Cardiovascular System + Key Terms + Disease Area

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Nouman Azmat Minhas Senior Professional Services Representative Pfizer Pakistan LTD. Base Town - Rawalpindi Presented By :-

description

Comprehensive presentation on Cardiovascular system. It covers the Anatomy and Physiology of CV system. It covers the Related Terms i.e Cardiac Output etc It covers major diseases related to CV systems . .............YOU will FIND it USEFUL...................

Transcript of Cardiovascular System + Key Terms + Disease Area

Page 1: Cardiovascular System + Key Terms + Disease Area

Nouman Azmat MinhasSenior Professional Services Representative

Pfizer Pakistan LTD.

Base Town - Rawalpindi

Presented By :-

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Cardio Heart

Vascular Vessels

A system in which blood is pumped by heart, and through vessels blood circulates to all parts of body.

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• Pulmonary Circulation: Circulation takes place between the heart and

lungs.

• Coronary Circulation: Blood circulates to the heart muscles

• Systemic Circulation: Blood circulates from heart to all parts of the

body.

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• – Pumps or pushes blood through body

• - Routes blood travels

• – Carries important “ * stuff * ” through body

* Stuff – includes oxygen, food, & waste

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The average adult has about FIVE liters of blood inside of their body, which makes up 7-8% of their body weight.

Blood is living tissue that carries oxygen and nutrients to all parts of the body, and carries carbon dioxide and other waste products back to the lungs, kidneys and liver for disposal. It also fights against infection and helps heal wounds, so we can stay healthy.

There are about one billion red blood cells in two to three drops of blood. For every 600 red blood cells, there are about 40 platelets and one white cell.

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Blood temperature is about 38°C.

PH range is about 7.35 To 7.45 (slightly alkaline).

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• PlasmaLiquid part of blood

• Red Blood Cells

They carry oxygen to all parts of the body

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• White Blood Cells

Fight and kill germs that may enter your bloodstream

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• Platelets

–Form “scabs” when you cut yourself

–Helps stop the bleeding

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Blood TypeAntigen on RBC

Antibodies In Plasma

Can Receive Blood From

Can Donate To

A A B O , A A , AB

B B A O , B B , AB

AB A , BNeither A nor B O, A,B,AB AB

O Neither A nor B

A , B O O,A,B,AB

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• Scientists sometimes study Rhesus monkeys to learn more about the human anatomy because there are certain similarities between the two species. While studying Rhesus monkeys, a certain blood protein was discovered. This protein is also present in the blood of some people. Other people, however, do not have the protein.

• The presence of the protein, or lack of it, is referred to as the Rh (for Rhesus) factor.

• If your blood does contain the protein, your blood is said to be Rh positive (Rh+). If your blood does not contain the protein, your blood is said to be Rh negative (Rh-).

A+ A-B+ B-

AB+ AB-O+ O-

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A blood transfusion is a procedure in which blood is given to a patient through an intravenous (IV) line in one of the blood vessels. Blood transfusions are done to replace blood lost during surgery or a serious injury. A transfusion also may be done if a person’s body can't make blood properly because of an illness.

Who can give you blood?

People with TYPE O blood are called Universal Donors, because they can give blood to any blood type.

People with TYPE AB blood are called Universal Recipients, because they can receive any blood type.

Rh + Can receive + or - Rh - Can only receive -

Universal Donor

Universal Recipient

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Arteries and arterioles carry blood away from heart

Capillaries site of exchange

Venules, veins return blood to heart

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• Hollow, muscular organ

• 300 grams (size of a fist)

• found in chest between lungs

• 4 chambers

• surrounded by membrane called Pericardium

• Pericardial space is fluid-filled to nourish and protect the heart.

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• Hold out your hand and make a fist. If one is a kid, heart is about the same size as the fist, and if one is an adult, it's about the same size as two fists. the heart weighs a mere 300 grams.

