No specific set of criteria has been developed for diagnosis of 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 lab, pacemaker interrogation plays a crucial role in determining if the pacemaker mode had any contribution to symptoms.

Symptoms commonly documented in patients history, classified according to cause:

- Neurological - Dizziness, near syncope, and confusion.

- Heart failure - Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and edema.

- Hypotension - Seizure, mental status change, 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 look for the following in the physical examination, as these are frequent findings at the time of admission:

- Vital signs may reveal hypotension, tachycardia, tachypnea, or low oxygen saturation.

- Pulse amplitude may vary, and blood pressure may fluctuate.

- Look for neck vein distension and cannon waves in the neck veins.

- Lungs may exhibit crackles.

- Cardiac examination may reveal regurgitant murmurs and variability of heart sounds.

- Liver may be pulsatile, and the RUQ may be tender to palpation. Ascites may be present in severe cases.

- The lower extremities may be edematous.

- Neurologic examination may reveal confusion, dizziness, or altered mental status.

Familial atrial fibrillation is an autosomal dominant heart condition that causes disruptions in the heart's normal rhythm. This condition is characterized by uncoordinated electrical activity in the heart's upper chambers (the atria), which causes the heartbeat to become fast and irregular.

Even though many types of sick sinus syndrome produce no symptoms, a person may present with one or more of the following signs and symptoms:

- Stokes-Adams attacks – fainting due to asystole or ventricular fibrillation

- Dizziness or light-headedness

- Palpitations

- Chest pain or angina

- Shortness of breath

- Fatigue

- Headache

- Nausea

Pacemaker syndrome is a disease that represents the clinical consequences of suboptimal atrioventricular (AV) synchrony or AV dyssynchrony, regardless of the pacing mode, after pacemaker implantation.

It is an iatrogenic disease—an adverse effect resulting from medical treatment—that is often underdiagnosed. In general, the symptoms of the syndrome are a combination of decreased cardiac output, loss of atrial contribution to ventricular filling, loss of total peripheral resistance response, and nonphysiologic pressure waves.

Individuals with a low heart rate prior to pacemaker implantation are more at risk of developing pacemaker syndrome. Normally the first chamber of the heart (atrium) contracts as the second chamber (ventricle) is relaxed, allowing the ventricle to fill before it contracts and pumps blood out of the heart. When the timing between the two chambers goes out of synchronization, less blood is delivered on each beat. 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.

In right atrial isomerism, both atria of the heart are morphological right atria leading to associated abnormalities in the pulmonary venous system. In addition, individuals with right atrial isomerism develop asplenia, a midline liver, malrotation of the small intestine and the presence of two morphologic right lungs. Individuals with left atrial isomerism, by comparison, have two morphologic left atria, polysplenia, intestinal malrotation and two morphologic left lungs.

The majority of cases present at the time of birth or within a few days or weeks. Presenting signs and symptoms of the congenital heart defect may include cyanosis, breathlessness, lethargy and poor feeding.

People with WPW are usually asymptomatic when not having a fast heart rate. However, individuals may experience palpitations, dizziness, shortness of breath, or infrequently syncope (fainting or near fainting) during episodes of supraventricular tachycardia. The telltale "delta wave" may sometimes be seen on an electrocardiogram (ECG/EKG).

Symptoms may occur at any time, but most often they accompany a change of body position. Pedunculated myxomas can have a "wrecking ball effect", as they lead to stasis and may eventually embolize themselves. Symptoms may include:

- Shortness of breath with activity

- Platypnea – Difficulty breathing in the upright position with relief in the supine position

- Paroxysmal nocturnal dyspnea – Breathing difficulty when asleep

- Dizziness

- Fainting

- Palpitations – Sensation of feeling your heart beat

- Chest pain or tightness

- Sudden Death (In which case the disease is an autopsy finding)

The symptoms and signs of left atrial myxomas often mimic mitral stenosis.

