The assessment of pulse and respiration within clinical practice is often referred to as ‘doing the obs’. But this phrase, whilst in common usage, does sound very simple and fails to convey the significance of these basic, yet essential vital signs. The importance of these assessments is sometimes unrecognized and delay in acting upon abnormal results can severely compromise maternal and child health and wellbeing (Lewis 2007). Of the reported maternal deaths due to genital tract sepsis during the triennium 2003–2005, suboptimal care was identified in 70% of the cases, with a number of practitioners either not recognizing or failing to act upon signs and symptoms of infection such as raised pulse and respiratory rate (Lewis 2007).

This chapter will focus upon the assessment of pulse and respiration within midwifery practice, based upon a scenario. The background physiology of heart rate and respiration will be discussed and the physiology in relation to pregnancy will be explored. Using the framework within this book, the procedure will be described and then the ‘jigsaw model’ will be used to consider relevant issues.

During each cardiac cycle, as the left ventricle of the heart contracts, a wave of pressure is transmitted through the arterial system causing expansion and recoil of the arteries (Tortora 2005). This can be palpated, with the fingertips, in arteries lying close to the surface of the skin as a wave-like sensation called a pulse (Tortora & Grabowski 2003). The pulse can be palpated as being strongest in the arteries closer to the heart, becoming weaker as it passes through the arterioles and disappearing as it reaches the capillaries (Tortora & Grabowski 2003).

The heart rate is regulated by the sinoatrial (SA) node; the heart’s internal pacemaker. The SA node sets a constant heart rate of approximately 100 beats per minute. During different circumstances, such as exercise, stress, haemorrhage or ill health, the body requires different volumes of blood flow to ensure that the oxygen and nutrient needs of the tissues and organs are met. To enable these requirements to be met a healthy heart is able to beat faster, or more slowly, under the influence of the autonomic nervous system, chemical regulation and a number of physical factors (Tortora & Grabowski 2003, Dougherty & Lister 2006).

In order to understand how the heart responds to these different circumstances, it is necessary to understand the terms heart rate, stroke volume and cardiac output.

So, cardiac output = stroke volume × heart rate.

The cardiovascular centre, in the medulla oblongata region of the brainstem, receives input from a range of sensory receptors; such as those monitoring movement, blood pressure and blood chemistry and from higher brain centres including the cerebral cortex, the limbic system and the hypothalamus. In response to this input, the cardiovascular centre then increases, or decreases, the frequency of nerve impulses to the heart via the cardiac accelerator nerves (sympathetic nervous system) or the vagus nerves (parasympathetic nerves) adjusting the heart rate. Increased sympathetic nerve stimulation leads to an increase in heart rate, whereas increased parasympathetic nerve stimulation leads to a decrease in heart rate (Tortora & Grabowski 2003, Tortora 2005, Dougherty & Lister 2006).

At rest, the normal pulse rate for an adolescent and an adult is between 60 and 100 beats per minute (bpm) (Dougherty & Lister 2006), whilst a newborn baby may have a pulse rate of over 120 beats per minute (Tortora & Grabowski 2003). During exercise, the body requires increased amounts of oxygen and nutrients so the heart must increase the rate at which it beats to increase cardiac output. Even before exercise occurs anticipatory changes may be noted as the limbic system generates anticipatory nerve impulses to the cardiovascular centre in the medulla, causing a rise in pulse rate. Once exercise begins the sensory receptors monitoring movement, blood chemistry and blood pressure send an increased frequency of nerve impulses to the cardiovascular centre and a rapid rise in pulse rate can be observed (Tortora & Grabowski 2003). If the circulating blood volume drops (hypovolaemia), for example during either an ante- or postpartum haemorrhage, the stroke volume declines and the blood pressure falls and in order to maintain cardiac output the heart must increase the rate at which it beats.

