Onset may be rapid or more gradual. Symptoms typically include those of cardiogenic shock including shortness of breath, weakness, lightheadedness, and cough. Other symptoms may relate to the underlying cause.

Cardiac tamponade, also known as pericardial tamponade, is when fluid in the pericardium (the sac around the heart) builds up and results in compression of the heart. Onset may be rapid or more gradual. Symptoms typically include those of cardiogenic shock including shortness of breath, weakness, lightheadedness, and cough. Other symptoms may relate to the underlying cause.

Common causes include cancer, kidney failure, chest trauma, and pericarditis. Other causes include connective tissue diseases, hypothyroidism, aortic rupture, and following cardiac surgery. In Africa, tuberculosis is a relatively common cause.

Diagnosis may be suspected based on low blood pressure, jugular venous distension, pericardial rub, or quiet heart sounds. The diagnosis may be further supported by specific electrocardiogram (ECG) changes, chest X-ray, or an ultrasound of the heart. If fluid increases slowly the pericardial sac can expand to contain more than 2 liters; however, if the increase is rapid as little as 200 mL can result in tamponade.

When tamponade results in symptoms, drainage is necessary. This can be done by pericardiocentesis, surgery to create a pericardial window, or a pericardiectomy. Drainage may also be necessary to rule out infection or cancer. Other treatments may include the use of dobutamine or in those with low blood volume, intravenous fluids. Those with few symptoms and no worrisome features can often be closely followed. The frequency of tamponade is unclear. One estimate from the United States places it at 2 per 10,000 per year.

Hemopericardium refers to blood in the pericardial sac of the heart. It is clinically similar to a pericardial effusion, and, depending on the volume and rapidity with which it develops, may cause cardiac tamponade.

The condition can be caused by full-thickness necrosis (death) of the myocardium (heart muscle) after myocardial infarction, chest trauma, and by over-prescription of anticoagulants. Other causes include ruptured aneurysm of sinus of Valsalva and other aneurysms of the aortic arch.

Hemopericardium can be diagnosed with a chest X-ray or a chest ultrasound, and is most commonly treated with pericardiocentesis. While hemopericardium itself is not deadly, it can lead to cardiac tamponade, a condition that is fatal if left untreated.

Symptoms of hemopericardium often include difficulty breathing, abnormally rapid breathing, and fatigue, each of which can be a sign of a serious medical condition not limited to hemopericardium. In many cases, patients also report feeling chest pressure and have an abnormally elevated heart rate.

An electrocardiogram helps establishing the exact diagnosis and guides treatment, it may reveal:

- Abnormal heart rhythms, such as bradycardia (slowed heart rate)

- myocardial infarction (ST-elevation MI, STEMI, is usually more dangerous than non-STEMIs; MIs that affect the ventricles are usually more dangerous than those that affect the atria; those affecting the left side of the heart, especially the left ventricle, are usually more dangerous than those affecting the right side, unless that side is severely compromised)

- Signs of cardiomyopathy

Myocardial infarction complications may occur immediately following a heart attack (in the acute phase), or may need time to develop (a chronic problem). After an infarction, an obvious complication is a second infarction, which may occur in the domain of another atherosclerotic coronary artery, or in the same zone if there are any live cells left in the infarct.

Dressler syndrome was, historically, a phenomenon complicating about 7% of myocardial infarctions; however, in the era of percutaneous coronary intervention, it is very uncommon. The disease consists of a persistent low-grade fever, chest pain (usually pleuritic in nature), pericarditis (usually evidenced by a pericardial friction rub), and/or a pericardial effusion. The symptoms tend to occur 2–3 weeks after myocardial infarction, but can also be delayed for a few months. It tends to subside in a few days, and very rarely leads to pericardial tamponade. An elevated ESR is an objective, yet nonspecific, laboratory finding.

Echocardiography may show poor ventricular function, signs of PED, rupture of the interventricular septum, an obstructed outflow tract or cardiomyopathy.

Obstructive shock is a form of shock associated with physical obstruction of the great vessels or the heart itself. Pulmonary embolism and cardiac tamponade are considered forms of obstructive shock.

Obstructive shock has much in common with cardiogenic shock, and the two are frequently grouped together.

