LearnOnly Heart

Patent Ductus arteriosus (PDA)

2012-02-14T13:10:00.004-06:00

Ductus arteriosus closes soon after birth, because lung expands with first breath and reduce the pulmonary vascular resistance; blood is directed to lung instead of systemic circulation i.e. avoiding ductus arteriosus to descending aorta

• Functional closer of ductus occurs within 12-24 hrs (spasm)

• Anatomical closerof ductus occours by proliferation of tissue within 2 to 3 weeks

If this ductus remains open in extra uterine life i.e. even after birth then, it is called patent ductus arteriosus. Incidence 5 to 10% of all congenital heart disease excluding premature infants

Small shunts do not cause any symptoms where as big shunts may lead to heart failure in infancy

• Left atrium and ventricle ascending aorta and arch of aorta are overloaded as these are part of circuit

• Right heart is spared from the shunt circuit

Clinical feature

1) Tachycardia (increase heart rate)

2) Tachypnea increase rate of breathing

3) Peripheral pulses are bounding wide pulse pressure (systolic minus diastolic pressure)

4) Precardium (chest wall overlying heart) is hyperactive (increased pulsations)

5) Systolic thrill (palpable murmur ) is present

6) Continuous murmur (heard both during systole and diastole with same quality)classicaly described as machinery quality wellhead in left infraclavicular space (below the clavicle)

7) With development of reversal of shunt “Eisenmenger syndrome” diastolic component of continuous murmur may disappear and only systolic component is heard

8) Severity of PDA

         a) Silent PDA detected only by Echocardiography no symptoms

         b) Small continuous murmur common Qp:Qs ratio less than 1.5:1

        c) Moderate continuous murmur common Qp:Qs ration 1.5:1 to 2.2:1

        d) Large continuous murmur present Qp:Qs ratio more than 2.2:1

        e) Eisenmenger syndrome murmur absent Differential cyanosis i.e. blue discoloration of lower limbs

Preterm Babies (Born prematurely)

Birth weight less than 1500 Grams most have PDA which may be large, these babies have ventilator dependence (respiratory machine used in case respiratory failure).

Investigation

1. ECG :-

   a. Small shunt normal ECG

    b. Large shunt produce:- left atrial and left ventricle enlargement signs present i.e. wide P waves and deep     Q wave tall R wave and tall upright T waves in lead V5 and V6

2. Chest X ray

   a. Cardiomegaly is present i.e. left atrium left ventricle ascending aorta are enlarged, pulmonary vascular markings are increased i.e. plethora is present

   b. With development of reversal of shunt heart size normalizes but pulmonary artery enlarges plethora disappears

3. Echocardiography: - is important investigation to know size of ductus and also asses pulmonary artery pressure

Treatement In preterm babies

In preterm babies having large shunt with hyaline membrane disease then they can be weaned from ventilator this babies need to closer of PDA surgically to prevent ventilator dependency

In case of babies who do not have hyaline membrane disease they can be given indomethacin to enhance closer. In about 10% of babies PDA does not close by drugs then surgical ligation is advised

Treatement Fulterm babies

Large /moderate PDA with heart failure and pulmonary artery hypertension needs early closer with 3 to 6 months

Moderate PDA without heart failure closer by 6 moths, if associated , failure thrive then early closer may be done

Small PDA closer to be done at 12-18months

Silent PDA no needs to close

Mode of close

If closer of PDA is to done within 6months of life :- then surgical ligation has to be done

If closer of PDA is to done after 6months of life:- then transe catheter closer is advised i.e coil is used for PDA of diameter size less than 4 mm and Amplazter device for PDA diameter more than 4mm in diameter, If anatomy of PDA is not suitable for closer then surgical ligation

Ventricular septal defect (VSD) :hole in heart

2012-02-12T07:08:00.005-06:00

This is defect or hole in inter-ventricular septum, which separates the right and left ventricle. This leads to mixing of unoxygenated right ventricular blood with oxygenated left ventricular blood.

VSD

Normally Right ventricle pumps blood in low pressure pulmonary circulation and left ventricle pumps blood into high pressure systemic circulation.

In presence of hole or defect in inter-ventricular septum, there is shunting of blood from left ventricle into pulmonary circulation .

Right ventricle just acts as conduit for passage of blood from left ventricle to pulmonary circulation in VSD . this is because

1. Shunting of blood occurs in systole

2. Right ventricle is contracting, when blood is being shunted

3. Because of above said reason, right ventricle does not dilate or hypertrophy in uncomplicated (without Eisenmenger syndrome) and in isolated VSD

Types of VSD

Types of VSD

Classified from the right side of septum according their location at inter-ventricular septum

1. Perimembrnaous VSD (defect extending from membranous septum into surrounding septum i.e. trabacular, inlet, outlet septum)

2. Membranous (subaortic VSD)

3. Muscular VSD (trabacular VSD)

4. Supracristal ( Sub pulmonary VSD)

5. Inlet VSD (below the tricuspid valve)

6. Doubly committed VSD (both to aorta and pulmonary artery)

7. Swiss cheese type

Ventricular septal Defect vary in size.

Qp:Qs ratio:- is amount of blood flowing in right heart compared to left heart. Big shunts produce larger Qp:Qs ratio and small defects produce lesser ratio

Restrictive and nonrestrictive :Iin restrictive shunts pressure gradient is present and in nonrestrictive type there is no pressure gradient across defect. Smaller defect are restrictive and larger defects are nonrestrictive

1. Large :- ( Non restrictive) Diameter of defect equal to diameter of aortic orifice Right ventricular systolic pressure equal to left ventricle systolic pressure

2. Moderate :- (Restrictive) Diameter of defect less than aortic orifice Right ventricular systolic pressure half to two third of left ventricle systolic pressure. Qp:Qs more than 2:1

3. Small :- (Restrictive) Diameter of defect is less than one third size of aortic orifice. Right ventricular systolic normal Qp:Qs less than 2:1

Clinical features

· Small defect are asymptomatic

· Moderate to large defects present with failure thrive

· Repeated respiratory tract infections in moderate to large defects

· Large defects may present with heart failure in infancy

· Large defects may produce pulmonary hypertension may progress to reversal of shunt by age of 10 to 15 years (Eisenmenger syndrome ) patient cannot be operated if this complication occurs

· Small defects produce long and loud systolic murmur (pan systolic ) where as large defects produce short and early systolic murmur (because of fast equalization of pressure across shunt during systole)

· Signs of pulmonary hypertension may be present i.e. loud second heart sound (P2) with narrow split second heart sound

· Subaortic, doubly committed , perimembrnaous VSDs may produce aortic regurgitation

· Left atrial, left ventricle are dilated, so apex is shifted outward and down ward

· With development of pulmonary hypertension and reversal of shunt (Eisenmenger syndrome) left atrium and left ventricle regress in size, right ventricle hypertrophies and also dilate. Main pulmonary artery is also dilated

Natural history of VSD

· About 10% of large VSDs may die by the end first year because of heart failure

· 30 to 40 % of moderate to small VSDs spontaneously close by mostly by 3 to 5 years of life

· Around 25% of VSDs decrease in size

Investigation

· ECG :- small VSD ecg is normal, Moderate VSD signs of left atrial enlargement with left ventricle diastolic over load

· Echocardiography is useful for sizing typing of VSD

· Chest X ray :-

o Small VSD normal X ray.

o Cardiomegly (Enlarged heart) in moderate to large VSD but with reversal of shunt (Eisenmenger syndrome) normal sized heart with dilation of pulmonary artery

Indication and Timing for closing the VSD

1. All VSDs need not be closed

2. Presence of reversal shunt is a contraindication for closer of VSD

3. Indication of closer

a. Qp:Qs ratio more than 1.5:1

b. Symptomatic patient

c. Pulmonary artery systolic pressure more than 50mmhg

d. Increased left ventricular and left atrial size

e. Worsening Left ventricular function

f. Aortic regurgitation irrespective of size and Qp:Qs ratio

4. Timing of closer of VSD

a. In children with large VSD with heart failure not responding to medication needs closer as soon as possible

b. In children with large VSD with Pulmonary hypertension (reversible) need to be closed within 3 to 5 months

c. Moderate sized VSD with pulmonary artery systolic pressure 50-60% of systemic pressure needs closer between age of 1-2 years, earlier closer is advised if associated with episode of life threatening respiratory infection.

d. Small VSD with episode of infective endocarditis

Closer of VSD

· Surgical method is preferred method (surgical Mortality less than 1%)

· Transe catheter device method of closer is done for children weighing more than 15kgs, and for muscular VSDs

· Swiss cheese type pulomonary artery banding

Atrial septal defect (ASD) hole in heart

2012-02-11T06:11:00.002-06:00

Left and right atrium are separated by septum called Inter atrial septum, which prevents mixing of deoxygenated blood coming from systemic circulation to right atrium with oxygenated blood coming from pulmonary circulation to left atrium.

ASD is congenital heart disease, in which there is hole or defect in inter atrial septum this leads to mixing of blood at the atrial level.

Blood from left atrium moves to right atrium, this is called left to right shunting. This is because right ventricle is more complained so it distends easily as compared to left ventricle.

Right atrium is overloaded with more blood, leading distention of right atrium, right ventricle and also pulmonary artery.

This increase flow on right side of heart leads following clinical signs

· Ejection systolic murmur at pulmonary valve.

· Fixed and wide splitting of second heart sound

· Mid diastolic murmur of tricuspid valve (Larger atrial septal defect)

Incidence of Atrial septal defect

1. 5 to 10 % of all congenital heart disease, as isolated anomaly

2. More common in females (male to female ratio 1:2)

3. ASD is associated with other congenital heart disease in 30-40% of cases

Types of Atrial septal defect

I. Ostium Secundum defect, most common 50-70% of all ASDs

II. Ostium primium defect, 30% of all ASDs

III. Sinus venosus defect, 10% of all ASDs

IV. Coronary sinus defect, rare variety of ASD

Types of ASD

Electrocardiographic findings

Right axis deviation Mild Right ventricle hypertrophy with RBBB rSR’ pattern in lead V1 .

