Chapter 1
Cardiovascular disease

Jonathan M. Congdon

Wisconsin Veterinary Referral Center, Waukesha, WI, 53188,, USA

Introduction

The most critical function of the cardiovascular system is to circulate blood continuously, ensuring the adequate delivery of oxygen and survival of cells and tissues. The body can survive deprivation of food and water far longer than it can survive deprivation of oxygen and lack of perfusion; lack 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 include 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

Figure 1.1 Determinants of oxygen delivery.

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 and is our best, yet indirect, clinical indicator of perfusion.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 in an attempt to estimate changes in CO, as CO is rarely measured in nonresearch patients.

Systolic arterial pressure (SAP) is the peak pressure measured in the artery or arteriole during one cardiac cycle and is due to a number of variables, including stroke volume (SV, volume ejected during one ventricular contraction), velocity of left ventricular ejection, arterial resistance, and the viscosity of blood.5 Diastolic arterial pressure (DAP) is the lowest arterial pressure measured during the cycle and is affected by blood viscosity, arterial compliance, and length of the cardiac cycle.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 as follows: (1) MAP = DAP + 1/3 (SAP-DAP) or (2) MAP = (SAP + (2 × DAP)/3). In regards to perfusion, the most important of these values is MAP, as the time during the cardiac cycle spent at SAP is very short, whereas the time spent at MAP is much longer (Figure 1.2).6

Figure 1.2 Diagram of arterial pulse waveform. Mathematically, mean arterial pressure is 1/3 the difference between systolic arterial pressure and diastolic arterial pressure, added to the diastolic arterial pressure. Mean arterial pressure is considered the pressure of perfusion, as more time in the cardiac cycle is spent closer to mean arterial pressure as compared to systolic arterial pressure. Total cycle length is estimated at 400 ms for illustration and determined by the heart rate and other cardiovascular variables.

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).7 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 MAPs of ~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.8

Figure 1.3 Principles of autoregulation. Between mean arterial pressures (MAPs) of ~60 and 160 mmHg, blood flow through a tissue capillary bed is held constant by autoregulatory mechanisms. At MAP > ~160 mmHg and at MAP < ~60 mmHg, autoregulation of blood flow is lost and blood flow through capillary beds becomes pressure dependent; tissues are either overperfused or underperfused.

Hypotension

MAPs <60 mmHg (or SAP <90 mmHg) have historically been considered the minimum recommended pressures in small animals associated with adequate tissue oxygen delivery.9 However, a MAP of ~60 mmHg may not actually reflect adequate perfusion for a number of reasons. Firstly, 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 the SNS tone is substantially reduced during

anesthesia, autoregulatory mechanisms are unavoidably depressed, either partially or completely, and autoregulation is impaired. Secondly, if a MAP of ~60 mmHg is considered the minimum acceptable BP and not hypotension, then treatments for patients assessed as hypotensive (i.e. MAP < 60 mmHg) will not begin until the patient is in a state wherein oxygen delivery is pressure dependent (i.e. to the left of thex

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 70 mmHg (or SAP of 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, taking into account both altered autoregulatory mechanisms and the time-dependent treatment effects.

Relationship between mean arterial pressure (MAP) and cardiac output (CO)

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 SVR (dynes s-1 cm1). 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 per minute) and SV (milliliter ejected per heart beat). 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, independent of preload and afterload; Figure 1.4).

Figure 1.4 Determinants of mean arterial blood pressure. Mean arterial blood pressure (MAP) is the product of cardiac output (CO), the volume of blood ejected by the heart per minute, and systemic vascular resistance (SVR), the degree of vasodilation (decreased SVR) or vasoconstriction (increased SVR). Note that MAP is not a component of oxygen delivery. Cardiac output is the product of heart rate (HR) and stroke volume (SV), the volume of blood ejected from the heart per cardiac cycle. Stroke volume is determined by the volume of blood returning to the heart during diastole (preload), the resistance to ejection of blood during systole (afterload), and the strength of cardiac muscle contraction (contractility).

Increases in SVR, SV, preload, and...