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  • Patho physiology
  • History
  • Nursing physical assessment
  • Related treatment

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  • Diagnosis and patient goal
  • Nursing intervention
  • Evaluation and
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Nursing Assignment


The objective of this paper is to analyse the case of health scenario of Mr. Carlos Sanchez as described below:

Mr. Sanchez is a 69-year old gentleman who lives at home with his wife Sandra. He is a retired public servant and has smoked heavily for the last 50 years. Since his retirement four years ago, Carlos had mildly elevated blood pressure for which he took diltiazemdaily. Two years ago, he was diagnosed with type II diabetes mellitus for which he was prescribed metformin. However, Carlos often forgets to take his daily sugar tablet. He is overweight and likes nothing better than to have a couple of glasses of wine and cheese every night with his wife. Over the last few weeks, he started to get breathless when gardening or walking up the gentle hill near his house. On Friday afternoon, while gardening while with Sandra, Carolos collapsed. Sandra rang ambulance and within twenty minutes he arrives to the emergency department on a stretcher.

1.1. Background

Prior to the admission, the patient was reported to be having mild blood pressure, suffering from Type II diabetes, panting for breadth. By disposition, he was obese, a regular drinker and heavy smoker. Besides, he was forgetful to take his medication of Metformin prescribed for diabetes.

At the time of admission, his conditions were reported to be as follows:

  • He was struggling to breadth, conscious, but characterised by confusion.

The nurse who conducted a preliminary check had recorded the following readings:

  • PR: 96 bpm, irregular, RR: 35 breaths/min, shallow and BP: 160/110 mmHg
  • SpO2: Unable to be determined

The intern on duty who did a physical examination recorded that he had left and right crackles to mid-lung field and oedema to ankles and knees. According to him the preliminary findings point towards the occurrence of congestive heart failure but in order to confirm he opines for the need to take additional tests towards which he orders for electro cardiogram and chest x-ray.

The results show the existence of atrial fibrillation, pulmonary oedema, and cardiac hypertrophy.


2.1. Pathophysiology

(a) Atrial fibrillation

Episodes of Atrial fibrillation (AF) can either be sudden or chronical in nature. It is considered to be chronic if it reappears after seven days. It is termed to be persistent if the attack does not cease within a period of 48 hours. In a majority of the patients, (between 70 and 80%), AF is associated with organic heart disorders, characterised by coronary heart disease, hypertension accompanied by left ventricular hypertrophy, valve disease and or congenital heart defects.

Some of the important causes for the occurrence of AF could be traced to reversible factors as alcohol ingestion, hypothyroidism, or pulmonary embolism. It often causes irregular and rapid heart rate resulting in palpitations, dyspnoea, and asthenia. It also causes impairment of hemodynamic function while at rest or physical activity. Its presence increases the risk of cerebrovascual insults (Wolf, 1991). In a number of surveys, (Kannel, 1982), it has been established that the cardiac and total mortality in patients with AF is doubled when compared with sex and age-adjusted groups in sinus-rhythm. A dominant part of such risk is attributed to the underlying structural heart diseases. It needs however to be noted the risk level of those diagnosed with lone A.F. is at much lesser risk, at least in those who age is below 60 years (Kopecky, 1987). This could be due to the fact that a decreasing tendency of the occurrence of primary AF is seen due to the availability of sophisticated diagnostic procedure which facilitates the exposure of the underlying diseases faster. Its occurrence in elderly patients is also relatively lesser.

The pathophysiological mechanisms of sudden attack and of chronic AF even though have not been fully understood, yet the factors that are known to contribute to it are (i) shortened refractory period, (ii) regional variations of refractoriness and conduction velocity and (iii) increased ectopic activity. The substrate of AF is described as a continuous activation of the atrial myocardium characterised by reentry of several circles which are not anatomically fixed but found to be spread and mingled in a seemingly chaotic pattern (Moe, 1962). The probable reason for the forming of several reentry cycles could be attributed to the short refractoriness and slow conduct velocity respectively which results in short wavelength. This is confirmed by the existence of electrophysiologic remodeling with the gradual shortening of the refractory period during the first hours to days of an attack of atrial fibrillation. This also contributes to the stabilisation of the atrial fibrillation and in fact this has led to the formulation of the statement that ‘atrial fibrillation begets atrial fibrillation (Wijffels, 1995).

