Cloquet's hernia :A femoral hernia perforating the aponeurosis of the pectineus and insinuating itself between this aponeurosis and the muscle, lying therefore behind the femoral vessels.

Cooper's hernia (bilocular femoral hernia ): A femoral hernia with two sacs, the first being in the femoral canal, and the second passing through a defect in the superficial fascia and appearing immediately beneath the skin.

De Garengeot's hernia : incarceration of the vermiform appendix within a femoral hernia.

Gibbon's hernia : hernia with hydrocoele

Gruber's hernia :Internal mesogastric hernia.

Hesselbach's hernia - hernia of a loop of intestine through the cribriform fascia presenting lateral to femoral artery

Hey's hernia :encysted hernia, scrotal or oblique inguinal hernia in which the bowel, enveloped in its own proper sac, passes into the tunica vaginalis in such a way that the bowel has three coverings of peritoneum

Holthouse hernia :an inguinal hernia that has turned outward into the groin.

Krönlein's hernia: An inguinoproperitoneal hernia; a hernia that is partially inguinal and partly properitoneal.

Larrey's hernia = (Morgagni's hernia)

Laugier’s femoral hernia- This is a type of femoral hernia through a gap in the lacunar ligament. It is more medial in position and nearly always strangulated.

Littre's hernia - hernia with Meckels's Diverticulum

lumbar hernia: hernia in the lumbar region (not to be confused with a lumbar disc hernia), contains following entities:

• Petit's hernia - hernia through Petit's triangle (inferior lumbar triangle).
• Grynfeltt's hernia - hernia through Grynfeltt-Lesshaft triangle (superior lumbar triangle).

Maydl's hernia -(hernia-in-W) The hernia contains two loops of bowel arranged like a 'W'. The central loop of the 'W' lies free in the abdomen and is strangulated where as the two loops present in the sac are not.

Mesocolic / transmesenteric hernias:  occur through iatrogenically created defects in the mesentery. These defects include herniation of an abdominal viscus, usually through the small bowel mesentery or transverse mesocolon. These hernias are common following abdominal surgery, especially Roux-en-Y loop reconstruction,  which creates a defect in the mesentery.

Morgagni hernia (also known as retrosternal or parasternal diaphragmatic hernia) occurs due to the defective fusion of the septal transverses of the diaphragm and the costal arches. This anatomic defect lies posterolateral to the sternum and is called Larrey’s space . The exact aetiology of this hernia is unknown but it is postulated that it begins as a weakness in the diaphragm which is later stretched due to intraperitoneal pressure.

Narath’s femoral hernia - The hernia lies hidden behind the femoral vessels. It occurs only in patients with congenital hip dislocation due to lateral displacement of the psoas muscle.

Pantaloon hernia: a combined direct and indirect hernia, when the hernial sac protrudes on either side of the inferior epigastric vessels

Perineal hernia(Mery’s hernia): A perineal hernia protrudes through the muscles and fascia of the perineal floor. It may be primary but usually, is acquired following perineal prostatectomy, abdominoperineal resection of the rectum, or pelvic exenteration.

Phantom hernia - Localised muscle buldge following muscular paralysis

Richter's hernia: strangulated hernia involving only one sidewall of the bowel, which can result in bowel perforation through ischaemia without causing bowel obstruction or any of its warning signs.

Rieux's hernia :retrocecal hernia, protrusion of the intestine into a pouch behind the cecum.

Rokitansky's hernia :A separation of the muscular fibres of the bowel allowing protrusion of a sac of the mucous membrane.

Serofini's hernia - behind femoral vessels

Spigelian hernia - Spigelian hernia occurs through congenital or acquired defects in the spigelian fascia. This is the area of the transversus abdominis aponeurosis, lateral to the edge of the rectus muscle but medial to the spigelian line, which is the point of transition of the transversus abdominis muscle to its aponeurotic tendon.

