@marimphil wrote:
A 45 year old woman presents to the ER with severe upper abdominal pain with vomiting. The pain is focused in epigastrium radiating to the back. There is no history of chronic epigastric pain. Which of the following are the most likely predisposing factors for this condition?
a. H. pylori infection and excess gastric acid secretion
b. Gallstone or alcohol use
c. Obesity and high serum cholesterol
d. Stress and cigarette use
e. Hepatitis B and D co-infection
A 56 year old obese female presents to ER after being found unconscious by her daughter. Paramedics report that the female is found in stuporous condition covered with vomit. On arrival at ER, she is clammy and her BP is 85/50mmHg. Her serum amylase is raised. Which of the following is the most likely cause of hypotension?
a. Alpha cell tumor of pancreas
b. Ectopic pancreas
c. Acute hemorrhagic pancreatitis
d. Pancreatic adenocarcinoma
e. Cystic fibrosis
A 51 year old male diagnosed with Decompensated Chronic Liver Disease suddenly starts vomiting blood and eventually loses consciousness. His wife finds him lying on the bedroom floor. He has no prior history of hematemesis, bleeding diathesis and had not been vomiting prior to the appearance of the blood. Which of the following is the most likely cause of this man’s presentation?
a. Achalasia
b. Esophageal varices
c. Mallory weiss tear
d. Plummer Winson syndrome
e. Zenker’s diverticulum
A 45 year old man presents with malaise,anorexia and vomiting to emergency room. The physician notices slight jaundice. Blood examination shows marked elevation of ALT and AST with AST/ALT ratio being 2.5. Alkaline phosphatase is near normal. Serum Copper and Iron are normal.histopathological reports show Mallory bodies in hepatocytes. Liver damage from which of the following diseases most likely accounts for these findings?
a. Biliary cirrhosis
b. Viral hepatitis
c. Alcoholic hepatitis
d. Hemochromatosis
e. Wilson’s disease
A 30 year old married woman presents to gynaecology OPD for routine checkup. She is taking Oral Contraceptive Pills for contraception for the last 4 years. She reports slight discomfort in the right hypochrondrium.Alpha protein level is essentially within normal limits. Ultrasound shows a space occupying lesion. She is physically fine otherwise. This lesion is most likely
a. Hepatocellular carcinoma
b. Hepatic adenoma
c. Angiosarcoma
d. Hepatic amebiasis
e. Echinococcus granulosus cyst
A 65 year old male presents with complaint of right upper quadrant pain. He was diagnosed HCV 20 years back. He also gives a history of ill health, fever, decreased appetite and fatigue. Biopsy specimen shows presence of bile and atypical lymphocytes. Apart from CT scan and other tests which tumor marker you will order to support your diagnosis?
a. Beta HCG
b. Carcino-embryonic antigen
c. Alpha feto protein
d. CA-125
e. CA-15
A 12 year old male child presents with pitting edema, ascites and prolonged bleeding from wound sites. His biological parents are not known and he was adopted from orphanage. His abdominal Ultrasound reveals cirrhosis and viral serology for HBV and HCV comes out as negative. What is the most likely cause of cirrhosis in children of his age?
a. Wilson’s disease
b. Gaucher’s disease
c. Alpha 1 Antitrypsin deficiency
d. Primary Biliary cirrhosis
e. Hemochromatosis
A 30 year old male presents with dementia, Hemiballism and de-arranged liver enzymes. On further evaluation his abdominal Ultrasound shows cirrhosis of the liver. His Viral serology is negative. What is the most likely next finding in this patient?
a. Periodic Acid Schiff Stain shows red cytoplasmic granules in hepatocytes.
b. Kayser Fleisher rings in cornea
c. Highly increased Alpha feto proteins
d. Antimitochondrial antibodies in blood
e. Central cyanosis
A 3 year old boy is brought to ER in a comatose condition. He had an episode of viral infection for which he was given aspirin by his mother to relieve fever. But his condition deteriorated and later he was brought to ER. His blood samples are taken and deranged liver enzymes are found. Most probably his diagnosis is:
a. Alpha 1 anti-trypsin deficiency
b. Reye Syndrome
c. Wilson’s disease
d. Neonatal cholestasis
e. Primary Biliary Cirrhosis
A 26 year old malnourished female presents to medicine OPD with mild abdominal discomfort in Right hypochondrium. On taking further history,she has had diarrhea for 2 weeks. Ultrasound abdomen shows space occupying lesion. Biopsy specimen shows abscess. Most likely cause of this liver abscess is:
a. E. coli
b. Klebsiella sp.
c. Entamoeba histolytica.
d. Acute hepatitis
e. Echinococcus granulosus cyst
A 25 year old man had been experiencing intermittent diarrhea which, over years, progressed to severe diarrhea, alternating with constipation, rectal bleeding, and passage of mucus. On physical examination, the abdomen is tender over the left iliac fossa . Stools examination fails to reveal parasites. Colonoscopy demonstrates inflammation limited to the rectum, with no higher lesions. Which of the following is the most likely diagnosis?
a. Celiac Disease
b. Crohn Disease
c. Hirschprung Disease
d. Tropical sprue
e. Ulcerative colitis
Exploratory laparotomy of a patient with an acute abdomen demonstrates a several foot long loop of small intestine with a dark red-to-brown, edematous appearance.The patient has a history of atrial fibrillation. The lesion ends abruptly on both the distal and proximal edges. Which of the following diagnosis is suggested by this appearance?
a. Adenocarcinoma of the colon
b. Crohn disease
c. Ulcerative colitis
d. Ischemic bowel disease
e. Tuberculosis
A 60 year old man presents to his physician because of progressive dysphagia, first to solids and then to liquids. Endoscopy reveals a large fungating mass 2cm above the Gastroesophageal junction. Biopsy of the mass shows that the glands have extended into muscular layer and contain large hyperchromatic nuclei. A diagnosis of esophageal adenocarcinoma is made. Which of the following conditions can result in the development of this lesion?
a. Esophageal rings
b. Esophageal webs
c. Reflux esophagitis
d. Scleroderma
e. Sliding hiatal hernia
A 65 year old man develops peri-umbilical pain which then shifted to the right iliac fossa. On physical examination, his temperature is 38C rectally and his abdomen is tender. Which of the following is the most likely diagnosis?
a. Acute Appendicitis
b. Diverticulitis
c. Hemorrhoids
d. Pancreatitis
e. Pyelonephritis
A 57 year old woman with anemia is found to have a decreased Vitamin B12 level. Antibodies to intrinsic factor are identified. Levels of all other vitamins are within normal limits. Which of the following is most likely to be associated with this condition?
a. Duodenal ulcer
b. Ulcerative colitis
c. Dietary Vit. B12 deficiency
d. Atrophic gastritis
e. Angiodysplasia
A 54 year old woman complains of burning pain in her epigastrium and vomiting a few days after she started taking medication for her rheumatoid arthritis. Which of the following forms of gastritis would most likely be found in this patient?