(b) Cardiac hypertrophy

Cardiac hypertrophy is characterised by an increase in the mass of the contractile and ancillary proteins of the heart. Hypertension is seen as the commonest cause for the occurrence of cardiac hypertrophy. It not only increases the risk of myocardial ischaemia and ventricular arrhythmias, but also constitutes an independent risk for the sudden death of the patient wherein the origin is unknown (Shapiro & Sugdeu, 1996)

A close relationship exists between total peripheral resistance (TPR) and hypertension. When the TPR is elevated diastolic rather than systolic blood pressure rises (Guyton & Hall, 2000, Opie, 2004). The starting phase of hypertension is marked by an increase in the TPR associated with the tropic factors in the blood vessel wall (Marrero et al, 1997).They cause cardiac hypertrophy. Besides, cardiac hypertrophy is more correlated to systolic dysfunction than diastolic dysfunction (Middlemost, 1999). Alcohol consumption constitutes one of the important pathophysiological bases for cardiac hypertrophy. Furthermore where there is the presence of cardiac hypertrophy, there is a greater potential for arrhythmia.

(c) Pulmonary Oedema

Pulmonary Oedema is a condition where there is an abnormal accumulation of fluid in the lungs. It is characterised by the accumulation of fluid accompanied by low-protein content in the lung interstitium and alveoli due to cardiac dysfunction.

The pathophysiological mechanisms that account for Pulmonary Oedema are (a) increased pulmonary capillary pressure, (b) possible damages to the alveolar-capillary barrier, (iii) lymphatic obstruction.

Pulmonary Oedema could be caused by excessive intravascular volume administration, pulmonary venous outflow obstruction, and or failure of the left atrial myxoma. Such patients develop acute breathlessness, anxiety and marked confusion.

In the case of the patient discussed in this paper, the conditions suggest the existence of Cardiogenic Pulmonary Edema, the effect of which could lead to congestive heart failure (CHS), or severe arrhythmias, or heart attack with left ventricular failure, and or can lead to crisis arising out of fluid overload resulting in kidney failure or a hypertensive crisis (Mehta, S & Nava, 2005, Cotter et al, 2008).

Congestive Heart failure (CHF)

CHF refers to a syndrome wherein there is an inability seen in the heart to pump sufficient quantity of oxygenated blood to meet the needs of the body. Patients likely to be subjected to it suffer from shortness of breath, pulmonary oedema and it can result among other things in liver congestion.

From a pathophysiology point of view, when CHF occurs and drop in cardiac output, the sympathetic nervous system (SNS) gets stimulated. This results in increased heart rate and force of contraction, in addition to increased preload of left end diastolic pressure and vascular resistance. Vasoconstriction also occurs.

The kidneys try to compensate for the initial decrease in cardiac output by decreasing the renal perfusion and activating the rennin-angiotensin-aldosterone-system (RAAS).

However, in either acute or chronic heart failure such initial compensatory mechanisms ultimately prove counterproductive. Once either the left or right ventricle loses its ability to handle the increase preload, there is a back up of fluid. In the case of left ventricle, the accumulation of the fluid reaches the pulmonary bed which is responsible for the causing of shortness of breath, dyspnea on exertion and result in pulmonary oedema. On the other hand, when the involved part is right ventricle, the fluid has a tendency to get into the systemic circulation and produces such symptoms as elevated central venous pressure, (CVP), hepatomegaly, anorexia, edema etc (Hunt et al, 2009).

2.2. Tests

2.2.1. Electrocardiogram

Electrocardiogram (ECG) is one of non-invasive tests conducted to identify underlying heart problems. It is used to diagnose heart diseases and provides measurements indicating how well the heart is pumping, especially the left ventricle ejection fraction , ILVEF), changes in the structure of heart post to a heart failure, and also to indicate the type and severity of heart failure that could have occurred (Hess & Carroll, 2007, Rich & McLaughlin, 2001).

Wherever the physician suspects irregular spacing of heartbeats deviating from the normal rate ranging between 60 and 150 beats a minute, they can order for the conduct of electrocardiogram test. In such cases, it can act as a principal tool for the diagnosis of cardiac arrhythmias. In addition, it also provides valuable information to the physician on the state of the heart muscle arising out certain alterations in the electrocardiographic complexes, in particular the QRS-T part. Nonetheless, the interpretation of results assume a critical significance for the reason a normal ECG can show up in patients with serious heart problems while at the same time showing up of abnormal electrocardiogram in itself need automatically indicate the existence of serious heart disease. However, this does not dispense away the utility of this tool for preliminary investigation in the assessment of the patient with suspected heart failure for the reason if the ECG is totally normal, it is reasonable for the physician to arrive at a conclusion that a patient is unlikely to have a heart failure (Hurst JW, 2005).

2.2.2. Chest X-rayagnosis

Chest radiology can provide additionally useful information particularly in regard to the presence or absence of cardiomegaly (Fonseca et al, 2004). It can also throw light on the existence of pulmonary congestion. Besides, it can provide clues to the causes of breathlessness as for instance as to whether it is due to the presence of chronic obstructive pulmonary disease or consolidation. Its limitation consists in the fact that its quality cannot be assured in older patients, especially those in whom chest wall abnormalities are found.

