A contribution to the studies of variability in human populations which arises from the heterogeneity of age group, particulary assessed biologically or physiologically, is often provided by clinicians. Physicians are often in a position to observe homogeneity in clinical parameters, changes in various pathological conditions due to age differences. There are still scarce data available on the phenomenon of aging.

Cardiogenic shock as a possible complication of acute myocardial infarction is twice as frequent in older than in younger patients. When cardiogenic shock occurs during acute myocardial infarction, the coronary perfusional pressure decreases, which results in expansion of the myocardial necrosis and consequently circulus vitiosus is created. If the mass of the left ventricle is reduced by more than 40%, cardiogenic shock occurs¹⁾. Most clinicians report some differences in the outcome of prolonged arterial hypotension during cardiogenic shock in relation to different age groups: reporting acute renal failure more often than functional oliguria in older patients, and more often functional oliguria than acute renal failure in younger patients¹⁾.

The aim of this study was to analyze prolonged arterial hypotension during acute myocardial infarction, in relation to oliguria in a relatively large clinical sample of 11 patients during an 11-year period. The sample is very narrowly defined according to the diagnosis and age. The study was planned to try to answer the question: does prolonged arterial hypotension during acute myocardial infarction in older patients lead to acute renal failure or to fuctional oliguria and if the entities differ from those in middle-aged patients?

From the beginning of January 1983 to the end of December 1993, a total number of over 500 patients with acute myocardial infarction were treated in the Department of Internal Medicine, Rebro, University Hospital, Zagreb. 3.6% of patients showed a picture of cardiogenic shock, of which half were of the older age group (≥65 years). The total death rate of myocardial infarction amounted to 17.2%, of which 10.7% occurred within 6 hours, and 6.5% during hospitalization. The characteristics of shock during myocardial infarction are^1–3) 1) electrocardiographic picture of acute myocardial infarction (not always present); 2) systolic pressure lower than 80mmHg; 3) cardiac index lower than 2.0 L/min/m²; 4) pulmonary wedge pressure higher than 18mmHg; 5) diuresis lower than 20 ml/hour; 6) signs of peripheral circulatory failure (symphathicus stimulation); 7) central venous pressure high (>12cmH₂O). The blood pressure was measured continuously by using a mercury manometer (indirect method). The term-blood pressure in shock means the mean systolic pressure during shock state. The definition of hypotension was: systolic blood pressure less than 80mmHg (in one hypertonic less than 90mmHg- patient no.7, 54.y.). All findings of the cardiogenic shock should be present for including a patient in this study (but pulmonary wedge pressure, because of potential complications in using the method on the elderly). The patients were oliguric at the moment of development of cardiogenic shock (less than 20ml/h). Clinical and laboratory parameters were followed in all patients: diuresis, sodium in urine, creatining urine/plasma quotient, urine osmolality, urine/plasma osmolality quotient, the renal failure index and the fractional excretion of filtered sodium. These parameters were analyzed the day after establishment of diuresis i.e. 16 to 24 hours after the onset of the cardiogenic shock, from 7a.m. in the morning to 7 a.m. the following morning (in all patients a urethral catheter was used). It is not done in the oliguric phase, because this phase durated a short time in most of those patients and, in most of them, the cardiogenic shock was a cause of admittance to the hospital and there were no data about renal function prior to cardiogenic shock. The therapy for cardiogenic shock was applied in accordance with the rational principles of clinical pharmacology in the treatment of this condition.

In all of the 11 patients of older age with cardiogenic shock due to acute myocardial infarction, the central venous pressure was higher than 19.5cm H₂O (other hemodynamic parameters: pulmonary wedge pressure and cardiac index were measured in 2 patients) and all other parameters indicated cardiogenic shock also. In 7 of the 11 older and in 5 younger patients, natriuresis indicated a value of more than 25mmol/L in the range of acute renal failure, while the ratio of creatinine in urine and plasma in 3 older and 5 younger patients indicated functional oliguria, in three older-and one younger in the range of acute renal failure and in five older and one younger between those two parameters. In 7 older and 2 younger patients the values of urine osmolality were in the range of functional oliguria and in four older and 5 younger in borderline range between functional oliguria and acute renal failure, as the osmolality quotient in urine and plasma: in 7 older and one younger indicated functional oliguria and in four older and 3 younger acute renal failure. The value of the renal failure index in all patients was lower than 3.0, but in 6 older and 3 younger patients lower than 1.0 indicated functional oliguria, and the values of the fractional excretion of filtered sodium were similar (Table 2, 2a, 3, 3a).

