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•Cardiac arrhythmias

• Conduction defects

•Myocardial infarction or ischemia

•Myocardial hypertrophy Electrolyte imbalance

• Toxicity of certain drugs

ECG interpretation is not much difficult, it is very important tool of investigation: therefore spend a lot of time in ECG reading during posting in cardiology unit. If ECG interpretation is weak it will become difficult for a physician to deal with cardiac emergencies with accuracy. Unfortunately in Government Hospitals most of emergency medical officers are posted from skin, surgery, neurology and other specialties who are not trained in ECG reading, occasionally they're indeed unfit to he cure of responsible fete cardiac exigency that results in loss of case's life. This practice will be continued until merit( not influence) becomes the criteria for selection of medical directors. Be a safe physician,learn ECG.

  There's nothing delicate in medical education except to find out sincere teachers who have tutoring chops and who are generous in transferring the practical knowledge to their scholars( unfortunately utmost of them are not → → greason g selection not grounded on merit)   


 Heart size  

 Heart size can be reliably assessed only from PA view of casketx-ray, because in AP view cardiac shadow is large. The maximum transverse periphery of the heart is compared with the maximum transverse periphery of the casket measured from inside of the caricatures this is called cardiothoracic rate( CTR) It should be lower than 50. Cardiomegaly and pericardial effusion beget an increase in cardiothoracic rate. 

 • Pericardial effusion produces spherical shadow. 

 • Left atrial dilatation manifests as elevation of left atrial accessory on the left heart border and a double atrial shadow to the right of the sternum( double right heart border).   

• Left ventricular blowup manifests as increased CTR and an increased protuberance of the left heart border. 

• Right atrial blowup manifests as protuberance of right border of heart into the right lower lung field.

 • Right ventricular blowup manifests as increased CTR and an upward relegation of the apex of the heart.  

• Blowup of pulmonary roadway manifests as a prominent bulge on the left heart border below the aortic knuckle   


X-ray chest may show calcification of pericardium, faucets, aorta and myocardium.  

 Lung fields  

 Lung fields may indicate pulmonary hypertension by blowup of hilar vessels eg. enlarged right lower lobe roadway. Kerly's B lines and pleural mes who aren't trained effusion may be present in cardiac failure.


It is a touchy strategy for assurance of

•Size of all four chambers of heart. 

 •Left ventricular function (ejection fraction).

•Regional wall motion abnormalities due to

myocardial infarction, ischemia.

•Complexities of myocardial localized necrosis like papillary muscle brokenness, mitrale Rgurgitation, VSD, left ventricular aneurysm and left ventricular thrombus.

•Structural valve abnormalities e.g. stenosis and regurgitation.  

•Cardiac output.

•Ventricular hypertrophy Pericardial effusion.

•Atrial and ventricular septal defects and other congenital defects.

Types of echocardiography

Two dimensional real time echocardiography This type of echocardiography is particularly valuable for detecting wall motion abnormality, intracardiac masses, such as thrombi and tumors or Stres endocarditic vegetations It is also helpful in In st detection of congenital heart diseases.

M-mod echocardiography

This type of echocardiography is particularly useful for the measurement of sizes of chambers of heart, calculation of ejection fraction and accurate timing of cardiac events such as opening and closing of valves.

Doppler echocardiography

Doppler echocardiography is valuable in detecting abnormal directions of blood flow eg aortic or gradient eg gradient across a stenosed aortic valve. There are three modes of Doppler mitral regurgitation and estimation of pressure gradient e.g. gradient across a stenosed aortic valve. There are three modes of Doppler echocardiography:

1.Pulse wave Doppler (PW). 2. Continuous-wave Doppler (CW)

3. Color Doppler

Experience sharing: a good echo machine should

have all three components.

1. Two-dimensional real time echocardiography

2. M-mod echocardiography

 3. Doppler echocardiography

Machines available in request have price ranging fromRs. 10,00000 to 100,00000 and echo charges are generally Rs. 1000 to 2500 in Karachi. Low priced machines don't have Doppler. important of the echo results are driver dependent, thus when you're pertaining the case for echo you must know how well- professed is the driver in performing  echo.   

Trans- Esophageal Echocardiography( TEE)   

In this fashion an ultrasound inquiry, in the shape of endoscope is passed into the esophagus and deposited behind the heart. It's veritably helpful in detecting veritably small leafages not detected on transthroacic( generally performed) echocardiogram. Thrombus in left patio or atrial accessory in cases of mitral stenosis and atrial fibrillation. ASD not detected by transdroracic.

  Stress Echo 

 In stress echocardiography echo is done during exercise or just after the exercise, or after pharmacological stress by administration of Dobutamine Stress Test( DSE) is now generally performed to descry stress convinced segmental wall stir abnormalities( an index of ischemia). 

