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CORONARY ARTERY DISEASE (CAD)

ANGINA PECTORIS

Coronary artery is the arterial blood vessel which is supplying nutritional pure blood to the muscles of the heart (Myocardium).For all actions of heart it need tremendous energy which is provided by the uninterrepted free flow of pure blood through this artery which is branched throughout the heart muscles into capillaries.

Atherosclerosis is a process by any injury on the inner portion of the blood vessels' wall caused by the rupture of LDL and releasing the sharp needle like molecules of cholesterol which make injury on the inner wall of the blood vessel.These injuries produces atherosclerosis and small portions of these sclerosis becomes plaques and shed as small particles causes clots which is a throbus which then shed small embols which will circulate the whole body and which when arrive he delicate coronary blood circulation it causes blockade.

A thrombus can be formed by any means directly at the coronary circulation.Either way if blood flow is blocked at a portion of coronary artery the area of the myocardium which receives blood from it is deprived of nutrition (oxygen) and become blackish and struggle to cooperate with the rhythmical heart contraction.This condition is known as Ischemia.In ischemia there is an insufficient supply of oxygen to the heart muscle so that oxygen demand exceed supply.

The ischemic muscle will produce pain,or discomfort or both on the chest which is known as Angina Pectoris.  
Angina Pectoris is one of the major contributors of Heart Attack and Heart Failure 
The symptoms of Angina is ranges from a mild to moderate pain on the chest.Some times as instead of a pain a heavy weight put on the chest.
When compared with Myocardial Infarction in which cell deaths occur and fatal ventricular fibrillation angina is reversible if properly attended.
The etiology is based on three aspects
1.Decreased blood flow
This is due to reasons like a)Atherosclerosis;
b)Coronary artery spasm.This condition is rare but often induced by external factors like inserting coronary catheter,or internal hemorrhage,exposure to exreme cold or ergot alkaloids.These angina may precipitate Prinzmetal syndrome or heart attack.
c.An severe traumatic impact of an heavy object on the chest like a car steering wheel,causes capillary hemorrhages
d.Entry of an embol into the capillaries can cause the blockade.
2.Oxygen demands exceed oxygen supply caused by
a)Hard exercises
b)Emotions
The above condition may not need medical intervention because it can be releived by sufficient rest and relax.Very rarely it may become pathogenic
3.Reduced blood flow such as in conditions like anaemias  

Types 

1.Classic stable angina,this is usually occurs during heavy work or exercises.

2.Unstable angina,this is pathologic and occur even in rest and suddenly become worse

3.Prizmetal's angina,this form is mostly due to coronary artery spasm and this condition is very rare.

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ANTI ARRHYTHMIC DRUGS

ARRHYTHMIA-TREATMENTS

 ARRHYTHMIA the irregular rhythmical beats of heart may result many times fatal if unattended

The Anatomy of Electrical Conduction Of the Heart Beats

As in the above diagram the electrical conduction of the heart muscle is clitched to start at the Sinu-Atrial (SA) node the most auto generated electrically depolarizable tissue in our body.

The atrium contracts and the conduction spreads down wards like waves to reach Atrio-Ventricular (AV) node as in the above figure.

The AV node is situated in between the Right Atrium (RA) and the Right Ventricle and this AV node is acting as protective shield to filter of any unwanted excessive impulses from above to pass further down to this shield.Also AV node acts as a Gate to pass needed impulses from the SA node sufficient for ventricular contraction.

Ventricular contraction not begins immediately when the impulses reaches AV node as the node is situated more towards the right as in the figure above,and because both right and left ventricle needed equal impulses to contract.To disperse the impulse equally from AV node  to both the sectors nature has provided a special tissue which is a portion of AV node.This special tissue is known as Bundle of His as you can note in the figure.This tissue is branched equally to right and left.AV node send impulses to Bundle of His which sends the impulses to both right and left down to the bottoms of both the ventricles known as Purkinje Fibers and the ventricles contracts.
This can be easily illustrated by an ECG as followsl;-

P-wave represent the Atrial depolarization and contraction
PR-interval represents the conduction of the impulse from the Atria to Purkinje fibers
QRS curve the rapid repolarize and depolorization of Ventricles
The ST segment represent the resting period or plateu period of the myocardium. 
There are two types of impulse defects may occur during a rhythm. 
1.Defects in the formation of the impulses as during stresses,straining to expell the feces in constipation,weight lifting,hard excercise.These impulses are non pathalogic and need no medical interventions.It can get corrected by taking rest and relax.
2.Defects in the conduction of formed impulses due to some underlying causes such as HT,Cardiac Failure,MI,Drugs,Infections,Anginas,Valvular defects and cardiac muscle damages may be pathologic and is known as Pathologic Arrhythmias and may be fatal.This condition needs medical intervensions.Also arrythmias can be pathologic if impulses originates from other parts of the myocardium especially from the fast acting cells instead of the pace maker tissues such as SA node and AV node.
Treatments 
 Class-IA-.Sodium channel blockers
Quinidine
Procainimide 
Disopyramide

