Cardiac:

- constrictive pericarditis. One study found that pulsus paradoxus occurs in less than 20% of patients with constrictive pericarditis.

- pericardial effusion, including cardiac tamponade

- cardiogenic shock

Pulmonary:

- pulmonary embolism

- tension pneumothorax

- asthma (especially with severe asthma exacerbations)

- chronic obstructive pulmonary disease

Non-pulmonary and non-cardiac:

- anaphylactic shock

- hypovolemia

- superior vena cava obstruction

- pregnancy

- obesity

PP has been shown to be predictive of the severity of cardiac tamponade. Pulsus paradoxus may not be seen with cardiac tamponade if an atrial septal defect or significant aortic regurgitation is also present.

Pulsus paradoxus can be caused by several physiologic mechanisms. Anatomically, these can be grouped into:

- "cardiac causes",

- "pulmonary causes" and

- "non-pulmonary and non-cardiac causes".

Considered physiologically, PP is caused by:

- decreased right heart functional reserve, e.g. myocardial infarction and tamponade,

- right ventricular inflow or outflow obstruction, e.g. superior vena cava obstruction and pulmonary embolism, and

- decreased blood to the left heart due to lung hyperinflation (e.g. asthma, COPD) and anaphylactic shock.

Atrial fibrillation increases the risk of heart failure by 11 per 1000, kidney problems by 6 per 1000, death by 4 per 1000, stroke by 3 per 1000, and coronary heart disease by 1 per 1000. Women have a worse outcome overall than men. Evidence increasingly suggests that atrial fibrillation is independently associated with a higher risk of developing dementia.

A family history of AF may increase the risk of AF. A study of more than 2,200 people found an increased risk factor for AF of 1.85 for those that had at least one parent with AF. Various genetic mutations may be responsible.

Four types of genetic disorder are associated with atrial fibrillation:

- Familial AF as a monogenic disease

- Familial AF presenting in the setting of another inherited cardiac disease (hypertrophic cardiomyopathy, dilated cardiomyopathy, familial amyloidosis)

- Inherited arrhythmic syndromes (congenital long QT syndrome, short QT syndrome, Brugada syndrome)

- Non-familial AF associated with genetic backgrounds (polymorphism in the ACE gene) that may predispose to atrial fibrillation

Rearrest may reduce the likelihood of survival when compared to patients who have had just one episode of cardiac arrest. Overall resuscitation rates have been estimated to be about 34%, however survival to hospital discharge rates are as low as 7%. This phenomenon may be contributed to rearrest.

A recent study by Salcido et al. (2010) ascertained rearrest in all initial and rearrest rhythms treated by any level of Emergency Medical Service (EMS), finding a rearrest rate of 36% and a lower but not significantly different rate of survival to hospital discharge in cases with rearrest compared to those without rearrest.

Athlete's heart is not dangerous for athletes (though if a nonathlete has symptoms of bradycardia, cardiomegaly, and cardiac hypertrophy, another illness may be present). Athlete's heart is not the cause of sudden cardiac death during or shortly after a workout, which mainly occurs due to hypertrophic cardiomyopathy, a genetic disorder.

No treatment is required for people with athletic heart syndrome; it does not pose any physical threats to the athlete, and despite some theoretical concerns that the ventricular remodeling might conceivably predispose for serious arrhythmias, no evidence has been found of any increased risk of long-term events. Athletes should see a physician and receive a clearance to be sure their symptoms are due to athlete’s heart and not another heart disease, such as cardiomyopathy. If the athlete is uncomfortable with having athlete's heart or if a differential diagnosis is difficult, deconditioning from exercise for a period of three months allows the heart to return to its regular size. However, one long-term study of elite-trained athletes found that dilation of the left ventricle was only partially reversible after a long period of deconditioning. This deconditioning is often met with resistance to the accompanying lifestyle changes. The real risk attached to athlete's heart is if athletes or nonathletes simply assume they have the condition, instead of making sure they do not have a life-threatening heart illness.

These possible causes are remembered as the 6 Hs and the 6 Ts. See Hs and Ts

- Hypovolemia

- Hypoxia

- Hydrogen ions (Acidosis)

- Hyperkalemia or Hypokalemia

- Hypoglycemia

- Hypothermia

- Tablets or Toxins (Drug overdose)

- Cardiac Tamponade

- Tension pneumothorax

- Thrombosis (e.g., myocardial infarction, pulmonary embolism)

- Tachycardia

- Trauma (e.g., hypovolemia from blood loss)

This list is not fully comprehensive. Most notably, it does not include anaphylaxis. Pressure effects associated with artificial ventilation may also contribute to significant reduction in cardiac output, resulting in a clinical diagnosis of PEA.

