As people age their physiologic reserve decreases. This loss of physiologic reserve is a slow process of deterioration often starting in the fourth decade of life and continues with increasing age. Despite this decrease in organ function, most elderly people can compensate physiologically to meet the needs of daily activities under normal condition. However, when stressed by illness, including traumatic injury, the physiologic demand may be excessive with a limited ability to compensate and mount the appropriate cardiovascular response to ensure adequate perfusion. The rate of physiologic change is variable from organ to organ and individual to individual [8].

Age is a major risk factor for the development of cardiovascular disease (CVD), and as such many elderly patients have some degree of CVD. CVD has been shown to be responsible for more than 40 % of deaths in patients over the age of 65 years [9]. Age-related changes in the myocardium affect anatomical as well as physiologic and electrophysiologic activity of the heart [10]. With aging, there is a decrease in myocardial contractility and ventricular compliance for a given preload as a result of loss of myocytes and increased myocardial collagen [11]. Autonomic tissue is replaced with connective tissue and fat, while fibrosis of the myocardium results in conduction abnormalities. The change in the conduction system increases the incidence of dysrhythmias including sick sinus syndrome, bundle branch blocks with resultant atrial arrhythmias which may be a cause for subsequent syncope in the elderly [12–14].

As one ages, systolic blood pressure increases due to augmented afterload from stiffening of the outflow tract. During times of physiologic stress, such as acute illness or injury, these changes result in decreases in peak ejection fraction and cardiac output [11, 15–17]. Compounding the situation is that between the ages of 20 and 85 years of age, it is estimated that maximal heart rate decreases by as much as 30 % [18]. Additionally aged myocardium does not respond as well to increased levels of endogenous and exogenous catecholamines [19]; thus, cardiac output in the elderly must be augmented by increasing ventricular filling and stroke volume rather than an increase in heart rate [11, 20]. This reliance on adequate volume (preload) makes the elderly very sensitive to even minimal hypovolemia which may result in cardiac collapse. However, one must be vigilant during times of volume resuscitation in the elderly and balance the need for adequate cardiac output with the potential for pulmonary edema due to decreased ventricular compliance.

Atrial fibrillation (AF) is the most common postoperative arrhythmia occurring in 3.7–6.7 % of patients [21–24]. Advanced age has been shown to be independently associated with a higher incidence of AF. AF is associated with higher daily fluid requirements, prevalence of severe infections, and the need for vasoactive and inotropic support [24]. It has been shown to be associated with significantly longer intensive care unit (ICU) and hospital length of stay (LOS) as well as increased mortality [23, 24].

The etiology for the development of AF can be multifactorial. Underlying myocardial disease in the elderly along with increased systemic inflammation can cause further myocardial dysfunction causing AF [25]. Increased intravascular volume from large volume resuscitation may dilate the left atrium and increase the risk of AF. Alternatively, hypovolemia leading to an increased adrenergic state can increase the likelihood of AF [26]. Regardless of the cause, atrial fibrillation in the geriatric critically ill patient appears to be a marker of severity of illness as demonstrated by higher Simplified Acute Physiologic Scores II, nursing workload in the ICU (OMEGA), and mortality [24].

There is a wide variation in the treatment of elderly patients with AF [27]. Clinicians should investigate for any treatable causes including thyroid dysfunction, electrolyte abnormalities, or acute cardiac ischemia. Therapy goals include rate control, rhythm control, and the prevention of thromboembolism.

Elderly patients in the ICU with AF often become hemodynamically unstable as a result of the loss of the atrial contribution to ventricular filling and stroke volume which leads to a decreased cardiac output [27]. Those with hypotension, angina, or heart failure should be immediately cardioverted. In contrast, the hemodynamically stable patient without symptoms can be treated pharmacologically. Currently, there are a number of treatment options available. Amiodarone has become the initial drug of choice for atrial fibrillation. It is a class III antiarrhythmic agent that depresses atrioventricular conduction and controls the ventricular rate. Side effects include bradycardia, thyroid dysfunction, as well as drug interaction, specifically warfarin. Intravenous (IV) amiodarone has been associated with acute elevation in liver enzymes; however, levels normalize with discontinuation of the IV form. Additionally, long-term amiodarone use has been associated with the development of pulmonary fibrosis. Dronedarone, similar to amiodarone, has been studied for rate and rhythm control in AF. It reduces morbidity and mortality in inpatients at risk for development of AF, however, is contraindicated in patients with acute severe heart failure [28]. Other pharmacological options include β-blockers and calcium channel blockers (CCB). Beta-blockers may be more appropriate for postoperative hyperadrenergic states, while CCB, specifically diltiazem, may be more appropriate for patients with severe asthma or chronic obstructive pulmonary disease. Side effects of CCB include hypotension, heart failure, and heart block.