2.2.3. Medication

Frusemide (iv)

It is a life saving drug, shorter diuretics, when administered intravenous acts in minutes and is effective for six hours. It is given to eliminate Pulmonary Oedema.

Digoxin (Oral)

It is a cardiac glucoside where there is a likelihood of heart failure.

Enoxaparin (sc)

It is anticoagulant and when given subcutaneous aims at handling deficiency of coronary blood circulation. When the dynamic circulation of blood gets altered, it results in stasis of fluid. This can result in the springing of blood clots. When administered subcutaneous, it helps in the prevention of fibrous clot formation and or alters the traveling of such clots.

Enalapril (oral)

It is an Angiotensin inhibitor and is given for the control of hypertension. It works on the kidney and prevents the conversion of Angiotensin 1 to Angiotensin 2.

When considered from the situation and experience of this nursing professional, the patient has been given the right kind of treatment and the tests asked for appear to be relevant. This can also be said about the medication, but for the following observations. Large doses of Frusemide can result in the depletion of potassium and hence there is a need for giving potassium supplement. There is no information whether this was done. Enalpril is now-a-days is replaced by Telemasarta. There is no reason given as to diltiazem was stopped. There is also no information on the dosages and no explicit information on the seriousness of the condition of the patient. This can only be inferred and points towards the fact that at the time of admission the patient condition was serious.



Cotter, G., Felker, G. M., Adams, K. F., Milo-Cotter, O., & O’Connor, C. M. (January 01, 2008): The pathophysiology of acute heart failure–is it all about fluid accumulation? American Heart Journal, 155, 1, 9-18.

Fonseca C, Mota T, Morais H et al. EPICA investigator (September, 01, 2004): The value of the electrocardiogram and chest x-ray for confirming or refuting a suspected diagnosis of heart failure in the community. Eur J Heart: 6(6):793–4

Guyton, A. C., & Hall, J. E. (2000): Textbook of medical physiology. Philadelphia: Saunders

Hess OM and Carroll JDClinical assessment of heart failure (2007): In: Libby P, Bonow RO, Mann DL, Zipes DP, eds. Libby: Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 8th ed. Saunders

Hurst, J. W. (January 01, 2005): Observational data suggesting there are electrocardiographic abnormalities that strongly suggest the presence of chronic heart failure. Clinical Cardiology, 28, 3, 154-7

Hunt SA, Abraham WT, Chin MH, et al. (2009): Focused update incorporated into the ACC/AHA 2005 Guidelines for the Diagnosis and Management of Heart Failure in Adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines: developed in collaboration with the International Society for Heart and Lung Transplantation. Circulation 2009; 119:e391

Kannel, W. B., Abbott, R. D., Savage, D. D., & McNamara, P. M. (January 01, 1982): Epidemiologic features of chronic atrial fibrillation: the Framingham study. The New England Journal of Medicine, 306, 17, 1018-22

Kopecky, S. L., Gersh, B. J., McGoon, M. D., Whisnant, J. P., Holmes, D. R. J., Ilstrup, D. M., & Frye, R. L. (January 01, 1987): The natural history of lone atrial fibrillation: A population-based study over three decades: The New England Journal of Medicine, 317, 11, 669-74.

Marrero, A. F., al’Absi, M., A, P. G., & Lovallo, W. R. (April 01, 1997): Men at risk for hypertension show elevated vascular resistance at rest and during mental stress. International Journal of Psychophysiology, 25, 3, 185-192.

Mehta, S., & Nava, S. (January 01, 2005): Mask ventilation and cardiogenic pulmonary edema: “another brick in the wall”: Intensive Care Medicine, 31, 6, 757-9


Middlemost, (January, 01 1999): Beyond systolic and diastolic blood pressure. Cardiology, 21:28-35.


Moe GK, (1962): On the multiple wavelet hypothesis of atrial fibrillation Arch Int pharmacodyn Ther: 140:183–188

Opie, L. H. (1998). The heart: Physiology, from cell to circulation. Philadelphia: Lippincott-Raven.

Rich, S., & McLaughlin, V. V. (2001): Pulmonary hypertension. Philadelphia: W.B. Saunders.


Shapiro LM, Sugdeu, P.H., (1996): Left ventricular hypertrophy: In: Julian DG, Camm AJ., FOX KM, Hall RTC, Pools-Wilson PA: Editors: Disease of the heart: 2nd ed, London: Saunders


Wijffels, M. C., Kirchhof, C. J., Dorland, R., & Allessie, M. A. (January 01, 1995): Atrial fibrillation begets atrial fibrillation. A study in awake chronically instrumented goats Circulation, 92, 7, 1954-68

Wolf, P. A., Abbott, R. D., & Kannel, W. B. (August 01, 1991): Atrial fibrillation as an independent risk factor for stroke: the Framingham Study. Stroke, 22, 8, 983-988




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