Chest X-ray

Cardiomegaly (enlarged heart), enlargement of Right atrium and ventricle and prominent pulmonary artery.

Echocardiography

This is most important investigation, which will detect ASD and helps in typing the ASD, and also gives valuable information in regard to weather given ASD needs closer by transcatheter (see below) approach or open heart surgery.

In older patients if trance thoracic imaging by Echocardiography is not proper some times, then patient may need trance esophagus echocardiographic study.

Echocardiography demonstrates

· Type of ASD

· Associated cardiac anomalies

· Size of ASD

· Rims around the defect whether they are good to hold ASD closer device

· Pulmonary artery pressure is estimated, if it is high then ASD cannot be closed.

Natural history of ASD

· Ostium secundum ASD have tendency to close by themselves

· Ostium secundum of less than 3mm in size detected within 3months after birth all of them ie 100% will close themselves within 1 and half year of age

· Ostium secundum of 3 – 8mm in size detected within 3months after birth 80% will close by themselves within one and half year of age

· Ostium secundum ASD of more than 8mm rarely close by themselves.

· Other type i.e. premium, sinus venosus type and coronary type do not close by themselves.

Symptomatic medical management

· Most children of ASD are asymptomatic

· Rarely develop heart failure in infancy

· Untreated large defect may lead to pulmonary hypertension at the age of 20 to 30 years

· ASD in adult may cause atrial fibrillation.

· No need for infective endocarditis prophylaxis

· Exercise restriction is unnecessary

Transe catheter closer of ASD

Transe catheter closer of ASD

1. What is transe cathter closer of ASD ?

a. Done for Ostium Secundum ASD

b. In this procedure chest is not opened.

c. From anterior aspect of thigh through femoral artery device is delivered at the inter atrial septum

d. Patient is discharged with one or two days after procedure

e. Device used to plug the ASD are most commonly Amplatzer, Cardio seal, Sideris buttoned device, Angel wings device

2. Transe catheter closer is indicated in

a. ASD of size more than 5mm

b. Qp to Qs ratio (blood movement in right heart verses left heart ) more then 1.5 :1 (more the ratio suggest more shunting of blood from left to right heart.

c. Heart failure present in infancy

3. Rim around the defect has to at least 4mm in size, to hold the umbrellas of device, if not this procedure cannot be done.

4. Advantages of transe catheter closer are, no scar , very little pain i.e one injection in groin, 1 to 2 day of hospital stay, rapid recovery

5. Disadvantages little more chance of minimal residual shunt, compared to open heart surgery.

6. Post procedure

a. Aspirin 81mg/day for 6months

b. Echocardiography

i. Confirm no obstruction of pulmonary veins by device

ii. Confirm no obstruction of coronary sinus

iii. Confirm free movement of tricuspid and mitral valve leaflets

Open heart surgery

1. Done only in cases where rims of ASD can not hold device

2. Other types of ASD i.e. Ostium primium, Sinus venosus, Coronary sinus type are closed by open heart sugary.

3. Complication of open heart surgery

a. Less than 0.5% mortality for open-heart surgery for ASD

b. Sick sinus syndrome following surgical closer of sinus venosus defect

c. Cardiomegaly (enlargement of heart)

d. 7% to 20% may develop atrial arrhythmias

e. Residual shunt

Heart attack in women is different from men

2012-02-08T10:16:00.002-06:00

Difference between women and men heart attack

· Incidence of heart attack in women is less than men in their young age i.e. premenopausal period and it equals men in at age of 50-60 years above 70 years it exceed men

· If women sustain heart attack, chances of survival after heart attack are less compared to men, even in young age

· Coronary vessels are less narrowed in women as compared men for same degree of symptoms

· Atypical chest pain (i.e. non classical type of pain) is common in women as compared to men leading confusion in diagnosis

· Sudden death following heart attack is more common in women then men

· Exercise stress test is less dependable in women, because it is more commonly gives false positives (i.e. even if women is not having disease exercise stress may say she has disease)

· Following MI chances of death in women more then men

· Following CABG (Cardiac bypass operation) chances of death are more common in women then men

IHD risk assessment in women (chances of having heart attack in future)

· Framingham risk score( click here) which predicts risk of heart attack for next ten years is less useful for women who are young as chances of heart attack in women increase more with age.

· Women with diabetes and smoking have higher chances of heart attack and more severe disease coarse then men with diabetes and smoking

· Women have more chances of combined dylipidemia (cholesterol involving LDL, HDL, triglyceride) then men. So difficult to treat

· Obese women have more sedentary life style then men

Diagnostic difference of heart attack in women.

· In 12 ECG QRS-T angle, QRS and QTrr duration are predictive of future heart attack

· Stress echocardiography is useful

· Multicomponent cardiac magnet resonance stress is good for diagnosing coronary lesion in women

· In women during heart attack routinely used blood biomarker to detect heart attack like CKMB, troponins are less useful. In women CRP and BNP are better.

Prevention of heart attack in women

1. life style interventions

a. cessation of smoking

b. minimum 30 to 60 minutes moderate degree of exercise (isotonic)

c. weight reduction

d. increase consumption of fruits , vegetables high fiber diet, whole grain, fish,

e. reduce intake of saturated fat acids less then 10%, and also transe fatty acids

f. reduce sodium intake (salt) less then 2.3 gram/day

2. Major risk factor reduction

a. Blood pressure should be controlled

i. Less then 140/90

ii. If associated with diabetes or kidney failure less then 130/80

b. Reduce cholesterol

i. LDL cholesterol less then 100 mg/dl click here

ii. Non HDL cholesterol less then 130 mg/dl click here

iii. In diabetes patient sugar has to controlled i.e. HbA_1c less then 7

3. Drug therapy for women with heart attack

a. Aspirin 81-325mg/dl has to be given, if intolerant to aspirin i.e. upper GI symptoms then clopedogrel has to be given

b. Beta blocker :- metaprolol

c. ACE inhibitors :-Ramipril, enalapril,

d. Statins :-atrovastatins, simvastatin, rosavastatin

e. In case associated heart failure (click here) aldosterone and ACE /ARB

f. Hormone therapy and estrogen receptor modulators, for menopausal symptoms is better avoided

Hemodynamics of left to right shunt (ASD, VSD, PDA, Endocardial cushion defect) acyanotic heart disease: for medical students

2012-02-08T10:14:00.000-06:00

In normal heart both sides of circulation are separated and there is no mixing of blood between left heart and right heart. In some patients at birth there is defect in heart either at level of atria’s or ventricles or at level of great arteries i.e. aorta and pulmonary arteries, this leads shunting of blood from high pressure left side of heart to low pressure right side of heart. This group of diseases is called “Acyanotic congenital heart diseases”.

· Defect at level of atria i.e. inter atrail septum is called atrial septal defect (ASD)

· Defect at the level of ventricle ie inter ventricular septum is called ventricular septa defect (VSD)

· At level of great arteries is called persistent ducts arteriosus (PDA)

· Endocardial cushion defect is defect at level of joining of inter atrial septum and interventricular septum (center of heart)

Acyanotic heart disease (ASD, VSD, PDA, Endocardial cushion defect)

In this group of disease direction of flow is from left to right heart so pulmonary circulation is loaded.

Quantity of shunt depends on two major factors

In fetal life pulmonary circulation has high vascular resistance this starts to decrease after birth and takes about 6 to 8 weeks

1. Small sized defect :- size of defect alone decide as the amount of leak

2. Big sized defect :- here because more loading of pulmonary circulation due large amount shunt, pulmonary vascular resistance decides the amount of shunt. At birth due to high pulmonary vascular resistance shunt is less. By 6 -8 weeks amount of shunt increases due to fall in pulmonary vascular resistance and in some can lead to heart failure in babies. in babies who survives unto teen or adult life can develop increase in pulmonary vascular resistance again (adaptive changes due to high flow) leading reversal of shunt called Eisenmenger’s syndrome

Atrial septal defect (ASD)

· Right ventricle is thinner and complained then the left ventricle. It distends in diastole much more easily then left ventricle. Although there is no pressure gradient at atrial level still shunt occurs is because of more complained right ventricle.

· Ejection systolic Murmur in ASD is produced at the pulmonary valve due excess flow but not the level of defect as there is no gradient across defect

· Right ventricle, right atrium and pulmonary artery dilate in large ASD but Left atrium and left ventricle will not dilate in ASD

· Second heart sound is wide split and fixed

· ECG shows incomplete RBBB

· In large sized ASD there can mid-diastolic murmur at tricuspid valve (not at mitral valve)

Ventricular septal defect (VSD)

· Left ventricle left atrium and main pulmonary artery dilate in large and moderate shunt.

· Unless patient develops pulmonary hypertension due to increase in pulmonary vascular resistance right ventricle will not enlarge.

· Shunt across VSD is during systole at this point of time right ventricle also contracting when blood from left ventricle is entering it so blood is pushed into pulmonary circulation directly and right ventricle is not extra loaded, so right ventricle will not enlarge, unless pulmonary hypertension develops

· If pulmonary hypertension develops, already enlarged left ventricle and left atrium will shrink in size, and right ventricle enlarges with persistent enlarged main pulmonary artery.

· Small sized defect produce loud and long mummer due maintenance of gradient across defect during complete systole, where as large defect produce short early systolic of murmur as there is equalization of gradient across defect early in systole.