a. Acute gastritis
b. Chronic antral gastritis
c. Chronic fundal gastritis
d. Hypertrophic gastritis
e. Lympocytic gastritis
A 32 year old woman presents with complaints of several months of burning substernal chest pain exacerbated by large meals, cigarettes and caffeine. Her symptoms are worse when she lies on her back, especially while sleeping at night. Antacids often improve her symptoms. This patient is at risk for which of the following conditions?
a. Cardiac ischemia
b. Columnar metaplasia of distal esophagus
c. Esophageal web
d. Leiomyoma of the esophagus
e. Mallory Weiss lesion in the esophagus
A patient develops anemia and weight loss and slight abdominal discomfort. On questioning, the patient is a known case of chronic gastritis. Which of the following type of malignancy is most strongly associated with this patient’s condition?
a. Gastric lymphoma
b. Intestinal type of gastric adenocarcinoma
c. Diffuse type of gastric adenocarcinoma
d. Squamous type of oesophageal carcinoma
e. Adenocarcinoma of oesophagus
A 50 year old man with a history of alcohol abuse is found to have elevated liver enzymes. A liver biopsy shows the microscopic features of fatty change (steatosis). If the patient abstains from further drinking, this condition will most likely evolve into which of thee following?
a. Acute hepatitis
b. Chronic hepatitis
c. Complete regression
d. Hyperplastic nodules
e. Malignant degeneration
A patient presents to a physician complaining of recurrent episodic diarrhea, triggered by eating too much or drinking alcohol. His wife states that “he turns as red as a beet and starts wheezing” during these episodes. Chest X-Ray demonstrates a lung mass. Which of the following would be the most likely cause of his symptoms?
a. Carcinoid tumor
b. Primary TB
c. Recurrent TB
d. Lung cancer
e. Superior vena cava syndrome
A 40 year old woman with polycythemia vera develops progressive severe ascites and tender hepatomegaly over a period of several months. Liver function tests are near normal. Which of the following is the most likely diagnosis?
a. Acute hepatitis
b. Hepatic vein obstruction
c. Hemochromatosis
d. Chronic hepatitis/cirrhosis
e. Carcinoid syndrome
A 10 year old boy complains of intermittent abdominal pain. Endoscopy fails to demonstrate peptic ulcer or chronic gastritis. The clinician suspects that the patient may have a heterotopic rest of gastric mucosa that is producing enough acid to cause ulceration of adjacent mucosa. Which of the following is the most likely diagnosis?
a. Ectopic pancreatic tissue
b. Meckel’s diverticulum
c. False diverticulum
d. Appendicitis
e. Cancer of the cecum
A 65 year old woman dies of metastatic liver cancer. The liver at autopsy shows a multinodular vascular tumor that histologically is composed of anastomosing channels lined by anaplastic endothelial cells. The liver parenchyma between tumor nodules appears normal. The histopathologist gives a preliminary diagnosis of angiosarcoma of the liver. Which of the following risk factors is associated with this form of liver cancer?
a. Cirrhosis
b. Hemochromatosis
c. Exposure to vinyl chloride
d. Hepatitis B virus infection
e. Oral contraceptive use
A 65 year old man presents to a physician because of a palpable mass immediately above the left clavicle. Biopsy of the mass demonstrates metastatic adenocarcinoma in a lymph node. Which of the following organs should be most strongly suspected as containing the primary tumor?
a. Bladder
b. Large bowel
c. Liver
d. Stomach
e. Pancreas
Chronic Gastritis is associated with:
a. Helicobacter pylori
b. Contaminated food
c. Drug poisoning
d. Trauma
e. Schistosoma infection
Major site of Peptic Ulcer is :
a. Ileum
b. Duodenum
c. Esophagus
d. Pancreas
e. Cecum
Inflammatory bowel diseases are associated with:
a. Viruses
b. Autoimmune disorders
c. Refined diet
d. Psycho – somatic factors
e. Elderly age
The granulomas of Crohns’s disease are differentiated from granulomas of tuberculosis due to:
a. Presence of necrosis
b. Presence of casseation
c. Presence of giant cells
d. Presence of lymphocytes
e. Presence of epitheloid cells
Which of the following features of the polyps of the colon indicates a better prognosis?
a. Villous histology
b. Large size
c. Higher degrees of dysplasia
d. Pedunculated
e. Proximal location
Which of the following is a major predisposing factor for the development of pseudomembranous colitis?
a. Young age
b. Malnutrition
c. Antibiotic use
d. Refined diet
e. Obesity
A 6 year old boy presents with abdominal pain and vomiting. The pain first started in the peri umbilical region and then shifted to the right lower quadrant. His temperature is 102F and pulse is 110. A laparotomy is performed and his appendix is removed. What will be observed if the appendix is examined by the histopathologist?
a. Lymphocytic infiltrate
b. Necrosis
c. Neutrophilic infiltrate
d. Perforation of the appendix
e. Adhesions
Schistosoma hematobium is associated with:
a. Adenocarcinoma of the kidney
b. Squamous cell carcinoma of the bladder
c. Hepatocellular carcinoma
d. Colon cancer
e. Ureteric colic
Barrets esophagus is a predisposing factor of
a. Squamous cell carcinoma
b. Adeno carcinoma
c. Basal cell carcinoma
d. Gastric carcinoma
e. Esophagus reflex disease
A 50yr old man who is on NSAIDs for his heart problem for last 4yrs and smokes 2 pack cigarette per day last 10-15yrs presents in OPD with the c/o recurrent epigastric pain 15-20 min after taking meal which is relieved by vomiting. What is the diagnosis?
a. Coelic disease
b. Peptic ulcer disease
c. Gastric ca
d. Gastro Esophageal Reflux Disease
e. Cholecystitis
A 42yrs old man presents in OPD with the complaints of passage of abnormally bulky, frothy, greasy, yellow stools for 3 days accompanied by weight loss anorexia, abdominal distention and flatus. On biopsy small intestine was found to be laden with distended macrophages in the lamina propria. What is the most likely diagnosis?
a. Whipples disease
b. Tropical sprue
c. Celiac disease
d. Giardiasis
e. Cholera
What is another name for apthous ulcer?
a. Leukoplakia
b. Erythroplakia
c. Bed sore
d. Canker sores
e. Oral candidiasis
A 60yrs old lady presents with a small swelling at the angle of the jaw for last 2 years which is painless. On exam it is non-tender and palpated as discrete mass. Surgeon wants to excise the lesion but he is worried about the facial nerve that may get damaged during the excision. What is most likely the diagnosis?
a. Saladenitis
b. Warthin tumor
c. Parotitis
d. Papillary cystadenoma
e. Pleomorphic adenoma
Classic lesion of crohns disease is
a. Skip lesion
b. Flask shaped ulcer
c. Pseudopolyps
d. Crypt abscess
e. Macrophages laden lamina propria
Deep ulcers, marked lymphoid reaction, fibrosis, serositis, granuloma mass and fistulas are the features of
a. Ulcerative colitis
b. Crohns disease
c. Intestinal polyposis
d. Malabsorbtion syndrome
e. Colorectal carcinoma
Most common colorectal carcinoma is
a. Squamous carcinoma
b. Basal cell carcinoma
c. Adenoma
d. Adenocarcinoma
e. Mucinous carcinoma
A 70yrs old lady who is case of colon cancer. On biopsy, her cancer as invaded the muscularis propria. Two pericolic nodes are involved with no metastasis. What is the TNM stage of her colon cancer?
