Nursing Case Study Chf

1. Remes J, Miettinen H, Reunanen A, Pyorala K. Validity of diagnosis of heart failure in primary health care. Eur Heart J. 1991;12:315–321.[PubMed]

2. Gillespie ND, McNeill GP, Pringle TH, Ogston S, Struthers AD, Pringle SD. Cross sectional study of contribution of clinical assessment and simple cardiac investigations to diagnosis of left ventricular systolic dysfunction in patients admitted with acute dyspnoea. Br Med J. 1997;314:936–940.[PMC free article][PubMed]

3. Davie AP, Francis CM, Love MP, et al. Value of the electrocardiogram in identifying heart failure due to left ventricular systolic dysfunction. Br Med J. 1996;312:222–224.[PMC free article][PubMed]

4. Dargie HJ, McMurray JVV. Diagnosis and management of heart failure. Br Med J. 1994;308:321–328.[PMC free article][PubMed]

5. Badgett RG, Mulrow CD, Otto PM, Ramirez G. How well can the chest radiograph diagnose left ventricular dysfunction? J Gen Int Med. 1996;11:625–634.[PubMed]

6. Choy AM, Darbar D, Lang CC, et al. Detection of left ventricular dysfunction after myocardial infarction: comparison of clinical, echocardiographic and neurohormonal methods. Br Heart J. 1994;72:16–22.[PMC free article][PubMed]

7. Raftery EB. Haemodynamic effects of diuretics in heart failure. Br Heart J. 1994;72(suppl S):44–S47.[PMC free article][PubMed]

8. Verma SP, Silke B, Hussain M, et al. First line treatment of left ventricular failure complicating acute myocardial infarction: a randomised evaluation of immediate effects of diuretic, venodilator, arteriodilator and positive inotropic drugs on left ventricular function. J Cardiovasc Pharmacol. 1987;10:38–46.[PubMed]

9. Collins R, Peto R, Flather M for the ISIS4 Study Group. A randomised factorial trial assessing early oral captopril, mononitrate or intravenous magnesium sulphate in 58 050 patients with suspected acute myocardial infarc 321–328tion. Lancet. 1995;345:669–685.[PubMed]

10. Flynn K, Coughlan MG, Phelan DM, Luke D, Neligan M, Wood AE. Intravenous captopril in acute heart failure. Lancet. 1988;301:173–174.[PubMed]

11. Swedberg K on behalf of the CONSENSUS Trial investigators. Effects of early administration of enalapril on mortality in patients with acute myocardial infarcation—results of the cooperative new scandinavian study II (CONSENSUS II) N Engl J Med. 1992;327:678–684.[PubMed]

12. Annane D, Bellisant E, Pussard E, et al. Placebo controlled, randomized double blind study of intravenous enalaprilat efficacy and safety in acute cardiogenic pulmonary edema. Circulation. 1996;94:1316–1324.[PubMed]

13. Garg R, Yusuf S. Overview of randomized trials of angiotensin converting enzyme inhibitors on mortality and morbidity in patients with heart failure. J Am Med Ass. 1995;273:1450–1456.[PubMed]

14. Hillis GS, Trent RJ, Winton P, MacLeod AM, Jennings KP. Angiotensin converting enzyme inhibitors in the management of cardiac failure: are we ignoring the evidence? Quart J Med. 1995;89:145–150.[PubMed]

15. Hart W, Rhodes G, McMurray J. The cost effectiveness of enalapril in the treatment of chronic heart failure. Br J Med Econ. 1993;6:91–98.

16. Benedict CR, Francis GS, Shelton B, et al. Effect of long term enalapril therapy on neurohormones in patients with left ventricular dysfunction. Am J Cardiol. 1995;75:1151–1157.[PubMed]

17. Cleland JGF, Poole-Wilson PA. ACE inhibitors for heart failure a question of dose. Br Heart J. 1994;72:s106–s110.[PMC free article][PubMed]

18. Poole Wilson PA The NETWORK Study—The effect of dose of an ACE inhibitor on outcome in patients with heart failure. Heart. 1996;75(s1):95.

