User:Micahkidd91/Pacemaker syndrome

Pacemaker syndrome is a condition that represents the clinical consequences of suboptimal atrioventricular (AV) synchrony or AV dyssynchrony after pacemaker implantation. It is an iatrogenic disease—an adverse effect resulting from medical treatment—that is often underdiagnosed. AV dyssynchrony occurs when timing of atrial contraction occurs too close to the pacemaker conducted ventricular contraction^[1]. In general, the symptoms of Pacemaker syndrome are a combination of decreased cardiac output, loss of atrial contribution to ventricular filling, loss of total peripheral resistance response with marked decreases in blood pressure, along with non-physiologic pressure waves^[1].

Individuals with bradycardia prior to pacemaker implantation are at higher risk for developing pacemaker syndrome. Normally the atria contract as the ventricles are relaxed, to allow adequate ventricular filling before it contracts, and blood to be pumped out of the heart. When the timing between the two chambers is unsynchronized, less blood is delivered with each beat, decreasing cardiac output. Patients who develop pacemaker syndrome may require adjustment of the pacemaker, or fitting of another lead to better coordinate the timing of atrial and ventricular contraction. Selecting the appropriate pacemaker is key in prevention of Pacemaker syndrome.

No specific set of criteria has been developed to diagnose pacemaker syndrome. Most of the signs and symptoms of pacemaker syndrome are nonspecific, and many are prevalent in the elderly population at baseline. In the electrophysiology lab, pacemaker interrogation plays a crucial role in determining if the pacemaker mode had any contribution to symptoms.

Symptoms commonly encountered in patients past medical history, classified according to cause^[1]:

• Neurological - Dizziness, syncopal episodes, confusion, and fatigue
• Heart failure - Exertional dyspnea, decreased activity tolerance, orthopnea, paroxysmal nocturnal dyspnea, and edema.
• Hypotension - Seizure, change in mental status, diaphoresis, and signs of orthostatic hypotension and shock.
• Low cardiac output - Fatigue, weakness, dyspnea on exertion, lethargy, and lightheadedness.
• Hemodynamic - Pulsation in the neck and abdomen, choking sensation, jaw pain, right upper quadrant (RUQ) pain, chest colds, and headache.
• Heart rate related - Palpitations associated with arrhythmias

In particular, the examiner should asses for the following while performing a physical examination, as these are frequent findings at the time of hospital admission^[1]:

• Vital signs may reveal hypotension, tachycardia, tachypnea, or low oxygen saturation.
• Pulse amplitude may vary, and blood pressure may fluctuate.
• Neck vein distension and pulsation and cannon A waves in the neck veins.
• Lungs auscultation of crackles
• Cardiac examination may reveal regurgitant murmurs and variability of heart sounds.
• Liver may be pulsatile with accumulation of ascites in severe cases, RUQ tenderness with palpation,
• Lower extremity edema
• Neurologic examination may reveal confusion, dizziness, or altered mental status.

Studies have shown that patients with Pacemaker syndrome and/or with sick sinus syndrome are at higher risk of developing fatal complications. These patients should be monitored closely during treatment of complications, typically in the intensive care setting. Complications include atrial fibrillation, thrombo-embolic events, and heart failure. Complications can impact the patients overall quality of life.

Pacemaker syndrome is seen in people with single chamber pacemakers with ventricular sensing and pacing ^[1]. With this type of pacer, the ventricle contracts at its set rate, without regard to the atrial contraction timing, because there is no atrial sensing occurring to direct the ventricle ^[1].

• In the preimplantation period, two variables are predicted to predispose to the syndrome. First is low sinus rate, and second is a higher programmed lower rate limit. In postimplantation, an increased percentage of ventricular paced beats is the only variable that significantly predicts development of pacemaker syndrome.
• Patients with intact VA conduction are at greater risk for developing pacemaker syndrome. Around 90% of patients with preserved AV conduction have intact VA conduction, and about 30-40% of patients with complete AV block have preserved VA conduction. Intact VA conduction may not be apparent at the time of pacemaker implantation or even may develop at any time after implantation.
• Patients with noncompliant ventricles and diastolic dysfunction are particularly sensitive to loss of atrial contribution to ventricular filling and have a greater chance of developing the syndrome. This includes patients with cardiomyopathy (hypertensive, hypertrophic, restrictive) and elderly individuals.
• Other factors correlated with development of pacemaker syndrome include decreased stroke volume, decreased cardiac output, and decreased left atrial total emptying fraction associated with ventricular pacing.