a. T2N1M0
b. T1N2M0
c. T2N2M0
d. T2N1M1
e. T2N0M0
What is the histological criteria for the diagnosis of acute appendicitis
a. Cytological atypia
b. Frond like villiform extensions of mucosa
c. Mucosal atrophy
d. Submucosal fibrosis
e. Neutrophilic infiltration of muscularis propria
Identify the risk factors associated with gastric carcinoma
a. Family history
b. H.pylori
c. Fatty food
d. Sedentary life style
e. More use of fruits in diet
The most common fungal infection of the oral cavity in immunocompromised individuals is:
Thrush (candidiasis)
Blastomycosis
Histoplasmosis
Mucormycosis
Coccidioidomycosis
A department of pathology reviews pathology reports of colorectal adenomas over the past 15 years and correlates them with clinical data. What set of factors is most likely to correlate with the risk of developing colorectal carcinoma?
a. Polyp size, histologic type, severity of dysplasia
b. Polyp size and anatomic location
c. Patient age, polyp size
d. Polyp size and gender of patient
e. Patients age and histologic type
During the pathogenesis of Pancreatitis which enzyme after activation from its proenzyme form can activate other enzymes and clotting, Kinin and compliment systems?
a. Lipase
b. Phospholipase
c. Trypsin
d. Elastase
e. Alpha amylase
An outbreak of acute hepatitis in the months of July and August is traced to the mixing of sewage with drinking water. The patients had jaundice, arthralgias and low-grade fever. Transaminases were markedly raised. None of the patients developed chronic disease. Only two patients died during the outbreak, both were pregnant females. What is the likeliest cause of this outbreak?
HAV
HEV
HBV
HDV
HCV
A 41year old man presents to his physician complaining of swollen ankles. He states that he never had this problem before. Physical examination demonstrates marked lower extremity edema and periorbital swelling. His pulse is strong and regular. Urine dipstick is 4+ positive for protein but negative for blood and glucose. A 24 hour urine collection demonstrates proteinuria if 6 gm / day.Spike like protrusion of GBM matrix is seen on histology Which of the following is the most likely cause of this man’s problem?
a. Berger’s disease
b. Diabetic nephropathy
c. Membranoproliferative glomerulonephritis
d. Membranous glomerulonephritis
e. Minimal change disease
A 6 year old child develops a large erythematous rash around the site of mosquito bite. One month later she is taken to a pediatrician because of a puffy face and swollen ankles. The scanty urine sample has a reddish brown hue and contains both Red Blood Cells and proteins. Which of the following distinctive features will be most likely to be seen on renal biopsy?
a. Fusion of podocyte foot processes
b. IgA in the mesangium
c. Linear IgG deposits
d. Onion skinning of renal arterioles
e. Sub epithelial electron dense humps
An IV drug abuser develops an aggressive form of nephrotic syndrome that does not respond to steroids. A renal biopsy is performed. Which of the following histological diagnosis will most likely be made from the biopsy tissue?
Focal segmental glomerulosclerosis
IgA nephropathy
Lipoid nephrosis
Membranoproliferative glomerulonephritis
Membranous glomerulonephritis
viral defences against host immunity examples
1.hiv viral vif against host APOBEC3G cellular protein (mutates HIV rna)
2.POX AND HERPES GROUP VIRUS greatly increase host cellular deoxyribonucleotidetriphosphate levels
3.non enveloped virus produce apoptosis but enveloped virus delay apoptosis
adeno and herpes bcl2 like protein
pox caspase inhibitors
HPV and adeno inhibits p 53
4.inhibit production or action of interferons
polio protease 2A interacts with mrna capstructure interacting protein and inhgibits mrna translation
influenza snatches cap structures and uses them as primers
5.mi rna silences mrna post translationally
herpes group virus are rich in mirna
adeno and polyoma virus have mirna
+strand rna virus(sense) directly translates
picorna no envelope
calci no
corona yes
toga yes
flavi yes
all have icosohedral nucleocapsid except corona ..helical
-strand rna virus(anti sense) transcribs to translatable rna then translates
paramyxo
orthomyxo
rabdo
filo
bunya
arena
all are enveloped
and all have helical nucleocapsid
ds rna are reo virus
dna virus(ds dna)
adeno no envelope
parvo no envelope and (ss dna)
papavo no
herpes yes
hepadna yes
pox yes
all are icosohedral nucleocapsids except pox complex structure
smallest dna parvo virus
largest dna pox virus
rna virus with dna intermediatein its cycle is RETROVIRUS
dna virus with rna intermediatein its cycle is hep b
1.C.obese &high cholestrol
2.C.Ac. Hemorrhagic pancreatitis
3.B.esophageal varices
4.C.Alcholic Hepatitis
5.B.Hepatic adenoma
6.C.AFP
7.?
8.KF ring
9.B. reye's
10.C.Entameba histolytica
11.E.UC
1.alcohol mostly presents chronically so though most cases of pancreatitis are due to alcohol and gall stones here i assume obesity and high cholesterol might be the answer
2.acute hemorrhagic pancreatitis
3.esophageal varices
4.deritis ratio >2 means alcoholic hepatitis and viral hepatitis but mallory bodies vote for alcoholic hepatitis
5.hepatic adenoma
6.alpha feto protein
7.wilsons disease:The main sites of copper accumulation are the liver and the brain, and consequently liver disease and neuropsychiatric symptoms are the main features that lead to diagnosis.[1] People with liver problems tend to come to medical attention earlier, generally as children or teenagers, than those with neurological and psychiatric symptoms, who tend to be in their twenties or older.
alpha1anti trypsin deficiency:respiratory symptoms dominate and liver failure presents in neonates if severe
gauchers disease:Painless hepatomegaly and splenomegaly: the size of the spleen can be 1500-3000 ml, as opposed to the normal size of 50-200 ml. Splenomegaly may decrease the affected individual's capacity for eating by exerting pressure on the stomach. While painless, enlargement of spleen increases the risk of splenic rupture.
Hypersplenism and pancytopenia: the rapid and premature destruction of blood cells, leading to anemia, neutropenia, leukopenia, and thrombocytopenia (with an increased risk of infection and bleeding).
Cirrhosis of the liver is rare
hemochromatosis:Symptoms from hemochromatosis usually begin between age 30 years and age 50 years
pbc:Primary biliary cirrhosis is most frequently a disease of women and occurs between the fourth and sixth decades of life
so the data is insufficient and i vote for wilsons disease presenting in liver
8.kf ring
9.reyes syndrome
10.e.histolytica
11 ulcerative colitis (limited to rectum.. proctitis)
12.ischemic bowel disease
13.reflux oesophagitis(barrets esophagus),sliding hiatal hernia,scleroderma by causing achalasia
14.acute appendicitis
15.atrophic gastritis
Ring enhancing lesions on CT Brain
The mnemonic : MR.THAMPA
What does it help in remembering : It helps us in remembering the differential diagnosis for a ring enhancing lesion on CT Brain.
