Cor triatriatum (or triatrial heart) is a congenital heart defect where the left atrium (cor triatriatum sinistrum) or right atrium (cor triatriatum dextrum) is subdivided by a thin membrane, resulting in three atrial chambers (hence the name).

Cor triatriatum represents 0.1% of all congenital cardiac malformations and may be associated with other cardiac defects in as many as 50% of cases. The membrane may be complete or may contain one or more fenestrations of varying size.

Cor triatrium sinistrum is more common. In this defect there is typically a proximal chamber that receives the pulmonic veins and a distal (true) chamber located more anteriorly where it empties into the mitral valve. The membrane that separates the atrium into two parts varies significantly in size and shape. It may appear similar to a diaphragm or be funnel-shaped, bandlike, entirely intact (imperforate) or contain one or more openings (fenestrations) ranging from small, restrictive-type to large and widely open.

In the pediatric population, this anomaly may be associated with major congenital cardiac lesions such as tetralogy of Fallot, double outlet right ventricle, coarctation of the aorta, partial anomalous pulmonary venous connection, persistent left superior vena cava with unroofed coronary sinus, ventricular septal defect, atrioventricular septal (endocardial cushion) defect, and common atrioventricular canal. Rarely, asplenia or polysplenia has been reported in these patients.

In the adult, cor triatriatum is frequently an isolated finding.

Cor triatriatum dextrum is extremely rare and results from the complete persistence of the right sinus valve of the embryonic heart. The membrane divides the right atrium into a proximal (upper) and a distal (lower) chamber. The upper chamber receives the venous blood from both vena cavae and the lower chamber is in contact with the tricuspid valve and the right atrial appendage.

The natural history of this defect depends on the size of the communicating orifice between the upper and lower atrial chambers. If the communicating orifice is small, the patient is critically ill and may succumb at a young age (usually during infancy) to congestive heart failure and pulmonary edema. If the connection is larger, patients may present in childhood or young adulthood with a clinical picture similar to that of mitral stenosis. Cor triatriatum may also be an incidental finding when it is nonobstructive.

The disorder can be treated surgically by removing the membrane dividing the atrium.

Signs/symptoms of tricuspid insufficiency are generally those of right-sided heart failure, such as ascites and peripheral edema.

Tricuspid insufficiency may lead to the presence of a pansystolic heart murmur. Such a murmur is usually of low frequency and best heard low on the lower left sternal border. As with most right-sided phenomena, it tends to increase with inspiration, and decrease with expiration. This is known as Carvallo's sign. However, the murmur may be inaudible indicating the relatively low pressures in the right side of the heart. A third heart sound may also be present, also heard with inspiration at the lower sternal border.

In addition to the possible ausculatory findings above, there are other signs indicating the presence of tricuspid regurgitation. There may be giant C-V waves in the jugular pulse and a palpably (and sometimes visibly) pulsatile liver on abdominal exam. Since the murmur of tricupsid regurgitation may be faint or inaudible, these signs can be helpful in establishing the diagnosis.

Tricuspid insufficiency (TI), a valvular heart disease also called tricuspid regurgitation (TR), refers to the failure of the heart's tricuspid valve to close properly during systole. This defect allows the blood to flow backwards, reducing its efficiency.

Regurgitation may be due to a structural change of components of the tricuspid valve apparatus, a lesion can be primary (intrinsic abnormality) or secondary (right ventricular dilatation).

Annuloaortic ectasia is a dilation of the proximal ascending aorta and aortic annulus. It may cause aortic regurgitation, thoracic aortic dissection, aneurysm and rupture. It is often associated with connective tissue diseases like Marfan syndrome and Ehlers Danlos Syndrome. It can also be a complication due to tertiary syphilis. In tertiary syphilis the aortic root becomes so dilated that the aortic valve becomes incompetent and cor bovinum results.

The term was first coined by the American heart surgeon Denton Cooley in 1961.

Cor bovinum refers to a massive hypertrophy of the left ventricle of the heart due to volume overload, usually in earlier times in the context of tertiary syphilis but currently more often due to chronic aortic regurgitation, hypertensive and ischaemic heart disease.