General symptoms may also be present, such as:

- Cough

- Pulmonary edema, as blood backs up into the pulmonary artery, after increased pressures in the left atrium and atrial dilation

- Hemoptysis

- Fever

- Cachexia – Involuntary weight loss

- General discomfort (malaise)

- Joint pain

- Blue discoloration of the skin, especially the fingers (Raynaud's phenomenon)

- Fingers that change color upon pressure or with cold or stress

- Clubbing – Curvature of nails accompanied with soft tissue enlargement of the fingers

- Swelling – any part of the body

- Presystolic heart murmur

These general symptoms may also mimic those of infective endocarditis.

Sick sinus syndrome (SSS), also called sinus dysfunction, or sinoatrial node disease ("SND"), is a group of abnormal heart rhythms (arrhythmias) presumably caused by a malfunction of the sinus node, the heart's primary pacemaker. Tachycardia-bradycardia syndrome is a variant of sick sinus syndrome in which the arrhythmia alternates between slow and fast heart rates. Tachycardia-bradycardia syndrome is often associated with ischemic heart disease and heart valve disease.

If untreated, this abnormal heart rhythm can lead to dizziness, chest pain, a sensation of fluttering or pounding in the chest (palpitations), shortness of breath, or fainting (syncope). Atrial fibrillation also increases the risk of stroke. Complications of familial atrial fibrillation can occur at any age, although some people with this heart condition never experience any health problems associated with the disorder.

Atrial fibrillation is the most common type of sustained abnormal heart rhythm (arrhythmia), affecting more than 3 million people in the United States. The risk of developing this irregular heart rhythm increases with age. The incidence of the familial form of atrial fibrillation is unknown; however, recent studies suggest that up to 30 percent of all people with atrial fibrillation may have a history of the condition in their family.

Premature atrial contractions (PACs), also known as atrial premature complexes (APC) or atrial premature beats (APB), are a common cardiac dysrhythmia characterized by premature heartbeats originating in the atria. While the sinoatrial node typically regulates the heartbeat during normal sinus rhythm, PACs occur when another region of the atria depolarizes before the sinoatrial node and thus triggers a premature heartbeat. The exact cause of PACs is unclear; while several predisposing conditions exist, PACs commonly occur in healthy young and elderly people. Elderly people that get PACs usually don't need any further attention besides follow ups due to unclear evidence. PACs are often completely asymptomatic and may be noted only with Holter monitoring, but occasionally they can be perceived as a skipped beat or a jolt in the chest. In most cases, no treatment other than reassurance is needed for PACs, although medications such as beta blockers can reduce the frequency of symptomatic PACs.

An enlargement of the aorta may occur; an increased risk of abnormality is seen in babies of women taking lithium during the first trimester of pregnancy (though some have questioned this) and in those with Wolff-Parkinson-White syndrome.

While Ebstein's anomaly is defined as the congenital displacement of the tricuspid valve towards the apex of the right ventricle, it is often associated with other abnormalities.

Wolff–Parkinson–White syndrome (WPW) is a disorder due to a specific type of problem with the electrical system of the heart which has resulted in symptoms. About 40% of people with the electrical problem never develop symptoms. Symptoms can include an abnormally fast heartbeat, palpitations, shortness of breath, lightheadedness, or syncope. Rarely cardiac arrest may occur. The most common type of irregular heartbeat that occurs is known as paroxysmal supraventricular tachycardia.

The cause of WPW is typically unknown. A small number of cases are due to a mutation of the PRKAG2 gene which may be inherited from a person's parents in an autosomal dominant fashion. The underlying mechanism involves an accessory electrical conduction pathway between the atria and the ventricles. It is associated with other conditions such as Ebstein anomaly and hypokalemic periodic paralysis. Diagnosis is typically when an electrocardiogram (ECG) show a short PR interval and a delta wave. It is a type of pre-excitation syndromes.

WPW syndrome is treated with either medications or radiofrequency catheter ablation. It affects between 0.1 and 0.3% in the population. The risk of death in those without symptoms is about 0.5% per year in children and 0.1% per year in adults. In those without symptoms ongoing observation may be reasonable. In those with WPW complicated by atrial fibrillation, cardioversion or the medication procainamide may be used. The condition is named after Louis Wolff, John Parkinson, and Paul Dudley White who described the ECG findings in 1930.

