RMT Cardiology

Dietetic table of № 10

2009-03-16T00:08:00.005+03:00

Posted By:Dr.Zharif

Dietetic table of № 10

Indication: diseases of cardiovascular system with Heart Failure NYHA I -II[a] degree.

Aim:

1. improvement in the blood circulation,

2. functions of cardiovascular system, liver and kidneys,

3. the normalization of exchange of substances,

4. protection of cardiovascular system and organs of digestion.

General characteristic: -

1. small reduction in the caloricity due to the fats and partly carbohydrates.

2. limitation of a quantity of sodium of chloride,

3. the decrease of the consumption of liquids.

4. The content of the substances, which excite cardiovascular and nervous system, which irritate the liver and nights, is limited superfluously burdening gastrointestinal tract, that facilitate meteorism.

5. increased the content of potassium, magnesium, lipotropic substances, products, which render the alkalizing action (milk, vegetables, fruits). Culinary working is performed with that moderated by mechanical .

6. Meat and fish they boil.

7. Food is prepared without the salt.

8. The temperature of food is usual.

9. Feed mode: 5 times a day by relatively uniform portions.

Chemical composition and energy-value (daily ration):

· the proteins 90[g] (55- 60% animals)

· the fats 70[g] (25 30% plant)

· the carbohydrates 350-400 g

· Energy-value 2500-2600 kcal.

· the common salt 6-7[g]

· the liquid 1,2[l]

Can

Can’t

• bread is wheaten from the flour the 1st and 2nd types, yesterday's baking or slightly dried slightly; dietetic salt-free bread, pastry and sponge cake;

• any vegetarian soups with different groats, milk soups;

• the nonfatty types of beef, veal, meat and trimming pork, rabbit, hen, turkey. they boil meat after cleaning from the tendons and fascias, and then bake or brown, dishes from the chopped or lump boiled meat, flood from the boiled meat, limited - doctoral and dietetic sausages, the nonfatty forms of fish - boiled or with subsequent roasting, dish from boiled sea products;

• milk, sour-milk beverages and cottage cheese;

• egg – 1per day, soft-boiled, the steam and baked omelettes, protein omelettes, in the dishes • dish from different groats; boiled macaroni articles;

• vegetables in the boiled and baked form potatoes, cauliflower, carrot, beet, summer squashes, pumpkin, tomatoes, lettuce, cucumbers, the cabbage and green peas – limited green bow, dill, parsley - in the dishes;

• lettuces from the fresh vegetables (ground carrot, tomatoes, cucumbers), vinaigrettes with vegetable oil, vegetable roe, lettuces are fruit, with sea products, fish the boiled flood

• soft ripe fruits and berry, honey, jam.

• Weak tea, coffee beverages with the milk, fruit and vegetable juices, the broth of sweetbrier, limited - grape juice.

• fresh bread, article made of the rich test and puff-pastry Guest, pancakes, fritter;

• soups from the bean, meat, fish and fungus bouillon;

• the fatty forms of the meat of goose, weft, the liver, kidney, the brains, smoked foods, sausage articles, meat canned foods, fish, bird;

• kidney, smoked foods, sausage;

• salt, the fatty forms of fish, roe, canned foods, salt and fatty cheeses;

• bean;

• the eggs hard-boiled, fried;

• the salt, and sour vegetables; fruits with rough cellulose tissue, spinach, sorrel, horseradish, radish, garlic, turnip-shaped bow, fungi;

• chocolate, strong tea, coffee and coco

You can download full description about Diet no.10 here

Диетический стол 10.docx

Ref:1.Russian Medical Portal
2. Russian Hospital Therapy Text Book

Management of Heart Failure By MOH

2009-02-16T01:01:00.008+03:00

Posted by:Dr.Zharif

Investigation

Blood test – FBC, renal function, liver function, glucose, lipid profile

urinalysis – proteinuria, glycosuria

Other important investigations include:

• echocardiogram – to identify structural abnormalities and assess LV systolic

and diastolic dysfunction

natriuretic peptides or their precursors (especially BNP and NT-proBNP) – If available, this investigation is useful in the evaluation of patients presenting IIa.A with acute dyspnoea in the urgent care setting in whom the clinical diagnosis of HF is uncertain. A low-normal concentration of this marker in an untreated patient makes the diagnosis of HF unlikely.Thus it is a useful “rule–out” test in doubtful cases.

Additional investigations when indicated;

Blood tests:

– cardiac biomarkers – thyroid function tests

– C-reactive protein (to look for inflammation)

Tests for myocardial ischemia and/or viability: – treadmill exercise test

– stress echocardiography (exercise or pharmacological)

– radionuclide studies

– cardiac magnetic resonance imaging (CMR)

Invasive tests:

– coronary angiography – cardiac catheterization – endomyocardial biopsy

Others:

– Holter electrocardiography, loop recorders and long-time ECG recording – pulmonary function tests

Management

The principles of management are:

Rapid recognition of the condition

Stabilization of hemodynamics

Improvement in clinical symptoms and signs

Identification and treatment of the

– underlying cause

– precipitating / aggravating factors.

The initial management includes a combination of the following first line therapy:

Oxygen – 5 to 6 liters/minute, by mask with the aim of achieving oxygen saturation of more than 95% in order to maximize tissue oxygenation and to prevent end organ dysfunction or multi organ failure. Elective ventilation using non invasive positive pressure ventilation (Continuous Positive Airway Pressure [CPAP] or Bi-level Positive Airway Pressure [BiPAP])should be considered early if necessaryShould the oxygen saturation be inadequate or the patient develop respiratory muscle fatigue, then endotracheal intubation and mechanical ventilation is necessary.

Frusemide – Intravenous (i.v.) frusemide 40 – 100mg. The dose should be

individualized depending on the severity of the clinical condition

Administration of a loading dose followed by a continuous infusion has been

shown to be more effective than repeated bolus injections alone .The

dose should be titrated according to clinical response and renal function.

Morphine sulphate – i.v. 3 – 5 mg bolus (repeated if necessary, up to a total maximum of 10mg). It reduces pulmonary venous congestion and sympathetic drive. It is most useful in patients who are dyspnoeic and restless. Intravenous anti-emetics (metoclopramide 10mg or prochlorperazine 12.5mg) should be administered concomitantly. Care must be exercised in patients with chronic respiratory diseases.

Nitrates - If the BP is adequate (SBP > 100 mmHg), nitrates are indicated as first line therapy in AHF. It should be administered sublingually or intravenously. The i.v. route is more effective and preferable. Patients should be closely monitored for hypotension. This commonly occurs with concomitant diuretic therapy. Studies have shown that the combination of i.v. nitrate and low dose frusemide is more efficacious than high dose diuretic treatment alone .

Extreme caution should be exercised in patients with aortic and mitral stenosis.