Some sources do not recognize obstructive shock as a distinct category, and categorize pulmonary embolism and cardiac tamponade under cardiogenic shock.

A myocardial infarction may compromise the function of the heart as a pump for the circulation, a state called heart failure. There are different types of heart failure; left- or right-sided (or bilateral) heart failure may occur depending on the affected part of the heart, and it is a low-output type of failure. If one of the heart valves is affected, this may cause dysfunction, such as mitral regurgitation in the case of left-sided coronary occlusion that disrupts the blood supply of the papillary muscles. The incidence of heart failure is particularly high in patients with diabetes and requires special management strategies.

Chest pain or pressure are common symptoms. A small effusion may be asymptomatic. Larger effusions may cause cardiac tamponade, a life-threatening complication; signs of impending tamponade include dyspnea, low blood pressure, and distant heart sounds.

The so-called "water-bottle heart" is a radiographic sign of pericardial effusion, in which the cardiopericardial silhouette is enlarged and assumes the shape of a flask or water bottle.

It can be associated with dullness to percussion over the left subscapular area due to compression of the left lung base. This phenomenon is known as Ewart's sign.

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.

Pericardial effusion ("fluid around the heart") is an abnormal accumulation of fluid in the pericardial cavity. Because of the limited amount of space in the pericardial cavity, fluid accumulation leads to an increased intrapericardial pressure which can negatively affect heart function. A pericardial effusion with enough pressure to adversely affect heart function is called cardiac tamponade. Pericardial effusion usually results from a disturbed equilibrium between the production and re-absorption of pericardial fluid, or from a structural abnormality that allows fluid to enter the pericardial cavity.

Normal levels of pericardial fluid are from 15 to 50 mL.

Dressler syndrome needs to be differentiated from pulmonary embolism, another identifiable cause of pleuritic (and non-pleuritic) chest pain in people who have been hospitalized and/or undergone surgical procedures within the preceding weeks.

Symptoms of myocardial rupture are recurrent or persistent chest pain, syncope, and distension of jugular vein. Sudden death caused by a myocardial rupture is sometimes preceded by no symptoms.

Difficulty breathing, a cardinal symptom of left ventricular failure, may manifest with progressively increasing severity as the following:

- Difficulty breathing with physical activity (exertional dyspnea)

- Difficulty breathing while lying flat (orthopnea)

- Episodes of waking up from sleep gasping for air (paroxysmal nocturnal dyspnea)

- Acute pulmonary edema

Other cardiac symptoms of heart failure include chest pain/pressure and palpitations. Common noncardiac signs and symptoms of heart failure include loss of appetite, nausea, weight loss, bloating, fatigue, weakness, low urine output, waking up at night to urinate, and cerebral symptoms of varying severity, ranging from anxiety to memory impairment and confusion.

Chronic stable heart failure may easily decompensate. This most commonly results from an intercurrent illness (such as pneumonia), myocardial infarction (a heart attack), abnormal heart rhythms (such as atrial fibrillation), uncontrolled high blood pressure, or the person's failure to maintain a fluid restriction, diet, or medication. Other well recognized precipitating factors include anemia and hyperthyroidism which place additional strain on the heart muscle. Excessive fluid or salt intake, and medication that causes fluid retention such as NSAIDs and thiazolidinediones, may also precipitate decompensation.

Acute myocardial infarction can precipitate acute decompensated heart failure and will necessitate emergent revascularization with thrombolytics, percutaneous coronary intervention, or coronary artery bypass graft.

Cardiac arrest is preceded by no warning symptoms in approximately 50% of people. For those who do, they have non specific symptoms such as, new or worsening chest pain, fatigue, blackouts, dizziness, shortness of breath, weakness, and vomiting.

When the arrest occurs, the most obvious sign of its occurrence will be the lack of a palpable pulse in the person experiencing it (since the heart has ceased to contract, the usual indications of its contraction such as a pulse will no longer be detectable). Certain types of prompt intervention can often reverse a cardiac arrest, but without such intervention the event will almost always lead to death. In certain cases, it is an expected outcome of a serious illness where death is expected.

