The patient factors include age, sex, race, underlying morbidity, diet, obesity, medications, socioeconomic status, and genetic determinants. Some of these are obviously out of an individual’s control, whereas others can be influenced by personal behavior. The following summarizes what is known about each patient factor and the relative importance of the factors to survival outcomes.
Patient Factors | Strength of Association with Outcome |
Age | + |
Sex | 0 |
Race | ++ |
Co-morbidity | +++ |
Diet | Unknown |
Obesity | Unknown |
Medications | + |
Socioeconomic | ++ |
Genetic | Unknown |
Age (weak association with survival):
One might assume that age would be a very strong predictor of survival but in fact age is only weakly associated with survival. Robert Swor in 2000 reported on 2600 cardiac arrests in Royal Oak, Michigan, a suburb of Detroit. He found a decrease in survival with advancing age. Starting with 40 to 49 years of age and increasing by 10-year increments, the likelihood of survival was 10%, 10%, 8.1%, 7.1%, and 3.3%. There were even survivors among patients 90 and older Similarly a report by Kim from King County reported reasonable survival rates among patients in their 80s and 90s.
Sex (no association with survival):
Men are more likely to have heart disease and therefore more likely to have cardiac arrest compared to women but sex is not a predictor of survival. Women and men have equal probabilities of survival at comparable ages.
Race (moderate associate with survival):
Several studies have shown that African-Americans have both a higher incidence of cardiac arrest and fare poorer in cardiac arrest survival compared to whites. A 1993 study from Chicago found a higher incidence of cardiac arrest in African-Americans and a dismal survival overall -- 0.8% compared to 2.6% in whites. Contrary findings were reported by Kevin Chu in a 1998 study in Royal Oak, Michigan, where there was no association of race with survival. An investigation from Seattle demonstrated racial differences in resuscitation from VF cardiac arrest. Compared to persons of African-ancestry, persons of European-ancestry had twice the likelihood of surviving VF cardiac arrest, after controlling for demographic and clinical factors. The reasons are not readily apparent.
Co-morbidity (strong association with survival):
Co-morbidity refers to other chronic or acute illnesses present at the time of cardiac arrest which are not directly the cause of the arrest. For example, a person who has a cardiac arrest caused by ischemic heart disease but also has emphysema, diabetes, and dementia. The latter three diseases are co-morbid conditions. Co-morbidity is definitely inversely correlated with survival. It is not surprising that a person with co-morbid conditions would do less well compared to an otherwise healthy person. The best study demonstrating this relationship was a 1996 study in Circulation by Al Hallstrom looking at the co-morbidity of 282 victims of out-of-hospital cardiac arrest. Co-morbidity was determined from interviews with the person calling 911 or other witnesses of the cardiac arrest approximately 7 weeks after the cardiac arrest. There was a strong association; the more co-morbidity the lower the likelihood of survival. Prior to Hallstrom’s study it was assumed that co-morbidity decreased the likelihood of survival but this was the first study to quantitate its effect. Hallstrom concludes that co-morbidity is an often-overlooked factor in studying cardiac arrest. I agree. Co-morbidity probably explains why some resuscitations are not successful even when VF is present and therapy is provided quickly. The power of co-morbidity as an explanation for unsuccessful resuscitations undoubtedly sets the maximum survival rate from cardiac arrest – the rate that is possible under ideal conditions. As will be argued in subsequent chapters this maximum community resuscitation rate for VF is around 50%. The figure of 50% is admittedly an estimate and it is based on community survival rates that include all persons in VF -- the relatively healthy and the severely ill. There are undoubtedly sub-populations within a community (for example, persons whose arrest occurs in public locations) that have maximum average resuscitation rates above 50%.
The challenge in measuring the effect of co-morbidity is obtaining this clinical information. Most EMS systems do not systematically collect co-morbidity information. Furthermore obtaining this information from hospital records or from patient families, in the event of death, is very difficult. Few centers have the resources to obtain such complete clinical particulars. There is some information routinely collected by EMTs and paramedics that could be a surrogate for co-morbidity data. This is the listing of medications prescribed to the patient. I suspect a simple tally of the prescription meds would be a good stand in for co-morbid conditions. The more meds, the more co-morbidity.
Diet (unknown association with survival):
David Siscovick, a cardiovascular epidemiologist from the University of Washington, reported in 1995 that a diet high in fish oils and omega-3 fatty acids protects against cardiac arrest. It is felt that the omega-3 fatty acids stabilize the cell membranes in the heart and therefore lowers the risk of an arrhythmia such as VF. This association of fish oils with sudden death reduction has been repeatedly demonstrated. It is possible that dietary factors explain in part the differences in sudden death rates among countries. Japan, for example, with a high national ingestion of fish has low rates of sudden death compared to the US. Many authors tout certain diets as cardioprotective. The Mediterranean diet which is high in monosaturated oils (such as olive oil) has been promoted for this benefit but good comparison data are hard to come by. Cross-cultural dietary comparisons are challenging to study. Though diets high in omega-3 fatty acids protect against the onset of VF there is no evidence that diet per se is associated with increased likelihood of successful resuscitation. Furthermore, fish oils do not reduce atherosclerosis or nonfatal myocardial infarction.
