cardiovascular system

CARDIOVASCULAR SYSTEM

By,Jitendra MouryaMayur GuptaSameer PatilSanjeev Kumar

GuideProf. Prashant Sir

What is the cardiovascular system?

Parts of cardiovascular system ?

3

Functions of the Heart

• Generates blood pressure• Routes blood

– Heart separates pulmonary and systemic circulation

• Ensures one-way blood flow– Heart valves ensure one-way flow

Functions of the Heart

• Regulates blood supply– Changes in contraction rate and force match

blood delivery to changing metabolic needs– Most healthy people can increase cardiac

output by 300–500%

Chambers of the heart; valves

HEART

Deoxygenated blood returns to the heart via the superior and inferior vena cava, enters the right atrium, passes into the right ventricle, and from here it is ejected to the pulmonary artery.

Oxygenated blood returning from the lungs enters the left atrium via the pulmonary veins, passes into the left ventricle, and is then ejected to the aorta.

The double pump

Serous membrane

Continuous withblood vessels

Coordination of chamber contraction, relaxation

The Heart: Cardiac OutputThe Heart: Cardiac Output

Cardiac output (CO)

Amount of blood pumped by each side of the heart in one minute

CO = (heart rate [HR]) x (stroke volume [SV])

Stroke volume

Volume of blood pumped by each ventricle in one contraction

Conduction system of the heart

Heart contracts as a unit

Atrial and ventricular syncytia help conductelectrical signals through the heart

Sinoatrial (S-A) node is continuous with atrialsyncytium

S-A node cells can initiate impulses on theirown; activity is rhythmic

Electrocardiogram (ECG) can trace conductionof electrical signals through the heart

Electrocardiograms (EKG/ECG) (cont.)

Aberrant ECG patterns indicate damage

More cells constriction of bloodvessel walls

Characteristics of blood vessels

Arteries and arterioles carry blood away fromheart

Capillaries- site of exchange

Venules, veins- return blood to heart

Endothelium- prevents platelet aggregationsecretes substances that control diameterof blood vessel

Tunica media- smooth muscle and connectivetissue. Innervated by sympathetic nerves(vasoconstriction)

Missing in smallest arteries

Tunica externa- connective tissue; isvascularized

KIDNEYS AND BLOOD PRESSURE RUGULATIONTHE “RENIN-ANGIOTENSIN SYSTEM”

Definition of Hypertension- Hypertension is very common disorder particularly past middle age.

Hypertension could be that level of BP (blood pressure) at or above which long term antihypertensive treatment will reduce cardiovascular mortality.

Blood Pressure- The force exerted by the blood against the walls of the blood vessels.

Normal blood pressure- 140/90 mmHg (systolic/diastolic)

Antihypertensive

Types of Hypertension:- Mild Hypertension- 90-99 mmHg/140-159 mmHg Moderate hypertension- 100-109 mmHg/160-179 mmHg Severe Hypertension- 110mmHg or more/180 mmHg or more

Classification:- Primary hypertension- elevated BP without known cause, accounts

for over 95% of hypertension cases. Secondary hypertension- cause of hypertension can be identified

accounts for 5% of hypertension cases.

Risk factor:-

Age, alcohol, cigarette smoking, diabetes mellitus, elevated serum lipids, excess Na in diet, gender, family history, obesity, sedentary lifestyle & ⁺socioeconomic stress.

Medical management

Lifestyle modification:-• Nutritional therapy• Avoid tobacco, smoking• Reduce alcohol consumption• Physical activity

Drug Therapy

DIURETICS- First line therapy for HT, promotes salt-water excretion thereby relaxing the vascular constriction.

Thiazide diuretics- Hydrochlorthiazide, Chlorthalidone

Mechanism of action- act on DCT To inhibit Na/Cl Co-transport

ADR- Hypokalemia, hypoglycemia, hypercalcaemia

Marketed Products- Hydrazide Tab( cipla), Aquazide(Sun) Loop diuretics- Furosemide, buetanide, torasemide

Mechanism of action- act on ascendind loop of henle by inhibiting Na/K/2Cl co-transport.

