Cardiovascular phsiology

CARDIOVASCULAR PHYSIOLOGY

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Fig. 1Anatomy of the heart

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Fig. 2 A - Valve partly open Fig. 2B - Valve almost completely closed

Photographs of the pulmonary valve viewed from the top—i.e., from the pulmonary trunk looking down into the rightventricle. Fig. 2 A - On the left the valve is in the process of opening as blood flows through it from the right ventricle into the pulmonary trunk

Fig. 2 B - On the right, the valve is in the process of closing, the cusps being forced together by the downward pressure of the blood— i.e., by the pressure of the blood in the pulmonary trunk being greater than the pressure in the right ventricle.

From R. Carola, J. P. Harley, and C. R. Noback, “Human Anatomy and Physiology,” McGraw-Hill, New York, 1990 (photos by Dr. Wallace McAlpine).

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Arranged in layers tightly bound together Cardiac muscle completely encircles blood-filled chambers Contraction of these muscles mimic a squeezing fist Converts chemical energy in the form of ATP into force generation Conducting system are in contact with cardiac muscle cells via gap

junctions Some cells in the atria secretes a peptide hormone called the

atrial natriuretic peptide (ANP)

ANP is a powerful vasodilator, and a protein (polypeptide) hormone secreted by heart muscle cells. It is involved in the homeostatic control of body water, sodium, potassium and fat (adipose tissue).

It is released by muscle cells in the upper chambers (atria) of the heart (atrial myocytes), in response to high blood pressure. ANP acts to reduce the water, sodium and adipose loads on the circulatory system, thereby reducing blood pressure. [1]

Cardiac Muscle

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Cardiac MuscleFig. 3 fist simulates the contracting of the heart muscle

Web Ref.- fist simulates the contracting of the heart muscleacofchattanooga.com

On average the heart beats approximately:

~ 70 beats per minute~ 4,200 beats per hour~ 100,800 per day~ 705,600 per week~ 2,822,400 per month~ 33,868,800 per year (multiply this number by your age to get an approximate total of how many times your heart has beat thus far).

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Cardiac Muscle vs. Smooth MuscleCardiac Muscle Cardiac muscles are striated muscles due to

regular repeating sarcomeres composed of myosin .

Troponin and tropomysin are present Involuntarily controlled

Arranged in tightly bound layers Semi-spindle in shape and short contain intercalated discs and T-tubules, which has

sarcoplasmic reticulum lateral sacs that store calcium

Completely encircle blood filled chambers. An excitable tissue, converts chemical energy in

the form of ATP Consists of a conducting system that are in contact

with cardiac muscle cells via gap junctions are relatively small (100 µm long & 20 µm wide) Have 1 nucleus

Smooth & Skeletal Muscle Smooth muscle contains actin &

myosin & contract by a sliding filament mechanism

Smooth muscle cells are spindle shaped and lack striations.

Smooth muscle has a single nucleus & is capable of cell division

Skeletal muscles are striated muscles. Somatic nervous system controlled Cylindrical in shape An excitable tissue, converts chemical

energy in the form of ATP Multi nucleated

Fig. 4 different muscle cells in the human bodyWeb ref.- Cardiac muscle cells ...nlm.nih.gov

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Fig. 5 Diagram of an electron micrograph of cardiac muscle.

Electron micrograph of cardiac muscle (Courtesy of Dr. Helen Rarick).uic.edu

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Rich supply of sympathetic and parasympathetic nerve fibers contained in the vargus nerves

Sympathetic postganglionic fibers – innervate the heart - releases norepinehrine

Parasympathetic nerve fibers – terminate on cells found in the atria – releases acetylcholine

Innervation

The vagus nerve is either one of two cranial nerves which are extremely long, extending from the brain stem all the way to the viscera. The vagus nerves carry a wide assortment of signals to and from the brain, and they are responsible for a number of instinctive responses in the body. The vagus nerve helps to regulate heart beat, control of muscle movement etc.

www.wisegeek.com/what-is-the-vagus-nerve.htm

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The receptors for norepinehrine on cardiac muscle are mainly beta-adrenergic.

Beta-adrenergic blockers (β-blockers) are an important class of drugs for the treatment of various heart diseases, including high blood pressure, insufficiency of blood flow to the heart muscle (angina pectoris), irregular heart beat (arrhythmias), thickened heart muscle (hypertrophic cardiomyopathy), and decreased ability of the heart to empty or fill normally (heart failure). β-Blockers can also be used to treat migraine headache and increased pressure of the eye (glaucoma). No other class of man-made drugs has had such widespread applicability in clinical medicine.

Ref: circ.ahajournals.org/content/107/18/e117.full

Innervation

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What Is a β-Blocker?

Hormones known as catecholamines (norepinephrine, epinephrine) activate or stimulate specific receptors on cell surfaces, known as adrenergic receptors. A receptor has a specific structure that allows a drug or hormone to bind to it, similar to a key fitting in a lock.

The catecholamines are released from nerve endings of the sympathetic nervous system, an involuntary nerve network that enables the body to withstand stress, anxiety, and exercise.

Innervation

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β-Adrenergic receptors are found in the heart, blood vessels, and the lungs, and can be stimulated by catecholamine binding, thus increasing the activity of cells in the body. β-Adrenergic receptor stimulation causes an increase in heart rate, heart muscle contraction, blood pressure, and relaxation of smooth muscle in the bronchial tubes in the lung, making it easier to exercise and expand the lungs.

When β-blocking drugs are given to patients through a vein or by mouth, they will block the access of catecholamines to their receptors so that the heart rate and blood pressure are reduced, and the heart will pump with less intensity. This, in turn, will reduce the oxygen needs of the heart. The effects of β-blockers are greatest when catecholamine levels and receptor numbers are high, as would occur during intense exercise, and are lessened when catecholamine levels are reduced, as during sleep. β-Blockers usually do not completely diminish the ability of the heart to respond to stress, but instead modify the heart’s response

Ref: circ.ahajournals.org/content/107/18/e117.full

Innervation

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The hormone epinephrine, from the adrenal medulla, combines with the same receptors as norepinehrine and exerts the same actions on the heart.