Patent ductus arteriosus (PDA)

· Similar to VSD left ventricle and left atrium dilate

· Ascending aorta and arch of aorta will not dilate as shunt is distal i.e. at or post origin left subclavien artery

· In PDA there persistence of gradient across aorta and pulmonary artery both in systole and also in diastole this leads to continuous murmur both in systole and diastole

· If patient develops pulmonary hypertension then diastolic component may shorten or may even disappear

· If pulmonary hypertension develops right ventricle dilates.

· Collapsing pulse wide pulse pressure (systole minus diastolic pressure) is present in patient of PDA due gush of blood in low resistant pulmonary circulation

Endocardial cushion defect

· Defect of joining of inter atrial septum with interventricular septum

· Inter atrial septum defect produces defect called ostium primum defect

· Cleft of anterior mitral leaf let

· VSD present in complete from endocardial defect. VSD is absent in partial from i.e. only primum type of ASD present

· Due to ASD right ventricle and right atrium dilate

· Due to VSD left ventricle and left atrium dilate

· Pulmonary artery also dilate

· In some cases there is shunt from left ventricle to right atrium here shunt is always present irrespective of pulmonary vascular resistance although this is large shunt this in not “Dependent” left to right shunt

How far one can treat Hypertension without drugs: Life style modification for Hypertension

2012-02-05T03:29:00.006-06:00

Hypertension is illness, which more often needs drug therapy throughout life. Most patients do not like to take drugs for hypertension. If blood pressure is not controlled then complication secondary to hypertension are very high.

There is place for life style modification in treatement for hypertension. Life style modification alone can be used treat hypertension in less severe hypertension i.e. stage one i.e. 140-159/ 90-99 without any Comorbid conditions. If blood pressure does not normalize, then need for drug is warranted. Undue delay or postponing drug therapy, may cause complication of hypertension

Below table gives general guidelines for imitation of drug therapy in cases of hypertension. I.e. blood pressure more then 140/90.

· In general, all patients with blood pressure more then 160/90 will need drug therapy with life style modification. More so if patient is age more than 65 years.

· For patient with blood pressure between 140/90 an d 160/100 without any Comorbid conditions initially patient can be given trial of life style modification for 1 to 3 months if blood pressure does not fall below 140/90 then drug therapy is added along with lifestyle modification

· Blood pressure between 140/90 to 160/100 with Comorbid conditions, (see table below for details) starting immediate drug therapy, with life style modification, is advised.

· Whatever modality of treatment the patient is on, blood pressure check up is advised once in two to three months (Home monitoring best). If patient is on only life style modification and blood pressure rises above 140/90 then drug therapy is needed for him also.

When start drug therapy for hypertension patients
High risk :- · If any one three criteria if present, then it high risk patient · Patient needs put on drugs immediately and also life style modification started	1. Blood pressure more then 140/90mmhg with evidence of heart disease and /or diabetes with without other risk factors 2. Stage 2 hypertension i.e. Blood pressure more then 160/100 3. Blood pressure more then 140/90 with any three of these co morbid conditions. o Male age more then 55 o Female age more then 65 o Smoking o Increased cholesterol o Obesity o Target organ damage Proteinuria (protein in urine)
Medium risk :- · Life style modification for 1 to 2 months if BP still more then 140/90 then add drugs continue life style modification	· Blood pressure more then 140/90 to 160/100 (stage one) with any one of these o Male age more then 55 o Female age more then 65 o Smoking o Increased cholesterol o Obesity o Target organ damage § Proteinuria (protein in urine)
Low risk :- · Life style modification for 1 to 3 months if BP still more then 140/90 then add drugs continue life style modification	· Male age less than 55 years · Female age less than 65 years · Stage one hypertension i.e. Blood pressure between 140/90 to 160/100 · No other risk factors

For patient with Blood pressure between 130/80 to 140/90 with diabetes or target organ damage heart disease, renal failure then patient requires drug therapy along with life style modification without Comorbid conditions, only life style modification is needed.

Life style modification for hypertension

1. Weight reduction

a. If BMI is more than 25 then weight reduction is needed.

b. Android type of obesity is more dangerous then genocide type of obesity. Android obesity is obesity of upper segment of body i.e. i.e. abdomen. Gynoid obesity is obesity of lower segment of body i.e. thigh and buttocks

c. Those patient who are not obese need not reduce weight

2. DASH Diet

a. Less sodium and saturated fat with high potassium and fiber rich diet

3. Exercise

a. Brisk walking for 4 to 5 time a week for 30 to 60 minutes is advised

4. Salt restriction

a. Reduce sodium intake increase potassium intake

b. Processed food and meet contain more sodium so avoid them

c. Increase fresh vegetable, fruit which contain more potassium

5. Stop smoking

a. This is very important to reduce chances of heart attack. See Framingham risk score

6. Alcohol moderation

a. For purpose of hypertension, alcohol is better avoided. Most doctor do not permit alcohol; for hypertension but some doctor may permit this. For men 2 drinks per day is allowed and for women one drink per days is permitted.

b. One drink is defined as 12 ml of alcohol equivalent 12oz of beer or 4oz of wine, or 1.5oz of liquor.

7. Coffee

a. Reduce excess coffee i.e. 3 to 4 cups per day. Caffeine with soda is more dangerous avoid this.

8. Acupuncture has questionable benefits for reduction of blood pressure. Relaxation exercise has shown only transient improvement in blood pressure control. Some doctors have different opinion on this.

Estimating life expectancy for heart failure patients

2012-02-03T21:46:00.010-06:00

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Reynolds Risk Score :calculation for risk of heart attack in next years

2012-02-03T21:08:00.007-06:00

Hypertension (increase in Blood pressure) over view, for common person

2012-02-02T12:19:00.001-06:00

What is blood pressure expression like 140/90 mmhg meaning?

Blood pressure reaches maximum during end of systole and reaches minimum at end of diastole. This what is expressed in blood pressure recordings as two readings i.e., 140/90 mmhg where 140 mmhg is systolic pressure and 90 mmhg is diastolic pressure

Definition of hypertension

Hypertension is sustained elevation of blood pressure (unlike intermittent elevation example Exercise) more then 140 systolic and or 90 diastolic

How to stage hypertension?

· Less then 120/80 is considered normal

· BP between 120-139 /80-89 mmhg is considered Prehypertension this is time when if appropriate life style, diet weight reduction are done, patients can be prevented from going into frank hypertension.(for primary hypertension only see below)

· More then 140/90 mmhg is hypertension

JNC 7 classification of hypertension
Blood pressure classification	Systolic blood pressure mmhg	Diastolic blood pressure mmhg
Normal	Less then 120	Less then 80
Prehypertension	120-139	80-89
Stage 1 hypertension	140-159	90-99
Stage 2 hypertension	More then 160	More then 100

· Increase in blood pressure is associated increased chance of getting heart attack, brain stroke kidney failure and heart failure.

· At the same time reduction of blood pressure in patients with hypertension is associated with reduction of above problems

· With increasing age blood pressure continues increases and also chances of above said problems, with reduction of blood pressure in this aged population, there is reduction of above problems. So in aged population more blood pressure as was thought normal in past is not acceptable now.

· Isolated systolic blood pressure i.e. systolic BP more then 140 and diastolic blood pressure less then 90 in patient more then 65 also to be treated, unlike in the past this was not treated.

Hypertension is typed into

· Primary (unknown cause) most common 95% of patients, needs life long antihypertensive drugs

· Secondary hypertension 5% of patients. Here detectable cause for hypertension is present. Some of these causes can be treated completely, then patient’s hypertension may get completely cured, i.e. he or she may not need any further antihypertensive treatment, in some cases blood pressure which was resistant to drugs may come under control.

o Secondary cause of hypertension are,

§ kidney diseases (both parenchymal and vascular supply disease of Kidney i.e. renal parenchymal and Reno vascular disease)

§ Cushing syndrome (excess corticosteroids)

§ Both hyper and hypo thyroid diseases

§ Primary hyperaldosteronism

§ Pheochromocytoma

Some important terms in blood pressure.

· Blood pressure is secondary to contraction of heart, against peripheral vascular resistance.

· Difference between systolic and diastolic pressure is called, pulse pressure i.e. if BP is 140/90 then pulse pressure is 140 mmhg -9 mmhg 0 = 50 mmhg

· Mean arterial pressure is product of vascular resistance and cardiac output (amount of blood ejected in one minute by heart)

· Mean arterial pressure can also be calculated by diastolic pressure plus one of pulse pressure i.e. for BP of 140/90 mmhg pulse pressure is 50 mmhg and diastolic pressure is 90 mmhg so mean arterial pressure is 90+(50/3)=90+16.3=106.3 mmhg

high Blood pressure is secondary to contraction of heart against peripheral vascular resistance so factor which modify these can change the blood pressure

· Increase in cardiac output

o Increase in fluid content of body

§ Chronic kidney failure

§ Increase in salt content (sodium)

o Increase in heart rate

§ Thyrotoxicosis

· Increase in peripheral vascular resistance.

o Some hormones increase constriction of vessels like catecholamine, in disease Pheochromocytoma,

Why treat hypertension?

· Most patients of hypertension do not have any symptoms, so why to treat hypertension is most common reason, for patients to stop treatment.

· Hypertension is silent killer, it destroys body organ and make them fail ,i.e. heart failure, kidney failure, heart attack, brain stroke. To prevent this complication treatment of hypertension is needed.

When to suspect secondary causes of hypertension?

· 95% of patients have primary hypertension and only 5% have secondary causes of hypertension, it is important to detect secondary cause for hypertension for purpose of possible complete cure, and better control of blood pressure in some cases.

· Because of this less chances of secondary hypertension (avoid unnecessary investigation), some clinical pointers are used to investigate, patient for secondary cause of hypertension.

o Onset of hypertension less then 15 years and more then 55 years of patients (primary Hypertension usually begins in between above said group)

o Muscle weakness (decrease in potassium) , increase urination due to increase in aldosterone

o History of kidney disease in same patient and in family members

o Thinning of skin (Cushing syndrome)

o Snoring during day time

o Heat intolerance Hyperthyroidism

How to measure blood pressure?