  Contrast Echo   

Intravenous discrepancy agents or agitated saline are used intravenously to assess intramyocardial inflow pattern; veritably helpful in discovery and to see the direction of inflow in shunts similar as ASD, VSD( left to right or right to left).  

 AMBULATORY ECG( Holter monitoring)  

 This outfit is a battery powered mail tape recording archivist which is used for nonstop recording of one or further ECG leads for 24 hours. This fashion is useful in detecting flash occurrences of arrhythmia or ischemia which infrequently do during the short time taken for routine 12- lead ECG recording. detail paroxysm of tachycardia, an occasional pause in meter or intermittent ST member changes may be linked.


It's also an event archivist that is used to record lower frequent arrhythmias. Case is handed with a fund- sized device that can record and store a short member of ECG.  


( Nuclear imaging)   

Thallium 201 scanning   

Thallium 201 scanning when fitted provides information regarding infarction andnon-infarction myocardium.  

 • Fixed disfigurement in perfusion shows myocardial infarction while the reversible disfigurement indicates myocardial ischemia.  

• originally the radioisotope is fitted during exercise, surveying blights indicate zones of ischemia or hypoperfusion if the myocardium is feasible( i.e. no infarction). 

•Now the checkup is performed latterly during rest, stuffing of these blights indicates a reversible ischemia and if the blights persist indeed at rest it means these are infracted areas. overlook charges are aboutRs. 3000. Advanced rates in private sector.   

Technetium-99- labeled sestamibi

 can be used rather of thallium if viability of myocardium is to be determined.  


 Thallium scanning is indicated :

•When resting ECG makes an exercise ECG delicate to interpret(e.g. due to LBBB). 

•In cases to descry myocardial infarction in whom exercise testing( ETT) isn't individual(eg. positive test in asymptomatic cases), or isn't allowede.g. in pack branch block, left ventricular hypertrophy or case taking digitalis.   

•To localize the region of ischemia. 

•To distinguish ischemic from infrared myocardium.   

  MUGA SCAN( Blood pool scanning)   

This isotope is fitted IV that mixes with circulating blood. The gamma camera detects the quantum of isotope- emitting blood in the heart at different phases of cardiac cyclee systole and diastole.

Clinical uses:

•MUGA scan is used for detection pf ventricular aneurysm.

•Left and right ventricular ejection fraction can be measured accuractaly. Ejection fraction indication ventricular function.


is the preface of a catheter into the rotation.  

•Right heart is catheterized by introducing the catheter into a supplemental tone( generally the right femoral tone) and advancing it to the right patio and right ventricle into the pulmonary roadway. The pressures in the right heart chambers and pulmonary roadway can be measured directly.   

•Left heart catheterization is generally performed via the right femoral roadway, catheter enters the left ventricle where pressures are attained, color is fitted for ventriculography to assess left ventricular function. Coronary angiography is performed by using especially designed right and left coronary roadway catheters.   During cardiac catheterization blood samples are withdrawn to measure attention of ischemic metabolites(e.g lactate) and oxygen to quantify intracardiac shunts. This invasive procedure by using catheter gives the following information.   

• dimension of pressure in different chambers of heart.

• Blood oxygen content or achromatism in different chambers.   

• dimension of cardiac affair. 

  Clinical Uses:

  1. Identification of coronary roadway complaint and assessment of its extent. Coronary spasm and thrombosis. 

  2. Left ventricular dysfunction and ischemic mitral regurgitation. 

3. Angiography and angioplasty for acute coronary pattern.   

4. To rule out ischemic cause of cardiomyopathy.

 5. To separate restrictive cardiomyopathy from constrictive pericarditis. 6. To assess extent and severityof stopcock complaint .  

7. For assessment of left and right ventricular function( abnormality similar as heart failure). 

  8. It detects atrial and ventricular septal blights. It's performed before surgical correction of natural heart complaint.


 Coronary angiography is performed during cardiac catheterization. It's the visualization byx-ray discrepancy material( color) fitted into the highways. Coronary angiography is performed by preface of catheter from femoral roadway, which is guided under radiological control( fluoroscope) to the left and right coronary highways and left ventricle. Differ medium is fitted white videotape images of the recordings are made( on CD). 

 Clinical uses:

 It detects and estimates the inflexibility of coronary roadway stenosis, thus revascularization can be performed with by- pass operation or angioplasty. suggestions Angiography is veritably generally performed procedure now a days. Medical scholars and croakers of other specialties must know the proper suggestions of angiography thus they can guide and counsel their cases confidently. suggestions are given below according to the clinical situations.