The receptors for acetylcholine are of the muscarinic type.

Innervation

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Fig. 6 Autonomic innervation of the heart.

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Heart pumps blood separately but simultaneously into the systemic and pulmonary vessels

The atria contracts first then the ventricles Contraction is triggered by depolarization of the

plasma membrane. This occurs in the sinoarterial (SA) node.

The gap junctions allow action potentials to spread from one cell to another resulting in excitation of all cardiac cells.

Heartbeat Co ordination

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The SA node (normal pacemaker) discharge rate determines heart rate

The atrioventricular (AV) node is located at the base of the right atrium. Here the propagation of action potentials is relatively slow ( .1s)

allows for artrial contraction to be completed before ventricular excitation occurs.

Sequence of Excitation

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Fig. 7 Conducting system of the heart

Diagram of the heart showing the cardiac conduction systemnottingham.ac.uk

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Fig 8 Sequence of cardiac excitation

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The resting membrane is much more permeable to K+ than Na+ Resting potential is closer to K+ potential than to Na+ equilibrium

potential Due mainly to opening of Na+ channels Na+ entry depolarizes the cell and sustains the opening of more Na+

channels in +ve feedback Permeability to K+ decreases as K+ channels close also contributing to

membrane permeability Permeability to Ca+ increases as plasma membrane open and Ca 2+ flows

into the cell. L-type Ca2+ channels – (long lasting) The flow of +ve Ca+ ions into the cell balances the flow of + K+ ions out

of the cell and keeps the membrane at the plateau value.

Membrane permeability

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Fig. 9 Membrane Potential recording from a ventricular muscle cell

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Firstly a progressive reduction in potassium permeability has potassium channels open during repolarization

This gradually closes due to the membrane return to negative potential

The pacemaker cells open when the membrane potential is at negative values

These nonspecific cation channels conduct mainly an inward depolarizing sodium current termed F-type sodium channels.


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Fig 10 Membrane potential recording from a cardiac nodal cell

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T-type sodium channels (T=transient) Only opens briefly but contributes to an inward

calcium current and a boost to the pacemaker potential Depolarizing phase is caused by calcium influx through

the L-type calcium channel The opening of K+ channels repolarizes the membrane The return to negative potentials activates the

pacemaker mechanism and the cycle continues


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Tool used for evaluating the events of the heart Charges/currents are caused by the action potentials occurring

simultaneously in many myocardial cells. In a typical ECG: 1. P wave corresponds to current flow during atrial

depolarization2. QRS complex occurs .15s later. It is the result of ventricular

depolarization. N.b differs as a result of the currents in body fluid change direction

3. T wave the result of ventricular repolarization. Occurs at the same time as the QRS complex

The Electrocardiogram (ECG)

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Fig. 11 The Electrocardiogram

The T wave is the electrocardiographic expression of repolarization of the ...vetgo.com

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Systole – ventricular contraction and blood ejection Diastole – alternating period of ventricular relaxation and blood filling Isovolumetric ventricular contraction – ventricles contract but no blood

is ejected as volume is constant Ventricular ejection – rising pressure causes the aortic and pulmonary

valves to open Stroke volume – the volume of blood ejected from each ventricle during

systole Isovolumetric ventricular relaxation – valves are closed, no blood is

entering or leaving, therefore ventricular volume is not changing Ventricular filling – AV valves open and blood flows in from the atria

Mechanical events of the Cardiac Cycle

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Fig 12 Divisions of the cardiac cycle

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Fig 13 Summary of events during the cardiac cycle

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The volume of blood that each ventricle pumps: Expressed in liters per minute (L/min)

The volume of blood flowing through either the systemic or pulmonary circuit per minute

Determined by heart rate (HR) x stroke volume (SV): CO= HR x SV

Normal range for a resting adult: 72 beats x .07L=5.0L/min

The Cardiac Output

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Activity in the parasympathetic nerves causes the heart rate to decrease

Activity in the sympathetic nerves causes the heart rate to increase

Epinephrine speeds the heart by acting on the beta adrengenic receptors in the SA node

Sensitivity to change in body temperature, plasma electrolyte conc. Other hormones and adenosine

Control of Heart Rate

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Three dominant factors affect stroke volume

Changes in the end diastolic volume (the volume of blood in the ventricles before contraction known as preload)

Changes in the magnitude of the sympathetic nervous system input to the ventricles

Changes in afterload i.e. the arterial pressures against which the ventricles pump

Control of Stroke Volume

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A length tension relationship as the end diastolic volume is a major determinant of how stretched the ventricular sarcomeres are before contraction.

An increase in venous return automatically forces an increase in cardiac output by increasing end-diastolic volume and stroke volume

IMPORTANT: The equality of the right and left output must be

maintained

The Frank-Starling Mechanism

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Fig 14 Ventricular function curve

CARDIOVASCULAR PHYSIOLOGY

BLOOD CELLS

PLASMA

ARTERIES

ARTERIOLES

CAPILLARIES

VEINS

Blood is defined as a mixture of cellular components

suspended in a fluid - plasma.