Nitrates are contraindicated in severe valvular stenosis

	Route of	Dosages
	Admin	Dosages
Diuretics
Frusemide	IV	40mg – 100mg
	Infusion	5 – 40mg/hour (better than very high bolus
		doses)

Vasodilators
Nitroglycerin	Infusion	5ug/min increasing at intervals of 3 – 5 min
		by 5ug/min increments up to 100 – 200
		ug/min
Nitroprusside	Infusion	0.1 – 5ug/kg/min

Sympathomimetics
Dobutamine	Infusion	2 – 20ug/kg/min
Dopamine	Infusion	<2>
		2 – 10ug/kg/min – inotropic doses
		10 – 20ug/kg/min –
		peripheral vasoconstriction
Noradrenaline	Infusion	0.02 – 1ug/kg/min till desired BP is
		attained

Phosphodiesterase-
3- Inhibitors
Milrinone	Infusion	50ug/kg bolus then 0.375 – 0.75ug/kg/min

Grading of Recommendations of Therapies in the Management of AHF

Intervention	Grades of	Level of
Intervention	Recommen-	Level of	Comments
	Recommen-	Evidence	Comments
	dation	Evidence
	dation
	INITIAL MANAGEMENT CONSISTS OF :
			Maintain the oxygen saturation above
Oxygen	I	C	Maintain the oxygen saturation above
Oxygen	I	C	95%
			95%

Diuretics	I	B	Indicated for fluid retention

Nitrates	I	B	Contraindicated if SBP<>
Nitrates	I	B	with caution in valvular stenosis.
			with caution in valvular stenosis.

Morphine	IIb	C	Indicated in pts who are dyspnoeic and
Morphine	IIb	C	restless
			restless

NOT RESPONSIVE TO INITIAL TREATMENT AND SBP≥100mmHg
			continuous infusion; combination with
			continuous infusion; combination with
Diuretics	IIb	C	nitrates, dopamine, dobutamine or
			thiazide
Dobutamine	IIa	C	Indicated for peripheral hypoperfusion +/-
Dobutamine	IIa	C	pulmonary congestion
			pulmonary congestion

Dopamine	IIb	C	To improve renal perfusion and promote
(<2>µg/kg/min)	IIb	C	diuresis
(<2>µg/kg/min)			diuresis

Milrinone	IIb	C	Improves symptoms and hemodynamics.

Sodium	I	C	Indicated in hypertensive crisis and acute
Nitroprusside	I	C	valvular regurgitation
Nitroprusside			valvular regurgitation

NOT RESPONSIVE TO INITIAL TREATMENT AND SBP<100mmhg
			Indicated to increase the BP
Dopamine	IIa	C
(>2µg/kg/min)	IIa	C
(>2µg/kg/min)

Noradrenaline	IIb	C	Indicated to increase the BP

			Indicated as a bridge till myocardial
IABP	I	B	recovery or heart transplant

Ventricular			Indicated as a bridge till myocardial
Assist Device			Indicated as a bridge till myocardial
Assist Device	IIa	B	recovery or heart transplant
(VAD)	IIa	B	recovery or heart transplant
(VAD)

For more detail Information about Management of Heart Failure By MOH
u can download the pdf file HERE

Antiarrhytmic drugs

2008-11-27T16:32:00.017+03:00

By:Dr.Zharif

Vaughan Williams classification of Antiarrhythmic agents(International Classification):

I(Membrane Stabilizing agents)

Ia((Na+) channel block (intermediate association/dissociation)

Mech of action

block the fast sodium channel(depresses the phase 0 depolarization (reduces Vmax))By:

1.prolongs the action potential duration by slowing conduction.

2.decreased conductivity

3.increased effective refractory period

Indications:

supraventricular tachycardia, ventricular tachycardia, symptomatic ventricular premature beats, and prevention of ventricular fibrillation.

Procainamide treatment of atrial fibrillation in the setting of Wolff-Parkinson-White syndrome, and in the treatment of wide complex hemodynamically stable tachycardias. While procainamide and quinidine may be used in the conversion of atrial fibrillation to normal sinus rhythm, they should only be used in conjunction with an AV node blocking agent (ie: digoxin, verapamil, or a beta blocker), because procainamide and quinidine can increase the conduction through the AV node and may cause 1:1 conduction of atrial fibrillation, causing an increase in the ventricular rate.

Drugs 1a

Quinidine-

200-600mg every 4-6 hour peroral during attack

Procainamide-

250-750mg every 4-6 hour peroral or

10-15mg/kg I/V droplet with 25mg/min after that 1-6 mg/min

Disopyramide –

100-200 mg every 6-8 hours peroral

Ib((Na+) channel block (fast association/dissociation))

Mech.of action

fast onset and offset kinetics, meaning that they have little or no effect at slower heart rates, and more effects at faster heart rates

shorten the action potential duration and reduce refractoriness

tend to be much more specific for voltage gated Na channels than Ia

more activity with increasing heart rates

Indication

ventricular tachycardia and symptomatic premature ventricular beats, and prevention of ventricular fibrillation.

Drugs 1b

Lidocaine

1-3mg/kg i/v droplet 25-50mg/min till 1-4mg/min

Mexiletine-

200-400mg every 8 hours peroral

Ic((Na+) channel block (slow association/dissociation))

Mech.of action

decrease conductivity but have a minimal effect on the action potential duration. Of the sodium channel blocking antiarrhythmic agents

Indication :

life-threatening ventricular tachycardia or ventricular fibrillation, and for the treatment of refractory supraventricular tachycardia

Imaline(AJMALINE)-I/V 50mg till 75 mg 7-10 min

Gilurytmal(in russian)

Drugs 1c

Propafenone-

150-300mg every 8 hour i/v

Moricizine-

150-300 mg every 8-12 hour i/v

II(Beta blocker)

Mech of action

Beta blockers block the action of endogenous catecholamines (epinephrine (adrenaline) and norepinephrine (noradrenaline) in particular), on β-adrenergic receptors, part of the sympathetic nervous system which mediates the fight or flight response.

Drugs II

Propranolol

10-100 mg every 6 hour peroral

III(K+ channel blocker)

Mech of action

block the potassium channels, thereby prolonging repolarization. The prolongation of the action potential duration and refractory period, combined with the maintenance of normal conduction velocity, prevent re-entrant arrhythmias.

Side effect:

These agents include a risk of torsades de pointes

Drugs III

Amiodarone

600-1600mg/day 1-3 week

next 3rd week 200-400 mg/day

Sotalol (is also a beta blocker)

80-320 mg every 12 hours peroral

IV(Ca2+ channel block)

Mech of action

blocking voltage-gated calcium channels (VGCCs) in muscle cells of the heart and blood vessels

decrease in cardiac contractility

less contraction of the vascular smooth muscle of vessel-vasodilation

decreases total peripheral resistance,

decreases cardiac output.

low blood pressure

Drugs IV

verapamil

80-320 mg every 6-8 hours peroral

5-10 mg for 1-2 min i/v

V(Work by other or unknown mechanisms)

digoxin

1,25-1,5 mg fractional peroral in 24 hours

next 0.125-0,375 mg/day i/v

adenosine

6mg rapidly i/v

if no effect inbetween 1-2 minutes

12 mg rapidly i/v

Mnemonics

"some block potassium channels"

Class I "Some" = S = Sodium blocker

Class II "Block" = B =Beta blockers

Class III "Potassium"=P= Potassium channel blockers

Class IV "Channels" = C =Calcium channel blockers

Class I agents

Class IA “Double Quarter Pounder” (Disopyramide, Quinidine, Procainamide),

Class IB “Lettuce, Tomato, Mayo” (Lidocaine, Tocainide, Mexilitine)

Class IC “More Fries Please” (Moricizine, Flecainide, Propafenone)

Class III agents:

"A Big Dog Is Scary" (Amiodarone, Bretylium, Dofetilide, Ibutilide, Sotalol)

Class IV agents:

"Very Nice Drugs" (verapamil, nifedipine, diltiazem)