Quinidine

Uses-Ventricular tachycardia and supraventricular arrhythmias,Atrial fibrillation and Atrial flutter
Quinidine prolongs the QT intervals and thereby calm down the rapid depolarization of fast acting muscles like Purkinje fibers and inturn calm down ventricular fibrillation.
Quinidine is administered orally
It is metabolised in the liver and half life is 6 to 8 hrs.
Toxicity 1.GI disturbances like Diarrhea,Nausea,Vomiting.
               2.Cinchonism such as blurred vision,dizziness,head ache,and tinnitus
               3.Syncope with light headedness and possible faint.
               4.Thrombocytopenia
               5.Excess prolongation of QT intervals result in a brady arrhythmia known as Torsade de Points causes immediate death.
               6.AV block
Drug Interactions 1.Increases plasma levels of digoxin and oral anti coagulants
                                2.Quinidine plasma levels are rapidly depleted by Phenytoin and Phenobarbital

Procainamide

Uses 

1.Venricular and supraventricular arrhythmias

2.Premature ventricular contractions

Procainamide is taken by oral,i.v.;or i.m.

Toxicity 1.Lupus like rashes or arthralgia.Renal involvement is unusual

               2.Pericarditis,

               3.Hellucination,and psycoses

               4.Torsade de Points.

Disopyramide

Action is very similar to the other two above mentioned drugs but produce prolonged negative inotropic (decreasing frequency of contractility) and stronger anticholinergic effect.
This medicine can be taken by I.V. or by Oral
Uses Both ventricular and supra ventricular arrhythmias
Kinetics Largely excreted by kidneys unchanged
Toxicity 1.Dry mouth, Blurred vision,Urinary retention,Constipation and Glacoma
               2.Torsade de Points
               3.Contra indicated in left ventricle dysfunction as it may leads to Heart Failure
               4.Because of the anticholinergic effects protate gland would be affected. 
Class - IB   
1.Lidocaine
2.Tocainide
3.Mexiletine
4.Phenytoin

Lidocaine (Xylocaine)

Lidocaine a local anethetic exert blocking effect on sodium channels

Use Lidocaine is the drug of choice for ventricular arrhythmias

Route I.V. only

Kinetics Lidocaine is metabolised in liver and care should be taken while using in liver dysfuntion

Toxicity CNS effects like Drowsiness,numbness,slurred speach,and convulsions

Nystagmus a condition at which rapid and involuntary movements of eyeballs occur

Tocainamide(Tonocard)

Usesd in ventricular arrhythmias

Taken orally

Toxicities 1.Bradycardia;2.Tachycardia;3.AV block;4.Hypotension

                  5.Nausea;6.Tremor;7.Lung fibrosis(Rare) ;8.Aplastic anemia(Rare)

Mexiletine (Mexitil)

Used in ventricular arrhythmias

Can be taken orally

Toxicity Dizziness;Nausea,& Vomiting;Erythrocytopenia;Thrombocytopenia;Leucopenia;Agranulocytosi s and Nystagmus

Phenytoin (Dilantin)

This drug block the inactivated sodium channel and keep it blocked for a long time and there by it is useful for convulsions and atrial and ventricular arrhythmias.

Can be taken orally or by I.V.

Side effects are similar as above.

Class-IC 

 1.Flecainide

2.Propafenone

3.Morizicine

Used in supraventricular and ventricular arrhythmias in patients with normal heart structure

Toxicity 1.This medicine should be used only if other medicines are ineffective because the Cardiac Arrhythmia Suppressor Trial (CAST) studies proved that this medicine is fatal to those who suffered recent heart attacks,and who suffer asymptomatic ventricular arrhythmias.

               2.CNS effects like blurred vision,and headaches

               3.Heart Arrest in patients who have defective conduction system.

Propafenone (Rhythmol)

Used in supraventricular and ventricular arrhythmias

Blocks sodium channels upto Purkinje fiber level and thereby correcting the ventricular contraction similar to flecainide but also have some beta adrenergic blocking effects.

Toxicity is having a proarrhythmogenic effect and beta blockade effects like Bronchospasm,bradycardia.