A number of chemicals, hormones and cations influence heart rate and the physiology of the cardiac muscle. Hypoxia, acidosis and alkalosis all depress cardiac activity (Tortora & Grabowski 2003) whereas the hormones adrenaline and thyroxine increase heart rate. Several cations are essential for the initiation and maintenance of action potentials in nerve and muscle fibres and an imbalance of ions can quickly compromise cardiac output. Elevated blood levels of sodium and potassium decrease the heart rate whereas elevated levels of calcium increase the heart rate (Tortora & Grabowski 2003, Tortora 2005).

Physical factors which influence the resting heart rate include age, gender, body temperature and physical fitness (Tortora & Grabowski 2003). Adult females have been noted to have a slightly higher resting pulse than adult males (Tortora & Grabowski 2003).

Tachycardia is the term used to describe an elevated resting heart rate. In adults this is over 100 beats per minute. A tachycardia may be noted when there is an increased body temperature, for example in response to a postpartum infection. The raised body temperature causes the sinoatrial nerve to trigger more rapid contractions of the heart, increasing the heart rate (Tortora & Grabowski 2003).

Bradycardia is the term used to describe a resting heart rate of less than 60 beats per minute. A bradycardia may be noted when the body temperature is low, as a result of certain drugs or if the parasympathetic nervous system is stimulated. A bradycardia may also be observed in athletes who are physically and cardiovascularly well conditioned. As a result of increased stroke volume due to hypertrophy of the heart, the athlete’s heart rate must be lower to maintain cardiac output.

The pulse rhythm is the sequence of beats (Dougherty & Lister 2006) and in a healthy individual this should be regular. Defects in the conduction system of the heart could cause uncoordinated contraction of the heart which could result in an irregular pulse.

The strength of a pulse reflects the elasticity of the arterial wall. If a woman is hypovolaemic, the greater the reduction in circulating blood volume, the more weak and thready the pulse will feel. A strong and bounding pulse may be an indication of infection (Trim 2004).

During respiration three events must occur; pulmonary ventilation, external respiration and internal respiration. Pulmonary ventilation, or breathing, is the movement of air into (inspiration) and out of (expiration) the lungs. The pressure changes within the lungs and thoracic cavity during inspiration and expiration result in the flow of gases to equalize pressure (Tortora & Grabowski 2003, Richardson 2006). Just before inspiration, the air pressure inside the lungs is equal to the pressure in the atmosphere so, for air to move into the lungs, the pressure inside the lungs must become lower than atmospheric pressure. This is achieved by increasing the volume of the lungs. As the lungs are tightly adherent to the diaphragm and thoracic wall, an increase in the volume of the thoracic cavity will result in an increase in the volume of the lungs. The volume of the thoracic cavity increases due to contraction of the dome-shaped diaphragm and the external intercostal muscles. Contraction of the diaphragm makes the diaphragm flatten, increasing the vertical dimension of the thoracic cavity (Tortora and Grabowski 2003, Richardson 2006). This is accompanied with contraction of the muscles lying between the ribs, the external intercostal muscles. This causes the rib cage to rise up and move outwards, increasing the front to back and side to side dimensions of the thoracic cavity (Tortora & Grabowski 2003, Dougherty & Lister 2004, Tortora 2005). The air in the lungs now has a larger area to fill and so the pressure falls and air flows into the lungs until the pressure in the lungs (intrapulmonary pressure) equals the atmospheric pressure.

Expiration occurs as the inspiratory muscles relax. The diaphragm moves upwards, returning to its dome shape. The external intercostal muscles return to their resting position causing the rib cage to descend and the volume of the thoracic cavity, and hence the lungs, decreases. This process is aided by the elastic recoil properties of the lungs. As the volume of the lungs decreases, the pressure inside the lungs increases and as this pressure is now greater than atmospheric pressure, air must flow out of the lungs to equalize pressure. The degree to which the lungs are able to stretch and recoil and the thorax is able to expand and relax during inspiration and expiration is called lung compliance.

External respiration is the exchange of gases between the air spaces of the lungs and the pulmonary capillary blood. The blood loses carbon dioxide and gains oxygen. The exchange of carbon dioxide and oxygen between the capillaries and tissue cells is called internal respiration (Tortora 2005). The blood loses oxygen and gains carbon dioxide.