Treitz's hernia is the eponymous name for a paraduodenal hernia. These are rare hernias that arise in the potential spaces and folds of the posterior parietal peritoneum adjacent to the ligament of Treitz.(duodenojejunal hernia)

Velpeau hernia: A velpeau hernia is a femoral hernia in front of the femoral blood vessels in the groin.

1.Both right & left ventricular systole ends at the same time .(ie, systolic muscle contraction of both ventricles ends at same time)

2.pulmonary arterial pressure is less than aortic pressure (i.e, pulmonary resistance to forward flow from ventricles is less than aortic resistance => therefore we can say that pulmonary impedance is less than aortic impedance.){impedance is nothing but resistance}

3.Therefore as pulmonary impedance is less, even after right ventricular systolic contraction blood continues to flow through valve until pulmonary arterial pressure increases more than right ventricle). But as aortic impedance is more ,it stops blood flow through the aortic valve before itself.

4.Due to the above reasons ,Right ventricular ejection begins prior to left ventricular ejection, has a slightly longer duration, and terminates after left ventricular ejection, resulting in P2 normally occurring after A2.

A2 and P2 are coincident with the incisura of the aorta and pulmonary artery pressure curves, respectively, and terminate left and right ventricular ejection periods.(incisura reflects closure of valves)

The differences between the aortic and pulmonary artery vascular impedance characteristics are also essential to understanding the effects of respiration on splitting of S2. When the pressure curves of the pulmonary artery and right ventricle are recorded simultaneously, the pulmonary artery curve at the level of the incisura (dicrotic notch) lags behind the right ventricular curve, or "hangs out" after it.

The duration of the "hangout interval" is a measure of impedance in the pulmonary artery system. In the highly compliant (low-resistance, high-capacitance) pulmonary vascular bed, the hangout interval may vary from 30 to 120 msec, contributing significantly to the duration of right ventricular ejection.

In the left side of the heart, because impedance is much greater, the hangout interval between the aorta and left ventricular pressure curves is negligible (less than or equal to 5 msec).

The hangout interval therefore correlates closely with impedance of the vascular bed into which blood is being injected. Its duration appears to be inversely related to vascular impedance.

Normal physiological splitting during respiration:

Alterations in the impedance characteristics of the pulmonary vascular bed and the right-sided hangout interval are responsible for many of the observed changes in splitting of S2.

In a normal physiologic setting, inspiration lowers impedance in the pulmonary circuit, prolongs the hangout interval and delays pulmonic valve closure, resulting in audible splitting of A2 and P2.

On expiration, the reverse occurs: pulmonic valve closure is earlier, and the A2–P2 interval is separated by less than 30 msec and may sound single to the ear. Since the pulmonary circulation has a much lower impedance than the systemic circulation, flow through the pulmonic valve takes longer than flow through the aortic valve. The inspiratory split widens mainly because of delay in the pulmonic component.

Traditionally it was believed that an inspiratory drop in intrathoracic pressure favored greater venous return to the right ventricle, pooling of blood in the lungs, and decreased return to the left ventricle. The increase in right ventricular volume prolonged right-sided ejection time and delayed P2; the decrease in left ventricular volume reduced left-sided ejection time and caused A2 to occur earlier. The delayed P2 and early A2 associated with inspiration, however, are best understood as an interplay between changes in the pulmonary vascular impedance and changes in systemic and pulmonary venous return. The net effect is that right ventricular ejection is prolonged, left ventricular ejection is shortened, and the A2–P2 interval widens during inspiration.

Clinical Significance

Normally the aortic closure sound (A2) occurs prior to the pulmonic closure sound (P2), and the interval between the two (splitting) widens on inspiration and narrows on expiration. With quiet respiration, A2 will normally precede P2 by 0.02 to 0.08 second (mean, 0.03 to 0.04 sec) with inspiration. In younger subjects inspiratory splitting averages 0.04 to 0.05 second during quiet respiration. With expiration, A2 and P2 may be superimposed and are rarely split as much as 0.04 second. If the second sound is split by greater than 0.04 second on expiration, it is usually abnormal.