Expand it : M = Metastatic tumors
R = Radiation necrosis
T = Tuberculoma
H = Hematoma
A = Aneurysm
M = Multiple Sclerosis
P = Primary Brain Tumor
A = Abscess.
To put it in a textbook way :
Primary brain tumor (glioblastoma), Metastasis (especially post chemotherapy), Abscess – ring is smooth and regular and usually thinner on the medial side; in HIV most common are toxoplasma, crytococcus, and TB (Toxoplasmosis is most common), Multiple sclerosis, Resolving hematoma (10-21 days), Tuberculoma, Radiation necrosis, Postoperative change, Aneurysm
. S1 normally is louder than S2 over the apex and along the lower left sternal border; intensity is reduced if S1 is softer than S2 over these areas. S1 intensity is likely to be accentuated if S1 is much louder than S2 over the left or right second interspace.
Increased intensity of S1 — Mitral valve closure begins a few milliseconds before onset of the rise of the left ventricular pressure pulse. The intensity of valve closure is increased when the mitral valve remains widely open at end-diastole and then closes rapidly. The greater distance of travel of the leaflets from the open to the closed position and the increased velocity of closure contribute to the increased intensity of S1. Clinical situations in which this occurs include (show table 1):
• Increased transvalvular gradient (mitral valve obstruction as in mitral stenosis or atrial myxoma)
• Increased transvalvular flow (left-to-right shunt in patent ductus arteriosus, ventricular septal defect, and high output state)
• Shortened diastole (tachycardia)
• Short PR intervals (preexcitation syndrome)
The relative contribution of the distance of travel and the velocity of mitral valve closure to increased S1 intensity is difficult to determine; both factors are likely to play a role. When mitral valve closure occurs on the steeper part of the left ventricular pressure pulse, the intensity of S1 increases; this phenomenon may also contribute to an accentuated S1 observed in patients with extremely short PR intervals and left atrial myxoma [9].
The increased intensity of tricuspid valve closure in atrial septal defect and tricuspid valve obstruction (tricuspid stenosis, right atrial myxoma) can also be explained by the same phenomenon. The tricuspid valve is held open by increased transvalvular flow and the transvalvular gradient until final closure with increased velocity occurs with right ventricular systole.
Decreased intensity of S1 — Restricted valve mobility and lack of apposition of the valve leaflets decrease the intensity of S1. Thus, S1 is soft when the mitral valve is immobile due to calcification and fibrosis, despite a significant transvalvular gradient. S1 may also be reduced when the leaflets are semi closed prior to the onset of systole or when the velocity of closure is reduced, as can occur with left ventricular dysfunction. These situations are illustrated by the following examples (show table 1):
• S1 is very soft or absent when mitral regurgitation results from fibrosis and destruction of the valve leaflets (as in patients with rheumatic valve disease), which prevent effective mitral valve closure. In contrast, mitral regurgitation due to perforation of the valve leaflets from bacterial endocarditis may not be associated with a reduced intensity of S1. Similarly, S1 is normal or even accentuated in patients with mitral valve prolapse with late systolic regurgitation. Increased intensity of S1 in some patients with the mitral valve prolapse syndrome may be caused by an increased strength of ventricular systole (hyperkinetic) [10].
• Reduced S1 intensity occurs when the mitral valve remains in the semi closed position before the onset of ventricular systole and when the distance of travel and the velocity of valve closure are decreased. S1 is usually soft when the PR interval is prolonged (exceeding 0.2 second) since semi closure of the mitral valve occurs following atrial systole and before ventricular systole begins. Premature closure of the mitral valve can occur in patients with severe acute aortic regurgitation due to a rapid rise in left ventricular diastolic pressure; the mitral valve may be virtually closed at the onset of systole, resulting in a markedly decreased intensity of or even absent S1 [11].
• S1 is soft in some patients with left bundle branch block without any other obvious abnormality; the mechanism is unclear. Decreased valve closure velocity due to myocardial dysfunction is possible.
• Hemodynamically significant aortic stenosis may be associated with a soft S1; this can occur in the absence of spreading calcification to the mitral valve and in the presence of a normal PR interval [9]. Semi closure of the mitral valve due to a powerful atrial contraction and an abnormally elevated left ventricular diastolic pressure before the onset of ventricular systole is the most likely explanation.
• S1 is frequently soft in patients with dilated cardiomyopathy, even in the absence of a prolonged PR interval or bundle branch block. The decreased S1 is almost invariably associated with a significantly reduced left ventricular ejection fraction and elevated pulmonary capillary wedge pressure. The mechanism for a soft S1 in these patients remains unclear; semi closure of the mitral valve due to an elevated left ventricular diastolic pressure and decreased velocity of valve closure due to myocardial dysfunction may contribute.
• Decreased conduction of sounds through the chest wall reduces the intensity of S1 in patients with chronic obstructive pulmonary disease, obesity, and pericardial effusion.
Variation in the intensity of S1 — Varying intensity of S1 may be evident in the following situations:
• It is a common feature of atrial fibrillation; the mechanism appears to be a variation in the velocity of valve closure related to changes in the RR cycle length.
• The intensity of S1 varies in the presence of premature beats.
• Changing intensity of S1 occurs in atrioventricular dissociation, whether the heart rate is slow or fast (eg, in complete heart block or ventricular tachycardia). The changing intensity is due to random variation of the PR interval; the short PR interval is associated with an increased intensity and the long PR interval with a decreased intensity. The pulse is regular in atrioventricular dissociation; thus, the varying intensity of S1 in a patient with a regular pulse almost always suggests atrioventricular dissociation.
• Auscultatory alternans, in which S1 is soft and loud with alternate beats, is a rare finding in severe cardiac tamponade; it is almost always associated with electrical alternans and pulsus paradoxus. Although the pulse is regular, changes in the intensity of S1 occur regularly with the alternate beats and not randomly as in atrioventricular dissociation.
Splitting of S1 — There are normally two components of S1: the mitral component precedes the carotid pulse upstroke and the tricuspid component occurs later. The interval between mitral and tricuspid closure is 0.02 to 0.03 second and can be appreciated with the diaphragm of the stethoscope along the lower left sternal border [1]. The mitral component is much louder than the tricuspid component and is normally heard more widely across the precordium; the tricuspid component is of low intensity and is best heard over the left third and fourth interspaces close to the sternal border.
Abnormal splitting of S1 can result either from conduction disturbances, hemodynamic, or mechanical causes.