19. Packer M. Do angiotensin converting enzyme inhibitors prolong life in patients with heart failure treated in clinical practice. J Am Coll Cardiol. 1996;28:1323–1327.[PubMed]

20. Pfeffer MA for the SAVE Study Investigators. Effect of captopril on mortality and morbidity in patients with left ventricular dysfunction after myocardial infarction. N Engl J Med. 1992;327:669–677.[PubMed]

21. Grinstead WC, Francis MJ, Marks GF, Tawa CB, Zoghbi WA, Young JB. Discontinuation of chronic diuretic therapy in stable congestive heart failure secondary to coronary artery disease or to idiopathic dilated cardiomyopathy. Am J Cardiol. 1994;73:881–886.[PubMed]

22. Rongen GA, Lenders JWM, Smits P, Thein T. Clinical pharmacokinetics and efficacy of renin inhibitors. Clin Pharmacokin. 1995;29:6–14.[PubMed]

23. MacFadyen RJ, Jones CR, Doig JK, Birnbock H, Reid JL. Responses to an orally active renin inhibitor remikiren (Ro-42-5892) after controlled salt depletion in humans. J Cardiovasc Pharmacol. 1995;25:347–353.[PubMed]

24. MacFadyen RJ. Angiotensin receptor antagonists from theory to practice. In: Elliott HL, editor. Current issues in cardiovascular therapy. London: Martin Dunitz; 1997. pp. 35–51. chapter 3.

25. Lacourciere Y, Brunner HR, Irwin R, et al. Effects of modulators of the renin angiotensin system on cough. J Hypertension. 1994;12:1387–1393.[PubMed]

26. Pitt B, Segal R, Martinez FA, et al. Randomized trial of losartan versus captopril in patients over 65 with heart failure (Evaluation of losartan in the elderly Study, ELITE) Lancet. 1997;349:747–752.[PubMed]

27. Gohlike P, Linz W, Scholkens BA, et al. Angiotensin converting enzyme inhibition improves cardiac function: role of bradykinin. Hypertension. 1994;23:411–418.[PubMed]

28. Cohn JN, Archibald DG, Ziesche S, et al. Effect of vasodilator therapy on mortality in chronic congestive heart failure: results of a Veterans Administration Cooperative Study. N Engl J Med. 1986;314:1547–1552.[PubMed]

29. Cohn JD, Johnson G, Ziesche S, et al. A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure. N Engl J Med. 1991;325:303–310.[PubMed]

30. Rich MW, Vinson JM, Sperry JC, et al. Prevention of readmission in elderly patients with congestive heart failure: results of a prospective randomized pilot study. J Gen Int Med. 1993;8:585–590.[PubMed]

31. Monane M, Bohn R, Gurwitz JH, Glynn RJ. Noncompliance with congestive heart failure therapy in the elderly. Arch Int Med. 1994;154:433–437.[PubMed]

32. Packer M, O’Connor CM, Ghali JK, et al. Effect of amlodipine on morbidity and mortality in severe chronic heart failure. N Engl J Med. 1996;335:1107–1114.[PubMed]

33. The Multicenter Diltiazem Postinfarction Trial Research Group. The effect of diltiazem on mortality and re-infarction after myocardial infarction. N Engl J Med. 1988;319:385–395.[PubMed]

34. Cohn JN. Physiological rationale for co-treatment with diuretics in heart failure. Br Heart J. 1994;72(suppl 2):s63–s67.[PMC free article][PubMed]

35. Channer KS, McLean KA, Lawson-Matthew P, Richardson M. Combination diuretic therapy in severe heart failure a randomized controlled trial. Br Heart J. 1994;71:146–150.[PMC free article][PubMed]

36. Dormans TP, et al. Diuretic efficacy of high dose furosemide in severe heart failure: bolus injection versus continuous infusion. J Am Coll Cardiol. 1996;28:376–382.[PubMed]

37. Vargo DL, Brater DC, Rudy DW, Swan SK. Dopamine does not enhance furosemide induced natriuresis in patients with congestive heart failure. J Am Soc Neph. 1996;7:1032–1037.[PubMed]

38. Van veldhuisen DJ, Man Int Veld AJ, Dunselman PHJM, et al. Double blind placebo controlled study of ibopamine and digoxin in patients with mild to moderate heart failure: results of the Dutch Ibopamine multicenter study (DIMT) J Am Coll Cardiol. 1993;22:1564–1573.[PubMed]