Russian classification for Antiarrhytmic drugs

Supraventricular arrhythmia

Drugs	During attack	Prophylactic	Start action	Prolong action
Izoptine	i/v 10mg(seldom 15-30 mg )with 1mg/min PerOS 40-120 mg till 160 mg	PerOS 40-120mg 4-6 times /day	i/v- 1st min. perOS-during 1 hours	4-8 hours
Quinidine	PerOS 0.2-0.6 g	PerOS 0.2-0.4g 4-6 times/day	30 min.	4-6 hours
Novocainamide	i/v 0.5-1 g or i/v every 2 min 0.1-0.2g or i/m o.5-1g or PerOS 1-1.5g	i/v 2-3mg/min or PerOS o.5g 4-6 times/day	i/v-1st minute perOS-30 min.	3-4 hours
Imaline	i/v 50 mg till 75 mg in duration 7-10 min or PerOS 0.05-0.1 g	perOs 0.05-1g 3-4 times/day	i/v-1st min.	6-8 hours
Ritmodan	i/v 2 mg/kg do 150 mg in duration 5 min. or perOS 0.2-0.3g	perOS 0.1-0.2g 3-4 times/day	i/v-1st min. perOS-30 min.	i/v-10 min perOS-4-6 hours
etmozine	i/v 2-2.5 mg/kg in duration 5-10 min	PerOS 0.2g 3-4 times/day	i/v-1st min perOS-24-48hours	i/v 20-25min perOS 6-8 hours
Obzidane	i/v 10mg in duration 7-10 min or PerOS 20-160mg	PerOS 20-80mg 4times/day	i/v- 1st min perOS-30 min.	i/v 2-4 hours perOS 3-6 hours
Kordaron	i/v 5mg/kg in duration 5 min	perOS: 1st week 200-400mg 3 times/day 2nd week 1-2 tab. 2 times/day 3rd week 1-2 tab./day 2 day rest in 1 week	i/v-1st min	i/v-20-30 min perOS- week

Ventricular arrhytmia

Drugs	During attack	Prophylactic	Start action	Prolong action
Lidocaine And trimecaine	i/v 80-100mg in duration 3-5 min seldom 150-200mg in duration 10-20 min.	i/v rapidly 80-100mg next droplet 2-3mg/min i/m 400-600mg in 3 hours	i/v-1st min. i/m- 10-15 min.	i/v-10-15min i/m 3hours
Mexitiline	i/v 75-250mg in duration 5-15 min or PerOS 0.3-0.4g	i/v rapidly 75-250mg next droplet or perOS 0.2-0.4g 3 times/day	i/v-1st min. perOS-30min.	i/v-3-8hours perOS- 6-8 hours
Diphenine		perOS:slow 0.1g 3-4 times fast 0.2g 5 times/day	3-5th day	Stop during 6-12 after stop taken

Ref:

Internal medicineRussian text book
Hospital therapyRussian text book
Cycle Russian therapy
American heart website
wikipedia

Cholecystocardial Syndrome (Botkin Syndrome)

2008-11-22T15:50:00.006+03:00

Cholecystocardial Syndrome (Botkin Syndrome)

By:Dr.Zharif

–

this is the complex of clinical symptoms, which is manifested by pains in the region of heart (cardialgia), by metabolic disorders in the myocardium with disturbance of rhythm and conductivity, shortness of breath, sometimes by worsening in the coronary blood circulation as a result of the reflector and infectious-toxic actions on the myocardium, which are appeared as a result of the defeat by the pathologic process of gall bladder.

acalculous cholecystitis-35%,

the patients of elderly age - 70%.

Clinical “masks” are diverse in their manifestation, which can lead doctor into error.

Are separated cardial, allergic, thyrotoxic, neurotic, rheumatic, solar, gastrointestinal and other “masks”. One of the sufficiently frequently meeting “masks” is cardial.

History

Botkin, who first noted the possibility of reflector be ill in the heart with the gall bladder disease in clinical lectures (1883), since itself from the 25- summer age suffered the gall bladder disease, which flowed with the frequent assaults of colic, and it connected stenocarditic pains in the region of heart with the disease of gall bladder.

You will not hear complaints of the disorder of digestion, pain, inflation of stomach, patient will complain predominantly about the assaults be ill in the side of the hearts, which go with explicit changes in his function, by arrhythmia, by the difficulty of respiration, in a word, with the clear picture of stenocardia.

This attacks continues 8-10 hours, instead of 1/2 hours or several minutes, suddenly it turns yellow after such several assaults of patient.

But investigate it attentively from the very beginning, and you will ascertain that the liver is increased, the gall bladder diseases There is and so that the disorder of heart it is not accompanied by pains, but only by arrhythmia and by the strong difficulty of respiration or by the phenomena of so-called asthma, which reaches sometimes the strong degree.

Etiology

cholecystocardial syndrome can be developed with the following diseases of the bile-secreting ways:

• chronic acalculous cholecystitis;

• acute and chronic calculous cholecystitis

(maximally it is manifested during the bilious colic);

• choleduchlithiasis without the development of bilious hypertension, with bilious hypertension (with the development of mechanical jaundice);

• the pathologic processes, which lead to the contraction of the terminal division of common bilious duct (stenosing papillitis, the tumor of the large papilla of duodenum, infiltrative pancreatitis).

Pathogenesis

The pathogenesis of cholecystocardial syndrome has several mechanisms of the realization: reflector influences on the coronary vessels, the shifts of the metabolism of myocardium (especially at the moment of bilious colic) and the infectious-toxic action on the cardiovascular system with the sharp inflammatory process in the bile-secreting ways.

1. Reflector influence. The afferent pathologic pulsation, which emanate

s from extra and intramural nervous interlacements of the bile-secreting ducts with the spas

m of the sphincters Of

lyutkensa,Mirizzi,Oddi and the expansion of bilious ducts with biliar hypertension, can by means of the sympathetic and parasympathetic nerve fibers influence heart, causing the spasm of coronary vessels, the disturbance of rhythm and the like

2. Change in the metabolism of heart muscle. With the prolonged course of the gall stones disease with the frequent attacks of the biliar colic, complicated by chronic recurrent cholecystitis and associated disturbances of the functions of the liver and the pancreas, is developed the dystrophia of myocardium, connected with the complex disorders of electrolytic, enzyme and carbohydrate balance, which can lead to the disturbances of cardiovascular system.

3. Infectious-toxic action on the heart muscle with the sharp inflammatory process in the bile-secreting system (acute cholecystitis, purulent cholangitis to mechanical jaundice) with the disturbances in the system of homeostasis and the development of the acute dystrophia of myocardium, which is the reason for the increased excitability, disturbances of conductivity and contracting ability of myocardium. Besides the direct mechanisms of the forming of cholecystocardial syndrome, it is necessary to consider that with the age the frequency of morbidity increases by the ischemic disease of heart, by stenocardia and by the disturbances of rhythm, which makes especially unfavorable the flow of cholecystocardial syndrome.

Clinical pictures

pain in the region of heart (cardialgia or reflector stenocardia). .

The cardialgesic and stenocarditic forms of cholecystocardial syndrome are most common with the gall bladder disease (79% of patients).

Character pain

sharp pain 85% of patients

compressing pain 56-65% of patients

splitting pain13-58% of patients

Irradiation of pain from the right subcostal area into the leftist and into the region of the heart (more frequent during the combination of cholecystitis and pancreatitis);

Is possible the analgesic form of the cholecystocardial syndrome, when its only manifestation - disturbance of the rhythm of heart.

