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Cardiovascular Disease

Jonathan M. Congdon

Veterinary Health & Wellness Center, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, 27607, USA

Introduction

The most critical function of the cardiovascular system is to circulate blood continuously, ensuring adequate oxygen delivery and survival of cells and tissues. The body can survive food and water deprivation far longer than it can survive oxygen deprivation and lack of perfusion; absence of oxygen delivery can trigger the complicated cascade that leads to temporary, permanent, or irreversible cell death [1]. As such, the simplest definition of cardiovascular disease is the decreased ability of this system to ensure adequate oxygen delivery for day-to-day survival.

Nearly all anesthetic drugs compromise cardiovascular function via a single or multiple mechanism(s) and can severely compromise oxygen delivery in patients with underlying cardiac disease [2]. Cardiovascular goals during anesthesia target maintenance of oxygen delivery and homeostasis when using drugs that knowingly disturb the system. However, this goal becomes complicated in patients with underlying cardiovascular disease and increasingly more difficult when severe pathology is present. In patients with significant cardiovascular disease, the optimization of oxygen delivery requires a complete understanding of the mechanisms underlying the pathology, as well as the anesthetic drugs, patient support, and monitoring tools available. The most difficult challenge when faced with these patients is how to balance the pathophysiology of disease against the effects of anesthetic drugs and to subsequently individualize an anesthetic plan that minimizes cardiovascular compromise.

It is difficult to predict all possible combinations of patient signalment and temperament, cardiovascular and comorbid conditions, clinicopathologic abnormalities, surgical procedures, and their effects on anesthetic drug choices. Thus, studies have tended to focus more on describing the specific cardiac disease or cardiac effects of specific anesthetics and less on their combinations. This approach leaves the difficult task of knowing how to choose the appropriate anesthetic plan for an individual patient. The goal of this chapter is to provide an overview of cardiovascular physiology and pathophysiology, anesthetic agents, and cardiovascular patient evaluation, monitoring, and support during anesthesia to help the clinician prepare anesthetic plans for patients with mild to significant cardiovascular disease.

Cardiovascular Physiology

Tissue Perfusion and Oxygen Delivery

The mathematical definition of oxygen delivery (DO2) is the product of oxygen content (CaO2, ml O2 dl-1 blood) and cardiac output (CO, l min-1; Figure 1.1) [3]. Perfusion and the ability to deliver oxygen suffer either if the ability of the heart to eject blood (CO) is compromised or if the ability of the blood to carry oxygen (CaO2) is reduced. Although decreases in CaO2 significantly affect tissue oxygenation, the focus of this chapter is on treating reductions in CO associated with cardiac disease.

Blood Pressure and Cardiac Output

It is critical to monitor blood pressure (BP) during anesthesia as it is our best, yet indirect, indicator of perfusion in veterinary medicine [4]. BP helps determine how anesthesia affects the patients' ability to perfuse their tissues and, as such, is used as a tool to treat perfusion abnormalities. However, BP is not a component of the mathematical definition of oxygen delivery: DO2 = CO?×?CaO2. It is useful to assess BP to indirectly estimate changes in CO, as CO is rarely measured clinically in nonresearch patients.

Systolic arterial pressure (SAP) is the peak pressure measured in the artery or arteriole during one cardiac cycle, and is determined by several variables, including stroke volume (SV, volume ejected during one ventricular contraction), velocity of left ventricular ejection, arterial resistance, and blood viscosity [5]. Diastolic arterial pressure (DAP) is the lowest arterial pressure measured during the cycle, and is affected by blood viscosity, arterial compliance, and cardiac cycle length [5]. Mean arterial pressure (MAP) is not the arithmetic mean pressure in the vessel and is always a calculated number. Various formulae exist to calculate MAP such as: MAP = DAP?+?1/3 (SAP?-?DAP) or MAP = (SAP + [2×DAP])/3.