BLOOD

• Average volume of blood: 5–6 L for males; 4–5 L for females

– Hypovolemia - low blood volume

– Hypervolemia - high blood volume

• Osmolarity = 300 mOsm or 0.3 Osm similar to that of coconut water

– This value reflects the concentration of solutes in the plasma

• Salinity = 0.85% ; reflects the concentration of NaCl in the blood

• Temperature is 38C, slightly higher than “normal” body temperature

• Viscosity (thickness) - 4 - 5 (where water = 1)

• The pH of blood is 7.35–7.45; x = 7.4

BLOOD CHARACTERISTICS

1. Transport:

–Oxygen from the lungs and nutrients from

the digestive tract

–Metabolic wastes from cells to the lungs and

kidneys for elimination

–Hormones from endocrine glands to target

organs

FUNCTION OF BLOOD

2. Blood maintains:

◦Body temperature by absorbing and distributing

heat to other parts of the body

◦Normal pH in body tissues using buffer systems

◦Adequate fluid volume in the circulatory

system

FUNCTION OF BLOOD

3. Blood protection: Blood prevents blood loss by:

◦Activating plasma proteins and platelets

◦Initiating clot formation when a vessel is broken Blood prevents infection by:

◦Synthesizing and utilizing antibodies

◦Activating complement proteins

◦Activating WBCs to defend the body against

foreign invaders

FUNCTION OF BLOOD

Blood is the body’s only fluid tissue

2 major components

Liquid = plasma (55%)

Formed elements (45%)

Erythrocytes, or red blood cells

Leukocytes, or white blood cells

Platelets - fragments of megakaryocytes in marrow

COMPOSTION OF BLOOD

Fig. 16 BLOOD COMPOSITION

Liquid part of blood

- Pale yellow made up of 91% water, 9% other

Three types of plasma proteins:

- Albumin: Important in regulation of water

movement between tissues and blood

- Globulins: Immune system or transport molecules

- Fibrinogen: Responsible for formation of blood

clots

PLASMA

• Organic nutrients – glucose, amino acid and

carbohydrates

• Electrolytes – sodium, calcium, potassium,

chloride and bicarbonate

• Non-protein nitrogenous substances – lactic

acid, creatinine and urea

• Respiratory gases – oxygen and carbon dioxide

PLASMA

• 7.5m in diameter

• One RBC contains 280 million hemoglobin molecules

• Life span 100-120 days and then destroyed in spleen

• Men- 5 million cells/mm3

• Women- 4.5 million cells/mm3

• Components : Hemoglobin, Lipids, ATP and carbonic anhydrase

• Function

Transport oxygen from lungs to tissues and carbon dioxide from

tissues to lungs

ERYTHROCYTES

• Structure:

Biconcave- Folding increases surface area (30% more surface area)

- plasma membrane contains spectrin

Give erythrocytes their flexibility

Anucleate-no centrioles, no organelles

◦ End result - no cell division

◦ No mitochondria means they generate ATP anaerobically

Prevents consumption of O2 being transported

ERYTHROCYTES

Consists of:

1. Globin molecules(4): Transport carbon dioxide and nitric

oxide

2. Heme molecules(4): Transport oxygen

Iron is required for oxygen transport

HEMOGLOBIN

Production of red blood cells

- Stem cells to proerythroblasts to early

erythroblasts intermediate to late to reticulocytes

Erythropoietin: Hormone to stimulate RBC

production

Erythropoiesis

1. Anemia - when blood has low O2 carrying capacity insufficient RBC or

iron deficiency. Factors that can cause anemia- exercise, B12 deficiency

2. Polycythemia - excess of erythrocytes, increase viscosity of blood 8-11

million cells/mm3. Usually caused by cancer, tissue hypoxia,

dehydration; however, naturally occurs at high elevations

4. Malaria - Disease that attacks the RBC, causes high fever

ERTHROCYTES DISEASE

Leukocytes, the only blood components that are

complete cells: 4,800 - 10,000/cubic millimeter

– Protect the body from infectious microorganisms

and remove dead cells and debris

–Can leave capillaries via diapedesis

–Move through tissue spaces (amoeboid motion)

–Many are phagocytic (possess numerous lysosomes)

LEUKOCYTES

Leukocytosis – WBC count over 11,000/mm3

– Normal response to bacterial or viral invasion

Leukopenia - a decrease in WBC count below

4,800/mm3

• Leukemia - a cancer of WBC

• Two major types of leukocytes

– Granulocytes: Neutrophils, Eosinophils, Basophils

– Agranulocytes: Monocytes, Lymphyocytes

LEUKOCYTES

1. Neutrophils- Account for 65-75% of total WBC’s

• Neutrophils have two types of granules that:

– Take up both acidic and basic dyes

– Give the cytoplasm a lilac color

– Contain peroxidases, hydrolytic enzymes, and defensins

(antibiotic-like proteins)

• Neutrophils are our body’s bacteria slayers

LEUKOCYTES CLASSES

2. Eosinophils- accounts for 1–4% of WBCs

◦ Have red-staining, bilobed nuclei

◦ Have red to crimson granules

◦ Function:

Lead the body’s counterattack against parasitic infections

Lessen the severity of allergies by phagocytizing immune

complexes (ending allergic reactions)

3. Basophils - account for 0.5-1% of all WBCs

– Have U- or S-shaped nuclei with two or three conspicuous

constrictions

– Are functionally similar to mast cells

– Have large, purplish-black (basophilic) granules that contain

histamine

• Histamine – inflammatory chemical that acts as a vasodilator

and attracts other WBCs (antihistamines counter this effect)

4. Lymphyocytes - account for 20-25% or more of WBCs and:

– Have large, dark-purple, circular nuclei with a thin rim of blue

cytoplasm

– Are found mostly enmeshed in lymphoid tissue (some circulate

in the blood)

• Most important cells of the immune system

• There are two types of lymphocytes: T cells and B

cells

– T cells - attack foreign cells directly

– B cells give rise to plasma cells, which produce antibodies

5. Monocytes account for 3–7% of leukocytes

◦ They are the largest leukocytes

◦ They have purple-staining, U- or kidney-shaped nuclei

◦ They leave the circulation, enter tissue, and differentiate into

macrophages

All leukocytes originate from hemocytoblasts

- The mother of all blood stem cells

Hemocytoblasts differentiate into myeloid stem cells and

lymphoid stem cells

- Myeloid stem cells become myeloblasts or monoblasts

Granulocytes form from myeloblasts

Monoblasts enlarge and form monocytes

- Lymphoid stem cells become lymphoblasts

Lymphoblasts develop into lymphocytes

FORMATION OF LEUKOCYTES

Leukemia refers to cancerous conditions involving white blood

cells

Leukemias are named according to the abnormal white blood

cells involved

◦ Myelocytic leukemia – involves myeloblasts

◦ Lymphocytic leukemia – involves lymphocytes

Acute leukemia involves blast-type cells and primarily affects

children

Chronic leukemia is more prevalent in older people

LEUKOCYTE DISEASE

Platelets are fragments of megakaryocytes

Their granules contain serotonin, Ca2+, enzymes, ADP,

and platelet-derived growth factor

Platelets function in the clotting mechanism by forming a

temporary plug that helps seal breaks in blood vessels

Platelets not involved in clotting are kept inactive by

nitric oxide (NO) and prostaglandins

PLATELETS

Fig. 17 VASCULAR SYSTEM

Arteries are muscular blood vessels that carry

blood away from the heart(oxygenated and

deoxygenated blood) .