• Heart beats about 100,000 times in one day, about 35 million times in a year and moves 7200 liters (1900 gallons) of blood every day. During an average lifetime, the human heart will beat more than 2.5 billion times.

• If we give a tennis ball a good, hard squeeze. We're using about the same amount of force uur heart uses to pump blood out to the body. Even at rest, the muscles of the heart work hard--twice as hard as the leg muscles of a person sprinting.

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• Pumps blood through 62,000 miles of vessels

• Suffers 7.2 mil. CAD deaths worldwide each year

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• The heart is enclosed in a sac called Pericardial Sac containing Pericardial Fluid to provide protection to the Heart

• The Heart wall consist of three layers

– Endocardium

– Myocardium

– Epicardium

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• Adjacent cardiac muscle cells connected by intercalated discs

• Forms atrial and ventricular syncytia, action potential spreads throughout myocardium so atria contract as a single unit, ventricles contract as a single unit (a fraction of a second later)

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• Myogenic: cardiac muscle cells can contract without direct stimulation from CNS

• Neurogenic: autonomic nervous system can change heart rate

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• Action potential– Rapid depolarization (fast Na+ channels)– Plateau phase (slow Ca+2 channels)– Repolarization (slow K+ channels)

*plateau phase makes action potential in cardiac muscle much longer (~300 msec) than action potential in skeletal muscle (~100 msec)

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• 4 valves, located in fibrous skeleton between atria and ventricles

• 2 atrioventricular valves (AV valves)– Right AV valve = tricuspid valve– Left AV valve = bicuspid v. = mitral v.

• 2 semilunar valves– Pulmonary semilunar valve– Aortic semilunar valve

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• Atrioventricular valves, prevent blood flowing back into atria during ventricular contraction

• Tricuspid valve = right AV valve• Bicuspid valve = mitral valve = left AV valve• Attached to edges of AV valves are chordae

tendineae (dense regular CT)• Papillary muscles pull on chordae tendineae

during ventricular contraction to hold valve closed against the high pressure in the ventricles

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• Between ventricles and the large blood vessels that leave the ventricles (pulmonary trunk, aorta)

• 3 flaps each, no chordae tendineae or papillary muscles needed

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• The heart is two pumps that work together, right (pulmonary) and left (systemic) half

• Repetitive, sequential contraction (systole) and relaxation (diastole) of heart chambers

• Blood moves through circulatory system from areas of higher to lower pressure.– Contraction of heart produces the

pressure

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• Coronary circulation is the functional blood supply to the heart muscle itself

• Collateral routes ensure blood delivery to heart even if major vessels are occluded

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• 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

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• Sympathetic and parasympathetic nervoussystems

• Parasympathetic: from medulla oblongata(vagus nerve)

• Nerve branches to S-A and A-V nodes, andsecretes acetylcholine (slows rate)

• Parasympathetic activity can increase (slowheart rate) or decrease (increase heart rate)

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• Sympathetic nervous system through celiac plexus to heart secretes

norepinephrine. increases force of contractions

• Cardiac control center in medulla oblongata maintains balance between the two

• Normally both sympathetic and parasympathetic function at a steady background level

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• 12 leads (3 bipolar and 9 unipolar)

• P wave – atrial depolarization – lasts 0.08s (0.1s to atrial contraction)

• QRS complex – ventricular depolarization – size dependant – lasts 0.08s

• T wave – ventricular repolarization – lasts 0.16s

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• Enlarged R may be enlarged ventricles

• Flattened T may mean cardiac ischemia

• Prolonged Q-T interval may be ventricular arrhythmias

• Absent or flattened P may be atrial fibrillation

• No QRS with every P is “heart block” (normally 1:1 whole number ratio)

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SA node generates impulse;atrial excitation begins

Impulse delayedat AV node

Impulse passes toheart apex; ventricular

excitation begins

Ventricular excitationcomplete

SA node AV node Purkinjefibers

Bundlebranches

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• Generates blood pressure

• Routes blood– Heart separates pulmonary and systemic

circulation

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

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• 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%