 1. Asymptomatic patient:  

substantiation of high threat on noninvasive testing( EGG, ETT, Thallium checkup, Echo).

 2. Nonspecific or atypical chest pain:

 opinion of ischemic heart complaint is made confidently in maturity of cases withnon-invasive testing. Angiography should be performed only if there are high- threat findings on noninvasive testing.

 3. Stable angina:

 substantiation of high threat on noninvasive testing or pain not relieved by medical treatment. 

 4. Unstable angina :

high or moderate threat cases refractory to original acceptable medical treatment or intermittent symptoms after original stabilization.

 5. After angioplasty:

 suspected abrupt check or subacute stent thrombosis after angioplasty or intermittent angina or high threat criteria on non- invasive testing within 9 months of angioplasty and 12 months of bypass operation.

 6. After myocardial infarction:

 as an volition to thrombolytic remedy within 12 hours of onset of symptoms.

 7. Perioperative evaluation beforenon-cardiac surgery :

in cases with suspected or known coronary roadway complaint.

 8. Before valve surgery:

 in grown-ups to rule out coronary roadway complaint, as the bypass grafting is possible in the same operation. Heart failure cases with heart failure having angina or substantiation of ischemia on noninvasive

 9. Heart failure:

Patient with heart failure having angina or evidence of ichemia on noninvasive testing.


 Syncope is a sudden loss of consciousness resulting from inadequate blood flow to the brain. When an individual experiences dizziness, it is referred to as presyncope, whereas blackout refers to a sudden loss of consciousness. The most common types of syncope include vasovagal syncope, postural syncope, medication-induced syncope, and cardiac syncope.


•Vasovagal syncope is caused by excessive vagal activation and decreased venous return. This is often triggered by prolonged standing, large meals, stressful or painful stimuli such as fear, pain, unpleasant sights, prostration, hot environments.

•It occurs due to a reduction in venous return to the heart, while the sympathetic nervous system is simultaneously inhibited.

Stimulation resulting in vigorous compression of the fairly under-filled ventricles, leading to kickback through the stimulation of ventricular mechano-receptors, can activate the parasympathetic (vagal) system and cause sympathetic pullout, resulting in bradycardia, vasodilation, or both. Variants of vasovagal blackout, such as cough blackout and micturition blackout, exist. Symptoms of vasovagal blackout include pallor, slow palpitation, low blood pressure, and dilated pupils. 


The head-up tilt test is a diagnostic test for vasovagal blackout. During this test, the patient is asked to lie on a table that is tilted at an angle of 70° for over 45 minutes while their ECG and blood pressure are monitored. A positive test is indicated by significant bradycardia or potentially hypotension. 


•Treatment for vasovagal blackout includes the use of beta-blockers to inhibit the initial sympathetic activation.

• Binary chamber pacing may be necessary if bradycardia is predominant.


Postural blackout is a medical condition that arises due to the failure of the normal compensatory mechanism of baroreceptors. These receptors are responsible for regulating heart rate and supplemental resistance in response to changes in posture. When the supplemental resistance drops, it causes vasodilatation and leads to hypotension, which is commonly known as postural hypotension. A decline in systolic pressure of more than 10 mm Hg immediately upon rising from a supine to standing position is indicative of postural hypotension. This sudden drop in blood pressure reduces cerebral blood inflow, resulting in blackout. Postural blackout is a frequent cause of outpatient department visits by patients taking ACE inhibitors and diuretics. 

Predisposing factors 

Several factors can contribute to the development of postural blackout, including 

•old age

•Parkinson's disease

•diabetes, and other cases with autonomic neuropathy. 

•Blood loss or hypovolemia, as well as the use of certain medications such as vasodilators, antidepressants, beta-blockers, and diuretics, can also increase the risk of postural blackout.


•The recommended course of action is to withdraw or reduce the dose of the responsible drug.
 •Additionally, patients should be advised to wear elastic stockings and to get up slowly from the bed.
• In some cases, NSAIDs and fludrocortisone may be required.


 is a condition that results from profound hypotension due to a combination of a reduction in cardiac output and a drop in peripheral vascular arrhythmia. 

The causes of this condition include.

•ventricular tachycardia
•supraventricular tachycardia.

•sick sinus syndrome
•heart block.

 Mechanical obstruction
•myocardial infarction
• aortic or pulmonary stenosis
• pulmonary hypertension or embolism
• atrial myxoma or thrombus
•hypertrophic obstructive cardiomyopathy
• Fallot's tetralogy
 • stuck-up prosthetic valve.