Class-II Antiarrhythmic Drugs-The Beta Adrenergic Blockers

In this class the most commonly used medicines as antiarrhythmics are as follows:-

1.Propranolol

2.Sotalol

3.Esmolol

Sotolol can be included in Class-III too.

The mechanism of these drugs are generally depressing the automaticity of the myocardium other than the pacemakers like SA and AV nodes and make the pacemakers to little calm by slowing their contractions and elongating their refractory periods and thereby preventing the arrhythmic excitations of the heart.

Sotolal is used clinically ventricular fibrillation

Esmolol is short acting and can be used safely during emergencies such as surgery.

Class-III -Potassium Channel Blockers

1.Bretylium 2.Amiodarone 3.Sotolol 4.Procainamide

The mechanism of action is by blocking the potassium channels so that there is no sodium influx and potassium efflux and there by prolong the ventricular excitations

These drugs can be used to treat venricular fibrillations

Postural hypotention can be an adverse effect of these medicines

Amiodarone is the drug of choice used in the name of Cardarone.

This drug also exhibits Class-I and Class-II properties also.

Amiodarone is used in Arterial flutter and ventricular arrhythmias 

Amiodarone can be taken orally as well as by I.V.route.

Toxicities 1.Lung fibrosis;2.Tremor ;3.Live damage;4.Photosensiivity;5.Corneal micro deposits;6.Thyroid defects leads to iodine accumulation and thereby bluish body skin discolouration;

Class-IV-Calcium channel Blockers

1.Verapamil

2. Diltiazem

3.Nifedipine

The mechanism of action is blocking the L-type calcium channels and thereby calm down the SA and AV nodes.The actions are mostly supra ventricular and hence can be used in atrial flutters

 

 

 

 

 

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CONGESTIVE HEART FAILURE (CHF)-TREATMENTS

CONGESTIVE HEART FAILURE

It is a pathological condition with multiple etiologies in which the left ventricle fails to contract sufficiently to deliver the blood through the aorta to our body tissues for their metabolic needs.The inability of the left ventricle to function properly the result is collection of waste fluids into its muscles and make it more congestive.Hence the name Congestive Heart Failure

CHF is commonly occuring in elderly patients of above 40 yrs.But it may occur at any age as a result of any one of the underlying heart and vascular diseases such as Angina,MI, Hypertension and Coronary Artery Disease etc.etc.

Myocardial stress such as heavy stress on the wall of left ventricle due to the absence of the interventricular wall (septal wall) or its dysfunctioning (Congenial Heart Failure),traumas,diseases like Rheumatic fever,pulmonary embolism, infections, anemia,pregnancy,drugs,fluid overload,arrhythmias and valve defects may all become the etiological factors.

Types of HFs

1.Low output vs High out put HF

If the metabolic demands are normal but the heart cannot meet the requirements is known as Low output Heart Failure (The most common type)

In case of high metabolic demand conditions due o hypertension or anemia and if the heart is unable to meet he requirements then it is known as High output Heart Failure.

2.Left side vs. Right side Failure

The sighns and symptoms are result from blood backing up in the failing ventricle except in the HF due to increased body demand in which blood will not be much backed up but there is left ventricle failure occurs.