• Heart failure is the inability of the heart to provide enough blood flow to maintain normal metabolism

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• Peripheral Resistance

• Cardiac Output

• Blood Pressure

• Heart Rate

• Stroke Volume

• Pre load

• After load

• Contractility

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• The resistance exerted by walls of the arteries & arterioles to passage of blood

• Total Peripheral Resistance (TPR) - the sum of all forces that oppose blood flow

– Length of vasculature (L)– Blood viscosity (V)– Vessel radius (r)

TPR = ( 8 ) ( V ) ( L )

( Λ ) ( r 4 )

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Cardiac Output: Volume of blood pumped from the left ventricle per minute

Heart Rate: Number of times the heart contracts per minute

Stroke Volume: Amount of blood pumped out by the left ventricle per beat

Cardiac output =heart rate x stroke volume

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BP = CO x PR

• Pressure exerted by blood on the arterial walls

• A result of pumping action of heart (CO) & resistance offered by arteries to blood flow (PR)

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• Systolic Blood Pressure (SBP) pressure measured in brachial artery during systole (ventricular emptying and ventricular contraction period)

• Diastolic Blood Pressure (DBP) pressure measured in brachial artery during diastole (ventricular filling and ventricular relaxation)

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(EDV) volume of the left ventricle at the end of diastole dependent on venous return & compliance (“stretch ability”) of ventricle

Load on the heart created by volume of blood injected into the LV by the LA, (I.e., at the end of ventricular diastole) and that it must eject with each contraction.

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Resistance to ventricular emptying during systole or The amount of pressure the left ventricle must generate to squeeze blood into the aorta. In a healthy heart this is synonymous with Aortic Pressure & Mean Arterial Pressure (MAP)

Mean Arterial Pressure (MAP) "average" pressure throughout the cardiac cycle against the walls of the proximal systemic arteries (aorta)

estimated as: .33(SBP - DBP) + DBP

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The squeezing contractile force that the heart can develop at a given preload

Regulated by:

• Sympathetic nerve activity (most influential)• Catecholamines (epinephrine norepinephrine)• Amount of contractile mass • Drugs

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End Diastolic Volume (EDV)Volume at the end of diastole(end of ventricular filling). In a healthy heart this is directly proportional to venous return

End Systolic Volume (ESV)Volume at the end of systole(end of ventricular contraction)

Stroke Volume (SV) = EDV - ESV

Ejection Fraction (EF) = SV EDV

Left ventricular norm for EF at Rest: approximately 62%

Left Ventricular norms for Max Exercise: approximately 80%

NOTE: Resting Ejection Fraction (EF) is the best indicator of both heart performance and heart disease prognosis

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Control of renin secretion:

• Mechanical

• Ionic

• NE release

Plays a major role in the regulation of hemodynamics and water and electrolyte balance via its circulating hormone, angiotensin II.

Renin: rate-limiting enzyme in angiotensin II production

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Blood PressureRises

Vasoconstriction

- +

A schematic portrayal of the homeostatic roles of the renin-angiotensin system

Blood VolumeRises

ReninRelease

Na+ Retention

AldosteroneSecretion

Na+ Depletion

Blood VolumeFalls

Blood PressureFalls

AngiotensinFormation

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Controls Body Fluid Balance and Associated Regulation Mechanisms and Pathways

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• 1. SMOKING

• 2. HYPERLIPIDAEMIA

• 3. HIGH SALT INTAKE

• 4. HOMOCYSTEINAEMIA

• 5. LACK OF EXERCISE

• 6. OBESITY

• 7. DIABETES

• 8. ALCOHOL

• 9. GENETIC

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Chronically elevated blood pressure:

Systolic > 140 mmHgDiastolic > 90 mmHg

90% of unknown cause – Essential Hypertension

Invariably associated with an increase inperipheral resistance

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Hypertension is a risk factor for atherosclerosis:

High B.P. damages the endothelial cells liningblood vessels promoting formation of atherosclerotic plaque

Extra strain on heart as must pump blood against Increased peripheral resistance, LVH develops.