Specifically pedal and holy edema in cardiac patients, is a result of heart failure, typically due to right or combined right and left heart failure, leading to fluid and water retention. Other cardiovascular causes of edema include constrictive pericarditis and cardiomyopathy. Additionally, calcium channel blockers have been known to produce pedal edema. Non-cardiac causes of edema include supplemental venous insufficiency, venous inhibition, nephrotic pattern, cirrhosis, or idiopathic factors.


 •cardiac failure, right heart failure, constrictive pericarditis, and cardiomyopathy. 

•Other causes include habitual venous insufficiency (such as varicose veins),


-nephrotic syndrome

-liver cirrhosis

- protein-losing enteropathy


-Retaining Sodium(such as non-steroidal anti-inflammatory drugs [NSAIDs]

 -Increase capillary permeability, e.g. nifedipine and amlodipine)

•idiopathic factors (more common in women than men).

• Habitual lymphatic inhibition may also contribute to edema.

Cardiovascular Disease

-Common cardiovascular symptoms

-chest pain



-peripheral edema


-investigation of cardiovascular system

-cardic failure

-acute pulmonary edema

-cardiogenic shock

Systemic hypertension

-ischemic heaet disease(IHD)

-angina pectoris 

-unstable angina and ACS

-myocardial infarction (MI)

-rheumatic fever 

-infective endocarditis

-examination of cardiovascular system

-mitral stenosis

-mitral regurgitation

-mitral valve prolapse

-Aortic stenosis

-aortic regurgitation

-tricuspid regurgitation

-pulmonary stenosis

-pulmonary regurgitation

-congential heart disease

-ventricular septal defect(VSD)

-atrial septal defect(ASD)

-patent ductus arteriosus (PDA)

-coarctation of aorta

-fallot's tetralogy

-transposition of great vessel (TGT)

-pulmonary hypertension

-cor pulmonale

-acute myocarditis


-acute pericarditis

-constrictive pericarditis

-atrial myxoma

-acute circulatory failure (shock)

-aortic aneurysm

-cardic procedures

-heart transplanation

-cardic arrhythmias

-sick sinus syndrome

-heart block

-bundle branch block 

-supraventricular tachycarida

-wolff-parkinson-white syndrome

-atrial flutter

-atrial fibrillation

-venticular tachycardia

-ventricular fibrillation

-cardiopulmonary resuscitation (CPR)


 Dyspnea or Windedness (Wail) is an unusual attention to breath. Dyspnea in coronary illness is hastened or exacerbated by effort yet may happen very still. It results from raised left atrial and pneumonic venous tensions or hypoxia, because of left ventricular systolic or diastolic brokenness or valvular hindrance.

Dyspnea or Windedness (Wail) is an unusual attention to breath. Dyspnea in coronary illness is hastened or exacerbated by effort yet may happen very still. It results from raised left atrial and pneumonic venous tensions or hypoxia, because of left ventricular systolic or diastolic brokenness or valvular hindrance

Grading of dyspnea

The New York Heart Affiliation has reviewed dyspnea going from grade 1-4. Continuously portray dyspnea with evaluating on the grounds that it shows practical class of patient and seriousness of the illness. Continuously depict dyspnea with NYH reviewing.

The New York Heart Affiliation practical and helpful arrangement applied to dyspnea.

Grade 1 No breathlessness

Grade 2 Breathlessness on severe exertion. Grade 3 Breathlessness on mild exertion

Grade 4 Breathlessness at rest.

Types of cardiac dyspnea

Acute pulmonary edema

Angina equivalent Chronic heart failure

Acute pulmonary edema Acute pulmonary edema develops from a major event such as acute myocardial infarction in previously healthy heart or minor event such as atrial fibrillation in a previously diseased heart.Patient out of nowhere creates windedness, pain, unsettling and cyanosis with hacking and wheezing. Sputum may be profuse, frothy and blood-streaked or pink. Heart auscultation reveals crepitations and rhonchi.

Angina equivalent

When shortness of breath is the dominant or sole feature of myocardial ischemia instead of chest pain, this is called angina equivalent.  A few patients particularly elderly folks individuals present ischemia with windedness without highlights of pneumonic edema(no prominent crepitation). ECG shows ST changes and treatment of angina relieves shortness of breath even without diuretics.

Chronic heart failure

 Orthopnea is dyspnea that occurs during

supine position (recumbency) as a result from increase in venous return. Paroxysmal Nocturnal Dyspnea (PND) is the shortness of breath that occurs abruptly 30 minutes to 2 hours after going to bed and is relieved by sitting up or standing up.


Palpitation is a disagreeable familiarity with the intense or fast pulsating of the heart. Patients describe it as pounding, jumping, racing or irregularity of heart beat. Palpitation can develop by change in heart rate, rhythm, ectopic beats, compensatory pauses, augmented stroke volume due to valvular regurgitation, high cardiac output states, all forms of tachycardia and sudden bradycardia.