The symptoms/signs of pulmonary heart disease (cor pulmonale) can be non-specific and depend on the stage of the disorder, and can include blood backing up into the systemic venous system, including the hepatic vein. As pulmonary heart disease progresses, most individuals will develop symptoms like:

Pulmonary heart disease, also known as cor pulmonale is the enlargement and failure of the right ventricle of the heart as a response to increased vascular resistance (such as from pulmonic stenosis) or high blood pressure in the lungs.

Chronic pulmonary heart disease usually results in right ventricular hypertrophy (RVH), whereas acute pulmonary heart disease usually results in dilatation. Hypertrophy is an adaptive response to a long-term increase in pressure. Individual muscle cells grow larger (in thickness) and change to drive the increased contractile force required to move the blood against greater resistance. Dilatation is a stretching (in length) of the ventricle in response to acute increased pressure.

To be classified as pulmonary heart disease, the cause must originate in the pulmonary circulation system. Two causes are vascular changes as a result of tissue damage (e.g. disease, hypoxic injury), and chronic hypoxic pulmonary vasoconstriction. If left untreated, then death may result, RVH due to a defect is not classified as pulmonary heart disease. The heart and lungs are intricately related; whenever the heart is affected by a disease, the lungs risk following and vice versa.

Due to Syphilitic aortitis (a complication of tertiary syphilis) the aortic valve ring becomes dilated. The free margins of valve cusps no longer approximate leading to aortic valve insufficiency. As blood regurgitates into the left ventricle between each systole, volume overload ensues and the ventricular wall hypertrophies in an attempt to maintain cardiac output and blood pressure. The massive ventricle can lead to a heart weighing over 1000 grams (the weight of a normal heart is about 350 grams), referred to as "Cor Bovinum" [Latin for cow's heart.]

Fluri and Gebbers define cor bovinum as a heart exceeding 500 g in weight. Looking through autopsies on Internal Medicine patients at the Kantonsspital Luzern, they found 415 cases out of 1181 autopsies in the two periods 1978-81 and 1997-2000. Cor bovinum was found in 25.3% of cases in the earlier period, with mean age at death 67.7 years, and in the later period 20.6% with mean age 74.3 years. The male female ratio was 4:1. "In 93% of all patients with CB, we found coronary atherosclerosis as a sign of high blood pressure and in 79% a COPD."

In 84% of cases the cause of death was directly related to the cor bovinum, but in 37% the cause of death was still unclear. They concluded that cor bovinum was a decreasing but still frequent autopsy finding. High blood pressure, COPD and male sex were the main risk factors. The decreasing incidence was ascribed to improved medical management: they mention treatments for high blood pressure and coronary artery disease, which suggests that "COPD" in their abstract refers to the latter.

Bilharzial cor pulmonale is the condition of right sided heart failure secondary to fibrosis and sclerosis of the pulmonary artery branches. It results from shifting of the "Schistosoma haematobium" ova from the pelvic and vescial plexus to the pulmonary artery branches where they settle and produce granuloma and fibrosis.

Bilharzial cor pulmonale occurs in "Schistosoma mansoni", when the portal pressure rises more than the systemic pressure. So blood will pass from the portal circulation to the systemic circulation carrying "Schistosoma mansoni" ova to reach the lungs.

This condition leads to Pulmonary hypertension, right ventricular hypertrophy and failure.

The left side of the heart is responsible for receiving oxygen-rich blood from the lungs and pumping it forward to the systemic circulation (the rest of the body except for the pulmonary circulation). Failure of the left side of the heart causes blood to back up (be congested) into the lungs, causing respiratory symptoms as well as fatigue due to insufficient supply of oxygenated blood. Common respiratory signs are increased rate of breathing and increased "work" of breathing (non-specific signs of respiratory distress). Rales or crackles, heard initially in the lung bases, and when severe, throughout the lung fields suggest the development of pulmonary edema (fluid in the alveoli). Cyanosis which suggests severe low blood oxygen, is a late sign of extremely severe pulmonary edema.

Additional signs indicating left ventricular failure include a laterally displaced apex beat (which occurs if the heart is enlarged) and a gallop rhythm (additional heart sounds) may be heard as a marker of increased blood flow or increased intra-cardiac pressure. Heart murmurs may indicate the presence of valvular heart disease, either as a cause (e.g. aortic stenosis) or as a result (e.g. mitral regurgitation) of the heart failure.