39. Struthers AD. Aldosterone escape during ACE inhibitor therapy in chronic heart failure. Eur Heart J. 1995;16:103–106.[PubMed]

40. Packer M, Lee WH, Medina N, Yushak M, Kessler PD. Functional renal insufficiency during long term therapy with captopril and enalapril in severe chronic heart failure. Ann Int Med. 1987;106:346–354.[PubMed]

41. Gottlieb SS, Robinson S, Weir MR, Fisher ML, Krichen CM. Determinants of the renal response to ACE inhibition in patients with congestive heart failure. Am Heart J. 1992;124:131–136.[PubMed]

42. Packer M. The neurohormonal hypothesis: a theory to explain the mechanisms of disease progression in heart failure. J Am Coll Cardiol. 1992;20:248–254.[PubMed]

43. Azizi M, Chatellier G, Guyene TT, Murieta-Geoffrey D, Menard J. Additive effects of combined angiotensin converting enzyme inhibition and angiotensin II antagonism on blood pressure and renin release in sodium depleted normotensives. Circulation. 1995;92:825–834.[PubMed]

44. MacFadyen RJ, Barr CS, Struthers AD. Aldosterone blockade reduces vascular collagen turnover, improves heart rate variability and reduces early morning rise in heart rate in heart failure patients. Cardiovasc Res. 1997;35:30–34.[PubMed]

45. Pitt B. ACE inhibitor co-therapy in patients with heart failure: rationale for the randomized aldactone evaluation study (RALES) Eur Heart J. 1995;16:107–110.[PubMed]

46. Uretsky BF, Young JB, Shahidi FE, Yellen LG, Harrison MC, Jolly MK. Randomized study assessing the effect of digoxin withdrawal in patients with mild to moderate chronic congestive heart failure: Results of the PROVED trial. J Am Coll Cardiol. 1993;22:955–962.[PubMed]

47. The Digitalis Investigation Group. The effect of diogoxin on mortality and morbidity in patients with heart failure. N Engl J Med. 1997;336:525–533.[PubMed]

48. Packer M, Colucci WS, Sackner-Bernstein JD for the PRECISE Study Group. Double blind placebo controlled study of the effects of carvedilol in patients with moderate to severe heart failure—The PRECISE Trial. Circulation. 1996;94:2793–2799.[PubMed]

49. Waagstein F, Bristow MR, Swedberg K for the Metoprolol in Dilated Cardiomyopathy Trial Study Group. Beneficial effects of metoprolol in idiopathic dilated cardiomyopathy. Lancet. 1993;342:1441–1446.[PubMed]

50. Vantrimpoint P, Rouleau JL, Wun CC, et al. Additive beneficial effects of beta blockers to angiotensin converting enzyme inhibitors in the survival and ventricular enlargement (SAVE) study. J Am Coll Cardiol. 1997;29:229–236.[PubMed]

51. Gilbert EM, Abraham WT, Olsen S, et al. Comparative hemodynamic, LV functional and anti-adrenergic effects of chronic treatment with metoprolol vs carvedilol in the failing heart. Circulation. 1996;94:2817–2825.[PubMed]

52. Doughty RN, Sharpe N. Beta adrenergic blocking agents in the treatment of congestive heart failure: mechanisms and clinical results. Ann Rev Med. 1997;48:103–114.[PubMed]

53. Eichorn EJ, Bristow MP. Practical guidelines for initiation of beta adrenergic blockade in patients with chronic heart failure. Am J Cardiol. 1997;79:794–798.[PubMed]

54. Hall SA, Cigarroa CG, Marcoux L, Risser RC, Grayburn PA, Eichorn EJ. Time course of improvement in left ventricular function, mass, and geometry in patients with congestive heart failure treated with beta adrenergic blockade. J Am Coll Cardiol. 1995;25:1154–1161.[PubMed]

55. Stevenson LW, Dracup KA, Tillisch JH. Efficacy of medical therapy tailored for severe congestive heart failure in patients transferred for urgent cardiac transplantation. Am J Cardiol. 1989;63:461–464.[PubMed]

56. The Cardiac Arrhythmia Suppression Trial II Investigators. Effect of the antiarrhythmic agent moricizine on survival after myocardial infarction. N Engl J Med. 1992;327:227–233.[PubMed]