Used in only severe HT with cardiac and renal insuffiency

ADR- Hyperuricaemia, hypercalciuria, hyperemagnesaemia, hypokalaemia

Marketed Products- Lasix (SANOFI AVENTIS)

ANGIOTENSIN CONVERTING ENZYME INHIBITORS– Enalapril, lisinopril, captopril.

Mechanism of action- blocks conversion of angiotensin 1 to ang. 2 which is vasoconstrictor and stimulates aldosterone release and thus promotes Na retention, also inhibit degradation of bradykinin which is vasodilator.

ADR- hypotension after first dose, dry cough, angioneuratic oedema, hyperkalaemia, fatal during pregnancy

Marketed products- Aceten tab(WOCKHARDT), Angiopril(TORRENT), Acinopril(NICHOLAS), Ciprol(CIPLA)

ANGIOTENSIN RECEPTOR ANTAGONIST

CALCIUM CHANNEL BLOCKER

VASODILATORS

BETA ADRENERGIC BLOCKER

ALPHA BLOCKER

FACTS WITH HYPERTENSION

One fifth of the deaths in India are from coronary heart disease. By the year 2020, it will account for one third of all deaths. Sadly, many of these Indians will be dying young.

there appears to be a steady increase in hypertension prevalence over the last 50 years, more in urban than in rural areas. Hypertension is 25-30% in urban and 10-15% in rural subjects.

Current projections suggest that India will have the largest cardiovascular disease burden in the world.

ARRYTHMIA

An Arrhythmia is an abnormal rhythm of the heart and is caused by problems with Hearts electrical impulse generation or conduction or both.

The electrical impulses may occur too fast or too slow or irratically causing the heart to beat very fast or very slow .

The normal rate of heart beat in a healthy person ranges between 60-80 beats per second

Types of ArrhythmiasThe arrhythmias are basically into following categories depending upon there impact on rate of heartbeat.

1) Bradycardia :In which the rate of heart beat is very low i.e. less than 60pulse /min.

2) Tachycardia : In which the rate of heart beat is very high i.e. more than 100 pulse /min

3)Atrial Fibrillation (AF or AFib) :AF is a quivering or irregular heartbeat that can lead to stroke and other heart-related complications.

4)Ventricular fibrillation: is life-threatening Ventricular fibrillation (v-fib for short) is the most serious cardiac rhythm disturbance. The

lower chambers quiver and the heart can't pump any blood, causing cardiac arrest

Types of Bradycardia

• Sinus bradycardia : The heart rate is less than 60 beats per min and it is considered as normal and not needed tobe treated.

• Sinus pause (also called sinus arrest) : During a sinus pause, the heart may miss one or more beats because its natural pacemaker.

• Sick sinus syndrome :Sick sinus syndrome happens when the normal pacemaker of the heart (the sinus node) does not work properly

• Heart block :Heart block refers to an abnormality in the way electricity passes through the normal electrical pathways of the heart. The abnormality "blocks" the electrical impulse from continuing through the normal pathways and usually results in a slower heart rate.

Types of Tachycardia

• Atrial or Supraventricular tachycardia (SVT) is a fast heart rate that starts in the upper chambers of the heart.some forms are called paroxysmal atrial tachycardia (PAT) or paroxysmal supraventricular tachycardia (PSVT).

• Sinus tachycardia = fast but steady Sinus tachycardia is a normal increase in the heart

rate The sinoatrial (SA) node --- the heart's natural pacemaker - sends out electrical

signals faster than usual. The heart rate is fast, but the heart beats properly.

• Ventricular tachycardia is a fast heart rate that starts in the heart's lower chambers (ventricles). It often occurs in life-threatening situations that dictate rapid diagnosis and treatment

Physical causes of arrhythmia

• Mechanical injury

• Smoking.

• Heart attack .

• Drug influences.