Three blood pressure recordings are to be taken separated by two minutes with patient either sitting or supine during examinations. After standing for at least two minutes.

Investigating a patients of hypertension

· ECG /EKG to know heart attack /hypertrophy

· Sr sodium/ Sr potassium

· Blood sugar

· Some special tests directed to diagnose secondary hypertension

Treatment of hypertension

· Life style modification, smoking cessation, weight reduction, DASH diet, salt restriction,

· Anti hypertensive drugs are to use as needed. It is better use low dose of multiple drugs rather then high dose of single antihypertensive to avoid side effects of high dose, only the problem with approach is, it increase number pills patient has to take.

· Details of treatment I will discuss in next post.

2012-02-01T13:01:00.001-06:00

VC3AYYR5NRS3

Cholesterol: what is it? : LDL, HDL, Triglyceride, and VLDL: how it causes heart attack?

2012-01-29T09:04:00.006-06:00

Increased Cholesterol is important risk factor for heart attack. Cholesterol reduction is associated with positive impact in prevention of heart attack

Total Cholesterol is divided into HDL Cholesterol (good cholesterol) and non HDL cholesterol (bad cholesterol)

HDL cholesterol is good cholesterol, increase in level of HDL cholesterol prevents heart attack. Apolipoprotein A-I (ApoA1) is protein associated with HDL cholesterol

NonHDL cholesterol is bad cholesterol, increased of nonHDL cholesterol is associated with increased chance of heart attack. Non-HDL cholesterol is a group i.e. LDL cholesterol, VLDL cholesterol, triglyceride. Apolipoprotein B (Apo-B) is protein associated with all types of nonHDL Cholesterol

ApoA1 is protective and ApoB is increases risk of heart attack.

How cholesterol causes heart attack?

· Cholesterol induces atherosclerosis is (plaque formation in vessel wall of arteries) this plaques narrow the lumen of arteries. The territory supplied by this narrowed vessel suffers decrease in blood supply, leading to heart attack

· Rupture of plaque surface induces clot formation over it, which suddenly blocks complete lumen. Read this article on STEMI

· LDL Cholesterol oxidized form enters wall of vessel (sub endothelial), where in it ignites inflammation and formation of foam cells (cells rich in cholesterol), if these foam cells are not cleared by HDL cholesterol then atherosclerosis occurs

Primary goal in treating a patient for cholesterol is reducing the LDL cholesterol. Once this is done other components of cholesterol i.e increasing HDL cholesterol and triglyceride reduction (most of triglyceride are associated with VLDL) are done.

Risk factors for heart attack (CHD) in future

Cholesterol treatement differs from patient to patient depending on their risk factors for heart attack in a given patient.

1. Already known case of heart attack in the past, is major risk factor for future heart attack. This group needs very aggressive reduction of cholesterol

2. CHD risk equivalents (CHD means heart attack) , means from prevention point of view, these patients are considered as, already a patient of heart attack even if they never suffered heart attack in their past. So the treatment of cholesterol is similar to a case of heart attack in the past as above.

· Symptomatic carotid artery disease

· Peripheral arterial disease

· Abdominal aortic aneurysm.

· Diabetes mellitus

3. Other risk factors heart attack

· Cigarette smoking

· Hypertension (BP >140/90 mmHg or on antihypertensive medication)

· Low HDL cholesterol (<40 mg/dL)*

· Family history of premature CHD (CHD in male first degree relative <55 years;

· CHD in female first degree relative <65 years)

· Age (men >45 years; women >55 years)

· High LDL cholesterol (LDL level has to titrated depending on above mentioned risk factors)

Depending on number of above mentioned risk factors in a given patient treatement for LDL cholesterol varies, check table below.

10 year risk is calculated from Framingham risk score click here Click here to calculate

In treating cholesterol most important factor life style modification, i.e. as below

· Saturated fat <7% of calories, cholesterol <200 mg/day

· Consider increased viscous (soluble) fiber (10-25 g/day) and plant stanols/sterols(2g/day) as therapeutic options to enhance LDL lowering

· Weight management

· Increased physical activity.

· Drugs for cholesterol are added, depending on the above table drugs used are Statins (Lovastatin, Pravastatin, Simvastatin, Fluvastatin, Atorvastatin, Cerivastatin)

After controlling LDL cholesterol, nonHDL goals to be reached are as below

If triglycerides 200-499 mg/dL after LDL goal is reached, consider adding drug if needed to

reach non-HDL goal:

• intensify therapy with LDL-lowering drug, or

• add nicotinic acid or fibrate to further lower VLDL.

If triglycerides >500 mg/dL, first lower triglycerides to prevent pancreatitis.

• very low-fat diet (<15% of calories from fat)

• weight management and physical activity

• fibrate or nicotinic acid

• when triglycerides <500 mg/dL, turn to LDL-lowering therapy.

Treatement for HDL cholesterol (less then 40mg/dl)

· First reach LDL goal, then:
· Intensify weight management and increase physical activity
· If triglycerides 200-499 mg/dL, achieve non-HDL goal
· If triglycerides <200 mg/dL (isolated low HDL) in CHD or CHD equivalent consider nicotinic acid or fibrate.

As Apo-B is associated with bad cholesterol(nonHDL cholesterol) and ApoA is associated good cholesterol some doctor target these i.e ratio of ApoB and Apo A

Calculate your risk of getting heart attack in future ten years : Framingham risk score

2012-01-27T06:39:00.010-06:00

Pregnancy and hypertension (increased blood pressure): Gestational hypertension, preeclampsia, and eclampsia

2012-01-26T05:44:00.011-06:00

During normal pregnancy, there is fall in blood pressure towards 13th to 14th weeks of pregnancy,towards 32 weeks of pregnancy again Blood pressure normalizes

Approximately 10% of first pregnancy is complicated by hypertension, preecplasia are common in first pregnancy and twin pregnancy

Measuring blood pressure in pregnancy

· Should be done in hospital

· systolic BP more then 140 and diastolic BP more then 90 is on same arm at least two readings

· for patients systolic BP more then 140 and diastolic BP less then 90, need close monitoring

Diagnosing Confusion of pregnancy with hypertension, is whether

· A patient who is had hypertension got pregnant

· Whether this is new on set of hypertension during pregnancy

· Or preexisting hypertension got worse during pregnancy

With this background confusion, during pregnancy, is typed into

1. Chronic hypertension :- A patient who is had hypertension got pregnant

2. Gestational hypertension:-New onset of hypertension after 20weeks pregnancy without protein in the urine(proteinuria), after delivery blood pressure comes to normal, in majority of patients

3. Preeclampsia:-New onset of hypertension during pregnancy with protein in urine (proteinuria) after 20 weeks of pregnancy, after delivery blood pressure comes to normal in majority of patients

4. Preeclampsia superimposed on chronic hypertension :- A preexisting hypertension got worse during pregnancy with proteinuria

Preeclampsia

Patient with preeclampsia are prone for complication, so they need to be treated more aggressively,

Complications of preeclampsia

1. HELLP syndrome is life-threatening complication usually considered to be a variant or complication of preeclampsia usually occur during the later stages of pregnancy or sometimes after child birth "HELLP" is an abbreviation of the three main features of the syndrome

· Hemolysis ( distraction of blood cells)

· Elevated liver enzymes

· Decrease platelet count

2. Eclampsia :- convulsions, along with preeclampsia .

3. Intra cerebral hemorrhage
4. Bbaby growth may be stunted, oligo hydromnia (decrease amniotic fluid,)

Treatment of hypertension with pregnancy

· Decreases in work load, bed rest,
· For preeclampsia hospitalized bed rest

Se Severe hypertension i.e. more then 160/110 should be, treated on emergency basis, as most of these patient high chance of complication, these patient may need parental antihypertensive like Hydralazine, labetalol, injection magnesium sulphate, nitroglycerine

For patient with less severe hypetesnsion ie 140-159/ 90-110 treatment is mostly bed rest and antihypertensive ifneeded, safer drugs in this group are methyl dopa, nifdepine are given

For Eclampsia treatment of choice deliver the baby, convulsions controlled with antiepiletics

Pregnancy following cardiac surgery for valvular heart disease; for common person

2012-01-23T13:00:00.009-06:00

Surgery for valvular (Mitral valve, Aortic valve) heart disease in young female’s poses a different set of problems. As some patients who under surgery for cardiac valve need valve replacement, this replacement is either mechanical of bioprosthetic valves

Mechanical valves are more durable but need anti-coagulation where as bioprosthetic valves are less durable need no anti-coagulation.

Anticoagulation for mechanical valves has to be given life long. This is because mechanical walls tend produce clot over them, this clot can obstruct the valve leading `to heart failure

Bioprosthetic valve as they degenerate and this may need reoperation and again valve replacement usually after 10years.

During pregnancy patient with mechanical valve need anticoagulation, usually warfarin is given. This drug can induce abnormality to baby inside the womb.

A young female undergoing cardiac valve surgery needs counseling, about future implication of valve replacement. She has to make choice between mechanical valve (durable but need anti-coagulation) or bioprosthetic valve (less durable but no need of anti-coagulation)

If surgeon can get away without valve replacement, by repairing the native valve, then it is best thing to be done, but all valve anatomy are not suitable for valve repair, particularly if underlying valve damage is of Rheumatic heart disease.

In case if female patient become pregnant who has mechanical valves, then anti-coagulation treatment is as follows during pregnancy.

· Exposure to warfarin in the first 13 to 14 weeks of pregnancy, may lead to abnormality to baby inside the womb i.e bone stippling (chondrodysplasia punctata); small nose, optic atrophy (eye sight problem), and mental retardation.