Eventually LV cannot meet work load - outputdeclines. If output from right side of heart remainsconstant - pulmonary oedema develops, oxygen exchange declines –heart further weakened Congestive Heart Failure

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• ACE inhibitors• ATII antagonists• Diuretics -adrenoceptor

blockers

• 1-adrenoceptor blockers

• Ca2+ channel blockers

MONOTHERAPY

• Centrally acting antihypertensives

• Guanethidine• Minoxidil• Hydralazine

Drugs used only in combination

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Active molecules:Captopril, Lisinopril, Enalaprilat

Prodrugs:Enalapril, Benazepril, Fosinopril, Quinapril(Accupril), Ramipril, Moexipril, Spirapril

Beneficial effects in:

Hypertension

CHF

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• Hypotension

• Renal insufficiency

• Cough

• Hyperkalemia

• Hyperreninemia

• Ageusia

• Skin rash

• Proteinuria

• Neutropenia

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Losartan,Valsartan, Candesartan, *sartan

Non-peptide competitive inhibitors of AT1 receptors. Block ability of angiotensins II and III to stimulate pressor and cell proliferative effects.

Antihypertensive effects Cell growth effects Lack of “bradykinin” effects

Renin Inhibitors

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Sources: liver and diet

Uses in body: molecule from which steroid hormones and bile manufactured, component of cell membranes

Transport in blood: high density lipoproteins (HDL) low density lipoproteins (LDL) (not VLDL--those are chylomicrons)

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atheromas (smooth muscle cell proliferation)+sclerosis (proliferation of fibrous connective tissue)

1. Injury to artery wall by invasion of LDLs, oxidized cholesterol, free radicals, high blood pressure, chemicals from fat cells, or bacterial-induced inflammation.2. Endothelial cells recruit WBCs to site3. WBCs attack LDL site and form fatty streak4. Proliferation of smooth muscle cells and fibrous connective tissue5. Ca++ deposited and “hardens” vessel 6. Plaque= LDL, muscle cells, fibrous tissue, Ca++, WBCs

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Artery less distensible due to plaque:

1. Reduced ability to produce nitric oxide

2. Ca++ makes plaque hard

3. Fibrous tissue less distensible than normal

And…1. Blockage can reduce or cut off blood flow2. Plaque’s rough edges can stimulate clot formation

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Most strokes occur when arteries are blocked by blood clots or by the gradual build-up of plaque and other fatty deposits.

Some strokes can be caused by arteries rupturing when weak spots on the blood vessel wall break.

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Stroke is the third most common cause of death in developed countries.

It is higher in black African than in Caucasian, more common in males and uncommon below the age of 40 years.

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• age >55 years

• Male

• Black

• Hypertension

• Diabetes

• a family history of stroke.

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• Previous stroke

• High cholesterol

• High blood pressure

• heart disease

• atrial fibrillation

• Carotid artery disease

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• Sudden numbness or weakness of the face, arm or leg especially on one side of the body

• Sudden confusion, trouble speaking or understanding

• Sudden trouble seeing in one or both eyes

• Sudden trouble walking, dizziness, loss of balance or coordination

• Sudden severe headache with no known cause.

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• Also known as MI or Heart Attack

• It Is the nacrosis of an area of Heart tissue due to an interrupted Blood supply.

• MI may result from a blood clot in one of the coronary artery.

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LOSS OF PUMPING

CORONARY THROMBOSISCORONARY THROMBOSIS

MYOCARDIAL INFARCTIONMYOCARDIAL INFARCTION

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• Hypertension• Angina Pectoris• CHOLESTEROL• Smoking• Obesity• Black

MYOCARDIAL INFARCTION

RISK FACTORS

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