Typically, pacemakers are single chambered, which can cause atrial and ventricular contractions to not be in sync, also known as AV dyssynchrony and VV dyssynchrony. This phenomenon often leads to reduced stroke volume, cardiac output or peripheral and/or pulmonary congestion ^[1]. In AV dyssynchrony, the atrial valve may contract too close to a ventricular contraction, causing increased pressure in the circulator system. Cardiac output then decreases due to a lack in atrial “kick”. The human body may compensate for this via increased peripheral vascular resistance ^[1]. However, at times, the body fails to compensate, which accounts for the signs and symptoms people experience, known as pacemaker syndrome. In VV dyssynchrony, the right and left ventricle contractions are not in sync ^[1]. Right ventricle pacing causes a left bundle branch block, as a result the left ventricle and interventricular septum asynchronously contract. The left ventricle loses output and the pressure in the pulmonary circulation increases ^[1].Pacemaker syndrome can causes cannon A waves and increased production of natriuretic peptides, but they are not involved in the pathophysiology behind pacemaker syndrome.

At the time of pacemaker implantation, AV synchrony should be optimized to prevent the occurrence of pacemaker syndrome. Where patients with optimized AV synchrony have shown great results of implantation and very low incidence of pacemaker syndrome than those with suboptimal AV synchronization.

Diet alone cannot treat pacemaker syndrome, but an appropriate diet to the patient, in addition to the other treatment regimens mentioned, can improve the patient's symptoms. Several cases mentioned below:

• For patients with heart failure, a low-sodium, 2-liter fluid restriction diet is appropriate.^[2]
• For patients with autonomic insufficiency, a high-salt diet may be appropriate.
• For patients with dehydration, oral fluid rehydration is needed.

No specific drugs are used to treat pacemaker syndrome directly because treatment consists of upgrading or reprogramming the pacemaker.

• For some patients who are ventricularly paced, usually the addition of an atrial lead and optimizing the AV synchrony usually resolves symptoms.
• For patients with systolic heart failure (left ventricular dysfunction with reduced ejection fraction) upgrading a single-chamber pacemaker with Cardiac Resynchronization Therapy using a bi-ventricular pacemaker is recommended.^[1]
• In patients with other pacing modes, other than ventricular pacing, symptoms usually resolve after adjusting and reprogramming of pacemaker parameters, such as tuning the AV delay, changing the postventricular atrial refractory period, the sensing level, and pacing threshold voltage. The optimal values of these parameters for each individual differ. So, achieving the optimal values is by experimenting with successive reprogramming and measurement of relevant parameters, such as blood pressure, cardiac output, and total peripheral resistance, as well as observations of symptomatology.
• In rare instances, using hysteresis to help maintain AV synchrony can help alleviate symptoms in ventricularly inhibited paced (VVI) patients providing they have intact sinus node function. Hysteresis reduces the amount of time spent in pacing mode, which can relieve symptoms, particularly when the pacing mode is generating AV dyssynchrony.
• If symptoms persist after all these treatment modalities, replacing the pacemaker itself is sometimes beneficial and can alleviate symptoms.
• Medical care includes supportive treatment, in case any of the following complications happen, medical team should be ready. Possible complications include heart failure, hypotension, tachycardia, tachypnea, and oxygenation deficit.

Sometimes surgical intervention is needed. After consulting an electrophysiologist, possibly an additional pacemaker lead placement is needed, which eventually relieve some of the symptoms.

The reported incidence of pacemaker syndrome has ranged from 2% to 83%. The wide range of reported incidence is likely attributable to two factors which are the criteria used to define pacemaker syndrome and the therapy used to resolve that diagnosis. The MOST trial reported an incidence of pacemaker syndrome approaches 20% in patients with single-chamber and ventricular-paced devices and is seen in similar distribution among males and females.^[1]

After the invention of pacemaker therapy in 1958, physicians have noted diminished cardiac output in select patients with ventricular pacing devices.^[1] Pacemaker syndrome was first described in 1969 by Mitsui et al. as a collection of symptoms associated with right ventricular pacing. The name pacemaker syndrome was first coined by Erbel in 1979. Since its first discovery, there have been many definitions of pacemaker syndrome, and the understanding of the cause of pacemaker syndrome is still under investigation. In a general sense, pacemaker syndrome can be defined as the symptoms associated with right ventricular pacing relieved with the return of A-V and V-V synchrony.