Obesity (unknown association with survival):
Obesity as a predictor of cardiac arrest survival has not been well studied. At the 2006 Resuscitation Science Symposium of the American Heart Association Annual Meeting in Chicago, Lance Becker presented a study on the body mass index for 76 cardiac arrest patients in Chicago. The morbidly obese patients (BMI >40) had worse survival but it was noted that this group of patients received shallower chest compressions compared to patients with normal body mass index. Presumably CPR is more difficult in obese patients and this may partly or wholly explain the worse outcomes. A study by Robert White showed no relationship between body weight and successful defibrillation.
Medications (weak association with survival):
There is, as noted above, an association between medications and co-morbidity which in turn lessens the probability of successful resuscitation. Patients with co-morbid diseases will likely be on medications for these diseases and thus medication is a co-factor with co-morbidity. With one exception, there are virtually no studies demonstrating that patients on specific medications are more difficult to resuscitate. The exception is diuretics -- commonly prescribed for patients with congestive heart failure. Some diuretics cause depletion of potassium which, if severe enough, can lead to cardiac arrest, and once in cardiac arrest the low potassium will make successful resuscitation much more difficult. It is also conceivable that some medications may improve the likelihood of resuscitation. Patients who are taking beta-blockers, for example, might be less likely to refibrillate following an initial defibrillation and therefore have a better survival. But without data this is purely speculative.
Separate from the effect on resuscitation is the potential to increase the likelihood of cardiac arrest. Occasionally there will be a drug recall or publicity in the media about a newly discovered side effect of a medication. For example, Vioxx was discovered to have an increased risk of myocardial infarction leading to new warnings (and lawsuits) about the medication. Recently a popular diabetic drug was found to increase cardiac events. Some drug studies are stopped prematurely when an increased risk of cardiac arrest is noted. The Cardiac Arrhythmia Suppression Trial (CAST) found an anti-arrhythmic medication led to more not fewer cardiac arrhythmias and once discovered the trial was stopped. Usually, however, a risk, unless it is large, will be difficult to detect in routine therapeutic use. Most adverse associations are discovered during large drug trials.
Socioeconomic factors (moderate association with survival):
Several studies have demonstrated a relationship of socioeconomic status and incidence of cardiac arrest. One study from Portland in 1995 showed that persons from low median income census tracts had higher rates of cardiac arrest compared to high median income tracts. The authors found no relationship of census tract median income to survival. A more detailed study in 2006, also from Portland, found similar results but did not report on the relationship to survival. In this two-year study census tract lower median income, higher poverty level, lower median home value, and lower educational attainment were strongly associated with higher incidence of sudden cardiac arrest.
Other studies have found a relationship between socioeconomic factors and survival – the lower the socioeconomic class the lower the survival. In a 1992 study Hallstrom found that greater survival following cardiac arrest was associated with higher assessed home valuation in Seattle. Every $50,000 increase in home valuation led to a 1.6 fold increase in survival. Rea in 2005, using median household income as the measure of socioeconomic status, found in King County that the higher the income the greater the likelihood of survival. It is not evident why a "wealthy" person should do better than a "poor" person in terms of cardiac arrest survival. Perhaps better pre-arrest health care and better-controlled co-morbid conditions may be a factor. In other words co-morbidity and socioeconomic factors may be related. If such is the case, and I suspect it is, it may be difficult to sort out the exact relationship. Just to further cloud the picture, another study from several communities in Michigan found no association between median household income and survival from cardiac arrest.
Genetic factors (unknown association with survival):
A recent report in the New York Times described the discovery of a genetic factor that increases the risk of heart disease up to 60% in persons of European descent. Though this finding does not relate to the likelihood or resuscitation, it certainly has the potential to identify people at risk of developing ischemic heart disease. This will allow for early interventions like control of blood cholesterol and blood pressure which in turn may reduce the likelihood of cardiac arrest.
While it is clear that genetic factors are linked to heart disease and cardiac arrest the question here is whether genetic factors influence the outcome once the arrest occurs. It is known that genetic factors determine the responsiveness to particular medications. Theoretically the potent pharmacotherapy used in resuscitations could be individually tailored based on genetic susceptibility. Similarly there may be genetic determinants to a patient’s responsiveness to defibrillatory shocks or hypothermia. While such factors are plausible there is very little known about them at this time and we are likely years away from understanding the genetic determinants of resuscitation.