Sinus tachycardia may be due to anxiety, anemia, fever or drugs etc while the paroxysmal tachycardia is usually due to SVT, atrial flutter or fibrillation. At the point when palpitation starts and finishes suddenly it is frequently because of a paroxysmal arrhythmia while the continuous beginning and discontinuance of assault propose sinus tachycardia or uneasiness state.

Palpitation = slow, fast or irregular rhythm

Untimely (ectopic) thumps Repetitive however fleeting episodes of a sporadic heart beat are as a rule due to atrial or ventricular ectopic beats. Patients depict it as a dropped beat on the grounds that the untimely beat is trailed by a delay previously the following ordinary beat which is more powerful as a result of longer diastolic filling period. Most of the time it is related to anxiety and aggravated by chocolate and excessive intake of tea.

Paroxysmal tachycardia

Bouts of very rapid heart beat (120/min) starting abruptly and terminating suddenly result from paroxysmal supraventricular (átrial or junctional) tachycardia or ventricular tachycardia. Paroxysmal supraventricular tachycardia (SV) and paroxysmal atrial fibrillation are common causes.

A few patients feel tachycardia on remaining from sitting position related with a gentle drop in pulse and side effects of dazedness.

These patients have a form of autonomic dysfunction termed the postural orthostatic tachycardia syndrome (POTS).Paroxysm of tachycardia especially

when prolonged may be associated with syncope, presyncope, dyspnea or chest pain. In patient's evaluation and diagnosis, measure blood pressure, check pulse and perform an ECG.

Consolation, aversion of stress, espresso and treatment with beta-blockers are generally sufficient to control the side effects.


Albeit by and large palpitation implies tachycardia, here and there patients of heart block and bradycardia additionally grumble of palpitation.

Ghabrahat is very commonly used Urdu term that patients describe for restlessness and in majority of cases due to tachycardia, sometimes due to bradycardia or irregular rhythm.

Chest pain

 Chest pain is of the most important one emergencies; therefore it is necessary to evaluate chest pain thoroughly. It could be as serious as myocardial infarction (MI) or just muscular pain. Continuously think first and preclude hazardous circumstances like myocardial localized necrosis, aortic analyzation, pneumonic embolism and pneumothorax. History is vital, find out if it is intense and continuous torment, intermittent or roundabout agony, or tireless agony in any event, for a really long time.



Coronary corridor sickness like angina, MI Aortic stenosis Pericarditis Hypertrophic cardiomyopathy.


Pulmonary embolism Aortic dissection.



Pneumonia Pneumothorax


Reflux esophagitis Esophageal spasm Peptic ulcer.


Cervical disc disease Arthritis of shoulder or spine Costochondritis.


Disorders of breast Herpes Zoster Emotional.


Angina means discomfort. Angina pectoris is generally depicted as greatness, tension, pressing or vibe of tightening in the chest, yet it could be portrayed as hurting or copying torment, trouble in breathing or even a heartburn (gas inconvenience). To take great history you ought to realize the distinction among steady and temperamental angina.

Anginal chest pain may be typical or atypical.

Typical chest pain

Typical pain of stable angina is the pain that develops gradually during exertion, after meal, with anger, excitement, frustration and other emotional states; it is not precipitated by coughing, respiratory movements or change in position.Anginal pain typically resolves within 5 to 30 minutes. More delayed torment addresses myocardial ischemia while more drawn out torment without proof of myocardial ischemia proposes a non-cardiovascular aggravation.Anginal torment vanishes for the most part after rest or in somewhere around 5 minutes when sublingual nitroglycerine (Angised) is utilized.Angina regularly happens in retrosternal area, anteriorly across the midthorax. It might emanate to or seldom happen alone in the interscapular area, arms, shoulders, teeth, or mid-region.This multitude of highlights of agony address ischemic torment because of stable angina, while the aggravation of unsteady angina happens very still, might be abnormal and less receptive to nitroglycerine.

Atypical chest pain

Abnormal chest agony might be because of ischemic coronary illness (particularly shaky angina) but it is doubtful to be cardiovascular in beginning. Abnormal chest torment might present as following:

Sharp or blade like agony welcomed on by respiratory developments or hack (pleuritic torment).Torment that has essential area of uneasiness in the middle or lower abdominal region.Torment that might be restricted at the tip of one finger, especially over the left ventricular pinnacle.
Pain produced with movement or palpation of the chest wall or arms.
Constant pain that persists for many hours. 
seconds or less.
Pain that radiates into the lower extremities.


