Q 1 What has happened?
The condition at hand being experienced by the patient is angina. This can be adduced from the fact that we are presented with a number of clues here, indicative of a possible myocardial or coronary dysfunction. Since the symptoms are not too aggravated the possibility of a heart attack can be set aside for a possible angina based disorder. Furthermore Angina manifests itself generally through central chest tightness and pain followed by a lack of oxygen levels, usually at a point of exertion. When such an observation is applied to the scenario at hand it is possible to see that all these symptoms were present here. Also the later tests of pH levels (as will be discussed earlier) confirm the presence of lactic acidosis, which is a primary indicator of oxygen loss and coronary disorder (Oh, 2006).
However, the reason why at this early stage of diagnosis it cannot be thoroughly adduced whether the patient’s pain and discomfort were severe enough to point more conclusively towards the presence of an aggravated coronary disease, is because angina may or may not occur without an underlying coronary disease or a previous history of cardiac malfunction. This is because theoretically a number of factors contribute to the loss of oxygen supply to the blood, which can cause the angina to occur (please see next section).
Q2 What could have caused it?
As mentioned above, one of the most obvious symptoms of angina is pain in the chest and shortness of breath. We have also been told that the patient is overweight and over-weight people tend to have high levels of fat and cholesterol. High fat levels in the blood are indicative of damage to the inner layers of coronary arteries. Furthermore this certainly seems more like an occurrence of “stable angina” due to the fact that such a type of Angina is most commonly triggered through intense physical exertion in patients with already narrowed arteries due to the build-up of plaque and cholesterol. In the case study at hand it is stated that the patient was moving heavy boxes at the time of the collapse. We have also been told that he is involved in a stressful and demanding job. Both these are trigger factors of angina because patients with narrowed arteries are likely to suffer from an oxygen shortage which is one reason the patient was breathless at the time he feels chest pain. Furthermore, angina itself is a symptom and a warning indication of serious coronary heart disease, which means that the patient might have been, prior to this incident, suffering from a reduced flow of blood to his heart or a part thereof. Similar to angina, CHD has similar trigger factors like high cholesterol, insulin imbalance/diabetes, and the effects of smoking. Coronary arteries have delicate inner layers and are likely to be damaged very easily by these factors. Plaque is created as a consequence of the nature cell repair process of these arteries and such a build up can further narrow the arteries. Either way, whenever the flow of blood is reduced to heart muscle either by plaque damage or plague narrowing of arteries, there is a likely occurrence of Angina or long term CHD for the patient. It should be noted that angina could also be caused by soft blood clots by plague rupturing the arteries as these clots can partially or fully block coronary arteries.
However, without further investigation it is not possible to link Angina fully to CHD here as Angina can easily occur in the absence of any coronary disease. At this point it would be advised to the patient to have further tests taken to determine whether they are suffering from a condition called aortic stenosis which is a heart valve problem called causing decreased blood flow to the coronary arteries. Since angina is caused by oxygen failure, anaemic people and those with thickened heart muscles are also prone to it.
Blood tests- pH of 7.27 and elevated levels of lactic acid– Normal adult Arterial Values of pH are between 7.35 and 7.45.The patient has a pH of 7.27 which is indicative of a low pH value, diminished sodium bicarbonate
The rationale and significance of taking the pH level test is very high for a patient suffering from these symptoms because this is indicative of the measurement of blood acidity and reflects upon the number of hydrogen ions present in the blood. Of course, lower pH recordings indicate blood acidity, which is further indicative of possible Cardiac Arrest and Congestive Heart Failure and even ventilatory failure. Therefore the 7.27 pH showed how the breathlessness and the chest pain were connected to a possible occurrence of Angina (Sifter, 2007). Low pH is also indicative of lactic acidosis, which is often triggered by intense exercise by the patient right before complications develop. At such a point the patient might feel nausea and weakness and a blood test to check electrolyte levels can quickly reveal such elevated levels of lactic acid. This is possible to note from the decreased HCO3 levels in the patient’s blood indicating decreased CO2 content (Hall et al, 1992). The kidney controls HCO3 levels. This is indicative of respiratory difficulties in the patient. In addition to lactic acidosis then, it seems that the patient might also be suffering from metabolic acidosis, which is mainly a consequence of a primary decrease in bicarbonate (HCO3) concentration, which also leads to decreased blood CO2 levels. The significance of these various observations is that they are a part and parcel of an emergency diagnosis of a possible coronary dysfunction like angina due to the presence of the symptoms, which were noted in the beginning (Saunders,1996). It is possible to establish the link between acidosis; ventilation complications and possible heart failure form these observations so further treatment can be planned accordingly.