Arrhythmias of heart are also different:

ectopic rhythms (0,47%)

extrasystole (9,6-13,9%)

fibrillation arrhythmia (3,5-13,5%),

atrioventricular blockade and/or blockade of the right branch of His's bundle

Differential diagnostics

Between Cholecystocardial syndrome and IHD

Cholecystocardial syndrome is manifested by pains in the region of the hearts (cardialgias), whose appearance is connected with the viscero- visceral reflex on the vagus. First pains appear in by right subcostal area, then in the region of heart. Frequently the pain is localized in the region of the top of heart, and patient indicates its localization sufficiently accurately (by one finger).The pains prolonged, sharp pain, can be paroxysmal pain and be accompanied by dyspeptic phenomena.

harp paincardial Cholecystocardial syndrome important to consider connection be pain with the consumption of food, but one should remember that the pain can arise after physical load. Sometimes accompanied by jaundice.

Cholecystocardial syndrome is characteristic the syndrome of vegetative disfunction with the predominance of parasympathetic tone, neurotic syndrome is the practically integral part of the clinic of the pathology of the bile-secreting ways.

The combination of cardial complaints with the asthenoneurotic phenomena, the lability of pulse and arterial pressure can lead to the formulation of the erroneous diagnosis of vegetovascular dystonia.

During the attack in the blood are noted leukocytosis, neutrophilia, accelerated ESR, bilirubinemia, hyperglycemia, increase in the level of amylase.

On the ultrasound usually are well visible the large and small concrements of gall bladder, the diffuse or local thickening of the wall of the gall bladder (more than 4 mm) and an increase in its echodensity

The shadows of concrements are visible with the presence of the mixed or lime stones in the survey X-ray photograph. With cholecystography and cholegraphy cholesterol and pigment stones give enlightenments or defects of filling, frequently the shadow of gall bladder is absent.

On ECG during the attack of pain are noted negative waves R in the right breast and in lead 3 standard removal. They frequently take place of the disturbance of rhythm (extrasystole, atrioventricular blockade I st.), diffuse changes in the myocardium are noted.

Treatment

Cholecystoectomy

Ref:translated and edited from Russian Cardiology Website

#1 case study

2008-11-06T22:55:00.009+03:00

By:Dr.Zharif

39 yo female was admitted to the hospital with a diabetic foot ulcer. She needed IV access for Unasyn IV and labs, and failed several peripheral line attempts.

A right IJ central line was placed. Immediately after the catheter was placed, she complained of SOB(dyspnea) and palpitations. Her SpO2 was 100%, breath sounds were equal and clear bilaterally.

What do you think is going on?
Is it a pneumothorax?

HR was 140 and irregular.

EKG showed AFib with RVR.(rapid ventricular respons) CXR showed that the triple lumen catheter (TLC) was at the level of the right AV junction.

TLC at the right AV junction on CXR

AFib due to a TLC at AV junction

What would you do?
Withdraw the central line. Repeat the CXR and EKG.

What happened?
The TLC was withdrawn 5 cm with conversion to sinus rhythm and no further complaints.

Central line in superior vena cava (SVC). This is the correct position for a TLC on CXR.

Conversion to NSR(normal sinus rhythm) after the TLC was repositioned

What your final Diagnosis????

correct diagnosis will answer on 26.11.2008
write your full diagnosis on discussion below k..
tq..

β-blocker drug (Antiadrenegic drug)treatment for IHD

2008-10-27T23:07:00.015+03:00

By:Dr.Zharif

β-blocker drug (Antiadrenegic drug)treatment for IHD

Purpose of treatment :

1.Improve quality of life

2.Improve outcome of life

β-blocker drug (Antiadrenegic drug)

General Mechanism of action

block the action of endogenous catecholamines (e pinephrine (adrenaline) and norepinephrine (noradrenaline) in particular),

on β-adrenergic receptors, part of the sympathetic nervous system which mediates the fight or flight response.

Action of β adregenic receptor (part of sympathethic nerves system)

-three known types of beta receptor, designated β₁, β₂ and β₃.

a) β₁-Adrenergic receptors are located mainly in the heart and in the kidneys.

b) β₂-Adrenergic receptors are located mainly in the lungs, gastrointestinal tract, liver, uterus, vascular smooth muscle, and skeletal muscle.

c) β₃-receptors are located in fat cells

Respiratory system(β2 agonists receptor)

1.bronchodilation

2. Increase Respiratory Secretions

Cardiovascular system

Heart(β1 agonists receptor)

1.Increase heart rate

2.Increase AV conduction

3.Increase BP -rise in systolic and diastolic-NA

-rise in systolic and fall diastolic-Iso

Blood vessel(β2 agonists receptor)

1.Vasodilation

Eye(β2 agonists receptor)

1.Increase secretory activity of ciliary epithelia(caution to patient with glaucoma)

2.Increase Intraocular Pressure

GIT(not clinical significant)

1.Reduced peristalsis

2.Sphincter constricted

Bladder

1.Relaxed detrussor muscle

Uterus

1.Decrease contraction of uterus

Metabolic

1.Increase glycogenolysis- hyperglycaemia,hypelactidemia(β2)

2.Decrease insulin

3.Increase lipolysis

4.Increase lipid profile in plasma

5.Transient hyperkalemia followed by hypokalemia

CNS

Not produce any effect on CNS because poorly penetration in brain (hydrophilic)

Lipophilic drugs

Lipophilic drugs (metoprolol, propranolol, timolol) are

rapidly and completely absorbed from the gastr

ointestinal

tract but are extensively metabolised in the gut wall

and in the liver (first pass effect), so that the

ir oral

bioavailability is low (10–30%). These drugs may accumulate

in patients with reduced hepatic blood flow (i.

e.,

elderly, congestive heart failure, liver cirrhosis). Lipophilic

drugs present short elimination half-lives (1-5 h)

and they easily enter the central nervous sys

tem (CNS),

which may account for a greater incidence of

central

side-effects.

Hydrophilic drugs

Hydrophilic drugs (atenolol, esmolol) are absorbed incompletely

from the gastrointestinal tract and are excreted

unchanged or as active metabolites by the kidney.

They have longer half-lives (6–24 h), and do not interact

with other liver-metabolised drugs. They barely cross the

blood–brain barrier. Elimination half-life is increased

when glomerular filtration rate is reduced (i.e., elderly,

renal insufficiency).

Mechanism of action in IHD

The prevention of the cardiotoxic effects of catecholamines plays

The following mechanisms are also considered:

(a) Antihypertensive action.

Associated with a decrease in cardiac

output, inhibition of the release of renin and production

of angiotensin II, blockade of presynaptic a-adrenoceptors

that increase the release of norepinephrine from

sympathetic nerve terminals and decrease of central

vasomotor activity.1–9

(b) Anti-ischaemic action

b-blockers decrease myocardial oxygen demand by reducing

heart rate, cardiac contractility, and systolic

blood pressure.10 In addition, prolongation of diastole

caused by a reduction in heart rate may increase myocardial

perfusion.

angiotensin II and aldosterone production by blocking of

b1-adrenoceptors on renal juxtaglomerular cells.

(d)Improvement of left ventricular structure and function,

decreasing ventricular size and increasing ejection fraction.

