Arrhythmias
Questions Received:
Responses:
6 months ago I was diagnosed with chronic sinus tachycardia. Unfortunately they can’t find the cause for this arrhythmia. Until they find a cause for this they will not give me any medication to relieve me of my symptoms because they want to see them when it is happening. These are my symptoms...
At night my bed becomes all wet
My heart beat never goes under 120 per min. and sometimes goes up to 160
Panic attacks
Heavy transpiration if I work on the house
Discomfort in the chest
In Quebec to see a cardiologist you have to wait 6 or 8 months because of congestion in our healthcare system, but until then I must endure these symptoms. My worry is that my heart will not last, I am very scared. I am a male, 34 years old with 2 children. By the way both my children were born with heart defects: tetralogy of Fallot. Am I in danger and what do you recommend?
25th November 1999
In some ways the lack of urgency being shown by the doctors to your condition is reassuring, since it implies that they think your condition is not life-threatening. It is clear though that you are particularly worried about the situation and it would therefore be worth visiting your doctor again to express this concern and ask whether you could see the cardiologist more quickly. Any undue stress can only add to your problem, and it will be helpful for you to try and reduce those stresses that you can influence.
The nervous system helps to regulate the behaviour of the heart, particularly via the sympathetic and parasympathetic fibres supplying it. When stress is experienced, the sympathetic part of the nervous system becomes more active and stress-related hormones are released - both these factors will accelerate the heart rate. Try to avoid smoking and drinks that contain caffeine or alcohol, since these will affect brain and heart function. Try also to reduce the stressfulness of situations that may occur at work and at home.
As your doctors have pointed out, it will be necessary to determine the underlying cause before an appropriate treatment can be given. There are several possible explanations for your condition - arrhythmias may result from problems with the natural pacemaker of the heart (SA node or sinus node), abnormal conduction of the controlling impulses through the heart, or a metabolic disorder (Schmidt, Ezri, and Denes, 1987).
Normally the testing involves a routine electrocardiogram, perhaps a 24 hr monitoring of your heart during normal activities, and an echocardiogram (ultrasound scan). If these tests are unable to reveal a cause, then more detailed information can be gained from imaging and electrophysiological studies carried out within the heart (Schmidt, Ezri, and Denes, 1987; Schwartz et al, 1995; Lesh, Kalman, and Karch, 1998). The activities of the sympathetic and parasympathetic nerves supplying the heart can be assessed by measurement of heart rate variability, which gives a good insight into any imbalance (Grossman, 1992; Baumert, Frey, and Adt, 1995; Cowan, 1995; Murata and Araki, 1996).
Many cardiac arrhythmias can be successfully treated with drugs, while the others can be controlled by an artificial pacemaker or surgery (Petri and Rudolph, 1979; Schmidt, Ezri, and Denes, 1987).
References
Baumert, J.H., Frey, A.W., and Adt, M. (1995) Analysis of heart rate variability. Background, method, and possible use in anesthesia. [Article in German] Anaesthesist, 44(10), 677-686 (Oct).
Cowan, M.J. (1995) Measurement of heart rate variability. West J Nurs Res, 17(1), 32-48; discussion 101-11 (Feb).
Grossman, P. (1992) Respiratory and cardiac rhythms as windows to central and autonomic biobehavioral regulation: selection of window frames, keeping the panes clean and viewing the neural topography. Biological Psychology, 34(2-3), 131-161 (Nov).
Lesh, M.D., Kalman, J.M., and Karch, M.R. (1998) Use of intracardiac echocardiography during electrophysiologic evaluation and therapy of atrial arrhythmias. Journal of Cardiovascular Electrophysiology, 9(8 Suppl), S40-47 (Aug).
Murata, K., and Araki, S. (1996) Assessment of autonomic neurotoxicity in occupational and environmental health as determined by ECG R-R interval variability: a review. American Journal of Ind Med, 30(2), 155-163 (Aug).
Petri, H., and Rudolph, W. (1979) Medical management of tachycardias. [Article in German] Herz, 4(4), 344-358 (Aug).
Schmidt, P.J., Ezri, M.D., and Denes, P. (1987) Cardiac arrhythmias - update 1987. Disease Monitoring, 33(7), 365-432 (Jul).
Schwartz, S.L., Pandian, N.G., Crowley, R., and Kumar, R. (1995) Intracardiac echocardiography without fluoroscopy: potential of a balloon-tipped, flow-directed ultrasound catheter. American Heart Journal, 129(3), 598-603 (Mar).
We are grateful to Bridget Todd, Senior Technician in the Department of Cardiology, Royal Devon and Exeter Hospital, for her help with this answer.
I recently nursed a patient in supraventricular tachycardia (SVT) and she was treated with verapamil can you tell me what causes a patient to present with this cardiac arrythmia and how the drug treats this. Are there any particular safety issues the nurse should be aware of when treating a patient with this condition (I am aware of the potential for cardiac arrest).
30th April 2001
Acute supraventricular tachycardia can occur as a result of acute myocardial infarction, digitalis intoxication, myocarditis and following cardiac surgery (Grahame-Smith and Aronson, 1994).
Calcium plays a key role in the depolarisation and contraction of myocardial cells during systole, entering the cells through slow channels in the cell's membrane.
Verapamil is a drug which belongs to the class 4 category of anti-arrhythmic preparations. The drug is a calcium-channel blocker (calcium antagonist) which means that it impedes the transport of calcium ions across the cell membrane. In doing so it modifies the electrochemical activity that takes place within myocardial cells, thereby changing the rate at which depolarisation takes place. Verapamil also acts on the specialised conduction cells in the heart and the smooth muscle cells in the walls of blood vessels (British National Formulary, 1999). The drug also has negative inotropic properties, which means it reduces contractility within the myocardium and therefore reduces myocardial oxygen demand.
When administered to someone who has developed supraventricular tachycardia the drug will increase the effective refractory period (the period of repolarisation) within the sinu-atrial and atrioventricular nodes, slowing the heart rate (Grahame-Smith and Aronson, 1994).
In terms of safety measures that need to be taken into account when caring for someone with this condition, these can be placed under two broad categories - monitoring and drug administration.
Monitoring
Aims:
To assess the person's progress and response to treatment
To identify the early onset of complications
Intervention:
Attach to ECG monitor - a daily12 lead ECG may be required
Record pulse and blood pressure - verapamil reduces cardiac output and slows the heart rate - and oxygen saturation levels, according to condition and treatment policy
Record body temperature regularly (usually 4-6 hourly)
Observe, measure and record urinary output
Assess pain levels if underlying cause is ischaemia/myocardial infarction
Observe and maintain infusion lines and intravenous pump/s, record delivery
Record fluid intake and output
Record bowel movements
Drugs
Aims:
To inform the person about the drugs they are to receive and the aims of treatment
To administer prescribed drugs safely, evaluate response/s and prevent complications
Intervention:
Calculate and administer prescribed drugs by the correct route
In terms of verapamil observe for, hypotension, bradycardia, nausea, oliguria, and allergic responses
Conduct close observations whenever dose adjustments are made.
References
British National Formulary (1999) Calcium-channel blockers. British Medical Association and the Royal Pharmaceutical Society. Wallingford: Pharmaceutical Press (Sect.2.6.2, p 97; September).
Grahame-Smith, D.G., and Aronson, J.K. (1994) Calcium antagonists. In: Oxford Textbook of Clinical Pharmacology and Drug Therapy (2nd. edition). Oxford: Oxford University Press (Section 4, p 570).