Conduction abnormalities — A widely split S1 occurs in complete right bundle branch block, during left ventricular pacing, with ectopic beats of left ventricular origin, and in ventricular tachycardia and idioventricular rhythm when the QRS complex morphology is of right bundle branch block configuration. S2 is also widely split when wide splitting of S1 occurs due to conduction abnormalities, with a further increase in the splitting of S1 and S2 during inspiration; this is due to increased venous return and right ventricular volume with further delay in tricuspid valve closure. A widely split S1 in conduction anomalies results from a delay in onset of the right ventricular pressure pulse.
Hemodynamic causes — Delayed closure of the tricuspid valve may occur in patients with atrial septal defect who have large left-to-right shunts. The widely split S1 in this case does not vary with inspiration since the right ventricular volume is fixed despite the increased venous return.
Wide splitting of S1 also occurs in patients with significant tricuspid stenosis due to a similar mechanism as in atrial septal defect. Wide splitting of S1 with increased intensity of the second component is a feature of Ebstein's anomaly [12]. It is related in part to the commonly associated right bundle branch block.
In patients with right atrial myxoma, a delay in closure of the tricuspid valve also causes wide splitting of S1. Wide splitting of S1 resulting from hemodynamic causes may not be associated with wide splitting of S2 (except in atrial septal defect).
Pseudo splitting of S1 — There are other cardiac sounds that may be confused with a split S1.
• A relatively loud atrial sound (S4) preceding S1 may be confused with a split S1. The left ventricular S4 is usually localized over the cardiac apex, is best heard with the bell of the stethoscope, and becomes softer as the bell is moved gradually to the left sternal edge. S4 decreases in intensity or disappears when the bell is converted to the diaphragm by applying firm pressure, while splitting of S1 becomes more obvious.
• The combination of a systolic ejection sound (also a high-frequency sound) and S1 may appear as split S1. However, the S1 and ejection sound interval is usually greater than the normal mitral and tricuspid interval. Furthermore, an aortic ejection sound is heard over the cardiac apex, along the left sternal border, and over the right second interspace. In contrast, tricuspid closure is usually heard along the left lower sternal border. Thus, splitting of S1 is not heard over the right or left second interspace.
Pulmonary ejection sounds can be easily distinguished from tricuspid closure. Pulmonary ejection sounds are usually localized and best heard over the left second interspace. More importantly, pulmonary ejection sounds decrease in intensity during inspiration, while the intensity of tricuspid closure remains unchanged or increases following inspiration.
• A combination of S1 and a midsystolic click is rarely confused with a split S1 since the interval between them is usually far greater than that between mitral and tricuspid valve closure. Furthermore, the S1-click interval can be changed by maneuvers such as standing and squatting, while no significant changes in normal S1 splitting can be appreciated with these maneuvers.
• The combination of a pacemaker sound and S1 should not be confused with the splitting of S1. The "pacemaker sound" that results from the stimulation of the intercostal muscles during pacing has a very high frequency and precedes S1; it therefore occurs well before the upstroke of the carotid pulse [13]. Furthermore, the pacemaker sound disappears with discontinuation of pacing.
Reversed splitting of S1 — Reversed splitting of S1 (tricuspid component preceding the mitral component) is seldom recognized. It may occur in patients with severe mitral valve stenosis, in whom mitral valve closure is markedly delayed; in the presence of a left atrial myxoma since mitral valve closure occurs after the tumor is expelled from the left ventricle to the left atrium, resulting in wide and reversed splitting of S1; and with premature beats arising from the right ventricle and associated with a left bundle branch block pattern. In most patients with left bundle branch block, however, reversed splitting of S1 is not appreciated, suggesting that no significant delay in the onset of left ventricular mechanical systole occurs.
SECOND HEART SOUND (S2) — The genesis of the second heart sound (S2) consists of two components, aortic and pulmonary valve closure sounds, traditionally designated as A2 and P2 [1]. S2 occurs after the peak of the carotid pulse and coincides with its downslope. The onset of A2 occurs with the dicrotic notch of the aortic root pressure pulse [14,15].
The two components of S2 are best heard with the diaphragm of the stethoscope and over the left second interspace close to the sternal border. A2 is widely transmitted to the right second interspace, along the left and right sternal border, and to the cardiac apex. P2 is normally best heard and recorded over the upper left sternal border and is poorly transmitted.
Intensity of A2 and P2 — S2 is usually single during expiration, particularly when auscultation is performed with subjects in the semi recumbent position. Separation of A2 and P2 occurs during inspiration, allowing comparison of the relative intensities of these two components. A2 is louder, even in pulmonary areas (left second interspace); it is the only component heard over the cardiac apex in almost all normal subjects [16]. P2 can be heard over the right second intercostal space and along the left sternal border. The relative intensity of A2 is almost always greater than P2 over the left second interspace; the intensity is equal in this area in approximately 2 percent of normal subjects.
The major determinants of A2 intensity (and therefore the major determinant of S2) include (show table 2):
• Aortic pressure
• Relative proximity of the aorta to the chest wall
• Size of the aortic root
• Degree of apposition of the valve leaflets and their mobility
Increased intensity of A2 cannot be quantitated objectively by auscultation; it is based upon a subjective impression.
The intensity of P2 is determined by:
• Pulmonary arterial pressure, particularly the diastolic pressure
• Size of the pulmonary artery
• Degree of apposition of the pulmonary valve leaflets
The intensity of P2 is determined by comparing its intensity with A2. An increased P2 intensity is suggested when it is louder over the left second interspace or when there is transmission to the cardiac apex.
Increased intensity of A2 — Increased intensity of A2 often occurs in systemic hypertension, coarctation of the aorta, and ascending aortic aneurysm; a "tambour" quality of A2 is commonly heard (show table 2). The intensity of A2 is significantly increased when the aortic root is relatively anterior and closer to the anterior chest wall, as in tetralogy of Fallot and transposition of the great arteries.
Increased intensity of P2 — The most common cause of an increased P2 intensity is pulmonary arterial hypertension of any etiology [17]. A2 is soft in patients with mitral regurgitation and P2 may appear to be increased. In these circumstances, one cannot rely on the relative intensity of P2 for the diagnosis of pulmonary hypertension.
In atrial septal defect the intensity of P2 is increased considerably and frequently greater than A2 over the left second interspace, even with a normal or slightly elevated pulmonary artery pressure [18]. P2 is heard over the cardiac apex in 50 percent of these patients. The mechanism for the increased intensity of P2, despite low pulmonary artery diastolic pressure and pulmonary vascular resistance, is unclear. A dilated pulmonary artery and considerable right ventricular dilatation may contribute.
Decreased intensity of A2 — Decreased intensity of A2 occurs when there is lack of apposition of the valve leaflets, as in severe luetic aortic regurgitation. Other causes of decreased A2 intensity include lower arterial diastolic pressure (eg, in significant aortic regurgitation), a relatively immobile aortic valve due to calcification (eg, in patients with calcific aortic stenosis), and relatively lower arterial pressure in hemodynamically significant aortic stenosis (show table 2).