Agony of myocardial dead tissue is like angina in dissemination however it is of longer term and is normally of more noteworthy power. In contrast to stable angina it is not relieved by rest or sublingual nitroglycerine. It may be  went with by nausea, perspiration and hypotension.

Diagnosis and plan of management

History: History is vital, get some information about risk factors for MI like hypertension, smoking, diabetes, dyslipidemia and strong family tendency. Decide whether the pain is typical or atypical, acute ongoing pain, recurrent or persistent pain. 
• Examination is usually unremarkable.

⚫ ECG: ST depression or elevation.

In the event that clinical doubt of myocardial ischemia is solid and ECG is typical, save the patient in perception for 6-12 hours, perform sequential ECGs and actually look at cardiovascular chemicals. After this period further cardiac testing with ETT, or thallium scan helps in making the diagnosis.

Following investigations may be considered to identify the cause of chest pain depending on clinical assessment;


Cardiac enzymes (CK-MB, Troponin Troponin I)


X-ray chest.

X-rays of spine, shoulder or rib

Echocardiogram CT chest

Upper Gl endoscopy

Always rule out life threatening conditions such.As myocardial infarction, aortic dissection, pulmonary embolism and pheumothorax.

History is very important, ask him/her risk factors for MI such as hypertension. smoking, diabetes, dyslipidemia and strong family tendency. Decide the pain is typical or atypical. For aspiratory embolism get some information about delayed bed rest, DVT.Use of oral contraceptives and valvular heart disease. History of heartburn and food regurgitation may indicate reflux esophagitis. Ask about any emotional problem. Sudden chest pain with shortness of breath, especially in patients of asthma, tuberculosis and COPD may indicate pneumothorax. While looking at the patient auscultation of lung and heart may be helpful. Local tenderness indicates musculoskeletal disorder.


Visceral pericardium and most of the parietal pericardium is insensitive to pain, therefore pain associated with pericardium is believed to be due to inflammation of adjacent parietal pleura. Torment because of non-irresistible causes, for example, MI or uremia is gentle while irresistible pericarditis makes more serious agony due spread of disease to the adjoining pleura.

Torment because of pericarditis might be felt at the tip of the shoulder, neck, foremost chest, upper

abdomen or back.

Pericardial pain is aggravated by cough and deep inspiration because of pleural irritation, change in posture and swallowing. It becomes sharper and more left-sided in supine position and milder when patient sits upright and leans forward.

In some patients pericardial pain is steady retrostenal discomfort mimicking the pain of myocardial infarction. 


Localized necrosis of a portion of lung that is nearby the pleura generally disturbs pleural surface and causes chest inconvenience, it might look like the torment of myocardial dead tissue.




Esophageal fit because of reflux esophagitis causes crushing torment that copies agony of MI. It may have similar pattern of distribution. History of heartburn and food regurgitation are important clues. Various youngsters come to cardiovascular crisis with chest torment that is typically because of esophageal fit as consequence of eating groundnut as sweat supari, container or gutca. We can petition God to save our kids as the public authority isn't intrigued to stop such wellbeing killing business.



Confined delicacy is normal. Agony might be sharp, going on for few moments or it could be dull that continues for quite a long time or even days. Torment is variable in site and power; there is no unmistakable example. It might fluctuate with stance or development: however doesn't stop right away on rest. Torment due to cervical spondylosis is extremely normal. Neighborhood delicacy over rib or costal ligament is usually present.


Hypertension and Marfan's disorder are the most well-known inclining factors. Patient is normally old giving serious tearing chest torment transmitting to interscapular locale, not answering enemy of anginal treatment. Pulse may be unequal. Features of cardiac temponad or acute aortic regurgitation may be present. Chest x-ray may show wide mediastinum. Transesophageal echocardiogram (TEE), CT or MRI are helpful in diagnosis.


Profound problems might cause chest uneasiness as chest snugness, going on for thirty minutes or more that is inconsequential to effort. It could be sharp and exceptionally short and situated close to the left areola. This type of pain is also called "precordial catch" effort syndrome or Da Costa's syndrome". Emotional strain may be evident or not. This kind of aggravation is normal in females of our general public. Anyway keep in mind the youthful populace since this chest torment might be a genuine issue because of mitral valve prolapse (MVP), aortic stenosis or hypertrophic cardiomyopathy.

Thusly generally preclude all prospects prior to proclaiming torment because of profound unsettling influence, insanity or malingering.

Blood and Blood Products




Red Cells-Erythrocytes

White Cells - Leukocytes - Granulocytes, Monocytes, Lymphocytes


Plasma Contains Water 91%

Plasma Proteins. Albumin 4.5g/100ml

Globulins 2.7g/100ml

Clotting factors- prothrombin & Fibrinogen

Electrolytes 0.9% Na, Cl, K, etc

Serum-Plasma - clotting factors



Erythrocyte, leukocyte and platelet formation occurs mainly bone marrow of axial skeleton.