57. Doval HC, Nul DR, Grancelli HO, Perrone SV, Bortman GR, Curiel R. Randomized trial of low dose amiodarone in severe congestive heart failure. Lancet. 1994;344:493–498.[PubMed]

58. Singh SN, Fletcher RD, Fisher SG for the CHF STAT Investigators. Amiodarone in patients with congestive heart failure and asymptomatic ventricular arrhythmia. N Engl J Med. 1995;333:77–82.[PubMed]

59. Stevenson WG, Ridker PM. Should survivors of myocardial infarction with low ejection fraction be routinely referred to arrhythmia specialists. J Am Med Ass. 1996;276:481–485.[PubMed]

60. Doval HC, Nul DR, Grancelli HO, et al. Nonsustained ventricular tachycardia in severe heart failure—independent marker of increased mortality due to sudden death. Circulation. 1996;94:3198–3203.[PubMed]

61. AVID Trial Executive Committee. Are implantable cardioverter-defribillators or drugs more effective in prolonging life. Am J Cardiol. 1997;79:661–663.[PubMed]

62. Curfman GD. Inotropic therapy for heart failure—an unfulfilled promise. N Engl J Med. 1991;325:1509–1510.[PubMed]

63. Dies F, Krell MJ, Whitlow P, et al. Intermittent dobutamine in ambulatory outpatients with chronic cardiac failure. Circulation. 1986;74:38.

64. Packer M, Carver JR, Rodeheffer RJ for the PROMISE Study Research Group. Effect of oral milrinone in severe chronic heart failure. N Engl J Med. 1991;325:1468–1475.[PubMed]

65. Poole Wilson PA. Heart failure. Unfinished business—a possible role for vasodilators. Int J Cardiol. 1993;40:1–6.[PubMed]

66. Adamopoulos S, Piepoli M, Qiang F, et al. Effects of pulsed beta stimulant therapy on beta receptors and chronotropic responsiveness in chronic heart failure. Lancet. 1995;345:344–349.[PubMed]

67. Hunn D, Pedersen WR, Beccker R, et al. Benefits of attending a heart failure clinic. Circulation. 1990;82:609.

68. West JA, Miller NH, Parker KM, et al. A comprehensive management system for heart failure improves clinical outcomes and reduces medical resource utilization. Am J Cardiol. 1997;79:58–63.[PubMed]

69. McKelvie RS, Teo KK, McCartney N, Humen D, Montague T, Yusuf S. Effects of exercise training in patients with congestive heart failure: a critical review. J Am Coll Cardiol. 1995;25:789–796.[PubMed]

70. Jenkinson C, Jenkinson D, Shepperd S, Layte R, Petersen S. Evaluation of treatment for congestive heart failure in patients aged 60 years and older using generic measures of health status (SF36 and COOP charts) Age and Ageing. 1997;26:7–13.[PubMed]

71. Myers J, Gullestad L, Vagelos R, Bellin D, Do D, Ross H, Fowler M. Clinical, hemodynamic and cardipulmonary exercise test predictors of outcome in patients referred for heart failure evaluation. J Am Coll Cardiol. 1997;29:98–160.

72. Chomsky Lang CC, Rayos GH, Shyr Y, et al. Hemodynamic exercise testing—a valuable tool in the selection of cardiac transplantation candidates. Circulation. 1996;94:3176–3183.[PubMed]

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.

History

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

Clinical Impression

  • ? Exacerbation of CHF
  • ? CVA
  • ? Post-seizure

AMPLE History

  • 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

Observations

  • 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.

Clinical Findings

Exacerbation of CHF, hypoxia secondary to same. Unresponsive to medication therapy.

Outcome

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

Learning Outcomes

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.

Furosemide

  • 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
  • Tachycardia
  • Hypertension/hypotension in extremis
  • Raised JVP
  • Central cyanosis
  • Tachypnea
  • 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)

  1. 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.
  2. Nitrates – GTN  is indicated for pulmonary oedema. This can be repeated as dictated by local guidelines.
  3. 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).
  4. 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.
  5. 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.

Glyceryl Tri-Nitrate/GTN

  • 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

References (non-Pubmed)

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

References

 
 
 
 
 
 
 
 

1.

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

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