The pulmonary arteries will carry

deoxygenated blood to the lungs

and the sytemic arteries will carry oxygenated

blood to the rest of the body.

ARTERIES

Arteries have a thick wall that consists of three layers.

- The inside layer is called the endothelium

- the middle layer is mostly smooth muscle

- the outside layer is connective tissue.

The artery walls are thick so that when blood enters

under pressure the walls can expand.

ARTERIES

When the left ventricle ejects blood into the aorta, the

aortic pressure rises.

The maximal aortic pressure following ejection is termed

the systolic pressure (Psystolic).

As the left ventricle is relaxing and refilling, the pressure

in the aorta falls.

The lowest pressure in the aorta, which occurs just before

the ventricle ejects blood into the aorta, is termed the

diastolic pressure (Pdiastolic )

Arterial Blood Pressure

When blood pressure is measured using a

sphygmomanometer, the upper value is the systolic pressure

and the lower value is the diastolic pressure.

Normal systolic pressure is 120 mmHg or less, and normal

diastolic pressure is 80 mmHg or less.

The difference between the systolic and diastolic pressures

is the aortic pulse pressure, which typically ranges between

40 and 50 mmHg. The mean aortic pressure(Pmean) is the

average pressure (geometric mean) during the aortic pulse

cycle.

Arterial pressure is measured using a sphygmomanometer (i.e.

blood pressure cuff) on the upper arm.

The systolic and diastolic pressures that are measured represent

the pressure within the brachial artery, which is slightly

different than the pressure found in the aorta or the pressure

found in other distributing arteries.

As the aortic pressure pulse travels down the aorta and into

distributing arteries, there are characteristic changes in the

systolic and diastolic pressures, as well as in the mean pressure.

MEASUREMENT OF SYSTEM ARTERIAL PRESSURE

The systolic pressure rises and the diastolic pressure falls,

therefore the pulse pressure increases, as the pressure pulse

travels away from the aorta.

This occurs because of reflective waves from vessel

branching, and from decreased arterial compliance (increased

vessel stiffness) as the pressure pulse travels from the aorta

into systemic arteries. There is only a small decline in mean

arterial pressure as the pressure pulse travels down

distributing arteries due to the relatively low resistance of

large distributing arteries.

An arteriole is a small artery that extends and leads to

capillaries.

Arterioles have thick smooth muscular walls. These

smooth muscles are able to contract (causing vessel

constriction) and relax (causing vessel dilation).

This contracting and relaxing affects blood pressure; the

higher number of vessels dilated, the lower blood

pressure will be.

ARTERIOLES

Local Controls: are mechanisms independent of hormones and

nerves. Hyperemia occurs when blood flow in an organ

increases by arteriolar dilation in response to an increase in

metabolic activity that causes local changes such as decrease in

O2, increase in CO2 and H+.

Extrinsic Controls: Sympathetic nerves that provide a rich supply

of impulses to arterioles. Release norepinephrine and cause

vasoconstriction

Hormones such as vasopressin (from posterior pituitary) and

angiotension II (from liver) constrict arterioles.

Heart

- High intrinsic tone; oxygen extraction is very high at rest, and so

flow must increase when oxygen consumption increases if

adequate oxygen supply is to be maintained.

- Controlled mainly by local metabolic factors, particularly

adenosine, and flow autoregulation; direct sympathetic influences

areminor and normally overridden by local factors.

- Vessels are compressed during systole, and so coronary flow

occurs mainly during diastole.

ARTERIOLAR CONTROL IN SPECIFIC ORGANS

Skeletal Muscle

- Controlled by local metabolic factors during exercise.

- Sympathetic nerves cause vasoconstriction (mediated by

alpha-adrenergic receptors) in reflex response to

decreased arterial pressure.

- Epinephrine causes vasodilation, via beta-adrenergic

receptors, when present in low concentration and

vasoconstriction, via alphaadrenergic receptors, when

present in high concentration.

Kidneys

- Flow autoregulation is a major factor.

- Sympathetic nerves cause vasoconstriction, mediated

by alpha-adrenergic receptors, in reflex response to

decreased arterialpressure and during stress.

Angiotensin II is also a major vasoconstrictor. These

reflexes help conserve sodium and water.

Lungs

- Very low resistance compared to systemic circulation.

- Controlled mainly by gravitational forces and passive

physical forces within the lung.

- Constriction, mediated by local factors, occurs in

response to low oxygen concentration—just opposite

that which occurs in thesystemic circulation.

Brain

- Excellent flow autoregulation.

- Distribution of blood within the brain is controlled by

local metabolic factors.

- Vasodilation occurs in response to increased

concentration of carbon dioxide in arterial blood.

- Influenced relatively little by the autonomic nervous

system.

GI Tract, Spleen, Pancreas, and Liver

- Actually two capillary beds partially in series with each other; blood

from the capillaries of the GI tract, spleen, and pancreas flows via the

portal vein to the liver. In addition, the liver also receives a separate

arterial blood supply.

- Sympathetic nerves cause vasoconstriction, mediated by alpha-

adrenergic receptors, in reflex response to decreased arterial pressure

and during stress. In addition, venous constriction causes displacement

of a large volume of blood from the liver to the veins of the thorax.

- Increased blood flow occurs following ingestion of a meal and is

mediated by local metabolic factors, neurons, and hormonessecreted by

the GI tract.