6–8 b-blockers may improve cardiac function because

they:

(i) reduce heart rate, prolong diastolic filling

and coronary diastolic perfusion time,

(ii) decrease myocardial

oxygen demands,

(iii) improve myocardial energetics

by inhibiting catecholamine-induced release

of free fatty acids from adipose tissue,

(iv) upregulate

b-adrenergic receptors

(v) reduce myocardial

oxidative stress.1;11;12

(e) The antiarrhythmic effect, the

result of direct cardiac electrophysiological effects

(reduced heart rate, decreased spontaneous firing of

ectopic pacemakers, slowed conduction and increased

refractory period of AV node),

reduces the sympathetic

drive and myocardial ischaemia, improves baroreflex

function and prevents catecholamine-induced hypokalemia.

Other mechanisms include:

Inhibition of cardiac apoptosis mediated via the activation of the b-adrenergic

pathway,

Inhibition of platelet aggregation,

Reduction of the mechanical stress imposed on t

he plaque,

Preventing plaque rupture

Resensitization of the b-adrenergic pathway and changes in myocardial gene expression,

i.e., an increase in sarcoplasmic reticulum calcium ATPase, mRNA and a-myosin heavy chain mRNA and a decrease in b-myosin heavy chain mRNA levels.15

exhibit antioxidant properties and inhibit vascular smooth

muscle cell proliferation.

Other Indication

· Hypertension

· Angina

· Mitral valve prolapse

· Cardiac arrhythmia

· Congestive heart failure

· Myocardial infarction

· Glaucoma

· Migraine prophylaxis

· Symptomatic control (tachycardia, tremor) in anxiety and hyperthyroidism

· Essential tremor

· Phaeochromocytoma, in conjunction with α-blocker

also been used in the following conditions

· Hypertrophic obstructive cardiomyopathy

· Acute dissecting aortic aneurysm

· Marfan syndrome (chronic treatment with propranolol slows progression of aortic dilation and its complications)

· Prevention of variceal bleeding in portal hypertension

· Possible mitigation of hyperhidrosis

· Social anxiety disorder and other anxiety disorders

Adverse effect

Cardiovascular

1.Reduce heart rate,

2.Extreme bradycardia and AV block.

3.Impaired sinusnode function and AV-node conduction

4.Produce cold extremities and Raynaud’s phenomenon and worsen the symptoms in patients with severe peripheral vascular disease.

5.Coronospasm

Metabolic

Hypoglycaemia -In patients with insulin-dependent type I diabetes nonselective

b-blockers mask and selective b-blocker should therefore be preferred at

least in insulin dependent patients

In one study carvedilol decreased the new onset diabetes in

patients with heart failure.

Pulmonary

Increase in airway resistance and are contraindicated in patients with

asthma or bronchospastic chronic obstructive pulmonary

disease.

Central effects

Central effects (fatigue, headache, sleep disturbances,

insomnia and vivid dreams, depression) are less common

with hydrophilic drugs

In some patients the fatigue may

be related to a decrease in blood flow to skeletal muscles;

in other cases, it may be secondary to a central effect.

Sexual dysfunction

Impotence and loss of libido.

Abrupt discontinuation of b-blockers after chronic

treatment can lead to rebound symptoms (i.e., hypertension,

arrhythmias, exacerbated angina)

This increased risk is related with upregulation of badrenoceptors during chronic treatment

Contraindications

Asthma,
Symptomatic hypotension
Bradycardia
Severe decompensated heart failure
Chronic obstructive lung disease without bronchospastic activity
Peripheral vascular disease are not considered as absolute contraindications and high risk patients may obtain a significant benefit from this therapy.
Patients with heart failure and bradycardia due to sick sinus node or second or third degree AV-block may benefit from pre-treatment with pacemaker in order to tolerate b-blockers, although this approach has, however, not been formally tested.
Diabetes or intermittent lower limb claudication are not absolute contraindications for b-blockers use

I. Non-selective β₁, β₂ adrenergic antagonists

Carteolol + Low 2.5–20 mg once/twice daily

Nadolol 0 Low 40–320 mg once daily

Penbutolol + Moderate 20–80 mg once/twice daily

Pindolol ++ High 10–40 mg twice daily

Propranolol 0 High + 40–180 mg twice daily

Sotalol 0 Low +

Timolol 0 High 5–40 mg twice daily

II. Selective β₁adrenergic antagonists

Acebutolol + Moderate 200–800 mg once/twice daily

Atenolol 0 Low + 25–100 mg once daily

Betaxolol 0 Moderate 5–20 mg once daily

Bisoprolol 0 Moderate 2.5–10 mg once daily

Celiprolol + Moderate 200–600 mg once daily

Esmolol 0 Low Only i.v.

Metoprolol 0 High 50–100 mg once/twice daily

Nevibolol 0 2.5–5 mg once daily

III. α1- and β₁-adrenergic antagonists

Bucindolol + Moderate 25–100 mg twice daily

Carvedilol_ 0 Moderate 3.125–50 mg twice daily

Labetalol + Low 200–800 mg twice daily

ISA: Intrinsic Sympathomimetic Activity;

i.v.: Intravenous administration possible; AMI: Acute Myocardial Infarction; CHF: Chronic Heart Failure.

Acute Myocardial Infarction (AMI)

Intravenous dosing of b-blockers

Drug Loading dose Maintenance dose

Atenolol 5 ю 5 mg Oral, 50–100 mg/day

Esmolol 0.5 mg/kg over 1–5 min 0.05–0.3 mg/kg/min

Labetalol 20 mg in 2 min 2–10 mg/min

Metoprolol 2.5–5 mg i.v. bolus over 2 min; up to three doses Oral, 25–100 mg/12 h

Propranolol 0.15 mg/kg 0.10–0.20 mg/kg/min oral, 80–240 mg/day

Practical guidance on using b-adrenergic blockers in heart failure

Who should receive b-blocker therapy

_ All patients with chronic, stable heart failure

_ Without contraindications (symptomatic hypotension or bradicardia, asthma)

What to promise

Treatment is primarily prophylactic against death and new hospitalisations for cardiovascular reasons. Some patients will

experience improvement of symptoms.

When to start

_ No physical evidence of fluid retention (use diuretics accordingly)

_ Start ACE-I first if not contraindicated

_ In stable patients, in the hospital or in outpatient clinics

_ NYHA class IV/severe CHF patients should be referred for specialist advice

_ Review treatment. Avoid verapamil, diltiazem, antiarrhythmics, non-steroidal anti-inflamatory drugs

Beta-blocker

_ Bisoprolol, carvedilol or metoprolol

Dose

_ Start with a low dose

_ Increase dose slowly. Double dose at not less than 2 weekly intervals

_ Aim for target dose (see above) or, if not tolerated, the highest tolerated dose

Starting dose mg Target dose mg

Bisoprolol 1.25 once daily 10 once daily

Carvedilol 3.125 twice daily 25–50 twice daily

Metoprolol CR/XL 12.5–25 once daily 200 once daily

Monitoring

_ Monitor for evidence of heart failure symptoms, fluid retention, hypotension and bradycardia

_ Instruct patients to weigh themselves daily and to increase their diuretic dose if weight increases

Problem solving

_ Reduce/discontinue b-blocker only if other actions were ineffective to control symptoms/secondary effects

_ Always consider the reintroduction and/or uptitration of the b-blocker when the patient becomes stable

_ Seek specialist advice if in doubt.

Symptomatic hypotension (dizziness, light headedness and/or confusion)

_ Reconsider need for nitrates, calcium channel blockers and other vasodilators

_ If no signs/symptoms of congestion consider reducing diuretic dose

Worsening symptoms/signs (increasing dyspnoea, fatigue, oedema, weight gain)

_ Double dose of diuretic or/and ACE-I.