· Because of above problem, Pregnancy has to be planned one, warfarin is discontinued before conception, and patient switched to Unfractionated or low molecular weight heparin and continued up to 13 to 14 weeks of pregnancy. After this period warfarin is started till 35 weeks of pregnancy, then after Unfractionated or low molecular weight heparin is restarted till delivery.

· If Unfractionated heparin is given it is either intravenously or subcutaneously injection, 2 to 4 times a day so as to maintain APTT of 2

· If low molecular weight heparin is used, it has to be given once in 12 hours subcutenous injection, so has to maintain anti–Xa at 1.0 to 1.2 unit/mL (anti- Xa àread this as anti ten a )

Potency of Unfractionated or low molecular weight heparin is less as compared to warfarin in preventing clot formation around mechanical valves.

But Unfractionated or low molecular weight heparin do not cause damage to baby in the womb

Weighing the risk of formation of clot around the mechanical valves, and benefit to baby in womb, treatment is decided

Damage to baby by warfarin is dose dependent . ie if mother is taking less then 5mg of warfarin, chances of damage to baby in womb is low.

Clot formation for mitral valve prosthesis (tilting disc) is high as compared to aortic valve

In case mother has tilting disc mitral prosthesis and dose of warfarin is less then 5mg, with atrial fibrillation some doctors give warfarin throughout pregnancy to mother. Balancing risk and benefit of clot formation and damage to baby in womb.

Mitral valve prolapse (MVP), Systolic click murmur syndrome, Barlow syndrome, Bilowing mitral cusp syndrome, Myxomatous mitral valve syndrome, floppy valve syndrome and Redundant cusp syndrome

2012-01-21T23:42:00.004-06:00

.Mitral valve anatomy

Mitral valve consist of leaflets , chordae, papillary muscles, and annulus

Leaflets :- These are shutters of valve

Chordae: - These are attachments between leaflets and papillary muscle and they restrict movement of leaflets in to atrium during systole

Papillary muscles are attached to ventricle.

Why valve prolapse in mitral valve prolapse?

Mitral valve prolapse is a disease of valve between left atrium and left ventricle. In this disease, valve leaflets which shut the valve during systole, tend to prolapse in to left atrium so the effective closer of mitral valve is not present so can cause Mitral regurgitation (leaky valve)

Mitral valve prolapse is common in young female, it can also occur even in old male patients

Mitral leaflets are large in MVP. Inter distance of Chordae is more. Leaflets tend to hood into left atrium during systole. so closer of leaflets does not occur in systole. which leads to leaky valve i.e. mitral regurgitation.

Although vast patients of Mitral valve prolapse do not have any symptoms throughout life, as this disease is more common, so it is a common reason for mitral valve surgery and infective endocarditis in united states.

Symptoms of Mitral valve

· May not have any symptoms (diagnosed by echocardiography or auscultation of heart for some other reason)

· Palpitation

· Fatigability

· Anxiety

· Syncope or presyncope

· orthostatic hypotension

· Chest pain

These patients are usually thin; blood pressure may normal or low

On auscultation with stethoscope, your doctor may hear click (non-ejection click) and murmur (late systolic murmur)

Investigation

Echocardiography is used to diagnose mitral valve prolapse.

ECG may shows T wave inversion in inferior leads may confuse with heart attack

CT scan and MRI can be used for confirmation, in cases suboptimal echocardiography

Arrhythmias with mitral valve prolapse

Premature atrial and also ventricular contraction are common

Association with Wolff-Parkinson-White syndrome, leads supraventricular tachycardia in some patients

Long QT syndrome association in some patients, can lead to ventricular tachycardia

Disease course

Most patients of mitral prolapse remain asymptomatic throughout life without any problems

Mitral valve prolapse is common in young female they have more benign coarse.

Mitral valve prolapse of old male is more prone for complication like Mitral regurgitation needing surgery.

Severe Mitral regurgitation and Infective endocarditis are common in patients who have by auscultation, murmur and clicks, less common in patients with only click

Patients of severe mitral regurgitation are prone to develop heart failure and atrial fibrillation

Some patients can develop hemiplegia (stroke)

Sudden death secondary to ventricular arrhythmia

Management and follow-up of patients

Patients with mitral regurgitation need to undergo echocardiography test, once in year to know progression of disease and patients without mitral regurgitation echocardiography, once in three to four years is needed.

If patients have palpitation, syncope or presyncope, giddiness with or without ECG/EKG showing QT prolongation, 24hour Holter monitoring and ECG stress test, is needed, to rule out arrhythmia. If arrhythmias detected, then beta-blockers are advised

Radiofrequency ablation is done for associated Wolff-Parkinson-White syndrome

For documented brain stroke Aspirin is advised

Mitral valve prolapse patient with severe mitral regurgitation are treated surgically, with mitral valve repair or mitral valve replacement.

Smoking and heart attack: risk factor for heart attack

2012-01-20T13:35:00.009-06:00

It is well known for common person, hazards of smoking in relation to lung cancer, but still some are not aware about smoking relation to heart attack. In fact this is one of the important preventable cause both for first and also subsequent heart attacks.

In united states alone smoking related 400,000 deaths occur every year. In India death due to smoking in year 2010 was 930,000

Burden of smoking worldwide is one billion

Passive smoking:- Smoke inhaled by bystander, like spouse, children, subordinate workers etc can also have heart attack.

Smoking increases chance of heart attack in does dependent manner more the person smokes, greater the chance of having heart attack.

Smoker with heart attack have increased chance of sudden death i.e. they may not reach the hospital if they had heart attack, because of increased incidence of dangerous arrhythmia leading to sudden death.

Apart from heart attack, smoking also causes other diseases of cardiovascular system

· Dilatation of aorta and prone for rupture

· Brain Stroke both ischemic and also hemorrhagic

· Gangrene of limbs (peripheral vascular diseases)

Of late women have started smoking, which was not seen in the past. They were protected from heart attack during the premenopausal period, but with smoking this protection is lost. Further if women use oral contraceptive, then things get worse.

Smoking increase blood pressure by increasing constriction of blood vessels, and accelerates plaqueing of blood vessels (atherosclerosis), by oxidizing bad cholesterol (LDL cholesterol)

Smoking cessation has very good positive impact on heart attack. This amount of of positive impact no other drug or intervention has achieved in connection heart attack. i.e 36% reduction in mortality as compared to non smokers.

Benefits of cessation of smoking starts within 15 minutes of cessation, and continues reduce risk of heart attack for 2 years, after this time, risk of heart attack in this ex-smoker is same as never smoker

Smokers paradox :-

Smoker with heart attack have relatively cleaner coronary arteries, may not need interventions. This is because these smokers with heart attack are relatively young; they do not have other Co morbid conditions. If they had not smoked at all then they would not had heart attack at all. Sad point with clean arteries in smoker who are young is, heart muscle damage. Which can lead to heart failure.

Help for cessation of smoking
Exercise daily which helps to quite smoking. People smoke because they can perform better following smoking. this is because smoking release adrenaline which improves performance, similarly exercise also releases adrenaline and improves performance without any side effects of smoking

There are nicotine replacement transdermal patches, nicotine chewing gums, along with psychiatrist help, one can quite smoking

I had heart attack (STEMI): what is my future? cardiac rehabilitation

2012-01-19T12:29:00.007-06:00

Heart attack to know what is STEMI, please read this post click here

In this article, I will explain what are dos and don’ts following heart attack (STEMI)

Patient who suffer heart attack more often go into depression, this depression further leads more complications. Today, patient of heart attack can be effectively be treated, with medical, percutaneous procedures or surgical approach if needed.

Role of family members along with treating doctor is important, in managing these patients. As depression leads to bad prognosis. Treatment of heart attack is not limited to just revascularization it extends into cardiac rehabilitation. Some hopsital do have this facility of cardiac rehabilitation

What is cardiac rehabilitation?

This means coordinated, multifaceted management deigned to optimize a cardiac patient, physical. Psychological and also social functioning in addition to slowing or even reversing progression of underlying disease of heart attack i.e. atherosclerosis

Aims of cardiac rehabilitation are

· Return the patient back to his vocational state with safe and effective manner.

· Risk factor modification

· Prevention of one more heart attack

1. Mobilization of patient following heart attack. In addition, discharge to just discharge from hospital

Unlike the few decades in the past, prolonged bed rest was advised. Now, if patient has no complications following heart attack i.e. heart failure , arrhythmias. They can be mobilized, Within 24 hours following heart attack, provided patient does not have chest pain for more than eight hours. On second day patient can sit up in the bed walk few steps just around the bed. By fourth or 5^th day patient should able walk in corridor of hospital. On 5^th day patients are usually discharged from hospital.

2. Risk factor management following heart attack

· Fasting state Cholesterol to maintained at

o LDL cholesterol <100mg/dl is OK but further reduction to <70mg/dl is very good. Treatment for LDL Cholesterol is dietery modification and Statin, unless contraindicated

o After controlling LDL cholesterol HDL cholesterol >40 mg/dl, total cholesterol <200 mg/dl, triglyceride <150mg/dl is recommended, to improve HDL cholesterol advise stop smoking, exercise, and drugs

· Hypertension treatment after heart attack

o BP of 120/80 is optimal

o BP> 130/85 and less than 140 /90 life style modification i.e. alcohol moderation, stop smoking, exercise. If renal failure or diabetes present then drug treatment is also needed

o BP >140/90 drug treatement and life style modification as above

· Diabetes management after heart attack

o HBA₁c <7 ( this test gives, mean blood sugar level of previous 120 days)

o Fasting blood sugar <100mg/dl

o With strict control of blood sugar, chances of hypoglycemia increase, patient need to educated about hypoglycemia, following exercise chances of hypoglycemia chances are more.

o If blood sugar is >300mg/dl then also, exercise has to be done with caution.

· Smoking cessation

o very important part of this cardiac rehabilitation. Complete cessation is needed,. If patient stops smoking, within two years his heart attack risk falls to level to never smoked patient .