Foctus :

erythropoiesis also occurs in liver, kidney and spleen.

Granulocytes, monocytes and some lymphocytes also produced in the bone. Lymphocytes may also be produced in the lymphoid tissue such as thymusand spleen.

Red cell mass maintained within normal limits by hormone erythropoietin Erythropoietin is a glycoprotein, produced mainly in the kidney as a response to cellular hypoxia - explains the mechanism of anaemia in patients with renal failure Many factors are required for normal RBC formation

Iron 100ml of blood requires 50mg of iron for daily requirements men 5mg,women 10mg

Vitamin B12 absorbed in combination with Intrinsic factor (secreted by the stomach)

Folic Acid - important for RBC maturation.


Administered as units ie. the quantity taken at one time from a donor, volume is altered by the processing.volume is altered by the processing WHOLE BLOOD

Volume 405-495 ml in container with anticoagulant 63-75 ml / Dextrose -life 28 days.

ACD Adenine/Citrate CPD-life 28 days.

CPDA Citrate / Phosphate / Dextrose /Adenine - life 35 days.

Whole blood contains all the cellular and plasma constituents of blood, subject to changes on storage, except in ionized calcium which is precipitated by the citric acid contained in the anticoagulants


Whole blood less than 24hrs old and still contains the clotting factors and

viable platelets, reserved for transfusion of neonates and occasionally following cardiac surgery.


Used for patients requiring replacement of RBC and circulating volume ie bleeding. Stored whole blood may have poor haemostatic properties and fresh frozen plasma and platelets may have to be given.


Red cells obtained by removing 200-250ml of plasma by centrifuge Often labeled plasma reduced blood Plasma obtained used in the manufacture of various blood products Packed cells are used to restore red cell mass in anaemic patients who do not require an increase in circulating volume.

 In practice all blood is to some extent plasma reduced as small volumes are removed which is use in the production of Cryoprecipitate Platelets are also often removed.


Red cells suspended in a protein poor solution.

Obtained by centrifugation of a unit of blood, removal of platelets and addition of 100ml of O.A.S.- Sodium Chloride,Adnine and Manitol. The resulting cell suspension has low viscosity allowing fast administration  and has shelf life of 5 weeks.

Produces a large amount of plasma for blood products Contraindications: Not recommended for open heart surgery.

Not for neonates or infants.

Not for patients with anaemia & low platelets ie liver, renal disease and burns.


Most demand for Human Albumin Solution, Plasma Protein Fraction,

Factor V111 & Platelets From every six units it is possible to obtain:

6 units red cell concentrate

6 platelet concentrates

6 cryoprecipitate (factor 8 for clotting)

2 vials Tactor IX concentrate

2 400ml bottles of PPF

8 for clating

7 vials of normal immunoglobulin


Protein solutions containing predominantly Albumin prepared by fractioning large pools of plasma.

Two types available - PPF & Human Albumin Solution Both have purity of 95% PPF 90% Albumin, also contains 160mmol sodium usually in 400mb bottles.

PPF is used to replace plasma proteins in patients who have impaired synthesis and for expansion of plasma volume . Human Albumin Solution 'salt poor albumin is a solution containing 29g A albumin, 130mmol sodium. It comes in 100ml bottles Used for severe low protein in acute nephrotic syndrome or with liver disease.

Albumin solutions are expensive and products are in short supply, should not be used to correct low protein from malnutrition.

For many patients synthetic expanders are more economical.


For clinical use it is separated from single units of blood and rapidly frozen

- within 6 hours of donation FFP is ABO &Rh group specific and is stored at -30 degrees centigrade, has a shelf life of 1 year Thawed before use at 37 degrees centigrade.

Indications for use

1. Replacement of clotting factors following DIC (factor eight), Liver disease, deficiency of vitamin K dependent on clotting factors, overdose of oral anticoagulants (warfarin), massive transfusion of stored blood 2. In treatment of diseases such as haemophilia when specific preparations are not available ic. factor eight

3. To replace other plasma constitutes such as Fibronectin (în septicaemia and delayed wound healing)


A plasma component containing factor eight and fibrinogen, obtained from a single donation of fresh plasma by rapid freezing within 6 hours of collection This frozen plasma is subsequently thawed at 4-8 degrees centigrade and 20ml of supernatant is removed, this is then refrozen and stored for up to one year at -30 degrees


Treatment and prevention of bleeding in haemophilia and Von Willebrands disease

Treatment of factor eight deficiency following massive blood transfusion In treatment of intractable bleeding in uraemia and some platelet function disorders.