_ Temporarily reduce the dose of b-blockers if increasing diuretic dose does not work

_ Review patient in 1–2 weeks; if not improved seek specialist advice

_ If serious deterioration halve dose of b-blocker

_ Stop b-blocker (rarely necessary; seek specialist advice)

Bradycardia

_ ECG to exclude heart block

_ Consider pacemaker support if severe bradycardia or AV block or sick sinus node early after starting b-blockers

_ Review need, reduce or discontinue other heart rate slowing drugs, e.g., digoxin, amiodarone, diltiazem

_ Reduce dose of b-blocker. Discontinuation rarely necessary

Severe decompensated heart failure, pulmonary oedema, shock

_ Admit patient to hospital

_ Discontinue b-blocker if inotropic support is needed or symptomatic hypotension/bradycardia is observed

_ If inotropic support is needed, levosimendan may be preferred

Reference
1. Cycle clinical farmacology 6th year RSMU
2.Essential of Medical Pharmacology,KD Tripathi,JAYPEE
3.wikipedia
4.Escardio(Europian Society of Cardiology)

Conducting systems of the Heart

2008-10-26T15:14:00.007+03:00

By:Dr.Norzaher
There are four basic components to the heart's conduction system

(1) sinoatrial node (SA node)

(2) inter-nodal fibre bundles

(3) atrioventricular node (AV node)

(4) atrioventricular bundle

The sinoatrial (SA) node is a small mass of specialised cardiac muscle situated in the superior aspect of the right atrium. It lies along the anterolateral margin of this chamber between the orifice of the superior vena cava and the auricle. The specialised cardiac muscle of the SA node is characterised by the property of automatic self-excitation and it initiates each beat of the heart. Therefore, the SA node is often referred to as the pacemaker of the heart.

Since the fibres of the SA node fuse with the surrounding atrial muscle fibres, the action potential generated in the nodal tissue spreads throughout both atria at a rate of approximately 0.3 meter per second and produces atrial contraction. Interspersed among the atrial muscle fibres are several inter nodal fibre bundles which conduct the action potential to the atrioventricular (AV) node with a greater velocity (approximately 1.0 meter per second) than ordinary atrial muscle. The AV node is located in the right atrium near the lower part of the interatrial septurn. Here there is a short delay (approximately 0.1 second) in transmission of the impulse to the ventricles.

This is important because it permits the atria to complete their contraction and empty their blood into the ventricles before the ventricles contract. The delay occurs within the fibres of the AV node itself as well as in special junctional fibres that connect the node with ordinary atrial fibres.

Once the action potential leaves the AV node, it enters specialised muscle fibres called Purkinje fibres. These are grouped into a mass termed the atrioventricular (AV) bundle, or the bundle of His. The Purkinje fibres are very large and conduct the action potential at about six times the velocity of ordinary cardiac muscle (i.e., 1.5 to 4.0 meters per second). Thus the Purkinje fibres permit a very rapid and simultaneous distribution of the impulse throughout the muscular walls of both ventricles.

As the AV bundle leaves the AV node, it descends in the interventricular septurn for a short distance and then divides into two large branches, the right and left bundle branches. Each of these descends along its respective side of the interventricular septum immediately beneath the endocardium and divides into smaller and smaller branches. Terminal Purkinje fibres extend beneath the endocardium and penetrate approximately one-third of the distance into the myocardium. Their endings terminate upon ordinary cardiac muscle within the ventricles, and the impulse proceeds through the ventricular muscle at about 0.3 to 0.5 meters per second. This results in a contraction of the ventricles that proceeds upward from the apex of the heart toward its base. The pathway taken by each action potential generated by the SA node is represented schematically as

The spontaneous generation of an action potential within the SA node initiates a sequence of events known as the cardiac cycle. Each cardiac cycle lasts approximately 0.8 second and spans the interval from the end of one heart contraction to the end of the subsequent heart contraction.

Ordinarily this occurs about 72 times each minute.

The cardiac cycle has two basic components:

(1) a contraction phase (systole) during which blood is ejected from the heart

(2) a relaxation phase (diastole) during which the chambers of the heart are filled with blood.

The spontaneous generation of an action potential within the SA nodal tissue represents the start of the cardiac cycle. This electrical impulse spreads throughout the atrial muscle and leads to contraction of the two atria.

As the atria contract, the AV valves remain open and additional blood is forced into the ventricles from the veins. A large amount of blood has already passed from the atria to the ventricles prior to atrial contraction.

The aortic and pulmonary (pulmonic) semilunar valves remain closed .

After the ventricles have filled (mostly by blood returning from the large veins) and the atria have contracted, the AV valves close as the ventricles begin their contraction.

Ventricular contraction forces blood through the semilunar valves into the aorta and pulmonary trunk.

Next, as the ventricles begin to relax, the aortic and pulmonic semilunar valves close, the AV valves open, and blood flows into the ventricles to begin another cycle.

While the atria are in systole, the ventricles are relaxed (in diastole). The atria relax during ventricular systole and remain in this phase even during a portion of ventricular diastole.

Blood (like any other fluid) tends to flow from a region of high pressure to one of lower pressure.

As each chamber of the heart fills with blood, the pressure increases within it. The blood moves out of the chamber, when the various one-way valves guarding those chambers permit it to do so.

For example, intra-atrial pressure increases as blood from the veins enters them, and this pressure increases further during atrial systole.

As the ventricles contract, the blood is forced in a retrograde fashion against the AV valves, which causes them to bulge inward slightly toward the atria and which also elevates atrial pressure.

In doing so, the AV valves are effectively closed and blood is prevented from regurgitating back into the atria. Near the end of ventricular systole the AV valves are still closed and since the atria are in the process of filling, this too contributes to a rise in intra-atrial pressure.

Even before the atria enter systole, the ventricles are filled with blood to approximately 70% of their capacity. When the atria do finally contract, additional blood enters the ventricles and elevates the intraventricular pressure. As the ventricles contract, blood is forced backward, closing the AV valves, and a sharp rise in ventricular pressure occurs.

Although the ventricles exist as closed chambers for a brief moment, the pressure within them soon exceeds that in the aorta and pulmonary trunk. When this happens the aortic and pulmonic semilunar valves are forced open under pressure and blood rushes out of the ventricles and is driven into these large vessels. Accompanying the opening of the semilunar valves is a rapid decline in intraventricular pressure that continues until the pressure within the ventricles becomes less than that of the atria. When this pressure differential is reached, blood within the atria pushes the AV valves open and begins to fill the ventricles once again.

Composition of the Heart

2008-10-26T14:33:00.010+03:00

The heart comprises of three layers, epicardium, myocardium, and endocardium surrounding the inner chambers and is enclosed in a fourth protective layer known as the pericardium.

The image below shows a section through the wall of the heart in the middle of the right ventricle. Note the branched appearance of the cardiac muscle in the myocardium.

The pericardium

Within the mediastinum, the heart and origins of the great blood vessels are enclosed in a loose fitting sac termed the pericardium. This protective sac is composed of two layers separated by a space called the pericardial cavity. The outer layer is termed the parietal pericardium, and the inner layer is called the visceral pericardium.

The parietal pericardium consists of an outer layer of thick, fibrous connective tissue and an inner serous layer. The serous layer, consisting largely of mesothelium together with a small amount of connective tissue, forms a simple squamous epithelium and secretes a small amount of fluid. Normally the total volume of this fluid is only about 25 to 35 ml.