"Backward" failure of the left ventricle causes congestion of the lungs' blood vessels, and so the symptoms are predominantly respiratory in nature. Backward failure can be subdivided into the failure of the left atrium, the left ventricle or both within the left circuit. The patient will have dyspnea (shortness of breath) on exertion and in severe cases, dyspnea at rest. Increasing breathlessness on lying flat, called orthopnea, occurs. It is often measured in the number of pillows required to lie comfortably, and in orthopnea, the patient may resort to sleeping while sitting up. Another symptom of heart failure is paroxysmal nocturnal dyspnea: a sudden nighttime attack of severe breathlessness, usually several hours after going to sleep. Easy fatigability and exercise intolerance are also common complaints related to respiratory compromise.

"Cardiac asthma" or wheezing may occur.

Compromise of left ventricular "forward" function may result in symptoms of poor systemic circulation such as dizziness, confusion and cool extremities at rest.

Heart failure symptoms are traditionally and somewhat arbitrarily divided into "left" and "right" sided, recognizing that the left and right ventricles of the heart supply different portions of the circulation. However, heart failure is not exclusively "backward failure" (in the part of the circulation which drains to the ventricle).

There are several other exceptions to a simple left-right division of heart failure symptoms. Additionally, the most common cause of right-sided heart failure is left-sided heart failure. The result is that patients commonly present with both sets of signs and symptoms.

The symptoms of pulmonary hypertension include the following:

Less common signs/symptoms include non-productive cough and exercise-induced nausea and vomiting. Coughing up of blood may occur in some patients, particularly those with specific subtypes of pulmonary hypertension such as heritable pulmonary arterial hypertension, Eisenmenger syndrome and chronic thromboembolic pulmonary hypertension. Pulmonary venous hypertension typically presents with shortness of breath while lying flat or sleeping (orthopnea or paroxysmal nocturnal dyspnea), while pulmonary arterial hypertension (PAH) typically does not.

Other typical signs of pulmonary hypertension include an accentuated pulmonary component of the second heart sound, a right ventricular third heart sound, and parasternal heave indicating a hypertrophied right atrium. Signs of systemic congestion resulting from right-sided heart failure include jugular venous distension, ascites, and hepatojugular reflux. Evidence of tricuspid insufficiency and pulmonic regurgitation is also sought and, if present, is consistent with the presence of pulmonary hypertension.

According to WHO classification there are 5 groups of PH, where Group I (pulmonary arterial hypertension) is further subdivided into Group I' and Group I" classes. The most recent WHO classification system (with adaptations from the more recent ESC/ERS guidelines shown in italics) can be summarized as follows:

WHO Group I – Pulmonary arterial hypertension (PAH)

- Idiopathic

- Heritable (BMPR2, ALK1, SMAD9, caveolin 1, KCNK3 mutations)

- Drug- and toxin-induced (e.g., methamphetamine use)

- Associated conditions:Connective tissue disease, HIV infection, Portal hypertension, Congenital heart diseases, Schistosomiasis

WHO Group I' – Pulmonary veno-occlusive disease (PVOD), pulmonary capillary hemangiomatosis (PCH)

- Idiopathic

- Heritable (EIF2AK4 mutations)

- Drugs, toxins and radiation-induced

- Associated conditions:connective tissue disease, HIV infection

WHO Group I" – Persistent pulmonary hypertension of the newborn

WHO Group II – Pulmonary hypertension secondary to left heart disease

- Left ventricular Systolic dysfunction

- Left ventricular Diastolic dysfunction

- Valvular heart disease

- Congenital/acquired left heart inflow/outflow tract obstruction and congenital cardiomyopathy

- Congenital/acquired pulmonary venous stenosis

WHO Group III – Pulmonary hypertension due to lung disease, chronic hypoxia

- Chronic obstructive pulmonary disease (COPD)

