Monitoring the pulse as part of track and trigger
VOL: 102, ISSUE: 43, PAGE NO: 28
Brendan Docherty, MSc, PGCE, RN, is nurse manager, patient access and nursing services
Steven Coote, MN (Critical Care), BN, RN, is advanced practice nurse, after hours nursing services; both at The Prince of Wales Hospital, Sydney, Australia
The pulse is one of the main vital signs measured and recorded clinically to ensure internal homeostasis and to det…
The pulse is one of the main vital signs measured and recorded clinically to ensure internal homeostasis and to detect related abnormalities. It is calculated as the number of contractions (heartbeats) in one minute and expressed as beats-per-minute (bpm). It is important to measure the pulse when patients are rested (that is, not immediately after exercise) and when their caffeine intake is minimised (Docherty, 2002).
Resting heart rates can be low in athletes and those with good exercise tolerance (or where medications reduce the heart rate to improve cardiac efficiency), and high in patients with anxiety, pain, or those who are obese or have physiological problems - for example infections/sepsis (Jenkins and Gerred, 2005; Tortora and Grabowski, 2002). Exercise, environmental stressors or psychological stress can cause the heart rate to increase above the resting rate (Tortora and Grabowski, 2002).
Measuring the Pulse
The radial artery is a convenient and reliable location for nurses to assess pulse rate and rhythm. The patient’s right radial pulse is best felt with three fingers of the nurse’s left hand. As this pulse is relatively distant from the aorta, it is not ideal for assessing the character of the pulse pressure but suffices for rate and rhythm (Bickley, 2005). Palpate the pulse rate for 60 seconds to identify any abnormalities (Bickley, 2005).
This ‘central’ pulse is closer to the heart than the peripheral radial pulse and so better to assess the quality of left ventricular function. It is more commonly used in critically ill patients (Bickley, 2005; Tortora and Grabowski, 2002). The pulse rate is assessed by placing three or four fingertips against the patient’s larynx and gently pushing against the neck. Only one side of the neck should be palpated at a time to avoid cutting off arterial circulation to the brain and overstimulating the baroreceptors, which may cause bradycardia and fainting (Bickley, 2005). Palpate the pulse rate for 60 seconds (Bickley, 2005).
Located between the triceps and biceps on the medial side of the elbow, the brachial pulse is often used to record children’s blood pressure and pulse recordings (Bickley, 2005; Tortora and Grabowski, 2002).
The femoral pulse is as reliable as the carotid in assessing cardiac performance (Bickley, 2005). It is best assessed with the patient unclothed and laying flat. Again, three fingers are placed directly above the superior pubic ramus. Direct downward pressure is exerted over the artery and it may take several attempts to locate a sufficient pulse pressure. Difficulty in palpation of the femoral pulse can occur with obese, confused or agitated patients. This pulse should be palpated for 60 seconds.
Bradycardia can be caused by lack of oxygen, lack of circulatory volume, drugs and toxins to name a few (Jenkins and Gerred, 2005). The slow heart rate leads to a decreased volume of blood carrying essential oxygen (and other vital components for cellular survival) around the body, causing tissue malnourishment. It is important to identify bradycardia quickly to ensure that it does not deteriorate into cardiac arrest - such as complete heart block or asystole (Resuscitation Council UK, 2005).
Treatment can be chemical or electrical, and can simultaneously correct underlying causes. The drug of choice is atropine (500mcg) given intravenously, and repeated every 2-3 minutes until the bradycardia resolves; six doses - that is, 3mg - is the maximum required (Jenkins and Gerred, 2005). Another option is isoprenaline or a low-dose adrenaline infusion (RCUK, 2005). Often bradycardic patients will require oxygen therapy either to rule out a hypoxia-related event or to manage any respiratory dysfunction caused (Docherty, 2002).
If bradycardia is severely affecting the patient then an external transcutaneous pacemaker should be considered (and as an intermediate intervention until an internal temporary pacing wire or a permanent pacemaker can be inserted) (RCUK, 2005). If the pulse becomes absent (for example in asystole or electrical mechanical dissociation), then the bradycardia has turned into a cardiac arrest. This should then be confirmed and external cardiac compressions administered immediately in the ratio of 30 compressions to two breaths (RCUK, 2005; Docherty and Hall, 2002). See www.resus.org.uk/pages/bradalgo.pdf.
Tachycardia is usually a compensation mechanism to a low circulating volume, and often indicates the patient is hypovolaemic (Bickley, 2005). However, pain, infection, anxiety and atrial/ventricular arrhythmias (usually related to electrolyte imbalance or hypoxaemia) are also common causes and must be managed effectively (Docherty, 2002; Tortora and Grabowski, 2002).
As the heart rate accelerates, the ability to fill the ventricular chambers reduces due to the shortened time that the ventricle is in a relaxed (diastole) position - which would normally facilitate filling of the ventricle more effectively (Docherty, 2002). So, the faster the heart rate, the smaller the stroke volume and the lower the blood pressure. If tachycardia is a ventricular conduction abnormality this results in an ejection volume that is lowered further due to the aberrant conduction across the ventricle walls (as opposed to the conduction down the His bundle) leading to two compounding issues (Docherty, 2002).
Treatment can be chemical or electrical and can also correct underlying causes, such as fluid replacement for hypovolaemia or analgesia for pain.
If the tachycardia is an atrial conduction problem, adenosine (6mg fast bolus initially intravenously, for example in supraventricular tachycardia) and digoxin (125mcg initially intravenously, for example in atrial fibrillation) should be considered (Jenkins and Gerred, 2005; RCUK, 2005). If it is a ventricular conduction problem, amiodarone (300mg initially intravenously, for example in pulsed ventricular tachycardia) should be considered (RCUK, 2005). This is useful in that it treats both atrial and ventricular tachycardias that require rate modification (RCUK, 2005).
Patients with severe tachycardia may need sedation in order to facilitate rapid cardioversion. See www.resus.org.uk/pages/tachalgo.pdf.
- Define pulse rate and the factors that influence it
- Identify a low pulse, the possible causes and the nursing care required
- Identify a high pulse, the possible causes and the nursing care required
- Reflect on this article and develop a systematic problem-solving approach in the care of patients with pulse-rate abnormalities
- Outline your place of work and why you were interested in this article
- Detail the last time you encountered a patient with bradycardia or tachycardia
- Write about a piece of information in the article that could have helped in your care of that patient
- Explain how you intend to disseminate what you have learnt among your colleagues
This article has been double-blind peer-reviewed.
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