This fluid layer lubricates the surfaces to allow friction free movement of the heart within the pericardium during it's muscular contractions.

The fibrous layer of the parietal pericardium is attached to the diaphragm and fuses with the outer wall of the great blood vessels entering and leaving the heart. Thus, the parietal pericardium forms a strong protective sac for the heart and serves also to anchor it within the mediastinum.

The visceral pericardium is also known as the epicardium and as such comprises the outermost layer of the heart proper.

The epicardium (or visceral pericardium) forms the outer covering of the heart and has an external layer of flat mesothelial cells. These cells lie on a stroma of fibrocollagenous support tissue, which contains elastic fibres, as well as the large arteries supplying blood to the heart wall, and the larger venous tributaries carrying blood from the heart wall. The large arteries (coronary arteries) and veins are surrounded by adipose tissue, which expands the epicardium.

The image on the left is a diagrammatic representation of a section through the left and right ventricles as viewed from above.

Notice the difference in thickness between the wall of the left ventricle and that of the right ventricle. Also note their different shapes.

Atrial myocardial fibres are not only smaller than those of the ventricles but also contain small neuroendocrine granules, which are usually sparse and located close to the nucleus; they are most numerous in the right atrium. These granules secrete atrial natriuretic hormone when the atrial fibres are stretched excessively.

Atrial natriuretic hormone increases the excretion of water and sodium and potassium ions by the distal convoluted tubule of the kidney. It also decreases blood pressure by inhibiting renin secretion by the kidneys and aldosterone secretion by the adrenals.

The right ventricle pushes blood through the pulmonary valve and through the lungs, to enter the left atrium. It therefore has a moderately thick muscle layer composed of fibres intermediate in diameter between atrial and left ventricular muscle cells.

The left ventricle pumps blood through the high-pressure systemic arterial system and therefore has the thickest myocardium with the largest diameter muscle fibres.

In both ventricles, raised mounds of cardiac muscle (papillary muscles) protrude into the ventricular lumina and point toward the atrioventricular valves. Papillary muscles are the site of attachment of chordae tendinae, narrow tendinous cords that tether the valve parts to the wall of the ventricle beneath them.

The endocardium

The internal lining of all four heart chambers is the endocardium, which is composed of three layers

	a layer in direct contact with the myocardium
	a middle layer
	an innermost layer.

The outmost layer is composed of irregularly arranged collagen fibres that merge with collagen surrounding adjacent cardiac muscle fibres. This layer may contain some Purkinje fibres, which are part of the impulse conducting system as we shall see later.

The middle layer is the thickest endocardial layer and is composed of more regularly arranged collagen fibres containing variable numbers of elastic fibres, which are compact and arranged in parallel in the deepest part of the layer. Occasional myofibroblasts are present.

The inner layer is composed of flat endothelial cells, which are continuous with the endothelial cells lining the vessels entering and emerging from the heart.

The endocardium is variable in thickness, being thickest in the atria and thinnest in the ventricles, particularly the left ventricle. The increased thickness is due almost entirely to a thicker fibroelastic middle layer. Localised areas of endocardial thickening (jet lesions) are common, particularly in the atria, and result from turbulent blood flow within the chamber.

Cardiac muscle

Cardiac muscle and skeletal muscle have some features in common. Like skeletal muscle, cardiac muscle is striated, has dark Z lines, and possesses myofibrils that contain actin and myosin filaments. During systole these filaments slide over one another in much the same manner as in skeletal muscle contraction.

On the other hand, cardiac muscle has several unique properties. It is capable of intrinsic contraction (contraction without being triggered by a nerve impulse). This is a characteristic of all cardiac muscle. Skeletal muscle, however, contracts only when stimulated via a nerve impulse.

When you view cardiac muscle with a microscope a particularly striking feature becomes apparent the muscle cells exhibit a characteristic branching pattern. Notice in the pictures on this page that the parallel muscle cells are interconnected by diverging branches. Furthermore, one or sometimes two nuclei are present within each cell and are more centrally located than the nuclei of skeletal muscle cells.

The image on the left shows a photomicrograph of cardiac muscle through a light microscope.

Another unique feature of cardiac muscle is the presence of dense bands called intercalated discs that separate individual cells from one another at their ends. These discs represent specialised cell junctions between cardiac muscle cells.

These junctions offer very little resistance to the passage of an action potential from one cell to the next. The resistance here is so low that ions move freely through this permeable junction and thus permit the entire atrial or ventricular muscle mass to function as one giant cell. For this reason cardiac muscle is frequently referred to as a functional syncytium, a single functional unit.

Because cardiac muscle functions as a syncytium, stimulation of an individual muscle cell results in the contraction of all the muscle cells. This is an application of the all-or-nothing principle. Although the principle applies only to individual cells in skeletal muscle, if the stimulus in cardiac muscle is great enough to initiate contraction of a single cell, the entire muscular syncytium will undergo contraction.

Due to differences between the way in which the action potential travels through cardiac muscle it contracts at a slower rate than does skeletal muscle.

The fibrocollagenous skeleton

The heart has a fibrocollagenous skeleton, the main component being the central fibrous body, located at the level of the cardiac valves.

This image shows an electron microscope view of the fibrocollagenous material which makes up the 'skeleton' of the heart. It is important not only from the point of enabling the heart to maintain it's shape but also because it prevents atrial contraction of heart muscle being automatically transferred to the ventricles unless it is triggered by the AV node.

Extensions of the central fibrous body surround the heart valves to form the valve rings which support the base of each valve. The valve rings on the left side of the heart surround the mitral and aortic valves and are thicker than those on the right side, which surround the tricuspid and pulmonary valves.

A downward extension of the fibrocollagenous tissue of the aortic valve ring forms a fibrous septum between the right and left ventricles called the membranous interventricular septum. This is a minor component of the septum between the right and left ventricles, most of which is composed of cardiac muscle covered on both sides by endocardium. It is important in that it provides for attachment of cardiac muscle and lends support to the AV valves.The membranous part is located high in the septal wall beneath the aortic valve.

The fibrocollagenous skeleton of the heart separates the atrial syncytium from the ventricular syncytium; therefore an impulse from the former must pass through specialised tissue called the AV node before triggering the latter. The connective tissue network of the fibrous skeleton lies within the septa between the atria and ventricles.

Coronary Circulation

2008-10-22T23:47:00.003+04:00

By: Dr.Norzaher

The heart muscle, like every other organ or tissue in your body, needs oxygen-rich blood to survive. Blood is supplied to the heart by its own vascular system, called coronary circulation.

The aorta (the main blood supplier to the body) branches off into two main coronary blood vessels (also called arteries). These coronary arteries branch off into smaller arteries, which supply oxygen-rich blood to the entire heart muscle.

The right coronary artery supplies blood mainly to the right side of the heart. The right side of the heart is smaller because it pumps blood only to the lungs.

The left coronary artery, which branches into the left anterior descending artery and the circumflex artery, supplies blood to the left side of the heart. The left side of the heart is larger and more muscular because it pumps blood to the rest of the body.

Anatomy of Heart

2008-10-22T21:46:00.002+04:00

By: Dr.Norzaher

Coronary Arteries
Because the heart is composed primarily of cardiac muscle tissue that continuously contracts and relaxes, it must have a constant supply of oxygen and nutrients. The coronary arteries are the network of blood vessels that carry oxygen- and nutrient-rich blood to the cardiac muscle tissue.