- Interstitial lung disease

- Mixed restrictive and obstructive pattern pulmonary diseases

- Sleep-disordered breathing

- Alveolar hypoventilation disorders

- Chronic exposure to high altitude

- Developmental abnormalities

WHO Group IV – chronic arterial obstruction

- Chronic thromboembolic pulmonary hypertension (CTEPH)

- Other pulmonary artery obstructions

- Angiosarcoma or other tumor within the blood vessels

- Arteritis

- Congenital pulmonary artery stenosis

- Parasitic infection (hydatidosis)

WHO Group V – Pulmonary hypertension with unclear or multifactorial mechanisms

- Hematologic diseases: chronic hemolytic anemia (including sickle cell disease)

- Systemic diseases: sarcoidosis, pulmonary Langerhans cell histiocytosis: lymphangioleiomyomatosis, neurofibromatosis, vasculitis

- Metabolic disorders: glycogen storage disease, Gaucher disease, thyroid diseases

- Others: pulmonary tumoral thrombotic microangiopathy, fibrosing mediastinitis, chronic kidney failure, segmental pulmonary hypertension (pulmonary hypertension restricted to one or more lobes of the lungs)

Symptoms of pulmonary embolism are typically sudden in onset and may include one or many of the following: dyspnea (shortness of breath), tachypnea (rapid breathing), chest pain of a "pleuritic" nature (worsened by breathing), cough and hemoptysis (coughing up blood). More severe cases can include signs such as cyanosis (blue discoloration, usually of the lips and fingers), collapse, and circulatory instability because of decreased blood flow through the lungs and into the left side of the heart. About 15% of all cases of sudden death are attributable to PE.

On physical examination, the lungs are usually normal. Occasionally, a pleural friction rub may be audible over the affected area of the lung (mostly in PE with infarct). A pleural effusion is sometimes present that is exudative, detectable by decreased percussion note, audible breath sounds, and vocal resonance. Strain on the right ventricle may be detected as a left parasternal heave, a loud pulmonary component of the second heart sound, and/or raised jugular venous pressure. A low-grade fever may be present, particularly if there is associated pulmonary hemorrhage or infarction.

As smaller pulmonary emboli tend to lodge in more peripheral areas without collateral circulation they are more likely to cause lung infarction and small effusions (both of which are painful), but not hypoxia, dyspnea or hemodynamic instability such as tachycardia. Larger PEs, which tend to lodge centrally, typically cause dyspnea, hypoxia, low blood pressure, fast heart rate and fainting, but are often painless because there is no lung infarction due to collateral circulation. The classic presentation for PE with pleuritic pain, dyspnea and tachycardia is likely caused by a large fragmented embolism causing both large and small PEs. Thus, small PEs are often missed because they cause pleuritic pain alone without any other findings and large PEs often missed because they are painless and mimic other conditions often causing ECG changes and small rises in troponin and BNP levels.

PEs are sometimes described as massive, submassive and nonmassive depending on the clinical signs and symptoms. Although the exact definitions of these are unclear, an accepted definition of massive PE is one in which there is hemodynamic instability such as sustained low blood pressure, slowed heart rate, or pulselessness.

The primary use of the ECG is to rule out other causes of chest pain. An electrocardiogram (ECG) is routinely done on people with chest pain to quickly diagnose myocardial infarctions (heart attacks), an important differential diagnosis in an individual with chest pain. While certain ECG changes may occur with PE, none are specific enough to confirm or sensitive enough to rule out the diagnosis. An ECG may show signs of right heart strain or acute cor pulmonale in cases of large PEs — the classic signs are a large S wave in lead I, a large Q wave in lead III, and an inverted T wave in lead III (S1Q3T3), which occurs in 12–50% of people with the diagnosis, yet also occurs in 12% without the diagnosis.

This is occasionally present (occurring in up to 20% of people), but may also occur in other acute lung conditions, and, therefore, has limited diagnostic value. The most commonly seen signs in the ECG are sinus tachycardia, right axis deviation, and right bundle branch block. Sinus tachycardia, however, is still only found in 8–69% of people with PE.

ECG findings associated with pulmonary emboli may suggest worse prognosis since the six findings identified with RV strain on ECG (heart rate > 100 beats per minute, S1Q3T3, inverted T waves in leads V1-V4, ST elevation in aVR, complete right bundle branch block, and atrial fibrillation) are associated with increased risk of circulatory shock and death.