SKIN

- Controlled mainly by sympathetic nerves, mediated by

alpha-adrenergic receptors; reflex vasoconstriction occurs

in response to

decreased arterial pressure and cold, whereas vasodilation

occurs in response to heat.

- Substances released from sweat glands and noncholinergic,

nonadrenergic neurons also cause vasodilation.

- Venous plexus contains large volumes of blood, which

contributes to skin color.

Capillaries are the smallest of a body’s vessels; they connect arteries and veins, and

most closely interact with tissues.

They are very prevalent in the body; total surface area is about 6,300 square meters.

Because of this, no cell is very far from a capillary, no more than 50 micrometers

away.

The walls of capillaries are composed of a single layer of cells, the endothelium,

which is the inner lining of all the vessels. This layer is so thin that molecules such as

oxygen, water and lipids can pass through them by diffusion and enter the tissues.

Waste products such as carbon dioxide and urea can diffuse back into the blood to be

carried away for removal from the body.

CAPILLARIES

The "capillary bed" is the network of capillaries present throughout

the body. These beds are able to be “opened” and “closed” at any

given time, according to need.

This process is called auto-regulation and capillary beds usually

carry no more than 25% of the amount of blood it could hold at any

time.

The more metabolically active the cells, the more capillaries it will

require to supply nutrients.

Blood velocity decreases as blood passes through the huge cross

sectional area of a capillary.

CAPILLARIES

There are three basic mechanisms by which substances move across

capillary walls to enter or leave the interstitial fluid:

(1) Diffusion is the only important means by which net movement of

nutrients, oxygen and metabolic end products can occur. Intercellular

clefts allow the passage of polar molecules. Brain capillaries, however,

are tight with no intercellular clefts. Liver capillaries are leaky with large

clefts for movement of substances. The trans-capillary diffusion gradient

is setup by utilization or production of a substance.

DIFFUSION & EXCHANGE ACROSS CAPILLARY WALL

(2) Vesicle transport allows for the passage of

molecules via endo- and exocytosis.

(3) Bulk flow enables protein-free plasma to

move from capillaries to the interstitial fluid due to

hydrostatic pressure. This is opposed by an osmotic force,

resulting from differences in protein concentration that

tends to move interstitial fluid into the capillaries. Bulk

flow also serves to function in distributing extracellular

fluid.

Fig. 18 DISTRIBUTION OF THE EXTRACELLULAR FLUID BY BULK FLOW

Veins carry blood to the heart.

The pulmonary veins will carry oxygenated blood to the

heart awhile the systemic veins will carry deoxygenated

to the heart.

Most of the blood volume is found in the venous system;

about 70% at any given time.

VEINS

The veins outer walls have the same three layers as the

arteries, differing only because there is a lack of smooth

muscle in the inner layer and less connective tissue on the

outer layer.

Veins have low blood pressure compared to arteries and

need the help of skeletal muscles to bring blood back to

the heart.

VEINS

Most veins have one-way valves called venous valves to prevent

backflow caused by gravity.

They also have a thick collagen outer layer, which helps maintain

blood pressure and stop blood pooling.

If a person is standing still for long periods or is bedridden, blood

can accumulates in veins and can cause varicose veins.

The hollow internal cavity in which the blood flows is called the

lumen.

VEINS

A muscular layer allows veins to contract, which puts

more blood into circulation.

Veins are used medically as points of access to the blood

stream, permitting the withdrawal of blood specimens for

testing purposes, and enabling the infusion of fluid,

electrolytes, nutrition, and medications.

VEINS

By the time blood has passed from the capillaries into the venous

system the pressure has dropped significantly.

The average blood pressure in the venous system is only 2 mmHg

(millimeters of mercury) as compared to an average of 100 mmHg

in the arterial system.

The low venous pressure is barely adequate to drive blood back

to the heart, particulary from the legs.

Other mechanisms are needed to aid in the return of blood to the

heart.

DETERMINANTS OF VENOUS PRESSURE

The flow of venous blood back to the heart is increased

by the sympathetic nervous system, the skeletal muscle

pump, and the respiratory pump.

Veins are enervated by sympathetic motor neurons.

Sympathetic input causes vasoconstriction, which

increases pressure, which drives blood back to the heart.

When the body needs to mobilize more blood for

physical activity, the sympathetic nervous system

induces vasoconstriction of veins.

Veins pass between skeletal muscles.The contraction of skeletal

muscle squeezes the vein, thus increasing blood pressure in that

section of the vein.

Pressure causes the upstream valve (furthest from the heart) to

close and the downstream valve (the one closest to the heart) to

open. Repeated cycles of contraction and relaxation, as occurs

in the leg muscles while walking, effectively pumps blood back

to the heart.

While the contraction of skeletal muscle in the legs drives venous

blood out of the lower limbs, the act of breathing helps to drive

venous blood out of the abdominal cavity.

As air is inspired, the

diaphragm descends and abdominal

pressure increases.

The increasing pressure squeezes veins

and moves blood back toward the heart.

The rhythmic movement of venous blood causes by the act of

breathing is called the respiratory pump.

Venous valves prevent backflow of blood in veins

Cardiovascular Physiology

The lymphatic system

Blood volume and long-term regulation of arterial pressure

Counteracting the effects of blood loss through

haemorrhage

The lymphatic system is a network of small organs (lymph

nodes) and tubes (lymphatic vessels/lymphatics) through

which a fluid derived from interstitial fluid (lymph) flows.

Fig.1illustrates the lymphatic system (green) in relation to

the cardiovascular system (blue and red).

The lymphatic system is a one-way system whose vessels

constitute a route for the movement of interstitial fluid to

the cardiovascular system. As such it is technically not a

part of the cardiovascular system.

Defining the lymphatic system

Figure 19- The lymphatic system

The lymphatic capillaries are the first of the lymphatic vessels. Numerous lymphatic capillaries are present in the interstitium of nearly all organs and tissues and are completely distinct from blood vessel capillaries.

They are tubes consisting of a single layer of endothelial cells resting on a basement membrane, but have large water-filled channels that are permeable to all interstitial fluid constituents including protein.