The blood leaving the left ventricle exits through the aorta, the body’s main artery. Two coronary arteries, referred to as the "left" and "right" coronary arteries, emerge from the beginning of the aorta, near the top of the heart.

The initial segment of the left coronary artery is called the left main coronary. This blood vessel is approximately the width of a soda straw and is less than an inch long. It branches into two slightly smaller arteries: the left anterior descending coronary artery and the left circumflex coronary artery. The left anterior descending coronary artery is embedded in the surface of the front side of the heart. The left circumflex coronary artery circles around the left side of the heart and is embedded in the surface of the back of the heart.

Just like branches on a tree, the coronary arteries branch into progressively smaller vessels. The larger vessels travel along the surface of the heart; however, the smaller branches penetrate the heart muscle. The smallest branches, called capillaries, are so narrow that the red blood cells must travel in single file. In the capillaries, the red blood cells provide oxygen and nutrients to the cardiac muscle tissue and bond with carbon dioxide and other metabolic waste products, taking them away from the heart for disposal through the lungs, kidneys and liver.

When cholesterol plaque accumulates to the point of blocking the flow of blood through a coronary artery, the cardiac muscle tissue fed by the coronary artery beyond the point of the blockage is deprived of oxygen and nutrients. This area of cardiac muscle tissue ceases to function properly. The condition when a coronary artery becomes blocked causing damage to the cardiac muscle tissue it serves is called a myocardial infarction or heart attack.

Superior Vena Cava
The superior vena cava is one of the two main veins bringing de-oxygenated blood from the body to the heart. Veins from the head and upper body feed into the superior vena cava, which empties into the right atrium of the heart.

Inferior Vena Cava
The inferior vena cava is one of the two main veins bringing de-oxygenated blood from the body to the heart. Veins from the legs and lower torso feed into the inferior vena cava, which empties into the right atrium of the heart.

Aorta
The aorta is the largest single blood vessel in the body. It is approximately the diameter of your thumb. This vessel carries oxygen-rich blood from the left ventricle to the various parts of the body.

Pulmonary Artery
The pulmonary artery is the vessel transporting de-oxygenated blood from the right ventricle to the lungs. A common misconception is that all arteries carry oxygen-rich blood. It is more appropriate to classify arteries as vessels carrying blood away from the heart.

Pulmonary Vein
The pulmonary vein is the vessel transporting oxygen-rich blood from the lungs to the left atrium. A common misconception is that all veins carry de-oxygenated blood. It is more appropriate to classify veins as vessels carrying blood to the heart.

Right Atrium
The right atrium receives de-oxygenated blood from the body through the superior vena cava (head and upper body) and inferior vena cava (legs and lower torso). The sinoatrial node sends an impulse that causes the cardiac muscle tissue of the atrium to contract in a coordinated, wave-like manner. The tricuspid valve, which separates the right atrium from the right ventricle, opens to allow the de-oxygenated blood collected in the right atrium to flow into the right ventricle.

Right Ventricle
The right ventricle receives de-oxygenated blood as the right atrium contracts. The pulmonary valve leading into the pulmonary artery is closed, allowing the ventricle to fill with blood. Once the ventricles are full, they contract. As the right ventricle contracts, the tricuspid valve closes and the pulmonary valve opens. The closure of the tricuspid valve prevents blood from backing into the right atrium and the opening of the pulmonary valve allows the blood to flow into the pulmonary artery toward the lungs.

Left Atrium
The left atrium receives oxygenated blood from the lungs through the pulmonary vein. As the contraction triggered by the sinoatrial node progresses through the atria, the blood passes through the mitral valve into the left ventricle.

Left Ventricle
The left ventricle receives oxygenated blood as the left atrium contracts. The blood passes through the mitral valve into the left ventricle. The aortic valve leading into the aorta is closed, allowing the ventricle to fill with blood. Once the ventricles are full, they contract. As the left ventricle contracts, the mitral valve closes and the aortic valve opens. The closure of the mitral valve prevents blood from backing into the left atrium and the opening of the aortic valve allows the blood to flow into the aorta and flow throughout the body.

Papillary Muscles
The papillary muscles attach to the lower portion of the interior wall of the ventricles. They connect to the chordae tendineae, which attach to the tricuspid valve in the right ventricle and the mitral valve in the left ventricle. The contraction of the papillary muscles opens these valves. When the papillary muscles relax, the valves close.

Chordae Tendineae
The chordae tendineae are tendons linking the papillary muscles to the tricuspid valve in the right ventricle and the mitral valve in the left ventricle. As the papillary muscles contract and relax, the chordae tendineae transmit the resulting increase and decrease in tension to the respective valves, causing them to open and close. The chordae tendineae are string-like in appearance and are sometimes referred to as "heart strings."

Tricuspid Valve
The tricuspid valve separates the right atrium from the right ventricle. It opens to allow the de-oxygenated blood collected in the right atrium to flow into the right ventricle. It closes as the right ventricle contracts, preventing blood from returning to the right atrium; thereby, forcing it to exit through the pulmonary valve into the pulmonary artery.

Mitral Value
The mitral valve separates the left atrium from the left ventricle. It opens to allow the oxygenated blood collected in the left atrium to flow into the left ventricle. It closes as the left ventricle contracts, preventing blood from returning to the left atrium; thereby, forcing it to exit through the aortic valve into the aorta.

Pulmonary Valve
The pulmonary valve separates the right ventricle from the pulmonary artery. As the ventricles contract, it opens to allow the de-oxygenated blood collected in the right ventricle to flow to the lungs. It closes as the ventricles relax, preventing blood from returning to the heart.

Aortic Valve
The aortic valve separates the left ventricle from the aorta. As the ventricles contract, it opens to allow the oxygenated blood collected in the left ventricle to flow throughout the body. It closes as the ventricles relax, preventing blood from returning to the heart.

Introduction

2008-10-22T19:44:00.005+04:00

By: Dr.Norzaher

The cardiovascular/circulatory system transports food, hormones, metabolic wastes, and gases (Oxygen, carbon dioxide) to and from cells all over the body.

Components of the circulatory system include:
blood: consisting of liquid plasma and cells
blood vessels (vascular system): the "channels" (arteries, veins, capillaries) which carry blood to/from all tissues. (Arteries carry blood away from the heart. Veins return blood to the heart. Capillaries are thin-walled blood vessels in which gas/ nutrient/ waste exchange occurs.)
heart: a muscular pump to move the blood

There are two circulatory "circuits":
Pulmonary circulation, involving the "right heart," delivers blood to and from the lungs. The pulmonary artery carries oxygen-poor blood from the "right heart" to the lungs, where oxygenation and carbon-dioxide removal occur. Pulmonary veins carry oxygen-rich blood from tbe lungs back to the "left heart."
Systemic circulation, driven by the "left heart," carries blood to the rest of the body. Food products enter the sytem from the digestive organs into the portal vein. Waste products are removed by the liver and kidneys. All systems ultimately return to the "right heart" via the inferior and superior vena cavae.

A specialized component of the circulatory system is the lymphatic system, consisting of a moving fluid (lymph/interstitial fluid); vessels (lymphatics); lymph nodes, and organs (bone marrow, liver, spleen, thymus). Through the flow of blood in and out of arteries, and into the veins, and through the lymph nodes and into the lymph, the body is able to eliminate the products of cellular breakdown and bacterial invasion.