· weight reduction :-click here

o Body mass index of 20-25 is ideal

o Waist <35 inches in men, <31inches in female

o In obese patient at least reduction of 10% of body weight leads lot benefit

o Reduce caloric intake, exercise,

o Carbohydrate 60%, fats 30% and protein 10%

· Drugs for heart attack

o Aspirin Life long

o Clopidogrel or presogrel at least for few months

o Beta blockers (metaprolol, Carvidalol) not less than 2 years can be continued indefinitely

o ACE indictors (Ramipril) continued if indefinitely if ejection fraction is less

o If patient develop cough to ACE inhibitors, then ARBs or used olmisartan, telmisaratn

o Statin (Atorvastatin, Rosavastatin) life long

o If patient shows signs of depression then antidepressants

o Omega 3 fatty acids

o Nitrates are only if chest symptoms are present or else they can be discontinued

o Anticoagulants (reduce clotting) if left ventricular cavity clot is present (every month PT INR to be checked maintain at 2 to 3, treatement for 6 months in post MI setting)

o AVOID NONSTERIODAL ANTIIMFAMMTORY DRUGS like Brufen, Diclefenac and selective COX 2 inhibitors

Fit or Faint: Funny turn, black out, giddiness, convulsions, syncope, loss of consciousness, vertigo

2012-01-14T01:56:00.002-06:00

Above terms in heading are used very frequently without clear distinction from patients. However, their distinction is useful for treatment of patient. This distinction is done from history given by the patient; investigation and clinical examination are only to confirm the diagnosis. Therefore, history given by patient is very important.

Broadly, Giddiness and blackout are terms more often described for wide spectrum of conditions like vertigo, loss of balance, even presyncope.

Syncope and faint are same. Fit and convulsions are same.

Syncope is transient loss of consciousness with loss of postural tone (all muscles of body become flaccid),

Vertigo is equated Funny turn i.e. sensation of movement, problem with inner ear, here there is no loss of conciseness. Some time loss of balance, secondary brainstem problems can give vertigo, but there will other findings like double vision, slurring of speech, difficulty in swallowing in brainstem lesions.

Distinction between faint and fit is some time challenging, even after investigations. Some point given may help in diagnosis. Most important part of distinction is, history given by the patient.

Distinction between Faint or Fit
	syncope	Convulsions or seizers
Symptoms before the event	Nausea lightheadedness, sweating	Confusion, hyperexcitabilty, noises heard
During i.e. unconscious period	Pallor	No pallor, tonic clonic movements, tongue biting, passing urine and defecation
After event	Nausea and lightheadedness present	Prolonged confusion, headache, paralysis of some body parts may be present.

Syncope is further divided into

1. vascular

2. cardiac

3. psychogenic

Vascular causes (problems from blood vessels)

· Vasovagal syncope

· Carotid body hypersensitivity

· Orthostatic hypotension

Vasovagal syncope :

Most common form of syncope, seen more common in young females and also in old age middle age this form of syncope is less common

This occurs following prolonged standing in warm environment. Pain of prick etc

Some patient develop syncope with some situation like passing urine, laughing, defecation, coughing

During event of syncope pallor with slow heart rate and hypotension are present. Most often prompt recovery is role unless patient is not able to lay down example sitting in dental chair

Treatement is to make patient lay down immediately in supine position, head of patient should be never above the level of rest of body. This done to augment flow of blood to brain with help of gravity as brain can not tolerate loss of blood supply. Within 10 seconds of cessation of blood supply to brain patient becomes unconscious. If more then 3 to 4 minutes of cessation of blood supply to brain occurs then damage to brain occurs.

“Giving supine position to all patient of loss of consciousness of any cause is very important part of treatement “

Carotid body hypersensitivity

Carotids are blood vessels, which carry blood to brain. These vessels, have pressure sensitive receptors present in the neck, which control blood pressure. They send signal to brain to either increase or decrease heart rate and for vessels to dilate or to constrict. With increase in heart rate and vasoconstriction, blood pressure increases and vasodilatation and decreased heart rate, blood pressure decreases.

Some old individuals have highly sensitive pressure receptors, even with minimal external stimulation like saving, tight collars around the neck can activate these receptors to reduce blood receptors and induce decrease blood pressure and heart rate, induce syncope

For these patient if they have predominant decrease in heart rate as manifestation of syncope, then pacemaker implantation will help them as it works on demand mode to increase the heart rate if it falls below set limit like 50/min for example.

Orthostatic hypotension

On standing from supine position, relative decrease in blood supply to brain happens, due to shift of blood to lower limb by gravity. To overcome, compensatory mechanisms work and prevent this fall in Blood pressure. In some old individuals these compensatory mechanisms is not effective.

Blood pressure fall is predominate manifestation but heart rate is does not decrease, some time increases. This happen within 3 min of standing from supine position, unlike vasovagal syncope, which happens following prolong standing, with decrease in both heart rate and blood pressure.

Causes of ineffective compensatory mechanisms are

· Diabetes which damage nerve cells

· Parkinson’s disease (rigidity of limb movement, tremors of limb due disease of the brain)

· Blood pressure controlling drug like ACE inhitors ramipril, enalapril, captopril, diuretics like frusamide, hydrchorothiazide,)

· Decrease in volume of blood, secondary to blood loss or dehydration, following loose motion and excessive vomiting.

Treatement for these patient is avoid above mentioned drugs if any. Elastic stoking to be worn to leg to decrease accumulation of blood in lower limb. Advise patients not get up suddenly from supine position.

Cardiac cause of syncope (problems from heart)

Syncope secondary to cardiac cardiac cause can secondary to arrythymic in origin or secondary to obstruction of flow of blood

Syncope of flow obstruction occur on execration example HOCM, Aortic stenosis, pulmonary embolism (clot getting plugged in pulmonary artery lead decreased blood reaching the left heart)

Arrythymic cause of syncope is secondary slow heart rate and fast heart rate

Slow heart rate disease

· sick sinus syndrome (sinus node pacemaker of heart if this stops firing impulses this leads to decreased heart rate)

· AV node block (heart block): AV node is filter present in between atria and ventricles, this is supposed to allow only required number of impulses to ventricle. Disease of this node prevents impulse reaching the ventricle, which leads to slow or absent ventricular contractions

· Fast heart rates (techycardias) these can originate from both ventricles or atria ventricular tachycardia is more dangerous than atrial ones. Syncope usually follows ventricular tachycardia, in case of atrial tachycardias rarely if syncope occurs that is only in the starting phase of atrial tachycardia then patient usually recovers although atrial tachycardia continues.

Treatement of syncope Out side hospital

· Put the patient in supine position immediately.(this is most important step of immediate treatement)

· If patient does not recover after putting in supine position within next minute then probably patient has some major issue, it is not syncope

· Check weather patient has convulsion, if yes mostly patient is not having syncope patient needs medical attention call for medical help in India some states have 108 phone number for ambulance services

· find out weather has patient cardiac arrest if yes start CPR if you are trained

· in some countries automated external defibrillator are placed in public places take use them

investigation and treatement in hospital

your doctor will ask for ECG, Echocardiography, Head up tilt test, if seizer is supeted then CT scan EEG are done

Heart murmur, sounds and cardiac cycle

2012-01-12T13:45:00.002-06:00

Heart has four chambers and four set of valves. chambers left atrium and left ventricle have valve between is called mitral valve, chambers right atrium and right ventricle have valve between them is called tricuspid valve. Left ventricle ejects blood into aorta (main vessel of systemic circulation) valve between left ventricle and aorta is called aortic valve. Right ventricle ejects blood into pulmonary trunk (vessel that carries blood to lung for oxygen loading of blood) valve between right ventricle and pulmonary trunk is called pulmonary valve

Read this post for knowing more on heart anatomy and circulation click here

Sound originating from heart i.e. First and second heart sound arises from closer of valves.

First heart sound: - closer of mitral and tricuspid valve

Second heart sound: - closer of aortic and pulmonary valve

Ventricles of heart expand to receive blood and contracts and eject blood. Contraction phase of ventricles of heart is called systole, and expansion phase of ventricles is called diastole

Systole and diastole of heart are classified for both right and left ventricular contraction and expansion, not for atrial contraction and expansion

Systole starts with first heart sound and end with second heart sound

Diastole starts with second heart sound and ends with first heart sound.

Both left and right atrial contraction occurs in last part diastole of heart (which fill the ventricle force fully, which contributes just 10% of ventricular filling)

Heart systole i.e. ventricular systole and ventricular diastole are divided into following phases

Heart or ventricular systole

1. Isovolumteric Contraction: here only pressure builds, due contraction but size of ventricle is not altered, in this phase mitral and tricuspid valve close, followed by opening of aortic and pulmonary valve.

2. Rapid ejection: - Blood is ejected in to aorta and pulmonary artery

3. Slow ejection: - blood continues to eject, but in slow phase.

Heart or ventricular diastole

1. Isovolumteric relaxation: - In this phase. Aortic and pulmonary valves close due to fall in ventricular pressure, but there is no expansion in size of ventricles.

2. Early rapid filling: Most of ventricular filling occurs in this phase and ventricles expand in this phase.

3. Slow rapid filling : Ventricular filling slows down

4. Protodiastole : No filling of ventricles, both atria and ventricle act as single column, mitral and tricuspid valves fully open

5. Atrial contraction: Atria contracts and empties, blood into ventricle.

Murmurs:

Murmurs are produced sec to increase flow through normal or secondary to normal flow through abnormal valve

Murmurs due to increased flow (functional murmur)

· Increase amount of flow is seen leaky valves i.e. regurgitant valves. Previous chamber is added with extra amount blood so in next cycle increased amount blood passes though leaky valve which produces murmurs.

· Increase flow is also seen in increased circulatory states i.e. anemia, hyperthyroidism, and some in normal person with thin chest wall.

