory status is improved and airway oedema is removed improving oxygenation and CO2 removal. CPAP can also help to reduce the incidence of intubation and invasive ventilation needed in CHF patients (Hubble et al., 2006)
Possibilities for advanced pre-hospital intervention
The ability of Paramedics to provide CPAP therapy for patients who require assisted ventilations, particularly in the presence of a strong history of CHF/pulmonary oedema is a key area for consideration. Prehospital based CPAP therapy is cheap, effective and can be safely deployed by all BLS, ILS & ALS providers. It in turn allows for a reduction in in-patient stays, reduced morbidity and mortality, and lower intubation rates in these patients (Vital et al., 2013).
CPAP can also provide an immediate effective treatment on-scene for a patient who is in respiratory distress (Kosowsky et al., 2001; Pang et al., 1998) It is estimated that a saving of approximately €3800 per patient can be achieved through the use of one particular prehospital CPAP system – the Vygon Boussignac CPAP system (Dieperink et al., 2007) Initial approximate costs are non-disposable parts of €300 per vehicle, with each patient treated costing approx. €45 in disposable parts.
- Presentation: 10 mg per ml; 2 ml, 5 ml and 25 ml per ampoule
- Administration: Intravenous
- Dosage: 40mg IV
- Effects: Inhibits re-absorption of sodium and chloride ions, retaining water in intestine, which is then dispelled in the urine. Also causes vasodilation, reducing venous return.
- Side-effects: Headache, dizziness, hypotension, arrhythmias, transient deafness, diarrhoea, nausea & vomiting.
Congestive Heart Failure
Congestive Heart Failure (CHF) is excessive blood or fluid in the lungs or body tissues caused by the failure of ventricles to pump blood effectively. CHF occurs when the left ventricle cannot pump out the amount of blood entering the ventricle, or when the ventricle is damaged and cannot effectively pump enough blood to meet the body’s requirements. It may also occur due to a build up of excess fluid in the body due to renal failure or dysfunction due to disease. Blood begins to congest in the lungs (pulmonary oedema).
The effort of breathing increases as the airways are obstructed by the fluid, reducing the intake of air into the lungs. The alveoli are unable to exchange gases effectively creating severe dyspnoea in patients. As the condition progresses, this congestion will eventually cause the right ventricle to fail. When this occurs, valuable blood supply (containing oxygen and nutrients) to the systemic cells is seriously disrupted, and the by-products of metabolism (such as CO2) are no longer eliminated effectively causing toxins to accumulate and ultimately causing cell death (AAOS, 2005)
Accurate assessment of CHF in the pre-hospital setting
The JRCALC Guidelines list specific criteria that should be assessed under respiratory status to accurately diagnose pulmonary oedema in the pre-hospital setting. These include:
- Excessive sweatiness/clamminess
- Hypertension/hypotension in extremis
- Raised JVP
- Central cyanosis
- Basal respiratory crackles
- +/- Wheeze
- Pitting ankle oedema
- ECG changes (old MI, ischaemic changes, indicative of previous myocardial damage)
Pre-hospital management of CHF/pulmonary oedema
The treatment of cardiogenic pulmonary oedema (caused by LVF) contains a number of items and exact protocols vary depending on country, EMS system, guidelines (Shapiro, 2005; Caroline, 2007)
- Sit the patient up, with legs dangling over edge of bed/seat – this encourages venous pooling, causing a decrease in venous return to the heart, and so reduces pulmonary oedema.
- Nitrates – GTN is indicated for pulmonary oedema. This can be repeated as dictated by local guidelines.
- Diuretics – Furosemide 40mg IV is another recommended adjunct. This is a looposmotic diuretic which when administered causes re-absorption of fluid through the Loop of Henle in the small intestine. There are however a percentage of patients who develop increased morbidity associated with dehydration, and electrolyte deficiencies as a result of furosemide administration. There is also evidence to suggest that torsemide or bumetanide use is favoured over furosemide in heart failure patients due to a decrease in mortality and morbidity in studies (Wargo & Banta, 2009).
- Morphine should also be considered in the presence of CCF with associated cardiac chest pain. Not only will the analgesic properties of morphine be useful but its’ vasodilation properties may also help in easing the patient’s dyspnoea.
- CPAP Therapy has proven to be extremely effective in the management of pulmonary oedema in a prehospital setting.
CPAP Therapy is an approved intervention for UK Paramedics under the JRCALC Guidelines. A study by Hoffman & Reynolds in 1987 suggested that GTN was the most effective EMS pharmacological treatment with the least harmful adverse effects. It also questioned the use of morphine and furosemide by EMS providers in the treatment of pulmonary oedema.
- Presentation: Aerosol spray, metered dose 400mcg (0.4mg)
- Administration: Sublingual
- Dosage: 400mcg per metered spray; dose of 800mcg (2 sprays) indicated for pulmonary oedema
- Effects: Vasodilation, dilation of coronary arteries, reduces BP
- Side-effects: Hypotension, dizziness, headache, facial flushing
AAOS – American Academy of Orthopaedic Surgeons (2005) Emergency Care and Transportation of the Sick and Injured 9th Edition. Massachusetts: Jones & Bartlett
Elling B, Caroline N, Smith M (2007) Nancy Caroline’s Emergency Care in the Streets, 6th Edition (UK Edition). London: LWW
Dieperink W1, Jaarsma T, van der Horst IC, Nieuwland W, Vermeulen KM, Rosman H, Aarts LP, Zijlstra F, Nijsten MW. Boussignac continuous positive airway pressure for the management of acute cardiogenic pulmonary edema: prospective study with a retrospective control group. BMC Cardiovasc Disord. 2007 Dec 20;7:40. PMID: 18096038.
Continuous positive airway pressure (CPAP) treatment for acute cardiogenic pulmonary edema can have important benefits in acute cardiac care. However, coronary care units are usually not equipped and their personnel not adequately trained for applying CPAP with mechanical ventilators. Therefore we i […]
Tags: cardiac, case study, CHF, CPAP, GTN, nitrate