Regarding perfusion, the most important of these values is MAP, as the total amount of time during the cardiac cycle (or during any one individual pulse) spent at SAP is very short, whereas the time spent at MAP is much longer (Figure 1.2) [6].

Mean Arterial Pressure and Autoregulation

Autoregulation is the automatic adjustment of blood flow through a tissue regardless of the MAP driving blood through the tissue (Figure 1.3). In other words, autoregulation is the unconscious adjustment of arterial and arteriolar smooth muscle tone to maintain a constant blood flow through a tissue across a wide range of pressures. Classically, this is thought to occur between a MAP of approximately 60-160?mmHg, and is due to adaptive metabolic, myogenic, and neurogenic feedback mechanisms. Outside of this interval, tissue or organ blood flow is substantially altered, potentially resulting in reduced or nonuniform perfusion patterns [7, 8].

Hypotension

MAPs <60?mmHg (or SAPs <90?mmHg) have historically been considered the minimum recommended pressures in small animals associated with adequate tissue oxygen delivery [9]. However, a MAP of approximately 60?mmHg may not actually reflect adequate perfusion for several reasons. First, studies investigating autoregulation are routinely performed in nonanesthetized patients [10]. Neurogenic mechanisms for autoregulation depend on sympathetic nervous system (SNS) input. Anesthetic agents depress both the conscious and unconscious (autonomic) nervous systems. Since SNS tone is substantially reduced during anesthesia, autoregulatory mechanisms are unavoidably depressed, either partially or completely, and autoregulation is impaired. Second, if a MAP of approximately 60?mmHg is considered the minimum acceptable BP but the patient is not yet considered to be truly hypotensive, then treatments may be delayed until the patient is in a state wherein oxygen delivery is pressure-dependent (i.e., to the left of the autoregulatory curve). As all hypotensive therapies are not instantaneously acting, there is concern that the patient may become increasingly hypotensive before treatments are efficacious. Thus, a MAP of approximately 70?mmHg (or SAP of approximately 90?mmHg) should be considered the minimum acceptable BP to build in a buffer zone so that treatments for hypotension can be applied and take effect before tissue perfusion is severely compromised, considering both altered autoregulatory mechanisms and the time-dependent treatment effects.

Figure 1.1 Determinants of oxygen delivery. Oxygen delivery (ml?min-1) is the mathematical product of cardiac output (l blood min-1) and oxygen content (ml?dl-1 blood).

Figure 1.2 Arterial pulse pressure waveform. Mean arterial pressure (MAP) is 1/3 of the difference between systolic arterial pressure (SAP) added to the diastolic arterial pressure (DAP). MAP is considered the pressure of perfusion, as more time in the cardiac cycle is spent closer to MAP as compared to SAP. Total cycle length is 400?ms for illustration and is determined by the heart rate and other cardiovascular variables.

Figure 1.3 Between MAP of approximately 60 and 160?mmHg, blood flow through a tissue capillary bed is maintained at a relatively constant flow by autoregulatory mechanisms. At MAP lower than approximately 60?mmHg and greater than approximately 160?mmHg, autoregulation of blood pressure is lost and blood flow through capillary beds becomes pressure-dependent; tissues are either underperfused or overperfused, respectively.

Relationship Between Mean Arterial Pressure and Cardiac Output

When considering the relationship of measured BP to the definition of oxygen delivery, one must understand the components that derive a measured BP [4]. MAP is the product of CO (l?min-1) and systemic vascular resistance (SVR) (dynes s-1 cm-5). SVR is considered the degree of vasodilation (which reduces SVR) or vasoconstriction (which increases SVR) present in the systemic circulation. CO is the product of heart rate (HR, beats?min-1) and SV (ml ejected per heartbeat). SV is determined by preload (the venous return during diastole preloading the ventricle before contraction/ejection), afterload (the resistance that ventricular contraction must overcome in order to eject blood), and contractility (the force of contraction of ventricular muscle,...