· Shunt between left and right heart produce increase flow in valve distal to receiving chamber example atrial septal defect, ventricular septal defect, and patent ductus arteriosus.

· Murmurs of increased flow are also called functional murmurs

· Sometimes they are innocent, example thin individual

Murmurs due to abnormal valve

· Abnormal valves produce murmurs by two mechanisms, leaky valve and stenotic valve.

· Leaky valve also produce murmur in same cycle apart from increase flow as discussed above

Aortic stenosis: for common person

2012-01-10T14:22:00.004-06:00

This is a disease is of the heart. Where in outflow of left heart has obstruction to flow. Left heart contracts more forcefully, but flow of blood into circulation is less then normal, patient suffers signs decreased circulation.

Symptoms of Aortic Stenosis

Patient of aortic stenosis have long period of asymptomatic phase, may be decades, During asymptomatic period, disease progress silently once symptoms develop the downhill course is rapid i.e. angina, syncope, breathlessness develop survival of patient is 5, 3 and 2 years respectively. So only the patient of aortic stenosis need to evaluated on early stages, for effective treatment.

Grading of Aortic Stenosis

Grading the severity of Aortic Stenosis is done with echocardiography, this is important with respect to assessing the prognosis and planning the right time of intervening. As severity of stenosis, increases the difference between the pressures across the stenosis increases.

Depending on mean pressure gradient across the stenotic valve, is graded into mild (0-20 mmhg), moderate (20-40 mmhg) and severe. (40 mmhg).

Reasons for fast worsening of Aortic Stenosis

Aortic Stenosis has long latency period ie although patient is having disease it does not create problem to him for long period of time. But in patient with these following factors Aortic Stenosis worsens faster

o Older age

o Calcification of leaflet

o Smoking

o Renal failure

Timing of surgery in sever aortic stenosis patients

· As surgery of Aortic stenosis has its own risk and patient need to take anticoagulants for rest of life, timing of surgery is important. It should not be either early or too late.

· If surgery is delayed unduly then heart muscle weakens and patient develop systolic heart failure which has bad prognosis after surgery also

Patient without symptoms with aortic stenosis

· Mild to moderate aortic stenosis are advised echocardiography study once in two to three years

· Severe aortic stenosis without symptoms. Need to confirm, weather patients really have no symptoms, for this stress test advised. If they are, truly asymptomatic, then once in year echocardiography follow-up is needed

Patient with symptoms with aortic stenosis

· Patient with symptoms of sever aortic stenosis are to be operated, immediately.

· Stress should not be done if patient has symptoms.

Surgical options available for aortic stenosis

In children and young adolescents balloon dilatation of stenotic valve is done. This is done in all patients of sever aortic stenosis, unlike in old people where balloon dilatation is not possible open heart surgery and aortic valve replacement is needed, so is reserved for symptomatic severe aortic stenosis see above. These children may require open heart surgery later, after 10 to 20 years

In adults here, surgical option is aortic valve replacement (AVR) as discussed above . if patient has associated heart attack disease bypass surgery (CABG) is also done along with aortic valve replacement.

As most patient of aortic stenosis are old, they may not tolerate open heart surgery in such a situation balloon dilatation as bridging intervention is done, once general condition improves, patient has undergo open heart surgery.

TAVI (transe catheter aortic valve replacement) is newer technique can be done. Like angioplasty wire and catheter is passed through the thigh to heart and aortic valve is replaced without opening chest.

This is indicated in patient who are very much sick for aortic valve replacement open heart surgery, as on date.

Heart and circulation over view anatomy and physiology for common person

2012-01-09T12:56:00.001-06:00

Heart is like pump, made up muscle, receives blood and pumps into circulation, so blood is always in flow. By creating continuous moving column of blood, transportation of oxygen and nutrients is made possible for body tissues. Blood gets oxygenated in lungs. Body needs continues supply of oxygen for survival if circulation is stopped then part of body in which circulation has stopped dies

Left and Right heart

Heart is compartmentalized in to left and right heart i.e. there is no direct connection between left and right heart. Right heart pumps blood to lung, from lung blood reaches left heart, from left heart blood is pumped into rest of the body. Blood from rest of the body reaches right heart with systemic veins. This is how left and right heart is in series connection, although heart is compartmentalized into left and right and no direct connection is present in between left and right heart

What are arteries and veins?

Arteries are vessels which arise from heart which carry the blood away from heart. For right heart they carry blood from heart to lung and for left heart to rest of body.

Veins are vessel which carries blood towards heart. Pulmonary veins carry blood from lung to left heart rest of the veins i.e. systemic veins, carry blood to right heart

What are valves of heart ?

Left and right heart two chambers each, upper chambers are meant to receive the blood i.e. atria and lower chamber i.e. ventricle are meant to pump blood to respective circulation.

What are atria and ventricle?

Chambers of heart are guarded by valves, which allow one way moment of blood i.e. from atria to ventricle and from ventricles into circulation. valves prevents backward moment of blood..

Veins connecting to atria, do not have valves so backward movement from atria to veins is possible.

Blood supply to heart, coronary vessels

Although heart has blood in it’s cavity it derives it share of blood not from cavity but from separate vessels known as coronary vessels, which like other vessel of body arise from arise from aorta (main trunk of systemic vessels)

There are two coronary arteries, left and right coronary arteries

Electrical activity and conduction and conduction of impulse in heart

Heart has its own pacemaker i.e. it contracts secondary impulse arising from this pacemaker.

Normal pacemaker is situated in upper part of right atrium, it is called sinus node, from here impulse travels all over the atria and reaches ventricle. There is gate between atria and ventricle called AV node, this gate prevents access impulses reaching ventricle from atria.

Disease of heart

· Muscle of heart can be damaged, due to infection, toxin like alcohol, heart attack

· Valves of heart can become stenotic or leaky secondary to rheumatic heart disease, senile calcification, infection etc

· Electrical activity problems, like sinus node may fail produce impulse, or AV node may not conduct impulse to ventricle completely or partially, it leads to slow heart rate, increased production of impulse can lead fast heart rate.

I get breathless; problem is in the heart or lung

2012-01-08T12:27:00.000-06:00

Breathlessness or dyspnea is a common symptom. Causes of breathlessness can be from problem with heart or lung. This distinction is important for doctor and also for patient .For patient this is important because next time when he get breathless it will guide him weather to approach a cardiologist (heart specialist) or pulamnologist (lung specialist) as some time patients are serious and time for treatment is very less.

Even to doctors to know weather breathless patient, is having problem in the heart or in the lung some times is difficult, more so if the patient has come to emergency room. Where in doctor has to decide between the two, within very short period of time. If previous history details are available, it gets easier to treat the patient effectively.

Below are few symptoms and signs, which may guide both doctor and also patient know where is problem, heart or lung.

Weather breathlessness or fatigability

Relatively one more common symptom is weakness or easy fatigability, some times, patients confuse this with breathlessness in non-emergency situation. Weakness complaint is more associated with heart problem then lung problem. So proper distinction between breathlessness and fatigability is important.

Cough and sputum

Generally, basic difference with lung and heart problem is, lung diseased patient have predominate cough with sputum along with breathlessness, where as patients of heart problem have less amount of cough associated with breathlessness.

Sputum associated with heart disease is usually white in color or some time blood sting rarely yellow in color. Where as that of lung disease is may be yellow, white or bloody.

These are not a rule; some times things may be reverse. To confuse further some patient, may have both lung and heart disease together, in such a patient, in given episode, which is predominate problem, has to be decided carefully,

Orthopnea:-

Orthopnea means after lying done immediately patient gets breathless, patient is comfortable while sitting, this can be present in both lung and cardiac disease

Paroxysmal nocturnal dyspnea:-

Here patients after sleeping for two to three hours, becomes suddenly (unlike immediate breathlessness in Orthopnea) breathless i.e. air hunger, he is made get from bed, sits for 15 to 30 minutes, then patients breathlessness is relived. This kind breathlessness is strongly suggestive of cardiac cause of breathlessness.

Wheeze or crepts:

Wheeze is sound which is high pitched musical in quality more common with lung disease where has crepts are crackling sounds which are heard both in lung and heart diseases

Pedal edema:

Pedal edema is due to many reasons apart from heart and lung diseases i.e. Just prolonged standing, varicose veins etc can lead to pedal edema

In connection to heart this is sign of right heart failure, a patient of lung disease may also develop right heart failure this is called cor pulmonale this is secondary to long duration lung disease

For heart failure please read my previous post click here

	Lung Disease	Heart disease
Cough with sputum	More common sputum may be yellow(yellow sputum is sign of infection) white or bloody	Less common if sputum is present rarely yellow in color
Paroxysmal nocturnal dyspnea	Never	If present strongly suggestive of heart disease
Orthopnea	Present +	Present ++
Wheeze or crepts	More of wheeze and less of crepts	More of crepts less of wheeze
Pedal edema	Unless long standing lung disease is complicated with right heart failure. is not present . cor pulmonale	Right heart failure

Investigation

Chest X ray, echocardiography, CT thorax, Spirometer, sputum examination will help your doctor to diagnose the problem and treat the condition

Bronchial asthma, chronic bronchitis, emphysema and interstitial lung disease

Kindly read this post about Chronic bronchitis and bronchial asthma from this link click here

Bronchial asthma More often distinction of from heart disease is easy, bronchial asthma is episodic, not normally precipitated by exertion and rarely leads to right heart failure where as heart disease is directly related to exertion .

Chronic bronchitis can be confused with heart disease, as it is also gets worsened by exertion, once patients develops emphysema (distraction of lung tissue) from prolonged chronic bronchitis and lead to right heart failure further confuses the issue.