Movement of interstitial fluid to the cardiovascular system

The interstitial fluid continuously enters the lymphatic

capillaries in small amounts by bulk flow.

The fluid now known as lymph then flows from the capillaries

into the next set of lymphatic vessels which converge to

from larger and larger lymphatic vessels. At various points

lymph flows through the lymph nodes.

The entire network ends in two large lymphatic ducts which

drain into the subclavian veins in the lower neck. This is the

point of entry into the cardiovascular system.


The movement of lymph into the cardiovascular system is very important because the amount of fluid filtered out of all the blood-vessel capillaries except those in the kidney, exceeds that reabsorbed by approximately 4L per day. The lymphatic system returns this 4L also containing leaked proteins to the blood.

Failure of the lymphatic system allows the accumulation of excessive interstitial fluid resulting in massive swelling of the area involved and is termed edema.

The lymphatic system also provides the pathway by which fats absorbed from the gastrointestinal tract reach the blood.


The lymphatic vessels beyond the lymphatic capillaries propel the lymph within them by their own contractions. The smooth muscle in the walls exerts a pump-like action by inherent rhythmical contractions.

The lymphatic vessels have valves similar to those in veins so contractions produce a one-way flow towards the point at which the lymphatics enter the circulatory system.

The lymphatic-vessel smooth muscle is responsive to stress. It is inactive when there is no accumulation of interstitial fluid and hence no entry of lymph into the lymphatics.

Mechanism of lymph flow

Increased fluid filtration out of blood vessel capillaries

increases lymph formation.

This increased fluid entering the lymphatics stretches

the walls and triggers rhythmical contractions of the

smooth muscle.

This constitutes a negative-feedback mechanism for

adjusting the rate of lymph flow to the rate of lymph

formation and thereby preventing edema.

Mechanism of lymph flow

The smooth muscle of the lymphatic vessels is

innervated by sympathetic neurons which

undergo excitation in various physiological states

such as exercise and may contribute to

increased lymph flow.

Lymph flow is also enhanced by forces external

to the lymphatic vessels such as the skeletal

muscle pump and the respiratory pump.

Mechanisms of lymph flow

The mean systemic arterial pressure is the

arithmetic product of

◦ the cardiac output (the volume of blood pumped into

the artery per unit time) &

◦ the total peripheral resistance (the sum of resistances

to flow offered by all the systemic blood vessels).

Defining the mean systemic arterial pressure

MAP is the major cardiovascular variable being regulated in

the systemic circulation.

It drives blood flow through all organs except the lungs.

Its maintenance is required for ensuring adequate blood

flow to these organs.

The average volume of blood in the systemic arteries (mean

arterial blood volume, MABV) is determined by the CO and

TPR over time in the systemic arteries. It is this blood

volume that causes the pressure.


The relationship which defines MAP as the arithmetic product of CO and TPR can be formally derived from the basic equation relating flow, pressure and resistance.◦ F = ∆P/R

◦ Therefore, ∆P = F x R

The systemic vascular system is a continuous series of tubes so the equation holds for the entire system, i.e. from the arteries to the right atrium. Therefore,o ∆P = mean systemic arterial pressure, MAP – pressure in the

right atriumo F = the cardiac output, COo R = the total peripheral resistance, TPR


The pressure in the right atrium is approximately 0mmHg. Thus the equation becomes◦ MAP =CO x TPR

An analogous equation can also be applied to pulmonary circulation.


At steady state the rate at which the heart pumps

blood into the arteries is equal to the total rate at

which blood leaves the arteries via the arterioles.

This is analogous to a pump pushing fluid into a

container at the same rate as which the fluid leaves the

container via outflow tubes. Shown in Fig 20a

Thus the height of the fluid in the column ∆P which is

the driving pressure for outflow remains stable.

TPR as a determinant of MAP

Recall

Hydrostatic Pressure = pgh

where p (rho) = density of fluid

g = acceleration due to gravity

h = height of the fluid column

It is defined as the pressure a vertical column of fluid

exerts due to the effects of gravity.

p and g are constants, so change in pressure is dependent

on change in height.


If the steady state is disturbed by loosening the cuff on one of

the outflow tubes the radius increases reducing its resistance

and increasing its flow.

More fluid leaves the reservoir than enters pump so the volume

and hence the height of the fluid column decreases until a new

steady state between inflow and outflow is reached.

Thus at any given pump input change in total outflow

resistance must produce changes in the volume and hence the

height (pressure) in the reservoir once no compensatory

adjustments are made.


Figure 20a - Dependence of arterial blood flow upon total arteriolar resistance

TPR is equated with Total Arteriolar Resistance

During exercise skeletal-muscle arterioles dilate thereby

decreasing resistance.

As shown in Fig.20b, if only one vascular bed (representative of

the skeletal-muscle arterioles) dilated and the CO and arteriolar

diameter remained unchanged in all the other beds (arterioles of

the other organs), the increased run-off through the skeletal-

muscle arterioles will decrease the MAP.

To compensate for this decreased resistance the arterioles in

other organs will constrict simultaneously to increase the

resistance rendering the TPR and hence the MAP unchanged.

The brain arterioles will however remain unchanged ensuring a

constant brain blood supply.


Figure 20b- compensation for dilation in one bed by constriction in others

When outflow tube1 dilates outflow tubes 2-4 are simultaneously tightened. Outflow tube 5 remains unchanged.

It is however important to note that the compensation

method previously described can only maintain the TPR

within certain limits.

The actual case during exercise is that the skeletal muscle

arterioles will dilate so wide that even complete closure of

the other arterioles will not prevent the total outflow

resistance from falling.

Thus this example only serves as an intuitive approach to

explain why TPR is one of the two variables that set the MAP.


Fig. 21 illustrates the grand scheme of factors that determine

the mean systemic arterial pressure. A change in a single

variable will produce a change in the mean systemic arterial

pressure by altering either cardiac output or total peripheral

resistance.

As a specific example Fig. 22 illustrates how the decrease in

blood volume occurring during haemorrhage leads to a

decrease in the mean arterial pressure.