Decreased intensity of P2 — A decreased intensity of P2 occurs when there is lower pulmonary artery diastolic pressure, except with atrial septal defect. P2 is soft and delayed with significant right ventricular outflow obstruction, as in patients with pulmonary valve stenosis. P2 is absent in patients with severe pulmonary insufficiency due to a congenitally absent pulmonary valve. In contrast, P2 is markedly accentuated in pulmonary insufficiency secondary to pulmonary hypertension.
Splitting of S2 — Inspiratory splitting of S2 can be appreciated 24 to 48 hours after birth when the pulmonary vascular resistance is considerably lower than at birth. A2 and P2 are usually fused during the expiratory phase of continuous respiration when auscultation is performed in adults in the semi recumbent position (30º to 40º from the horizontal); occasionally, slight expiratory splitting is heard in the recumbent position. During the inspiratory phase, separation of A2 and P2 occurs; the degree of splitting varies from 0.02 to 0.06 second [19]. Splitting of S2 is best heard with the diaphragm of the stethoscope over the left second interspace.
Mechanism — Multiple mechanisms contribute to the normal inspiratory splitting of S2. A2, which is coincident with the incisura of the aortic pressure pulse, occurs on average 0.02 seconds after left ventricular systolic pressure falls below the aortic pressure. P2, coincident with the pulmonary arterial incisura, occurs 0.03 to 0.09 seconds after the crossover point of right ventricular and central pulmonary arterial pressure [20,21].
The interval between the pressure crossover point and the incisura (the onset of A2 or P2) has been termed hangout time. The hangout time is inversely proportional to the impedance to blood flow in the systemic arterial and pulmonary arterial systems. Systemic vascular resistance normally is considerably higher than pulmonary vascular resistance and systemic arteries are less compliant than the pulmonary arteries. These differences account for the shorter hangout time in the aorta than in the pulmonary artery. During inspiration, pulmonary vascular impedance declines with a further increase in the pulmonary hangout time, which appears to be the principal mechanism for inspiratory splitting of S2.
The other contributions to a normal inspiratory splitting of S2 result from an increased right ventricular ejection time. More negative intrathoracic pressure during inspiration is associated with increased venous return to the right ventricle and greater right ventricular stroke volume, which increases its ejection time and delays P2. Inspiratory delay of aortic valve closure is minimal, probably due to a much shorter aortic compared with pulmonary hangout time [22,23]. After one to three cardiac cycles the immediate inspiratory increase in right ventricular stroke volume is followed by a similar increase in left ventricular stroke volume, associated with increased left ventricular ejection time [24]. Prolongation of the left ventricular ejection time and a delayed A2 during normal respiration usually occur during the expiratory phase, while lengthening of the right ventricular ejection time and delayed pulmonary valve closure coincide with the inspiratory phase.
The relative contributions of these different mechanisms to the normal inspiratory splitting of S2 are difficult to determine. Traditionally, it has been thought that prolongation of the right ventricular ejection time accounts for a major part of the normal inspiratory splitting. Recent studies, however, suggest that the increase in pulmonary hangout time is the major contribution to normal inspiratory splitting.
Wide splitting of S2 — A2 and P2 are fused in normal adults and S2 appears single during the expiratory phase of respiration, particularly in the semi recumbent, sitting, and standing positions. Wide splitting of S2 should be suspected if the A2-P2 separation is appreciated in these positions during expiration. The A2-P2 interval needs to be 0.03 second or more to be appreciated by auscultation at the bedside.
A wide splitting of S2 can result either from conduction disturbances or hemodynamic causes (show table 2 and ).
• Conduction disturbances — Conduction anomalies that cause wide splitting of S2 include complete right bundle branch block, artificial pacing from the left ventricle, and the Wolff-Parkinson-White syndrome with left ventricular preexcitation. Premature beats and an idioventricular rhythm of left ventricular origin (QRS complex of right bundle branch block morphology) are also associated with wide splitting.
Wide splitting of S2 due to conduction disturbances results from delayed activation of the right ventricle and, consequently, delayed completion of right ventricular ejection. Widened splitting of S2 during inspiration and concomitant splitting of S1 occur in these circumstances.
• Hemodynamic causes — Increased resistance to right ventricular ejection and prolongation of right ventricular ejection time are other important causes of wide expiratory splitting of S2. Pulmonary valve and infundibular stenosis, supravalvular and pulmonary branch stenoses, and pulmonary arterial hypertension of any etiology lengthen right ventricular ejection time and cause relatively wide splitting of S2. The intensity of P2 is related to the pulmonary arterial diastolic pressure; a lower pressure is associated with a reduced intensity and a higher pressure with increased intensity. Thus, in patients with pulmonary valve and infundibular stenoses, wide splitting of S2 is associated with reduced intensity of P2, while P2 is accentuated in pulmonary hypertension and pulmonary branch stenosis.
In pulmonary valve stenosis, the degree of expiratory splitting of S2 (the A2-P2 interval) is directly related to the severity of stenosis and right ventricular systolic hypertension [25]. Further splitting of S2 during inspiration usually occurs in these conditions, but wide splitting of S1 is not observed.
Although expiratory splitting is obvious in pulmonary hypertension, the degree of splitting is much less than in other conditions which also increase the resistance to right ventricular ejection. This is because of a significant reduction in pulmonary hangout time due to decreased pulmonary vascular compliance in pulmonary hypertension [20]. For the same reason, the magnitude of inspiratory widening of the splitting of S2 is smaller. Thus, in patients with chronic pulmonary arterial hypertension, a relatively narrow expiratory splitting of S2 is expected with only a slight inspiratory increase.
Isolated reduction of the left ventricular ejection time may also cause wide splitting of S2 due to the early occurrence of A2. The best example is significant mitral regurgitation, which decreases impedance to left ventricular ejection and forward stroke volume [26]. In some patients with a ventricular septal defect with increased pulmonary flow and decreased pulmonary vascular resistance, wide splitting of S2 can occur due to the same mechanism, although a delay in the onset of right ventricular mechanical systole has also been observed [27]. Inspiratory widening of S2 is maintained in patients in this category, and S1 usually remains normal. Inspiratory reduction in left ventricular ejection time can also occur in constrictive pericarditis, which may account for the wide inspiratory splitting of S2 that occasionally is observed in these patients [28].
Wide and "fixed" splitting of S2 — Fixed splitting of S2 occurs when the A2-P2 interval does not vary more than 0.1 second during the inspiratory and expiratory phases of respiration. One common cause is a relatively large interatrial communication (atrial septal defect, common atrium) and left-to-right or bidirectional shunt; abnormally wide splitting of S2 occurs and respiratory variations of the A2-P2 intervals are minimal or absent. The mechanism of wide expiratory splitting of S2 in atrial septal defect appears to involve isolated shortening of left ventricular ejection time while the right ventricular ejection time remains normal, and an increase in pulmonary hangout time due to decreased pulmonary vascular impedance (show table 2 and ) [18,29].
The other cause of fixed splitting of S2 is right ventricular failure, when the right ventricle is unable to vary its stroke volume during inspiration, and inspiratory prolongation of its ejection time and delay of P2 does not occur. Any condition that induces severe right ventricular failure, such as right ventricular outflow obstruction, pulmonary hypertension, and primary right ventricular dysfunction can be associated with fixed splitting (show table 2 and ).
