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Guided Learning

Using sympathomimetic drugs to manage hypotension 1: the cardiovascular system

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This article outlines background on the cardiovascular system, and how its various components affect blood pressure and common factors that lead to hypotension

Abstract

Higginson, R., Jones, B. (2009) Using sympathomimetic drugs to manage hypotension 1: the cardiovascular system. Nursing Times; 105: 14. Early online publication.

This first in a two-part unit on sympathomimetics outlines background information on the cardiovascular system, and how its various aspects affect blood pressure.

Keywords: Blood pressure, Cardiovascular system, Hypotension

Authors

Ray Higginson,PhD, MSc, PGCE, BN, is senior lecturer in critical care; Bridie Jones, MSc, PGCE, PGDip, BSc, is senior lecturer in emergency care; both at University of Glamorgan.

 

Learning objectives

  1. Understand what is meant by the terms ‘preload’ and ‘afterload’ and how they affect blood pressure.
  2. Identify the factors that can influence BP.

 

Introduction

The cardiovascular system (CVS) pumps blood around the body. Blood contains a number of important physiological elements, such as oxygen, carbon dioxide, nutrients and hormones (Aron, 2004).  

Most processes carried out inside the body require oxygen, without which the body would not be able to perform many of its vital functions and the energy needed for homeostasis could not be manufactured. All cells need oxygen and many cannot survive for long without it.

For oxygen to reach the body’s cells, it must first make its way from the atmosphere (outside) to the inside. The respiratory system’s primary role is to deliver oxygen from air to inside the body. The lungs allow oxygen to pass from the respiratory system into the blood.

Once oxygen has made its way through the respiratory system, it is then carried via the cardiovascular system to cells and tissues.

Similarly, the body’s main waste product (carbon dioxide) needs to be transported throughout the body and then, ultimately, to be expelled by the lungs (Tortora and Derrickson, 2006). Carbon dioxide is transported via the cardiovascular system, being formed from cells and expelled by the respiratory system.

There is, therefore, an essential relationship between the respiratory system and the cardiovascular system.

Cardiovascular system  

The cardiovascular system – sometimes referred to as the circulatory system – moves blood containing oxygen, carbon dioxide, waste products, hormones, nutrients, blood cells, any injected drugs and metabolised ingested drugs to and from the body’s cells. It consists of the heart, which is a muscular pumping device, and a closed system of vessels - arteries, capillaries and veins.

The blood contained in the CVS is pumped by the heart around a closed circuit of vessels as it passes again and again through the various ‘circulations’ of the body (for example, the systemic circulation, venous circulation, pulmonary circulation, coronary circulation, capillary circulation). Blood moving from the heart delivers oxygen and nutrients to all the body’s cells. Blood pumped back to the heart carries carbon dioxide and other waste products which are then delivered to the respiratory system for removal. Put simply, the CVS can be said to move blood.

The heart

This organ is a muscular pump that provides the force necessary to circulate blood to all the body’s tissues. Its principal function is to continuously pump blood around the cardiovascular system. The heart’s function is vital because, to survive, tissues need a continuous supply of oxygen and nutrients, and metabolic waste products have to be removed.

Therefore, while blood is the transport medium, the heart is the organ that keeps blood moving through the vessels (Klabunde, 2004).

Blood pressure

Under normal conditions, an adult heart will contract (beat) approximately 70 times a minute. The strength and frequency of the beat is controlled by the autonomic nervous system – specifically, the parasympathetic and sympathetic branches of this system innervate the heart and control the heart rate.

The normal adult heart pumps about 70ml of blood each time it contracts (one cardiac cycle), contracting approximately 70 times a minute. The volume of blood ejected in every contraction is referred to as the stroke volume (SV). Over one minute, the heart pumps approximately 5L of blood, known as the cardiac output (CO). Thus, CO can be expressed as: CO = SV x HR.

During ventricular systole, the left ventricle pushes blood into the aorta and out into the systemic circulation. The pressure which the left ventricle has to push against to eject blood into the aorta is called ‘afterload’. According to Klabunde (2004), afterload can be thought of as the ‘load’ that the heart must eject blood against.

Increases in afterload can affect stroke volume; if afterload increases, stroke volume decreases. This can then, ultimately, adversely affect CO and BP.

Another concept important in understanding blood pressure is the term ‘preload’. Although this concept can be applied to either the ventricles or atria, it is usually used in relation to the left ventricle.

When the heart’s ventricles are in diastole they are filling with blood, which causes them to stretch. The amount of blood in the left ventricle just before the ventricles contract is referred to as the left ventricular end-diastolic volume, and is related to the term preload. Preload can be defined as the initial stretching of the cardiac cells (myocytes) before contraction.

Changes in ventricular preload dramatically affect ventricular stroke volume via the Frank-Starling mechanism (Klabunde, 2004). Put simply, the Frank-Starling mechanism states that the greater the volume of blood entering the left ventricle during diastole, the greater the volume of blood ejected by the left ventricle during systolic contraction.