Any deviation in arterial pressure like that occurring during

haemorrhage will elicit homeostatic reflexes so that CO

and/or TPR will be changed in the direction required to

minimize the initial change in arterial pressure.

Factors that determine the MAP

Figure 21-Summary of factors that determine MAP

Determinants of CODeterminants of TPR with the addition of the effect of hematocrit on resistance

Figure 22- Sequence of events by which a decrease in blood volume leads to a decrease in the MAP

Baroreceptor reflexes bring about homeostatic adjustments to MAP on a short-term basis (seconds to hours) i.e. they function as short term regulators of MAP.

They utilize mainly changes in the activity of autonomic nerves supplying the heart and blood vessels, as well as changes in the secretion of the hormones (epinephrine, angiotensin II, and vasopressin) that influence these structures.

The baroreceptor reflex is activated instantly by any blood pressure change and attempts to restore blood pressure rapidly towards normal. It cannot regulate on a long-term basis as arterial baroreceptors adapt to arterial pressure once it deviates from its normal operating point for more than a few days. They will therefore have a decreased frequency of action potential firing at any given pressure.

Short-term regulation of MAP by baroreceptor reflexes

Baroreceptor reflexes originate primarily with arterial receptors that respond

to changes in pressure called arterial baroreceptors. They are constituted by

the two carotid sinuses and the aortic arch baroreceptor. Afferent neurons

from the arterial baroreceptors travel to the brain stem and provide input to

the neurons of the cardiovascular control centres there.

The carotid sinuses are located high in the neck at the point where the

carotid arteries divide.

At the carotid sinus the artery wall is thinner and contains a large number of

branching vine-like nerve endings that are highly sensitive to stretch.


The degree of wall stretching is directly related to the pressure

within the artery so the carotid sinus serves as pressure receptors, or

baroreceptors.

The arch of the aorta is functionally similar to the carotid sinuses.

Fig. 23 illustrates the location of the arterial baroreceptors.


Figure 23- Location of arterial baroreceptors

It is important to note that the large systemic veins the pulmonary vessels and the walls of the heart also contain baroreceptors which keep the brain cardiovascular control centres constantly informed about changes in pressure in these areas thus providing a further degree of regulatory sensitivity. They contribute a feed forward component of arterial pressure control.

The primary integrating centre for the baroreceptor reflexes is a diffuse network of highly interconnected neurons called the medullary cardiovascular centre, located in the brainstem medulla oblongata.

The input received by neurons in this centre determines the outflow from

the centre along neural pathways that terminate upon the cell bodies and dendrites of the vagus (parasympathetic) neurons to the heart and the sympathetic neurons to the heart, arterioles and veins.


As illustrated in Figure 24 a decrease in sympathetic outflow to the

heart, arterioles and veins and an increase in parasympathetic

outflow to the heart results when the arterial baroreceptors increase

their rate of discharge (firing of action potentials) and vice versa.

Decreased arterial pressure elicits increased plasma concentrations

of the hormones angiotensin II and vasopressin which raise arterial

pressure by constricting arterioles.


Figure 24- Neural components of the arterial baroreceptor reflex

If the initial changes were a decrease in arterial pressure all the arrows in the box will be reversed.

A decrease in the arterial pressure causes the discharge rate of the

arterial baroreceptors to also decrease. Thus fewer impulses travel

up the afferent nerves to the medullary cardiovascular centre and

induces

◦ Increased heart rate because of increased sympathetic activity to the heart

and decreased parasympathetic activity.

◦ Increased ventricular contractility because of increased sympathetic activity

to the ventricular myocardium.

◦ Arteriolar constriction because of increased sympathetic activity to the

arterioles and increased plasma concentrations of angiotensin II and

vasopressin.

◦ Increased venous constriction because of increased activity to the veins.


The net result is an increased CO (increased heart rate and stroke

volume), increased TPR (arteriolar constriction) and return of blood

pressure toward normal.

The arterial baroreceptor reflex compensation for decreased arterial

pressure as occurs during a haemorrhage is illustrated in Fig. 25.

The compensatory mechanisms do not restore arterial pressure

completely to normal. Toward normal refers to the values before

haemorrhage. For simplicity, reflex increases in angiotensin II and

vasopressin which help to constrict arterioles are not shown.


Figure 25- Arterial baroreceptor reflex compensation for haemorrhage

The major factor for long-term regulation of MAP is blood volume.

This is because it influences venous in turn venous pressure, venous

return, end-diastolic volume, stroke volume and cardiac output. Thus

factors controlling blood volume play a dominant role in determining

blood pressure.

An increased blood volume increases arterial pressure but this

increased arterial pressure reduces blood volume (particularly the

plasma component of the blood) by increasing the excretion of salt and

water by the kidneys.

Long-term regulation of MAP by blood volume

Fig. 26 illustrates how the two causal chains constitute negative-

feedback loops that determine both blood volume and arterial

pressure. ◦ An increase in blood pressure causes a decrease in blood volume which tends

to bring the blood pressure back down.

◦ An increase in blood volume raises the blood pressure which tends to bring

the blood volume back down.

Because arterial pressure and blood volume influence each other,

blood pressure can stabilize in the long run only at a value at which

blood volume is also stable. Thus steady state blood-volume

changes are the single most long-term determinant of blood

pressure.

Long-term regulation of MAP by blood volume

Figure 26- Causal reciprocal relationships between arterial pressure and blood volume.

Increase in arterial pressure induces a decrease in blood volume

Increase in blood volume induces an increase in arterial pressure

Low blood volume in a haemorrhage produces hypotension (low

blood pressure) .

Blood loss leads to decreased blood volume, venous pressure, venous

return, arterial pressure and ventricular end-diastolic pressure. These

decrease the stroke volume in the cardiac muscle which hence

decreases cardiac output and the arterial blood pressure

The most serious consequences of hypotension are reduced blood

flow to the brain and cardiac muscle.