Reversed (paradoxic) splitting of S2 — Paradoxic splitting occurs when A2 follows P2 during the expiratory phase of respiration. The splitting of S2 is then maximal during expiration and the splitting is less or S2 becomes single during inspiration with the normal inspiratory delay of P2 [1,30].
Reversed splitting of S2 may result from either conduction disturbances or hemodynamic causes (show table 2 and ).
• Conduction abnormalities — Left bundle branch block, artificial right ventricular pacing, preexcitation of the right ventricle (Wolff-Parkinson-White syndrome), and premature beats of right ventricular origin are examples of conduction disturbances associated with reversed splitting of S2. Delayed activation of the left ventricle, and consequently delayed completion of left ventricular ejection, causes a delayed A2 and reversed splitting of S2. In left bundle branch block or the preexcitation syndrome, splitting of S1 does not usually occur. Splitting of S1, however, may accompany splitting of S2 with right ventricular pacing or ectopic beats. With a lesser degree of left bundle branch block or right ventricular preexcitation, the P2-A2 interval during expiration may be very short (reversed splitting), and normal splitting can occur during inspiration.
• Hemodynamic factors — A markedly prolonged left ventricular ejection time may delay A2 sufficiently to cause reversed splitting of S2. With fixed left ventricular outflow tract obstruction, as in patients with aortic valve stenosis, left ventricular ejection time is lengthened and reversed splitting of S2 usually indicates hemodynamically significant outflow obstruction. However, P2 may be inaudible due to the long ejection systolic murmur of aortic stenosis, making it difficult to recognize the reversed splitting.
The distinction between hypertrophic cardiomyopathy and mitral regurgitation or ventricular septal defect, conditions in which the character and locations of the systolic murmur may appear similar on auscultation, is facilitated by recognizing the character of S2 splitting. Reversed splitting suggests hypertrophic cardiomyopathy, while physiologic splitting favors mitral regurgitation or ventricular septal defect.
Reversed splitting of S2 is observed in some patients with hypertension. However, the P2-A2 interval in expiration is usually short and normal inspiratory splitting occurs.
A prolonged left ventricular ejection time and reversed splitting of S2 can occur with myocardial dysfunction, as in myocardial ischemia [31]. However, reversed splitting is rarely observed with severe heart failure because of the concomitant decrease in stroke volume, which is an important determinant of left ventricular ejection time.
A selective increase in left ventricular forward stroke volume may prolong left ventricular ejection time sufficiently to cause reversed splitting of S2; this explains reversed splitting of S2 in some patients with patent ductus arteriosus with a large left-to-right shunt and in patients with significant chronic aortic regurgitation. Reversed splitting of S2 is often difficult to recognize by auscultation because the inspiratory noise often obscures a relatively soft P2.
Single S2 — A single S2 may result from the absence of either of the two components of S2 or from the fusion of A2 and P2 without inspiratory splitting (show table 4).
• Absence of A2 is occasionally observed in severe calcific aortic stenosis with an immobile aortic valve. A2 may be absent in some patients with severe aortic regurgitation due to destruction of the valve leaflets.
• P2 is absent in the congenital absence of the pulmonary valve, pulmonary atresia, and truncus arteriosus. In severe pulmonary valve stenosis or in tetralogy of Fallot, P2 may be markedly attenuated and escape recognition by auscultation.
• Fusion of A2 and P2 without inspiratory splitting occurs in Eisenmenger syndrome with ventricular septal defect and in patients with a single ventricle.
A truly single S2 is rare. An apparently single S2 usually results from the inability to hear or record P2 due to emphysema, obesity, or pericardial effusion.
THIRD (S3) AND FOURTH (S4) HEART SOUNDS — S3 and S4 are low-frequency diastolic sounds that appear to originate in the ventricles. (See "Examination of the precordial pulsation").
Mechanism — The precise mechanism of the genesis of S3 and S4 has not been identified with certainty. It is generally agreed that both sounds, occasionally termed ventricular filling sounds, are associated with ventricular filling and an increase in ventricular dimensions. They are heard and recorded during rapid filling and atrial filling phases of the ventricle, respectively [32].
• S3 occurs as passive ventricular filling begins after actual relaxation is completed [33]. It appears to be related to a sudden limitation of the movement during ventricular filling along its long axis [34]. It coincides with the y descent of the atrial pressure pulse and the end of the rapid filling phase of the apical impulse, occurring usually 0.14 to 0.16 second after S2.
• S4 occurs after the P wave on the electrocardiogram and coincides with atrial systole and a waves of the atrial pressure pulse, and with the apical impulse.
Auscultation — S3 and S4 are best heard with the bell of the stethoscope. Auscultation over the cardiac apex in the left lateral decubitus position is preferable for identification of left ventricular S3 and S4. Right ventricular S3 and S4 are best heard along the lower left sternal border; occasionally right-sided filling sounds are also heard over the lower right sternal border and over the epigastrium. The intensity of S3 and S4 of right ventricular origin usually increases during inspiration, while that of left ventricular origin remains unchanged. S3 is closer to S2 and S4 occurs prior to S1.
S3 can be heard and recorded in healthy young adults. However, it is usually abnormal in patients over the age of 40 years, suggesting an enlarged ventricular chamber.
S4 can be heard in many healthy older adults without any other cardiac abnormality due to decreased ventricular compliance with age. S4 may become audible in otherwise healthy subjects with a prolonged PR interval due to the separation of S4 from S1. In patients with complete atrioventricular block, S4 is heard at a faster rate than S1 and S2 and may not indicate any hemodynamic abnormality. S4 is usually abnormal in young adults and children.
Gallops — An abnormal S3 and S4 tend to be louder and of higher pitch (sharper) and are frequently referred to as gallops. S3 is the ventricular gallop and S4 is the atrial gallop sound. S3 and S4 can be fused during tachycardia to produce a loud diastolic filling sound, termed a summation gallop [35]. At the bedside, carotid massage can cause separation of S3 and S4 as the heart rate slows. S3 and S4 may occasionally be intensified or precipitated by exercise or by sustained hand grip. Gallops can sometimes be seen and palpated. (See "Examination of the precordial pulsation").
Effective atrial contraction and ventricular filling are both required for production of atrial gallop sounds. Thus, these sounds are usually absent in atrial fibrillation and in significant atrioventricular valve stenosis.
It is often difficult to distinguish between gallop sounds of right and left ventricular origin at the bedside when they are present in the same patient. However, if one follows the "inching" method of auscultation (eg, auscultation starting over the cardiac apex and then gradually moving the stethoscope inch-by-inch to the left lower sternal border), the decreasing intensity of gallops of left ventricular origin and the increasing intensity of gallops of right ventricular origin can be appreciated. Furthermore, the intensity of the right-sided gallop sounds increase during inspiration.