Multifocal atrial tachycardia is characterized by an electrocardiogram (ECG) strip with 3 or more P-waves of variable morphology and varying P–R intervals, plus tachycardia, which is a heart rate exceeding 100 beats per minute. Narrow QRS complexes are visible as well.

Junctional ectopic tachycardia (JET) is a rare syndrome of the heart that manifests in patients recovering from heart surgery. It is characterized by cardiac arrhythmia, or irregular beating of the heart, caused by abnormal conduction from or through the atrioventricular node (AV node). In newborns and infants up to 6 weeks old, the disease may also be referred to as His bundle tachycardia.

Abdominal organs, including the liver, stomach, intestinal tract, and spleen may be randomly arranged throughout the left-right axis of the body. Distribution of these organs largely dictates treatment, clinical outcomes, and further evaluation.

The liver is typically symmetrical across the left-right axis in patients with situs ambiguous, which is abnormal. A majority of left atrial isomeric patients have defects throughout the biliary tree, which is responsible for bile production, even when the gall bladder is functional and morphologically normal. This biliary atresia can lead to acute problems such as nutrient malabsorption, pale stools, dark urine, and abdominal swelling. If this condition continues without proper treatment, cirrhosis and liver failure become a major concern. Biliary atresia is not usually observed in patients with right atrial isomerism.

Random positioning of the stomach is often one of the first signals of situs ambiguous upon examination. Malrotation of the entire intestinal tract, or improper folding and bulging of the stomach and intestines, results in bowel obstruction. This impairment leads to vomiting, abdominal distention, mucus and blood in the stool. Patients may also experience abdominal pain. Intestinal malrotation is more commonly identified in patients with right atrial isomerism than in those with left atrial isomerism.

Isomeric patients often experience disruptions to splenic development during embryogenesis, resulting in an overall lack a spleen (asplenia) or development of many spleens (polysplenia). Asplenia is most often observed in patients with right atrial isomerism. Polysplenia results in 90% of patients with left atrial isomerism. Although they have many spleens, each is usually ineffective resulting in functional asplenia. Rarely, left atrial isomeric patients have a single, normal, functional spleen. Patients lacking a functional spleen are in danger of sepsis and must be monitored.

People with TIC most often present with symptoms of congestive heart failure and/or symptoms related to their irregular heart rhythm. Symptoms of congestive heart failure can include shortness of breath, ankle swelling, fatigue, and weight gain. Symptoms of an irregular heart rhythm can include palpitations and chest discomfort.

The timecourse of TIC is most well-studied in experiments on animals. Researchers have found that animals began to exhibit abnormal changes in blood flow after just one day of an artificially generated fast heart rate (designed to simulate a tachyarrythmia). As their TIC progresses, these animals will have worsening heart function (e.g.: reduced cardiac output and reduced ejection fraction) for 3–5 weeks. The worsened heart function then persists at a stable state until the heart rate is returned to normal. With normal heart rates, these animals begin to demonstrate improving heart function at 1–2 days, and even complete recovery of ejection fraction at 1 month.

Human studies of the timecourse of TIC are not as robust as animal studies, though current studies suggest that the majority of people with TIC will recover a significant degree of heart function over months to years.

Asplenia with cardiovascular anomalies, also known as Ivemark syndrome and right atrial isomerism, is an example of a heterotaxy syndrome. These uncommon congenital disorders are characterized by defects in the heart, spleen and paired organs such as the lungs and kidneys. Another name is "asplenia-cardiovascular defect-heterotaxy".

Right atrial isomerism is named for its discoverer, Swedish pathologist Biörn Ivemark.

Hypertension, or abnormally high blood pressure, often signifies an elevated level of both psychological and physiological stress. Often, hypertension goes hand in hand with various atrial fibrillations including premature atrial contractions (PACs). Additional factors that may contribute to spontaneous premature atrial contractions could be:

- Increased age

- Abnormal body height

- History of cardiovascular disease (CV)

- Abnormal ANP levels

- Elevated cholesterol

Third-degree atrioventricular block (AV block), also known as complete heart block, is a medical condition in which the impulse generated in the sinoatrial node (SA node) in the atrium of the heart does not propagate to the ventricles.