It should be noted first and foremost that the patient here has not been prescribed a aspirin / clopidogreln based medicinal intervention which is meant alleviate the conditions of pathway of platelet aggregation and plaque formation, thereby reducing the incidence of blood clots and arterial narrowing (Weatherall et al,1996). This is usually an early intervention and the author sees no reason why this was not used first. However, it is also true that some patients are resistant to aspirin and this can further lead to adverse coronary events. Without further information the author cannot comment on this.
Since the patient has to go on living a stressful lifestyle due to the nature of his job, the use of nitroglycerin prior to any stressful activity he takes in the future can prevent the recurrence of such stable angina, Another popular intervention for such a patient involves the use of Beta Blockers in form of atenolol and metoprolol in order to reduce myocardial and angina based symptoms in patients, usually post a myocardial infarction (Knight et al, 1997). If the initial use of Beta Blockers does not have significant results then the use of Calcium channel blockers or Calcium antagonists is often recommended. Such medicines include the likes of nifedipine or nicardipine or even the use of nitrates like isosorbide mononitrate. Furthermore, if at a later stage of treatment the presence of blood clots is confirmed then Potassium channel openers can serve as a good method of monotherapy (Ibid).
However, if the calcium antagnostic being prescribed is of a short acting nature and dihydropyridine based, then it should not be used in isolation from a good beta-blocker as it can cause reflex tachycardia, which is a leading cause of sudden cardiac death in patients with previous cardiac disorders. Also during such an intervention the use of long lasting nitrates can balance out such negative impacts of calcium antagnostics (Suanders, 1996).
Despite their possible negative side effects calcium channel blockers can actually allow the relaxation of the blood vessels but manipulating calcium flow in these channels through these vessels which can in turn cause a secondary form of arteriolar dilation which can allow for reduced resistance to blood flow and hence normalize the blood pressure (Knight et al, 1997). The can also slow down the heart contractions and their negative impact upon the heart. Moreover, the use of nitrates can bring about similar effects in terms of bringing about maximal dilation of veins and slight arterial dilation.
Having said this, all the medicines used here in this scenario may or may not be effective in patient management in the long term. In addition, we have not yet established the actual presence of CHD here but the presence of angina symptoms have been confirmed. The key to their positive impact upon this already over-weight and stressed patient remains dependent upon the actual presence of the concomitant disease with in his body. Furthermore, we have also not been told whether the doctors plan to manage this drug administration through monotherapy or dual therapy for an effective cure.
D.J. Weatherall , J.G.G. Ledingham , D.A. Warrell (1996) the chapter on “ Intensive Care “ – in Oxford Textbook of Medicine, Oxford Medical Publications 1996
Jesse B. Hall, Gregory A. Schmidt, Lawrence D. H. Wood (1992), the chapter on “ Acid Base Disorders “ – in Principles of Critical Care Medicine, Mc Graw Hill
Knight CJ, Panesar M, Wilson DJ, Chronos NA, Patel D, Fox K, Goodall AH (1997) ,“ Different effects of calcium antagonists, nitrates, and beta-blockers on platelet function. Possible importance for the treatment of unstable angina”, Circulation. 1997 Jan 7;95(1):125-32.
Saunders (1996) the chapter on “ Critical Care Medicine “ – in Cecil Textbook of Medicine.
Oh MS (2006). Evaluation of renal function, water, electrolytes and acid-base balance. In: McPherson RA, Pincus MR, eds. Henry’s Clinical Diagnosis and Management of Laboratory Methods. 21st ed. Philadelphia, Pa: Saunders Elsevier; 2006: chap 14.
Seifter JL (2007). Acid-base disorders. In: Goldman L, Ausiello D, eds. Cecil Medicine. 23rd ed. Philadelphia, Pa: Saunders Elsevier; 2007: chap 119.