• Antiarythmatic drugs

• Congenital heart defects (present at the time of birth) e.g. Wolff-Parkinson-White syndrome .

• Strong emotions, anger and other feelings may cause imbalance in heart beats.

Actual causes

• Abnormal atomaticity.

• Impaired conduction.

• Combination of above two.

• Ischemia.

• Electrolyte and pH imbalance.

• Altering electrophysiological properties of cardiac fibres.

Mechanism of Arrythmias• Ectopic PacemakersWhen the SA node is suppressed the other specialized conduction tissues like artrial fibres, artrioventricular

nodal tissue, bundle if HIS, pirkinje fibres takes up the role of pacemakers and develop automaticity.such conditions occur in the cases of myocardial ischaemia,hypopotassaemia circulating cathecoalmines.

• Electrophisiological ActionsThis phenomenon occurs when the slope of depolarization in phase 1 increase causing premature ventricular

beats,ventricular tachycardias,ventricular,rhythm escape.

• Reentry or Altered Impulse Propagation or Conductivity DefectIn this type of mechanism heart may transmit impulses slowly or act as a conduction blocks.simply slowing the

rate of transmission of impulses through ventricals causing ventricular tachycardias, A-V blocks, ventricular premature beats.this can occur in case of

Reentry Mechanism

Antiarrythmatic Drugs• Vaughan Williams and Singh in 1969 divided

the antiarrythmatic drugs into four classes according to their actions on the heart cells.

Antiarrythmatic Drugs

Class INa+ channel blocker

Class IIBeta-Adrenergic blockers

Propanolol,Esmolol,Sotalol

Class IVCa channel blocker

Verapamil,Diliatizem

Class IIIProlong Repolaraization

Amiodarone,Bretylium,Dofelitide,Ibulitide

Class I Drugs

• They are further classified into IA, IB, IC• IA : They moderately decrease dv/dt (electrical potential) of 0 phase.

Drugs: Quninidine, Procanamide, Disopyramide, Moricizine

• IB : They make a little decrease in dv/dt of 0 phase. Drugs : Lidocaine, Mexiletine

• Ic : They markably decrease in dv/dt of 0 phase.

Drugs : Propafenone, Flecainide

Additional Drugs

• Adenosine, Digitalis : For PSVT (Paroxysmal Supraventricular Tachycardia)

• Sympathomomimetics-Isoprenaline

Anticholinergics-Antropine : for A-V Blocks(Artrio-Ventricular blocks)

Anti arrythmatic Drugs can only reset the heart beat by monitoring or controlling the flow of ions or elements such as Na+,Ca2+.Cl-,K+ in the cardial cells.

Or they can Prolong the ERP(effective refractory period) and ADP(action potential duration).

Simply antiarrythmatic drugs are used only for resseting or prolonging the action potential.

The important Drugs which are used freqently are tabulised as follows

Drugs Class Brand Name

T ½ Dosage Used for Excretion

Disopyramide I Norpace 6-7 hrs Oral 100-150 mg Anti chlorinergic

renal

Propranolol II Idneral 3-4 hrs i.v. 40-80 mg Fillbration and toxication

renal

Amiodarone III Cordarone, Pacerone

3-8 weeks

Orally 400-600mg i.v. 100-300 mg

Ventricular arrythmias

Hepatic and biliary

Verapamil IV Calan, veralan 5-12 hrs I.V. 5 mg PSVT Urine and faeces

Adenosine new Adenocar,Adenoscan

< 10 sec I.V. 6-12 mg PSVT and nearly all

above

urine

Important Drugs Used for Arrythmia

Adverse effects of antiarrythmatic Drugs

• The major adverse effect of antiarrythmatic drugs are they themselves cause arrythmia.

• Major part of these drugs are toxic if not administered accurately .e.g. lidocaine

• They can cause fall or rise in blood pressure.

• Other adverse effect seen in most antiarrythmatic drugs is nausea,bradyarrythmia,drowsiness,pulmonary aveoltis and fibrosis.

• Photosensitization