Digoxin, one of the oldest antiarrhythmic agents for AF, is still used by many clinicians. Digoxin works by slowing down conduction at the atrioventricular node by parasympathetic activation. It may be the ideal pharmacological choice if patients have simultaneous heart failure or left ventricular dysfunction. Digoxin may have a synergistic effect with β-blockers or CCB. Unfortunately, digoxin has many drug-drug interactions which often limit its use in critically ill patients. Additionally, digoxin is renally metabolized, and drug levels need to be closely monitored and adjusted accordingly in patients with abnormal renal function.

If patients do not respond to pharmacological interventions and remain in AF, cardioversion is sometimes required. Patients who remain in AF for more than 48–72 h have an increased risk of atrial clot formation. Prior to cardioversion, it is recommended that a transesophageal echocardiogram be performed to evaluate for an atrial thrombus. Once successfully cardioverted, systemic anticoagulation is required. Clinicians need to take into account the risks of systemic anticoagulation in the critically ill geriatric patient including falls risks and drug interactions. Alternatively, additional medical attempts at rate control alone may be safer in this patient population.

Age and preexisting cardiovascular disease predispose the elderly to cardiac complications when critically ill. Cardiac complications have been reported to range from 12 to 16.7 % in this patient population especially for those over the age of 80 years [29–31]. Cardiac complications are one of the more common causes of mortality in the elderly surgical patient, and for those over the age of 80 years, myocardial infarction (MI) has been shown to be the leading cause of postoperative death [32]. The prevalence of postoperative MI in the elderly ranges between 0.1 and 4 % [33–35]. The majority of MIs occur within 72 h after conclusion of the operation [33].

Beta-blockers are thought to be the mainstay of treatment to help prevent perioperative cardiac complications in the elderly. By decreasing heart rate and afterload, the shear forces on the atherosclerotic vessels are reduced. These changes to the cardiovascular system also minimize the chances of plague rupture, which is the etiology of up to 50 % of perioperative heart attacks [36]. Additionally β-blockers assist in minimizing ventricular dysrhythmias, improve myocardial oxygen balance, and decrease sympathetic tone, leading to fewer perioperative cardiac complications. In 2002, Auerbach and Goldman reviewed the efficacy of perioperative β-blockade in reducing myocardial ischemia, infarction, and cardiac-related mortality [37]. The authors concluded that there was a benefit with β-blockade in preventing perioperative cardiac morbidity. In 2008 the Perioperative Ischemic Evaluation (POISE) study group evaluated the use perioperative β-blockade and concluded that although the treatment group had significantly lower rates of MI, there was a significantly higher death rate and stroke rate in the patients receiving β-blockers [38].

As a result of the vast literature on the use of β-blockers in the perioperative period, there is little consensus as the appropriate patient population that would benefit from their use. Some authors believe patients having one or two risk factors (high risk surgery, known ischemic heart disease, history of congestive heart failure or cerebrovascular disease, baseline creatinine >2 mg/dL) would benefit, while others believe patients with more than three risk factors are more appropriate [36, 39, 40]. As a result of the existing literature, the American Heart Association/American College of Cardiology Foundation has modified the recommendation for the use of β-blockers in the perioperative period [41, 42].

During times of acute illness or trauma, many elderly patients cannot appropriately augment their cardiac output, and therefore, systemic vascular resistance is increased to maintain perfusion [43]. As a result, elderly patients may demonstrate a normal blood pressure, while having severely depressed and compromised cardiac function leading to overall poor systemic perfusion. In a study of geriatric trauma patients, Scalea and colleagues demonstrated as many as 50 % geriatric trauma patients who appeared clinically stable with “normal” blood pressure had unrecognized cardiogenic shock and a poor outcome [44]. Using a pulmonary artery catheter, resuscitation was optimized using volume, inotropes, and afterload reduction, and survival increased from 7 to 53 %. The authors determined that identifying occult shock early in the geriatric population with the use of invasive monitoring improves survival.

The question as to the ideal method for hemodynamic monitoring in the elderly, or any critically ill patient, is an ongoing dilemma. Unfortunately, there is scant data specifically looking at invasive monitoring in the elderly, and as such, data must be extrapolated from existing literature based on various patient populations. The pulmonary artery catheter (PAC) has long been considered the gold standard of hemodynamic monitoring. It was first described and used in 1970 by Doctors Swan and Ganz [43]. However, the studies evaluating its utility to improve patient outcomes are variable with some showing no effect [45–47]; some concluding mortality rates are decreased with the use of a PAC [44, 48, 49], and others reporting increased morbidity and mortality [50]. It has been suggested by some experts that the reason for the variable outcomes with the use of the PAC is the incorrect interpretation of the hemodynamic parameters and subsequent clinical decision making [51–53].