Left ventricular gallops — S3 is almost always present in patients with hemodynamically significant chronic mitral regurgitation; the absence of S3 is an important finding to exclude severe chronic mitral regurgitation. An S3 gallop in patients with chronic aortic regurgitation is frequently associated with a decreased left ventricular ejection fraction and increased diastolic volume; its recognition should prompt further evaluation [36].
An S3 gallop is an important and common early finding of heart failure in dilated cardiomyopathy. It occurs with equal frequency in patients with or without coronary artery disease. In patients with aortic valve disease, coronary artery disease, and congestive cardiomyopathy, an S3 gallop is associated with left atrial pressures exceeding 20 mmHg; absence of an S3 gallop usually indicates normal left atrial pressure [35].
S3 often occurs in high-output states such as thyrotoxicosis or pregnancy. It does not necessarily indicate left ventricular dysfunction in these circumstances [37].
An audible S4 is abnormal in younger subjects and children; it is always abnormal when it is palpable, regardless of patient age. An abnormal S4 is most frequently observed in patients with decreased left ventricular distensibility [38]. Thus, S4 is common in hypertensive heart disease, aortic stenosis, and hypertrophic cardiomyopathy. Left ventricular hypertrophy, which is present in all these conditions, contributes to decreased left ventricular distensibility.
In aortic stenosis, the presence of an S4 has been reported to indicate hemodynamically significant left ventricular outflow obstruction, with a peak transvalvular gradient 70 mmHg and an elevated left ventricular end-diastolic pressure [39]. However, in patients over 40 years of age, S4 can occur due to myocardial disease in the absence of significant aortic stenosis. Thus, in elderly patients, the presence of an S4 cannot be used to assess the severity of aortic stenosis. Associated coronary artery disease may also cause an S4 in patients with mild to moderate aortic stenosis.
An S4 is heard in the vast majority of patients during the acute phase of myocardial infarction [40]. Although pulmonary venous pressure may also be elevated, there is a poor correlation between the presence and absence of an S4 and hemodynamic abnormalities. Thus, S4 is a poor guide to assess the severity of left ventricular dysfunction in patients with acute myocardial infarction.
Audible and/or palpable atrial gallops are a frequent finding in chronic left ventricular aneurysm and are usually found with left ventricular dyskinesia associated with elevated end-diastolic pressures. In patients with chronic coronary artery disease, the transient appearance of an S4, particularly during chest pain, is a strong indication of transient myocardial ischemia.
A loud S4 that is also usually palpable is a frequent finding in patients with acute and severe mitral or aortic regurgitation. It is almost always associated with an increased left ventricular end-diastolic pressure [41]. (See "Examination of the precordial pulsation").
Right ventricular gallops — An S3 gallop of right ventricular origin frequently occurs in patients with significant tricuspid regurgitation, whether it is primary or secondary to pulmonary hypertension and right ventricular failure. An S3 gallop is also heard in right ventricular failure in the absence of tricuspid regurgitation.
An S4 of right ventricular origin is most commonly heard in patients with right ventricular outflow obstruction (pulmonary valve stenosis) and pulmonary arterial hypertension [42]. It likely denotes decreased right ventricular distensibility due to hypertrophy.
EJECTION SOUNDS — An aortic ejection sound is a high-frequency "clicky," early systolic sound, usually recorded 0.12 to 0.14 second after the Q wave on the electrocardiogram. It is best heard with the diaphragm of the stethoscope and is widely transmitted, heard at the cardiac apex and also over the right second interspace. Its intensity does not vary with respiration.
When aortic or pulmonary ejection sounds occur in the presence of normal semilunar valves, the origin may be the proximal aortic or pulmonary artery segments. Thus, the term vascular ejection sound has been suggested. These sounds generally tend to occur later and are not associated with "doming" of the semilunar valves, which is characteristic of a valvular ejection sound. The mechanism of the vascular ejection sound remains unclear.
Aortic ejection sound — Aortic ejection sounds occur in association with a deformed but mobile aortic valve and with aortic root dilatation. Thus, it is present in aortic valve stenosis, bicuspid aortic valve, aortic regurgitation, and with aneurysm of the ascending aorta. An aortic ejection sound is also heard in some patients with systemic hypertension, probably due to associated aortic root dilatation.
Aortic ejection sounds are heard frequently in patients with mild to moderate aortic valve stenosis; they may be absent in severe calcific aortic stenosis, presumably due to the loss of valve mobility [44]. Since ejection sounds are usually absent in subvalvular and supravalvular aortic stenosis, the presence of an ejection sound helps to identify the site of obstruction at the level of the aortic valve. An ejection sound also does not favor the diagnosis of hypertrophic cardiomyopathy.
Identification of the aortic ejection sound is the most important and consistent bedside clue for the diagnosis of an uncomplicated bicuspid aortic valve [45]. In patients with coarctation of the aorta, an aortic ejection sound usually signifies the presence of an associated bicuspid aortic valve.
Pulmonary ejection sound — A pulmonary ejection sound occurs earlier than an aortic ejection sound and is recorded 0.09 to 0.11 second after the Q wave on the electrocardiogram, beginning at the time of maximal opening of the pulmonary valve. It is also a "clicky" sound of high frequency and is best heard with the diaphragm of the stethoscope. In contrast to the aortic ejection sound, it is not widely transmitted and usually best heard at the left second interspace and along the left sternal border; it is not usually heard over the cardiac apex or right second interspace.
The most helpful distinguishing feature of a pulmonary ejection sound is its decreased intensity, or even its disappearance during the inspiratory phase of respiration. During expiration, the valve opens rapidly from its fully closed position; sudden "halting" of this rapid opening movement is associated with a maximal intensity of the ejection sound. With inspiration, the increased venous return to the right ventricle augments the effect of right atrial systole and causes partial opening of the pulmonary valve prior to ventricular systole. The lack of a sharp opening movement of the pulmonary valve explains the decreased intensity of the pulmonary ejection sound during inspiration.
The tricuspid closure sound should not be confused with the pulmonary ejection sound. The intensity of tricuspid closure tends to increase rather than decrease during inspiration.
Pulmonary ejection sounds tend to be present in clinical conditions associated with a deformed pulmonary valve and pulmonary artery dilatation, including pulmonary valve stenosis, idiopathic dilatation of the pulmonary artery, and chronic pulmonary arterial hypertension of any etiology [46-49]. The interval between the S1 and the pulmonary ejection sound is directly related to the right ventricular isovolumic contraction time, which usually is prolonged in pulmonary hypertension, explaining a relatively late occurrence of the ejection sound in these patients. With increasing severity of pulmonary valve stenosis, the isovolumic systolic interval shortens, and the pulmonary ejection sound therefore tends to occur soon after S1. In patients with very severe pulmonary valve stenosis, the ejection sound can fuse with S1 and may not be recognized.
Measure Typical value Normal range
end-dia stolic volume (EDV) 120 mL[2] 65–240 mL[2]
end-systolic volume (ESV) 50 mL[2] 16–143 mL[2]
stroke volume (SV) 70 mL 55–100