If, for example, venous return increases, this will increase preload, which in turn will increase stroke volume and, ultimately, BP. 

In addition to the above, systemic vascular resistance (SVR) is also an important factor in BP regulation. Commonly referred to as the total peripheral resistance (TPR), SVR is the resistance to blood flow by the blood vessels of the systemic vasculature (Guyton and Hall, 2005). The blood vessels’ diameter affects resistance to blood flow. If these dilate then SVR falls and if they constrict then it increases.

The heart rate, stroke volume, cardiac output and vascular resistance all influence BP, which is normally approximately 120/80mmHg. The relationship between these variables is what provides BP, which can be expressed as: CO x VR.

Fig 1 highlights the component factors affecting BP.

Factors affecting the heart rate include: intravascular blood volume; nervous system stimulation; and hormones such as adrenaline. Those affecting stroke volume include: intravascular blood volume; changes to preload and afterload volumes; and the heart’s ability to contract. Changes to either heart rate or stroke volume affect cardiac output and, ultimately, BP. 

Hypotension and cellular hypoxia

As discussed above, blood pressure is related to heart rate, stroke volume and vascular resistance.

Because BP can vary between people, it is best assessed in terms of how well the body’s tissues are supplied with blood.

There are many clinical conditions that can affect BP, leading to hypotension.

If BP falls, then cells can be deprived of oxygen. If this happens they quickly become ischaemic and switch to anaerobic cellular metabolism. Prolonged cellular ischaemia can lead to cell death (Bersten and Soni, 2008). Common factors leading to hypotension include loss of intravascular blood volume (shock), neurologically induced peripheral vasodilatation and heart disease (Boon et al, 2006). Table 1 outlines factors that affect stroke volume, heart rate and vascular resistance.

Table 1. Factors affecting stroke volume, heart rate and vascular resistance

Factors that decrease heart rateFactors that decrease stroke volumeFactors that decrease vascular resistance
Heart disease (such as coronary plaque, sick sinus syndrome)Loss of intravascular blood volume (caused by, for example, traumatic shock, burns)Vasodilation due to hypoxia
Systolic/diastolic heart failureSystolic/diastolic heart failureVasodilation due to hypercapnia
Drug overdoseReduced venous return Neural factors and hormones such as atrial natriuretic peptide
Metabolic and endocrine disordersCardiac tamponadeNitric oxide – produced by vascular endothelium
Electrolyte imbalance (changes to, for example, sodium, calcium, potassium levels)Chest traumaVasoactive drugs (such as glyceryl trinitrate)
Sinoatrial and atrioventricular node associated bradycardiasMyocardial ischaemiaSepsis leading to multiple organ failure

Compensatory mechanisms in hypotension

If hypotension occurs, the body uses a number of physiological mechanisms to restore adequate blood pressure. The body’s compensatory mechanisms can be divided into neural, hormonal and chemical ones. These occur simultaneously to restore blood pressure and tissue oxygenation (Bersten and Soni, 2008).

Neural compensation: a decrease in BP will stimulate sympathetic nervous system activation, leading to a series of neurological responses in an attempt to raise blood pressure. Neural mechanisms cause both the heart rate and the rate and depth of breathing to increase and the blood vessels to constrict.

Hormonal compensation: in response to hypotension and resultant sympathetic nervous system stimulation, hormones are secreted which help to restore BP.

Antidiuretic hormone, secreted from the posterior pituitary gland, acts to prevent the production of dilute urine, thus helping to maintain intravascular volume. Aldosterone from the adrenal glands causes the kidneys’ tubules to retain sodium and water, again helping tomaintainintravascular volume and restoring BP. In addition, adrenaline and noradrenaline are secreted from the adrenal medulla, resulting in vasoconstriction and increased heart rate.

Chemical compensation: decreased BP means a decrease in blood flow to the lungs, which affects gaseous exchange. Hypoperfusion of the lungs results in a high ventilation-to-perfusion ratio (ventilation with low perfusion). This has the effect of increasing physiological dead space (a part of the respiratory system that does not participate in gaseous exchange), resulting in decreased arterial oxygen levels. The hypoxia stimulates chemoreceptors, which results in increased rate and depth of respirations.

Most of the body’s blood vessels dilate during episodes of hypoxia. Although this will not help to raise BP, the widening of the blood vessels allows for greater blood perfusion and oxygen delivery to the tissues.

Managing hypotension

If a patient’s blood pressure falls, clinical staff can manipulate venous return, stroke volume, cardiac output and vasoconstriction, thus mimicking the body’s natural physiological responses to hypotension. Decreases in intravascular volume can be dealt with by administering IV fluids. Depending on the nature and causes of hypotension, fluids such as crystalloid and/or colloid solutions can be administered to increase BP.

Vasoactive drugs can also be administered to manipulate heart rate and vascular resistance. Drugs such as adrenaline/noradrenaline, which mimic the sympathomimetics released from the sympathetic division of the autonomic nervous system, can be administered to increase BP.

  • Part 2 of this unit, to be published in next week’s issue, examines the use of sympathomimetic drugs.

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