Factor VI11 concentrate - Hemophilia A Factor IX concentrate - Hemophilia B
Both prepared from large pools of plasma by fractionation, stored at a freeze dried preparation for reconstitution with sterile water.


Advances in cytotoxic chemotherapy have increased the demand for platelet transfusion. Platelets are ideally prepared from blood which is less than 24hours old - in practice blood up to 72 hours old is used Wide variety of platelets available, differences arise in methods of separation.

Platelets may be harvested from single units or a pool of 4-6 units Once harvested life is 5-7 days

Transfusion is normally by special giving set There is always some contamination of platelets with donor red cells so

platelets should be ABO &Rh compatible In emergency incompatible platelets can be used HLA matching important in certain types of patients ie bone marrow

transplant or those previously sensitized as a result of repeated previous

transfusions Platelets play important role in haemostasis by forming platelet plugs and

by releasing activators in the clotting cascade Normal platelet count is 150-400

Platelet counts below 20 are associated with spontaneous bleeding Platelets are often required inpatients who are actively bleeding and have counts less than 50.
Low platelet counts - thrombocytopenia - result from: Dilution with massive blood transfusions due to low count in administered blood .
Excessive consumption as in DIC.
Hyperspleenism Liver disease.
Bone Marrow Depression following radiotherapy or cytotoxic chemotherapy



Destruction of donor cells by antibodies in the recipients plasma Usually immediate but may be delayed for 1-2 weeks when an antibody that was not present at time of transfusion develops rapidly - this only occurs in patient who has bee previously transfused

Immediate reactions are due to antibodies present at time of transfusion and should be detected by cross matching Usually due to ABO incompatibility Commonest cause of such reaction is failure of labeling or checking of the donor blood


Restlessness, breathlessness, retrosternal or anginal pain, abdominal or
lumbar pain, throbbing headache, rigors
Signs of cardio-respiratory collapse, renal failure &DIC


Stop transfusion, support circulation with plasma expanders Use of steroids and antihistamines.
Urine output maintained with diuretics and dopamine
Minor transfusion reactions:
More common
Usually present with pyrexia, nausea, diarrhoea, pains in chest and abdomen.


If mild, slowing of transfusion and use of antihistamines and paracetamol Incidence of minor reactions reduced by the use of inline filters or by using washed cell preparations



Rapidly lose ATP & 2,3-DPG. Adenine is added to transfusions to help maintain RBC ATP. Effects the ability of blood to transport oxygen Potassium leaks out of RBC, after 10 days the potassium concentrate rises to 15mmol and there is a risk of toxic hyperkalaemia following rapid massive transfusion and if serum potassium is already raised. ie renal failure

During storage red cells metabolisr ATP and produce lactic acid. The stored blood becomes progressively more acidotic - pH falls to 6.4 after 3 weeks storage. A very rapid transfusion may produce metabolic acidosis. However as each mmol of the citrate anticoagulant is metabolised 3mmol of bicarbonate are produced and a progressive metabolic alkalosis is the expected outcome.


Granulocytes begin to lose their phagocytic and bactericidal properties within 4-6 hours and are totally nonfunctional after 24 hours. They retain their ability to sensitize the recipient and may cause a febrile transfusion reaction. The incident of this is reduced by blood filters during transfusion. Some lymohocytes may remain viable for 2-3 weeks. This can be a problem in patients who have had bone marrow transplants. Blood products for these patients are irradiated to destroy these lymphocytes.


Lose their haemostatic function within 24 hours.
COAGULATION FACTORS - 11, V & V111 and to a lesser extent XI rapidly become inactive - less than 50% active within 48 - 72 hours

MICROAGGREGATES Of old platelets, WBC, Fibrin strands and cellular debris are produced during storage. These can be removed by in line filters but tend to pass through the giving set filter.

The use of blood filter is controversial, accepted indications are for cardiopulmonary bypass, when transfusions are expected to exceed 5 units, patients who receive regular transfusions or who had febrile reactions to previous transfusions.

A problem of inline filters is that packed cells do not readily pass through them and this can be a problem during rapid transfusion. Fortunately most aggregates in packed cells are removed by a standard giving set filter. In line giving sets MUST NOT BE USED for platelets as they will filter 30% of the platelets. Platelets are usually given with a special giving set. A clean conventional giving set can be used in an emergency as the normal filter will only remove 3% of the platelets.

Indication of Blood Transfusion(B.T)

-major surgery
-Road Accidents.
-Haemolytic Diseas in neborn
-Thalasemia mejor
-Alpha thalassemia
-Beta thalassemia
-Destruction of red blood cells


-Drais 1.


 -white blood
 -Pus Cells
 -iron Daficimy