In terms of signs and symptoms the severe form of this condition presents as acute pulmonary heart disease this may lead to death.Clinical fat embolism syndrome presents with tachypnea, elevated temperature, anuria, drowsiness, and occasionally mild neurological symptoms.A petechial rash appears on the upper anterior portion of the body, including the chest, neck, upper arm, oral mucosa and conjunctivae; it appears late and often disappears within hours.

Central nervous system signs in an affected individual include acute confusion, stupor, coma, rigidity (neurology), or convulsions; cerebral edema contributes to the neurologic deterioration.

Embolized fat travels through the venous system to the lungs and can occlude pulmonary capillaries, fat emboli may cause cor pulmonale if adequate compensatory pulmonary vasodilation does not occur.Circulating free fatty acids are directly toxic to pneumocytes and capillary endothelium in the lung, causing interstitial hemorrhage, edema and chemical pneumonitis.Complications from a fat embolism can be serious such as:

1. "Pulmonary fat embolism": Obstruction causes sudden death.

2. "Systemic fat embolism": These may get lodged in capillaries of organs like the brain, kidneys, or skin, causing minute hemorrhage and microinfarcts.

The defining symptom of pleurisy is a sudden sharp, stabbing, burning or dull pain in the right or left side of the chest during breathing, especially when one inhales and exhales. It feels worse with deep breathing, coughing, sneezing, or laughing. The pain may stay in one place, or it may spread to the shoulder or back. Sometimes, it becomes a fairly constant dull ache.

Depending on its cause, pleuritic chest pain may be accompanied by other symptoms:

- Dry cough

- Fever and chills

- Rapid, shallow breathing

- Shortness of breath

- Fast heart rate

- Sore throat followed by pain and swelling in the joints

Obesity hypoventilation syndrome (also known as Pickwickian syndrome) is a condition in which severely overweight people fail to breathe rapidly enough or deeply enough, resulting in low blood oxygen levels and high blood carbon dioxide (CO) levels. Many people with this condition also frequently stop breathing altogether for short periods of time during sleep (obstructive sleep apnea), resulting in many partial awakenings during the night, which leads to continual sleepiness during the day. The disease puts strain on the heart, which eventually may lead to the symptoms such as heart failure, leg swelling and various other related symptoms. The most effective treatment is weight loss, but it is often possible to relieve the symptoms by nocturnal ventilation with positive airway pressure (CPAP) or related methods.

Obesity hypoventilation syndrome is defined as the combination of obesity (body mass index above 30 kg/m), hypoxemia (falling oxygen levels in blood) during sleep, and hypercapnia (increased blood carbon dioxide levels) during the day, resulting from hypoventilation (excessively slow or shallow breathing). The disease has been known since the 1950s, initially as "Pickwickian syndrome" in reference to a Dickensian character but currently under a more descriptive name.

Pleurisy, also known as pleuritis, is inflammation of the membranes (pleurae) that surround the lungs and line the chest cavity. This can result in a sharp chest pain with breathing. Occasionally the pain may be a constant dull ache. Other symptoms may include shortness of breath, cough, fever, or weight loss depending on the underlying cause.

The most common cause is a viral infection. Other causes include pneumonia, pulmonary embolism, autoimmune disorders, lung cancer, following heart surgery, pancreatitis, chest trauma, and asbestosis. Occasionally the cause remains unknown. The underlying mechanism involves the rubbing together of the pleurae instead of smooth gliding. Other conditions that can produce similar symptoms include pericarditis, heart attack, cholecystitis, and pneumothorax. Diagnosis may include a chest X-ray, electrocardiogram (ECG), and blood tests.

Treatment depends on the underlying cause. Paracetamol and ibuprofen may be used to help with the pain. Incentive spirometry may be recommended to encourage larger breaths. About one million people are affected in the United States each year. Descriptions of the condition date from at least as early as 400 BC by Hippocrates.

Feeding problems are common in infants with BPD, often due to prolonged intubation. Such infants often display oral-tactile hypersensitivity (also known as oral aversion).