Because the impulse is blocked, an accessory pacemaker in the lower chambers will typically activate the ventricles. This is known as an "escape rhythm". Since this accessory pacemaker also activates independently of the impulse generated at the SA node, two independent rhythms can be noted on the electrocardiogram (ECG).

- The P waves with a regular P-to-P interval (in other words, a sinus rhythm) represent the first rhythm.

- The QRS complexes with a regular R-to-R interval represent the second rhythm. The PR interval will be variable, as the hallmark of complete heart block is lack of any apparent relationship between P waves and QRS complexes.

Patients with third-degree AV block typically experience severe bradycardia (an abnormally-low measured heart rate), hypotension, and at times, hemodynamic instability.

An episode of SVT may present with palpitations, dizziness, shortness of breath, or losing consciousness (fainting). The electrocardiogram (ECG) would appear as a narrow-complex SVT. Between episodes of tachycardia the affected person is likely to be asymptomatic, however, the ECG would demonstrate the classic delta wave in Wolff–Parkinson–White syndrome.

A sinus venosus atrial septal defect is a type of atrial septal defect primarily associated with the sinus venosus.

They represent 5% of atrial septal defects.

They can occur near the superior vena cava or inferior vena cava, but the former are more common.

They can be associated with anomalous pulmonary venous connection.

MAT usually arises because of an underlying medical condition. Its prevalence has been estimated at about 3 per 1000 in adult hospital inpatients and is much rarer in paediatric practice; it is more common in the elderly, and its management and prognosis are both those of the underlying diagnosis.

It is mostly common in patients with lung disorders, but it can occur after acute myocardial infarction and can also occur in the setting of low blood potassium or low blood magnesium.

It is sometimes associated with digitalis toxicity in patients with heart disease.

It is most commonly associated with hypoxia and COPD. Additionally, it can be caused by theophylline toxicity, a drug with a narrow therapeutic index commonly used to treat COPD. Theophylline can cause a number of different abnormal heart rhythms when in excess, and thus further predisposes COPD patients to MAT. Theophylline toxicity often occurs following acute or chronic overtreatment or factors lowering its clearance from the body.

Presentation is similar to other forms of rapid heart rate and may be asymptomatic. Palpitations and chest discomfort are common complaints. The rapid uncoordinated heart rate may result in reduced cardiac output, with the heart being unable to provide adequate blood flow and therefore oxygen delivery to the rest of the body. Common symptoms of uncontrolled atrial fibrillation may include shortness of breath, shortness of breath when lying flat, dizziness, and sudden onset of shortness of breath during the night. This may progress to swelling of the lower extremities, a manifestation of congestive heart failure. Due to inadequate cardiac output, individuals with AF may also complain of light-headedness, may feel like they are about to faint, or may actually lose consciousness.

AF can cause respiratory distress due to congestion in the lungs. By definition, the heart rate will be greater than 100 beats per minute. Blood pressure may be variable, and often difficult to measure as the beat-by-beat variability causes problems for most digital (oscillometric) non-invasive blood pressure monitors. For this reason, when determining heart rate in AF, direct cardiac auscultation is recommended. Low blood pressure is most concerning and a sign that immediate treatment is required. Many of the symptoms associated with uncontrolled atrial fibrillation are a manifestation of congestive heart failure due to the reduced cardiac output. Respiratory rate will be increased in the presence of respiratory distress. Pulse oximetry may confirm the presence of hypoxia related to any precipitating factors such as pneumonia. Examination of the jugular veins may reveal elevated pressure (jugular venous distention). Lung exam may reveal crackles, which are suggestive of pulmonary edema. Heart exam will reveal a rapid irregular rhythm.

Isomerism of the bronchial tree is not typically damaging and presents no significant clinical complications. Pulmonary valve stenosis results in issues of blood flow to the lungs.