Initially the symptoms tends to be specific to one sided failure but later eventually both side involvement is seen.
Leftside failure can be attributed by when the blood cannot be properly pumped by the inability of the left ventricle into the aorta through the aortic valve,leads to he accumulation of blood in it.
Because of this the left ventricle cannot receive further blood flow from the left atrium through the Miral valve (the valve between the left atrium and left venricle),and inturn because of the blood accumulation in the left atrium it itself cannot accept further blood flow from the pulmonary(lungs) vein and hence the fluid portion of the blood will be pumped back to the lungs leads to Pulmonary Edema.
Right side failure can be atributed by the inability of right ventricle to pump the blood into the pulmonary artery through the pulmonic valve.The blood get accumulated inside the ventricle and is known as Right side failure.
Because of this accumulation the fluid portion of the blood backs up throughout the body (in the veins,liver,legs and bowels) leads to Systemic Edema
Treatment Options is composed of avoiding drugs which can exacerbate the cause as follows.
The followings are the substances which should not be taken in CHF:-
1.Androgens
2.Corticosteroids
3.Estrogens
4.Licorice
5.Guanethidine
6.Lithium carbonate
7.Methyldopa (a centrally acting antihypertensive drug)
8.Salicylates and other NSAIDs
Because all the above drugs causes sodium and water retensions
Second options are releiving the symptoms and improve pump functions by,
a)Reducing metabolic congestion and needs by relaxations,rest,and medications.
b)Reducing fluid intakes
c)Taking digitalis and other inotropic(improving heart contractions)
  drugs
d)Patient educations
Pathophysiology God has given to our body every aspects of self defence and self corrections to some extend inorder to minimise the inconveniences caused by the disorders.Similarly in case of CHF if we left uncare at first our body trys to care it by some compensative activities as follows:-
Sympathetic Responses by which the norepinephrine outflow will act on the heart to increase the contractility,heart rate and the bloodflow which with no otherway redisributed to ensure perfusion of the heart.
Hormonal Stimulation The redistribution of bloodflow to the heart will result in renal insult which decreases glomerular filteration rate (GFR),leads to sodium retension,water retension,activation of the renin-angiotensin-aldosteron system to add to more sodium and water retension.
Cardiac Hypertrophy, The above process of fluid retension will lead to thickening and enlargement of cardiac wall.This will make larger contractile cells and diminishing the capacity of the cavity in an attempt to precipitate expulsion of blood at lower volumes.
Frank-Sterling Mechanism is that increase fiber dilation hightens the contractile force which then increase the energy released.
as a result,1)the heart pumps all the blood it receives.2)as blood volume increases the various cardiac chambers dilate by stretch and enlarge in attempt to accommodate excess fluid.c)as these stretched muscles contract and the contractile force increase proportionally to their dilation.Then the stretched fibers snap back like a rubber band expelling the extra fluid into the arteries.
The above compensation processes may or may not result in a permenant solution as it depending upon the severity of the condition.If the condition is mild the above compensation process may be successful with the Grace of Almighty.If not the tragic events of decompensation process follows as below:-
Overtime the body gets exhausted of its all compensation mechanism and become self defeated.
As the strain continues,total peripheral resistance and afterload pressure further increase and thereby making the ventricular muscle further weaker to expell the blood.
After load is the amount of contractile force required to overcome the interventricular forces and the pressure in aorta (in case of left ventricle) to eject the blood.
Afterload is defined as the pressure in ventricular muscles during contraction.It is the interventricular systolic pressure.
Preload is the force exerted on the ventricular muscle at the end of diastole.
As the fluid volume expands proportionally  the demand also expands on the already exhausted pump,allowing increased volume remain in the ventricle.
The resulting fluid backup produces signs of CHF 
Physical Symptoms
1.Tiredness and fatigue
2.Coughing
3.Shortness of breath or difficult to breath (Due to Left Ventricle failure)
4.Swelling of abdomen and systemic edima(Due to right sided CHF)
Mostly the symptoms are very similar to that of Heart Attack
The following image will illustrate the symptoms diagrammatically

MEDICATIONS
The pharmaceutical therapeutics is based on three approaches as follows:-
1.Improving heart muscle contractions
2.Reduce preload (The filling of ventricles)
3.Reduce afterload(The resistance pressure against which the heart must pump)
The Drugs Options are as follows:-
1.Cardiac Glycosides (e.g)Digoxin(Lanoxin);Digitoxin
2.Bipyridinederivatives(e.g)Amrinone(Inocor);Milrinone(Primacore)
3.Beta-Adrenergic Agonists (e.g) Dolbutamine (e.g) and Dopamine
4.Vasodilators (e.g) Nitrates (Nitroglycerine,Isordil,Amylnitrate);Hydralazine and ACE Inhibitors (Enalapril and other ...prils)
5.Diuretics (No monotherapy,as an adjunct only)
 

 

 

   

MYOCARDIAL INFARCTION-HEART ATTACK

HEART ATTACK(M.I.)

When the heart muscle cells dies with necrosis there is complete blockade of coronary blood supply to heart with prolonged ischemia,and complete occlution of the coronary artery the ultimate result is Myocardial Infarction or Heart Attack.During and after the attack the left ventricle become enlarged and hypertrophied due to the outside pressure.

Etiology:The most common cause is acute thrombus (clot) formation following fissuring and rupture of the lipid rich atherosclerosis plaque and platelet aggregation in the already congested coronary artery. Rare association of the coronary arterial spasm may also contribute to the cause.
Heart Attack is one of the morbid result of prolonged ischemia followed by angina pectoris.
The long time Ischemic Heart Desease caused by decreased blood flow to the heart muscle due to obstruction of the blood flow by the clots,the diffused plaque from the atherosclerosis,followed by platlet aggregation,would certainly leads to MI if left untreated.
Because these condion may kill the heart muscle cells by depriving of oxygen which leads to necrosis and ischemia which will eventually lead to MI.