Interstitial lung disease: is one more group of lung disease is having exertion related breathlessness, without wheeze but with fine crepts. This is less common disease. Spirometer and CT thorax will help make diagnosis.I get breathless; problem is in the heart or lung click here

Heart failure, over view

2012-01-08T12:20:00.001-06:00

Heart is like motorized pump, supposed to pump the blood, to maintain flowing blood column, it has to push blood against blood pressure. Blood pressure is maintained by the body to allow movement of nutrients and oxygen from circulatory channel to deeper tissue by hydrostatic pressure

To do above job, heart has to contract with force and eject enough blood into circulation so body needs are met. In heart failure patients this generation of enough force or enough blood ejection is not adequate, due to variety of causes and body suffers from decreased circulation.

In initial stages or in patients with less severe form of heart failure, patients needs of body may be done with increase in heart rate, this correction may be sufficient in resting state of patient but when same patient start exerting heart may not be able to meet the needs. Then signs of failure of heart manifest. In severe form heart failure even in resting state, heart may not be able to meet the needs of body.

There are mainly two forms of heart failure

1. Systolic heart failure (problem secondary to contraction of heart)

2. Diastolic heart failure (problem secondary to dilatation of heart)

Systolic heart failure:

Here muscle of heart can not contract so heart can not generate enough force,

Causes are

· Heart attack leading to damaged muscle

· Damage to valves of heart, leaky or stenotic valves, make force generated by hear to go waste.

Diastolic heart failure

Here problem is dilatation or relaxation of heart, during this phase blood fills the chambers of heart, if heart does not dilate enough, then filling will be less, so quantity of blood ejected will also be less, and needs of body are not fully met, this leads to heart failure

· Hypertropic cardiomyopathy HOCM/HCM read my previous post click here

· Constrictive pericarditis here covering heart prevents dilatation of heart

Symptoms of heart failure

For convince of understanding symptoms can be grouped in to backward and forward, left heart and right heart symptoms.

For left heart back ward symptoms manifest in lung and forward symptoms manifest in peripheral arterial circulation

For right heart back ward symptoms manifest on systemic venous circulation and forward symptoms in lung

When left heart fails

· Backward symptoms manifest with congestion of lungs and patients becomes breathless

· Forward symptom of left heart manifest with easy fatigabilty.

When right heart fails,

· Back wards symptoms manifest with systemic congestion in the form of pedal edema, patient get bloated, acites can be there.

· Forward systems manifest with decreased blood entry of blood into lung so less amount of blood is oxygenated and when blood reaches the left heart then to systemic circulation

Some patients have both right and left heart failure.

Investigations

· ECG diagnose heart attack

· Echocardiography is important investigation for diagnosing the heart failure and reasons for heart failure

o Assessment of Ejection fraction (EF): - This is fractional quantity of blood, that is ejected before heart started contracting.

o In normal heart Ejection fraction is 60-70%

o Systolic heart failure ejection fraction less then 60%

o Diastolic heart failure this is usually 60% or some time more then 60%

Treatment

· Diuretics :- Increase the urine output by this they reduce backward symptoms of congestion example Lasix, spironolactone

· Ionotropic drugs :-Which increase force of contraction by this they give benefit for forward symptoms and also backwards symptoms example Digoxin, Dobutamine

· Vasodilators :- Dilates the arteries so these will reduce work of contraction for heart example Ramipril

· Beta-blocker :- These will reduce, undue tachycardia (fast heart rate) and prevent the damage to heart and also reduce arrhythmias

· CRT (cardiac resynchronization therapy) and ICD (implantable cardiac defibrillator): - These are small machines, are fitted in chest wall and connected to heart.

o CRT is used in patients with systolic heart failure with help of this machine one can coordinate the contraction of heart such that blood is made to flow smoothly out of heart, thus reduce work of contraction.

o ICD, patient of heart failure are prone for dangerous arrhythmias ICD machine give shock to heart immediatly and correct arrhythmia in a timely fashion and avoid sudden death sec to arrhythmias.

o Heart transplant is a last resort.

Hypertrophic Cardiomyopathy HOCM, HCM: for common person

2012-01-04T10:48:00.003-06:00

"Hypertrophic Cardiomyopathy HOCM, HCM is treatable disease with normal life span"

Our heart is a muscle, like our muscles of arm and leg, it also can get hypertrophied, if heart is made contract against increased pressure, like hypertension, if there is a obstruction to flow of blood i.e. aortic stenosis and pulmonary stenosis, this kind of hypertrophy is different from the hypertrophy seen in hypertrophic Cardiomyopathy (HCM/HOCM). Here heart muscle hypertrophy is without any obvious reason, this is secondary to hereditary condition (autosomal dominant inheritance)

Hypertrophy of heart, is not uniform in HCM more often is localized to some section of heart. This hypertrophy can encroach on the cavity of heart. If it involves out flow tract of heart, leads to obstruction to flow of blood. So name Hypertrophic obstructive Cardiomyopathy. (Not all cases of HCM have obstruction to out flow of blood)

As heart is hypertrophied, it cannot dilate during diastole (ventricle filling) and this can lead backpressure changes to previous chamber i.e. atrium. Which leads to heart failure (diastolic heart failure).

Symptoms of HCM are

· No symptoms

· Angina on effort (heart attack)

· Breathlessness on effort

· Syncope on effort

· Sudden death

HCM patient are asymptomatic more often, some time the only clinical presentation sudden death/ cardiac arrest. for this reason, in patient HCM, all blood relatives are advised undergo echocardiography as prevention.

Screening strategies for Family members of HCM

As HCM can present with sudden death, in a totally asymptomatic and yet having disease HCM. As prophylaxis we need to screen family members of HCM for possibility of asymptomatic HCM, so prevent later problems

Screening can done with echocardiography, ECG ,CMR with or without genetic testing

If genetic testing is not used, then from age of 12 years, one need to do echocardiography, ECG once in 18months till person reaches 21years, even up to age of 21years if reports show no evidence of HCM then one can increase interval of screening once in 5 years afterwards.

If genetic testing is done, if that is negative for HCM genes , then no need for screening further with Echocardiography or ECG.

Among the patient with HCM who are prone for sudden death?

· Previous history of cardiac arrest, but patient survived the arrest

· Family history of sudden death

· Recurrent syncope

· Exercise induced hypotension

· Multiple episodes of heart arrhythmias i.e. ventricular tachycardia

· Severe hypertrophy of heart muscle

If a patient of HCM develop arrhythmias, like ventricular tachycardia, which more often occur out side hospital. AS we need to treat patient immediately i.e. within 1 to 2 minutes(if not done, patient is prone for sudden death). This is only possible with ICD (implantable cardiac defibrillator, a machine put in chest wall, which automatically gives shock to heart, if it notices arrhythmias and correct the arrhythmias).

Therefore, for Patient who is prone for sudden death as mentioned above, advice is ICD implantation.

How to relive obstruction to blood flow?

· Obstruction can be treated with beta blocker drug, if it is mild.

· If severe then, surgery is needed where obstructing part of muscle is resected and smooth blood flow is reestablished.

· Instead of surgery in severe obstructing HOCM, one can induce infarct (artificially controlled heart attack) at the site of obstruction and relieve obstruction . this procedure is similar to angioplasty ,where chest is not opened.

What are palpitations: how are they produced and what I should do for them? For common man

2012-01-01T06:16:00.004-06:00

Palpitations are sensing or painful sensing of owns heart beat.

Normal heartbeats are reraly sensed in normal life, but after running or after strenuous activity most of us feel palpitations, this is normal.

Palpitations are produced by two different mechanisms

· Increase force of contraction
· Secondary to fast heart rate
Non cardiac problem like thyroid disease, panic attacks, anemia can aslo cause palpitations

Increase in force of contraction: -Ectopics PAC premature atrial contraction or VPC premature ventricular contraction), secondary to structural heart diseases.

Ectopics PAC premature atrial contraction or VPC premature ventricular contraction)
Heart contracts with increased force. If heart volume is increased.(this rule is called starling law)

Increase force of contraction following extra beat (PAC premature atrial contraction or VPC premature ventricular contraction), is because, heart slowly down following extra beat and this slowed beet has pronged filling time, so more blood enters the ventricle, so heart is more enlarged, this leads increase force of contraction.

Secondary to structural heart diseases
Apart from extra beat increase in force contraction in heart is secondary to regurgitant lesions of heart
valves. Heart has four chambers and four valves they are

Chambers of heart
Right atrium	Left atrium
right ventricle,	left ventricle

Valves of heart
Mitral valve	Tricuspid valve
Aortic valve	Pulmonary valve

· Valves of heart allow moment of blood in only one direction.

· Mitral valve and tricuspid valves allows moment of blood from atrium to ventricle on left and right side respectively

· Aortic and pulmonary valves allows moment of blood from ventricle to arota or pulmonary trunk on left and right side respectively

If these valves are incompetent, there can regurgitation of blood from distal chamber to proximal i.e.

· Arota to left ventricle

· Pulmonary artery to right ventricle

· Left ventricle to left atrium

· Right ventricle to right atrium

· Blood regurgitated into atrium reach ventricle in next cycle along with regular volume of blood, and ventricle is extra loaded and enlarged

· Blood regurgitated from arota or pulmonary trunk adds up the blood coming from atriums so ventricle is extra loaded.

· Enlarged ventricle when they contract forcefully, will give sense palpitation.

· Secondary to fast heart rate: palpitation secondary to fast heart rate are sec to arrhythmia.

Fast heart rate can come from either atrial (upper chamber) or from ventricle (lower chamber)

Atrial fast rate are benign most often, common causes are atrial fibrillation (old people), SVT, WPW syndrome (young people) etc treatement for WPW, SVT is by ablation.

Ventricle fast rate are sec to usually to heart attack related problems, some rare cause like pronged QT syndrome. Hypertrophic Cardiomyopathy are also there. Treatment for this condition is ICD (implantable cardiac defibrillator) implantation