None of these patients was dialyzed. We have not seen any significant change in their urine sodium or osmolality as time progessed (especially in the patients who died). In most of them, we did not measure a serum creatinine level just before death. Of the older patients with a picture of cardiogenic shock, nine died and 4 died in the younger age group. Autopsy was lone in 5 older (no. 1, 2, 4, 10, 11) and 3 younger (no. 1, 4, 6) and the pathological finding of the heart and blood vessels was in correlation with the clinical and ECG changes. Finding of the kidneys in two older patients was normal (no. 1, 11) in one showed bilateral chronic pyelonephritis (no. 2) and in two patients acute tubular necrosis was the finding (no. 4 with previous finding of the renal failure index of 0.3 and the fractional excretion of filtered sodium of 0.2 and in no. 10, with previous finding of the renal failure index of 2.3 and the fractional excretion of filtered sodium of 2, 0). Finding of the kidneys in two younger patients was normal (no. 1. and no. 6) and in one showed disseminated intravascular coagulation (no. 4).

Clinical and laboratory parameters of acute renal failure were presented in 11 older and in 7 younger patients with cardiogenic shock. This is, therefore, a higher frequency than reported in the literature: in some data, this amounts to approximately 1% of 500 patients⁶⁾. However, this difference depends on numerous factors such as the time of arrival in hospital at the beginning of the clinical signs. However, in older patients it should be borne in mind that the clinical signs of infarction is more serious, and that lung edema is more frequent⁷⁾, and even more frequent than cardiogenic shock⁸⁾. A fatal outcome during cardiogenic shock is very frequent: of four patients reported in one paper, all four died⁹⁾. According to some authors, it is possible to find that, during myocardial infarction acute renal failure is infrequent because the patients do not live long enough to develop acute renal failure: the lethality rate reached 75–90% in cardiogenic shock in the elderly¹⁰⁾. Data exist on renal blood flow: in healthy persons this is 1130ml/min, while in patients with myocardial infarction in cardiogenic shock this is 420ml/min¹⁰⁾. The cardiogenic shock is a main causal factor of acute renal failure. Our data show that all older and younger patients had creatinine quotient in urine and plasma, the renal failure index and the fractional excretion of filtered sodium in the range of functional oliguria or at the borderline values indicating that those parameters did not separate who has prerenal failure and who has established acute renal failure^11–20). In cases of cardiogenic shock with heart failure, urinary sodium excretion may not be a good clinical indicator of acute renal failure, since acute cardiac dilatation with stimulated ANP could lead to an erroneous natriuresis even in a state of prerenal oliguria. Even more, urinary sodium excretion could be low in cases of frank acute tubular necrosis in severe congestive heart failure. The distinction between functional oliguria (prerenal failure) and acute renal failure in this situation may be meaningless and should be judged from the clinical outcome of the patients.

The urine osmolality and the urine/plasma osmolality ratio were to a high for the diagnosis of acute tubular necrosis. All the patients presented were (at the time of U/P osmolality tests) suffering from prerenal failure (functional oliguria) with quite a good renal reserve. This was corraborated by the value of creatinine clearance which amounted to over 18.1ml/min. in all older and to over 17.0ml/min. in younger patients the day after the phase of oliguria. This does not agree with data from the literature which suggests that hypotension, due to acute myocardial infarction which lasts for one hour or longer, leads to acute renal failure in all older patients²¹⁾.

Although, in the literature, the values of RFI and FE_Na% indicating of functional oliguria are reported as values less than 1.0 when acute renal failure is considered, when this amounts to over 1.0⁵⁾, in our earlier work^11–15), we have demonstrated that the renal failure index in cases of functional oliguria amount to 0.9 or less, while in acute renal failure it amounts to more than 3.0. In contrast to the data of other authors¹⁹⁾, the sodium in urine is not suficiently discriminative: there were only two older and three younger patients with urine sodium more than 40mmol/L and they got furosemide. All others did not lose sodium. The creatinine quotient is not discriminative, also. Two of five patients died and had been examined by autopsy. They had findings of acute tubular necrosis, and both had laboratory signs of functional oliguria. There is no good correlation between structural and functional changes in human ischemic renal failure.

Acute renal failure due to cardiogenic shock in older and younger patients is pre-renal or is rare acute tubular necrosis in the elderly. Acute renal failure develops in fatal cardiogenic shock only. All the older and younger patients had adequate urine concentration at the onset of the shock. Out of nine older patients who died. Acute tubular necrosis was present in two only.