The possible mechanisms by which the above conditions can cause pulseless in PEA or the same as those recognized as producing circulatory shock states. These are (1) impairment of cardiac filling, (2) impaired pumping effectiveness of the heart, (3) circulatory obstruction and (4) pathological vasodilation causing loss of vascular resistance and excess capacitance. More than one mechanism may be involved in any given case.

Pulseless electrical activity leads to a loss of cardiac output, and the blood supply to the brain is interrupted. As a result, PEA is usually noticed when a person loses consciousness and stops breathing spontaneously. This is confirmed by examining the airway for obstruction, observing the chest for respiratory movement, and feeling the pulse (usually at the carotid artery) for a period of 10 seconds.

The overall chance of survival among those who have cardiac arrest outside hospital is 10%. Among those who have an out-of-hospital cardiac arrest, 70% occur at home and have a survival rate of 6%. For those who have an in-hospital cardiac arrest, survival rate is estimated to be 24%. Among children rates of survival is 3 to 16% in North America. For in hospital cardiac arrest survival to discharge is around 22% with many having a good neurological outcome.

Prognosis is typically assessed 72 hours or more after cardiac arrest. Rates of survival are better in those who someone saw collapse, got bystander CPR, or had either ventricular tachycardia or ventricular fibrillation when assessed. Survival among those with Vfib or Vtach is 15 to 23%. Women are more likely to survive cardiac arrest and leave hospital than men.

A 1997 review found rates of survival to discharge of 14% although different studies varied from 0-28%. In those over the age of 70 who have a cardiac arrest while in hospital, survival to hospital discharge is less than 20%. How well these individuals are able to manage after leaving hospital is not clear.

A study of survival rates from out-of-hospital cardiac arrest found that 14.6% of those who had received resuscitation by ambulance staff survived as far as admission to hospital. Of these, 59% died during admission, half of these within the first 24 hours, while 46% survived until discharge from hospital. This reflects an overall survival following cardiac arrest of 6.8%. Of these 89% had normal brain function or mild neurological disability, 8.5% had moderate impairment, and 2% had major neurological disability. Of those who were discharged from hospital, 70% were still alive four years later.

In left ventricular dysfunction, the ejection fraction will decrease significantly, causing reduction in stroke volume, hence causing an increase in end-diastolic volume. As a result, during the next cycle of systolic phase, the myocardial muscle will be stretched more than usual and as a result there will be an increase in myocardial contraction, related to the Frank–Starling physiology of the heart. This results, in turn, in a stronger systolic pulse. There may initially be a tachycardia as a compensatory mechanism to try to keep the cardiac output constant.

The risk factors for SCD are similar to those of coronary artery disease and include age, cigarette smoking, high blood pressure, high cholesterol, lack of physical exercise, obesity, diabetes, and family history. A prior episode of sudden cardiac arrest also increases the risk of future episodes.

Current cigarette smokers with coronary artery disease were found to have a two to threefold increase in the risk of sudden death between ages 30 and 59. Furthermore, it was found that former smokers risk was closer to that of those who had never smoked.

Because several well-known and high-profile cases of athletes experiencing sudden unexpected death due to cardiac arrest, such as Reggie White and Marc-Vivien Foé, a growing movement is making an effort to have both professional and school-based athletes screened for cardiac and other related conditions, usually through a careful medical and health history, a good family history, a comprehensive physical examination including auscultation of heart and lung sounds and recording of vital signs such as heart rate and blood pressure, and increasingly, for better efforts at detection, such as an electrocardiogram.

An electrocardiogram (ECG) is a relatively straightforward procedure to administer and interpret, compared to more invasive or sophisticated tests; it can reveal or hint at many circulatory disorders and arrhythmias. Part of the cost of an ECG may be covered by some insurance companies, though routine use of ECGs or other similar procedures such as echocardiography (ECHO) are still not considered routine in these contexts. Widespread routine ECGs for all potential athletes during initial screening and then during the yearly physical assessment could well be too expensive to implement on a wide scale, especially in the face of the potentially very large demand. In some places, a shortage of funds, portable ECG machines, or qualified personnel to administer and interpret them (medical technicians, paramedics, nurses trained in cardiac monitoring, advanced practice nurses or nurse practitioners, physician assistants, and physicians in internal or family medicine or in some area of cardiopulmonary medicine) exist.

If sudden cardiac death occurs, it is usually because of pathological hypertrophic enlargement of the heart that went undetected or was incorrectly attributed to the benign "athletic" cases. Among the many alternative causes are episodes of isolated arrhythmias which degenerated into lethal VF and asystole, and various unnoticed, possibly asymptomatic cardiac congenital defects of the vessels, chambers, or valves of the heart. Other causes include carditis, endocarditis, myocarditis, and pericarditis whose symptoms were slight or ignored, or were asymptomatic.