Physical findings:

- hypoxemia;

- hypercapnia;

- crackles, wheezing, & decreased breath sounds;

- increased bronchial secretions;

- hyperinflation;

- frequent lower respiratory infections;

- delayed growth & development;

- cor pulmonale;

- CXR shows with hyperinflation, low diaphragm, atelectasis, cystic changes.

The newer National Institute of Health (US) criteria for BPD (for neonates treated with more than 21% oxygen for at least 28 days) is as follows:,

- Mild

- Breathing room air at 36 weeks post-menstrual age or discharge (whichever comes first) for babies born before 32 weeks, or

- breathing room air by 56 days postnatal age, or discharge (whichever comes first) for babies born after 32 weeks gestation.

- Moderate

- Need for <30% oxygen at 36 weeks postmenstrual age, or discharge (whichever comes first) for babies born before 32 weeks, or

- need for <30% oxygen to 56 days postnatal age, or discharge (whichever comes first) for babies born after 32 weeks gestation.

- Severe

- Need for >30% oxygen, with or without positive pressure ventilation or continuous positive pressure at 36 weeks postmenstrual age, or discharge (whichever comes first) for babies born before 32 weeks, or

- need for >30% oxygen with or without positive pressure ventilation or continuous positive pressure at 56 days postnatal age, or discharge (whichever comes first) for babies born after 32 weeks' gestation.

Obesity hypoventilation syndrome is a form of sleep disordered breathing. Two subtypes are recognized, depending on the nature of disordered breathing detected on further investigations. The first is OHS in the context of obstructive sleep apnea; this is confirmed by the occurrence of 5 or more episodes of apnea, hypopnea or respiratory-related arousals per hour (high apnea-hypopnea index) during sleep. The second is OHS primarily due to "sleep hypoventilation syndrome"; this requires a rise of CO levels by 10 mmHg (1.3 kPa) after sleep compared to awake measurements and overnight drops in oxygen levels without simultaneous apnea or hypopnea. Overall, 90% of all people with OHS fall into the first category, and 10% in the second.

Central hypoventilation syndrome (CHS) is a respiratory disorder that results in respiratory arrest during sleep. CHS can either be congenital (CCHS) or acquired (ACHS) later in life. It is fatal if untreated. It is also known as Ondine's curse.

ACHS can develop as a result of severe injury or trauma to the brain or brainstem. Congenital cases are very rare and involve a failure of autonomic control of breathing. In 2006, there were only about 200 known cases worldwide. As of 2008, only 1000 total cases were known. The diagnosis may be delayed because of variations in the severity of the manifestations or lack of awareness in the medical community, particularly in milder cases. However, as there have been cases where asymptomatic family members also were found to have CCHS, it may be that these figures only reflect those found to require mechanical ventilation. In all cases, episodes of apnea occur in sleep, but in a few patients, at the most severe end of the spectrum, apnea also occurs while awake.

Although rare, cases of long-term untreated CCHS have been reported and are termed late onset CCHS (LO-CCHS). Cases that go undiagnosed until later life and middle age, although the symptoms are usually obvious in retrospect. There have, however, even been cases of LO-CCHS where family members found to have it have been asymptomatic. Again, lack of awareness in the medical community may cause such a delay. CCHS susceptibility is not known to be affected by gender.

Symptoms of DPB include chronic sinusitis (inflamed paranasal sinuses), wheezing, crackles (respiratory sounds made by obstructions such as phlegm and secretions in the lungs), dyspnea (shortness of breath), and a severe cough that yields large amounts of sputum (coughed-up phlegm). There may be pus in the sputum, and affected individuals may have fever. Typical signs of DPB progression include (enlargement) of the bronchiolar passages and hypoxemia (low levels of oxygen in the blood). If DPB is left untreated, bronchiectasis will occur; it is characterized by dilation and thickening of the walls of the bronchioles, inflammatory damage to respiratory and terminal bronchioles, and pooling of mucus in the lungs. DPB is associated with progressive respiratory failure, hypercapnia (increased levels of carbon dioxide in the blood), and can eventually lead to pulmonary hypertension (high blood pressure in the pulmonary vein and artery) and cor pulmonale (dilation of the right ventricle of the heart, or "right heart failure").