cardiovascular system
DESCRIPTION
Complete Cardiovascular systemTRANSCRIPT
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