The normal treatments for episodes due to the pathological look-alikes are the same mainstays for any other episode of cardiac arrest: Cardiopulmonary resuscitation, defibrillation to restore normal sinus rhythm, and if initial defibrillation fails, administration of intravenous epinephrine or amiodarone. The goal is avoidance of infarction, heart failure, and/or lethal arrhythmias (ventricular tachycardia, ventricular fibrillation, asystole, or pulseless electrical activity), so ultimately to restore normal sinus rhythm.

Ventricular tachycardia can occur due to coronary heart disease, aortic stenosis, cardiomyopathy, electrolyte problems (e.g., low blood levels of magnesium or potassium), inherited channelopathies (e.g., long-QT syndrome), catecholaminergic polymorphic ventricular tachycardia, arrhythmogenic right ventricular dysplasia, or a heart attack.

The risk of death in individuals with aortic insufficiency, dilated ventricle, normal ejection fraction who are asymptomatic is about 0.2 percent per year. Risk increases if the ejection fraction decreases or if the individual develops symptoms.

Individuals with chronic (severe) aortic regurgitation follow a course that once symptoms appear, surgical intervention is needed. AI is fatal in 10 to 20% of individuals who do not undergo surgery for this condition. Left ventricle dysfunction determines to an extent the outlook for severity of aortic regurgitation cases.

Therapy may be directed either at terminating an episode of the abnormal heart rhythm or at reducing the risk of another VT episode. The treatment for stable VT is tailored to the specific person, with regard to how well the individual tolerates episodes of ventricular tachycardia, how frequently episodes occur, their comorbidities, and their wishes. Individuals suffering from pulseless VT or unstable VT are hemodynamically compromised and require immediate electric cardioversion to shock them out of the VT rhythm.

The prognosis of tricuspid insufficiency is less favorable for males than females. Furthermore, increased tricuspid insufficiency (regurgitation) severity is an indication of a poorer prognosis according to Nath, et al. It is also important to note that since tricuspid insufficiency most often arises from left heart failure or pulmonary hypertension, the person's prognosis is usually dictated by the prognosis of the latter conditions and not by the tricuspid insufficiency "per se".

Palpate radial or femoral arteries, feel for regular rhythm but alternating strong and weak pulses

Use blood pressure cuff to confirm: Raise blood pressure cuff to over systolic level then, lower slowly towards the systolic level, if hearing alternating loud & soft korotkoff sounds, pulses alternans is indicated.

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.

Since PDA is usually identified in infants, it is less common in adults, but it can have serious consequences, and is usually corrected surgically upon diagnosis.

In terms of the cause of aortic insufficiency, is often due to the aortic root dilation ("annuloaortic ectasia"), which is idiopathic in over 80% of cases, but otherwise may result from aging, syphilitic aortitis, osteogenesis imperfecta, aortic dissection, Behçet's disease, reactive arthritis and systemic hypertension. Aortic root dilation is the most common cause of aortic insufficiency in developed countries. Additionally, aortic insufficiency has been linked to the use of some medications, specifically medications containing fenfluramine or dexfenfluramine isomers and dopamine agonists. Other potential causes that affect the valve directly include Marfan syndrome, Ehlers–Danlos syndrome, ankylosing spondylitis, and systemic lupus erythematosus. In acute cases of aortic insufficiency, the main causes are infective endocarditis, aortic dissection or trauma.

If untreated, severe symptomatic aortic stenosis carries a poor prognosis with a 2-year mortality rate of 50-60% and a 3-year survival rate of less than 30%. Prognosis after aortic valve replacement for people who are younger than 65 is about five years less than that of the general population; for people older than 65 it is about the same.

Junctional ectopic tachycardia derives its name from the problem it causes. "Junctional" is used as the abnormal tissue driving the ventricular rate is located close junction between the atria and ventricles, known as the AV node. Ectopic (from the Greek "ektopos", meaning "out of place") refers to the fact that the ventricles are being triggered by tissue that is not the normal pacemaker tissue within the heart. Tachycardia (from the Greek "takhys", meaning "swift", and "kardia", meaning heart) means a swift heart rate.

By this definition, junctional ectopic tachycardia is an abnormally swift heart rhythm due to cells firing within the heart near the AV node.

A PDA is sometimes idiopathic. Known risk factors include:

- Preterm birth

- Congenital rubella syndrome

- Chromosomal abnormalities (e.g., Down syndrome)

- Genetic conditions such as Loeys-Dietz syndrome (would also present with other heart defects), Wiedemann-Steiner syndrome, and CHAR syndrome.

In Heyde's syndrome, aortic stenosis is associated with gastrointestinal bleeding due to angiodysplasia of the colon. Recent research has shown that the stenosis causes a form of von Willebrand disease by breaking down its associated coagulation factor (factor VIII-associated antigen, also called von Willebrand factor), due to increased turbulence around the stenotic valve.