Therefore, the presence of audible splitting during expiration (i.e., the ability to hear two distinct sounds during expiration) is of greater significance at the bedside in identifying underlying cardiac pathology than is the absolute inspiratory increase in the A2–P2 interval.

ABNORMAL SPLITTING OF THE SECOND HEART:

(1) persistently single;

(2) persistent (audible expiratory) splitting, with normal respiratory variation;

(3) persistent splitting without respiratory variation (fixed splitting); and

(4) reversed (paradoxical) splitting.

(1) persistently single;

• When S2 remains single throughout the respiratory cycle, one component is absent or the two components are persistently synchronous.
• The most common cause of a single S2 is inaudibility of the P2 in older adults with increased anteroposterior chest dimensions.
• In the setting of
  congenital heart disease, a single S2 due to absence of the pulmonary component is a feature of pulmonary atresia, severe pulmonary valve stenosis, dysplastic pulmonary valve, or complete transposition of the great arteries.
• Conversely, a single S2 due to inaudibility of the A2 occurs when the aortic valve is immobile (severe calcific aortic stenosis) or atretic (aortic atresia).

(2) persistent (audible expiratory) splitting, with normal respiratory variation;

• Persistent splitting may be due to a delay in P2, as in cases of simple complete right bundle branch block,or to early timing of the A2, as occasionally occurs in cases of mitral regurgitation(since early emptying of left ventricle –> early closure of Aortic valve).
• Normal directional changes in the interval of the split (greater with inspiration, lesser with exhalation) in the presence of persistent audibility of both components defines the split as persistent but not fixed.
• these conditions have wide inspiratory split

(3) fixed splitting;

• This term applies when the interval between the A2 and P2 is not only wide and persistent but also remains unchanged during the respiratory cycle.
  Fixed splitting is an auscultatory hallmark of  atrial septal defect(ASD). 
• A2 and P2 are widely separated during exhalation and exhibit little or no change in the degree of splitting during inspiration.

Reason behind wide splitting:

The wide splitting is caused by a delay in the P2 because a marked decrease in pulmonary vascular impedance prolongs the interval between the descending limbs of the pulmonary arterial and right ventricular pressure pulses (“hangout”), and therefore delays the pulmonary incisura and the P2.

Reason behind fixed splitting:

• We know that in normal individuals , the amount of pulmonary ejection is more during inspiration compared to that in expiration (since pulmoary impedance decreases during inspiration)
• In ASD .the amount of blood which passes throught he pulmonary valve ramains the samee in both inspiration& expiration because of Phasic changes in systemic venous return during respiration in patients with atrial septal defect are associated with reciprocal changes in the volume of the left-to-right shunt, minimizing respiratory variations in right ventricular filling. (ie, whenever venous return increases in inspiration, it causes a reciprocal decrease in left to right shunting in atria & whenever venous return decreased as in expiration ,shunting increases =>this maintains equal amount of blood in right ventricle irrespective of inspiration or exoiration)
• The net effect is the characteristic wide, fixed splitting of the two components of the S2.

(4) reversed (paradoxical) splitting. 

• This term refers to a reversed sequence of semilunar valve closure, the P2 preceding the A2.
• Common causes of paradoxical splitting are complete left bundle branch block or a right ventricular pacemaker, both of which are associated with initial activation of the right side of the ventricular septum, and delayed activation of the left ventricle owing to transseptal (right-to-left) depolarization.
• When the S2 splits paradoxically, its two components separate during exhalation and become
  single (synchronous) during inspiration .
• Inspiratory synchrony is achieved as the two components fuse because of a delay in the P2, less to earlier timing of the aortic
  component.

Please review this article & if you have any doubts do tell me.