Also, as a result of inadequate blood flow to the brain (cerebral perfusion), the patient will quickly become unconscious and will have stopped breathing. The main diagnostic criterion to diagnose a cardiac arrest (as opposed to respiratory arrest which shares many of the same features) is lack of circulation; however, there are a number of ways of determining this. Near-death experiences are reported by 10–20% of people who survived cardiac arrest.

PP is quantified using a blood pressure cuff and stethoscope (Korotkoff sounds), by measuring the variation of the systolic pressure during expiration and inspiration. Inflate cuff until no sounds (as is normally done when taking a BP) slowly decrease cuff pressure until systolic sounds are first heard during "expiration" but not during inspiration, (note this reading), slowly continue decreasing the cuff pressure until sounds are heard "throughout" the respiratory cycle, (inspiration and expiration)(note this second reading). If the pressure difference between the two readings is >10mmHg, it can be classified as pulsus paradoxus.

Sudden cardiac arrest (SCA) and sudden cardiac death (SCD) occur when the heart abruptly begins to beat in an abnormal or irregular rhythm (arrhythmia). Without organized electrical activity in the heart muscle, there is no consistent contraction of the ventricles, which results in the heart's inability to generate an adequate cardiac output (forward pumping of blood from heart to rest of the body). There are many different types of arrhythmias, but the ones most frequently recorded in SCA and SCD are ventricular tachycardia (VT) or ventricular fibrillation (VF).

Sudden cardiac arrest can result from cardiac and non-cardiac causes including the following:

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.

Tachycardia-induced cardiomyopathy (TIC) is a disease where prolonged tachycardia (a fast heart rate) or arrhythmia (an irregular heart rhythm) cause an impairment of the myocardium (heart muscle), which can result in heart failure. People with TIC may have symptoms associated with heart failure (e.g. shortness of breath or ankle swelling) and/or symptoms related to the tachycardia or arrhythmia (e.g. palpitations). Though atrial fibrillation is the most common cause of TIC, several tachycardias and arrhythmias have been associated with the disease.

There are no formal diagnostic criteria for TIC. Thus, TIC is typically diagnosed when (1) tests have excluded other causes of cardiomyopathy and (2) there is improvement in myocardial function after treatment of the tachycardia or arrhythmia. Treatment of TIC can involve treating the heart failure as well as the tachycardia or arrhythmia. TIC has a good prognosis with treatment, with most people recovering some to all of their heart function.

The number of cases that occur is unclear. TIC has been reported in all age groups.

While a few seconds may not result in problems longer periods are dangerous. Short periods may occur without symptoms or present with lightheadedness, palpitations, or chest pain. Ventricular tachycardia may result in cardiac arrest and turn into ventricular fibrillation.

Myocardial rupture is a laceration or t

e ventricles or atria of the heart, of the interatrial or interventricular septum, or of the papillary muscles. It is most commonly seen as a serious sequela of an acute myocardial infarction (heart attack).

It can also be caused by trauma.

Ventricular fibrillation is a cause of cardiac arrest and sudden cardiac death. The ventricular muscle twitches randomly rather than contracting in a co-ordinated fashion (from the apex of the heart to the outflow of the ventricles), and so the ventricles fail to pump blood around the body - because of this, it is classified as a cardiac arrest rhythm, and patients in V-fib should be treated with cardiopulmonary resuscitation and prompt defibrillation. Left untreated, ventricular fibrillation is rapidly fatal as the vital organs of the body, including the heart, are starved of oxygen, and as a result patients in this rhythm will not be conscious or responsive to stimuli. Prior to cardiac arrest, patients may complain of varying symptoms depending on the underlying cause. Patients may exhibit signs of agonal breathing, which to the layperson can look like normal spontaneous breathing, but it is in fact a sign of hypoperfusion of the brainstem.

It has an appearance on electrocardiography of irregular electrical activity with no discernable pattern. It may be described as 'coarse' or 'fine' depending on its amplitude, or as progressing from coarse to fine V-fib. Coarse V-fib may be more responsive to defibrillation, while fine V-fib can mimic the appearance of asystole on a defibrillator or cardiac monitor set to a low gain. Some clinicians may attempt to defibrillate fine V-fib in the hope that it can be reverted to a cardiac rhythm compatible with life, whereas others will deliver CPR and sometimes drugs as described in the advanced cardiac life support protocols in an attempt to increase its amplitude and the odds of successful defibrillation.