Sudden death is caused by MI which can trigger the abrupt onset of ventricular fibrillation,the most disorganized and lethal arrhythmia,which can suddenly stop the cardiac output.If this emergency situation is not medically intervened immediately by cordial thump,or defibrillation by counter shock the result is death. 
Generally if there is uncontrolled ventricular fibrillation followed by recusciation occur the situaion is emergency and is known as Sudden Death Syndrom 
In MI a portion of the of the heart muscle suffer prolonged severe supply block of oxygenated blood because of a clot formation,leading to blood vessel damage to form atherosclerosis and platelet aggregations.

Symptoms: 

1.Severe pain radiating from the lower left side to the shoulder.back and neck

2.Shortness of breath

3.Nausea with vomiting or without vomiting;some times stomach pain

4.Hypertention or hypotention

5.Dizziness with headpain,and Fatigue

6.Throat or jawpain

7. Unusual loud snoring with cjocking voice may indicate the presence of sleep apnea,a warning signal to heart attack

8.Sweating

9.Non stopable coughing

10.Diaphoresis (Excretion or oozing of moisture through sweating)

11.Heart murmurs,with tachyarrythmias or bradyarrythmias

25% of the heart attacks are not showing the above symptoms and are silent in eldely patiens,patients with Diabetes and Hypertension

MI can be cassified as 1.Anterior;2.Lateral and 3. Inferior.

But more conveniently and medically classified by ECG as 1.Q-wave MI

2.Non Q-wave MI

What is a Q-wave:-

A Q-wave in an ECG represent any down ward left to right depolarization of the interventricular septum during which ventricles dilates to get filled by blood.See the figure down

In the above ECG look at small downward graphic dip indicated by the arrows and circle.

If there is a problem in the normal depolarizing effects of inter ventricular muscle the Q-wave will be elongated

If this is the condition then there is much chances to get an Q-wave mediated MI.But a problem in Q-wave may not always result to an MI.The presence and elongated  Q-wave indicates there are necrosis.This can be corrected by Coronory bypass surgery if done within a few hours of the post MI.
Generally Q-wave syndroms accounts for 40 to 70% of MI events when compared with non Q-wave MIs.In Q-wave mediated MI there is usually an elevated ST segment.In non Q-wave MIs there is depression in ST-segments.
The most serious warning is a sudden ventricular arrythmia with fibrillation occur without any warnings.

Therapy

 Goals:1.Elimination of clot formations by using Thrombolytics

            2.Releiving Pain

            3.To Prevent arrhythmias

            4.To reduce cardiac workload and stabilize rhythm.

            5.Limiting the affected area and preserving the pump function.

            6.Solving the other complications like nausea,vomiting,stomach aches,arrythmias,blood pressure variations etc.etc.

If not contra indicated four groups of medications can be used in MIs

1.Thrombolytics

2.Beta blockers

3.Nitrates

4.Aspirin

Apart from these Morphine,Lidocaine,Heparine and Warfarine can also be used at times.

The first choice is using thrombolytics such as streptokinase,Urokinase,and Alteplase.as thrombus and embols are the major causes of coronary atherosclerosis plaque apart from LDL and Triglycerides.ACE inhibitors and Calcium channel blockers can also be tried but their efficacy is yet to be proved.

If in case thrombolytics are contraindicated then Percutaneous Transluminal Coronory Angioplasty(PTCA) is proved efficaceous.

Thrombolytic agents were used in patients with suspected MI with prolonged chest pain.

But any benifits that attained by Thrombolytic may seen not immediate but occur as late as 12 hrs.after the pain starts.

Administration of streptokinase IV should be started within 12 hrs and optimally 6 hrs of the pain starts.

Aspirin can be used along with a thrombolytic agent to regulate the circulation in the dosage of 160 mg to 325 mg.for life after the first attack.Get a physicians advice for dosage.

Heparin can be used along with a thrombolytic agent to prevent reocclusion of the coronary artery even heparin is proved in reducing mortality even if it is used without a thrombolytic agent after the first attack.

An IV bolus of 5000 units followed by a continous infusion of 1000 units/hr is its usual dosage.The goal is to maintain the Activated Partial Thromboplastin Time (APTT) between 1 & 1/2 or 2 & 1/2 times normal.

Warfarin can be used in patients with mural thrombus.

Beta Adrenergic blockers propranolo,metoprolol,atenolol,and timolol are commonly used with success.

Nitrates Nitroglycerin is in the most common usage.It should be administered sublingually at the onset of the pain.