Haemorrhage as a cause of hypotension

The immediate counteracting response to haemorrhage is the arterial

baroreceptor reflex. Fig. 26 shows how five variables change over time

when there is a decrease in blood volume. It illustrates five simultaneous

graphs showing the time course of the cardiovascular effects of

haemorrhage.

It is important to note that the entire decrease in arterial pressure

immediately following haemorrhage is secondary to the decrease in stroke

volume and hence the CO. All variables shown are increased relative to the

state immediately following the haemorrhage, but not necessarily to the state

prior to the haemorrhage.

Compensatory mechanisms for haemorrhage

Figure 27- The time course of the cardiovascular effects of haemorrhage

The values of the factors changed as a direct result of haemorrhage (stroke

volume, CO and MAP) are restored by the baroreceptor reflex toward but

not to normal.

In contrast values not altered directly by haemorrhage but only by the

reflex response to haemorrhage (heart rate and TPR) are increased above

their prehaemorrhage values.

Increases peripheral resistance results from increases in sympathetic

outflow to the arterioles in many vascular beds but not those of the heart

and brain. Thus skin kidney and intestinal blood flow may decrease

markedly.


A second type of compensatory mechanism involves the

movement of interstitial fluid into capillaries.

The drop in blood pressure and increase in arteriolar constriction

decrease capillary hydrostatic pressure, thereby favouring

absorption of interstitial fluids.

Thus the initial blood loss and the decreased blood volume is in

large part compensated for by the movement of interstitial fluid

into the vascular system. Fig. 27 illustrates this mechanism.


Figure 27- Mechanism compensating for blood loss by movement of interstitial fluid into the capillaries

Approximately 12 to 24 hours after a moderate haemorrhage the

blood volume may be restored virtually to normal by this

mechanism.

At this time the entire restoration of the blood volume is due to

expansion of the plasma volume. This is shown in Table 1.

Both of these early compensation mechanisms for haemorrhage

(the baroreceptor reflexes and the interstitial fluid absorption) are

highly efficient so that losses of as much as 1.5L of blood

approximately 30% of the blood volume can be sustained with only

slight reductions in MAP and CO.


Table 1- Fluid shifts after haemorrhage

Absorption of interstitial fluid only redistributes the extracellular

fluid. Ultimate replacement of fluid loss involves the control of

fluid ingestion and kidney function.

Replacement of lost erythrocytes requires the stimulation of

erythropoiesis by erythropoietin. This replacement requires days

to weeks in contrast to the rapidly occurring reflex

compensations described.


“Shock” denotes any situation in which a decrease in blood flow to the

organs and tissues damages them.

Decrease in blood volume secondary to haemorrhage or loss of fluid

other than blood can result in a type of shock called hypovolemic

shock.

The heart suffers damage if shock is prolonged. As it deteriorates, CO

declines markedly and shock becomes progressively worse and

ultimately irreversible even if blood pressure is temporarily restored.

Haemorrhage leads to hypovolemic shock

Cardiovascular Patterns in Health & Disease

135

Hypotension and hypertension as it relates to the cardiovascular system.

Understand the upright posture. Discuss the role of exercise in cardiovascular system. Discuss what causes heart failure. Explain coronary artery disease and heart attack. Explain drugs used in hypertension / heart failure

GENERAL OBJECTIVES

WHAT IS BLOOD PRESSURE?

©The heart pumps blood into the arteries which goes throughout the body and cells.

©When the heart muscles contract, blood is forced out.

© The contraction is as a result of the heart beating and the pressure building up.

© This is the systolic blood pressure.

© The relaxation between beats is the diastolic pressure.

BLOOD PRESSURE

© Blood pressure is measured in millimeters of Mercury (mm Hg)

© Systolic pressure is when the heart contracts while diastolic pressure is when it relaxes.

© Normal Blood Pressure:

120 140

80 90HIGH =

BLOOD PRESSURE

HYPOTENSION (LOW BLOOD PRESSURE)?

© Loss of Blood volume e.g.. hemorrhage. Erythrocytes needs hormone erythropoietin to stimulate erythropoiesis.

CAUSES

© Reduced blood flow in brain and cardiac muscle.

© Loss of salt which causes a loss of water e.g.. diarrhea, vomiting.

© Strong emotions e.g.. fainting.

© Shock (may be reversible by blood transfusion and therapy).

HYPOTENSION (LOW BLOOD PRESSURE)?

THREE TYPES Of SHOCK© Hypovolemic – decreased blood volume.

© Low Resistance – decreased in total peripheral resistance.

© Cardiogenic – decrease in cardiac output.

© Peripheral resistance: the resistance to pump blood in the small arterial branches that carry blood to tissues.

© Cardiac output: the volume of blood pumped by heart within a

specified time.

DEFINITION OF PERIPHERAL RESISTANCE AND CARDIAC OUTPUT

HEMORRHAGE

© Bleeding or abnormal flow of blood.

© Transfusion helps in restoring blood volume.

© Interstitial fluid goes into the capillaries causing the blood pressure to drop.

© Increased arteriolar constriction decreases capillary hydrostatic pressure and interstitial fluid is absorbed.

HOW THE BODY REGULATES BLOOD VOLUME

THE UPRIGHT POSTURE

© This is movement from a horizontal/lying position to a vertical/standing one. The blood vessels are in the same level with the heart.

© Gravity increases the pressure of the body below the heart and decreases the pressure force in organs above the heart.

© Increase in capillary pressure caused by gravity, increases filtration of fluid out of capillaries. This causes swelling of feet after a long period of standing.

© This involves blood vessels of the heart. © A major contributor to this disease is a build up of

plaque in vessels which slows down blood flow.

WHAT IS CARDIO VASCULAR DISEASE

HYPERTENSION AS IT RELATES TO CARDIO VASCULAR

© Can be noticed from both increase of cardiac output and peripheral resistance.

© Increased peripheral resistance caused by reduced arteriolar radius.

© Hypertension of unknown cause is called primary hypertension.

© Caused by excessive sodium as a contributing factor.

© Caused by increased release of renin from the kidney.

HEART FAILURE/CONGESTIVE HEART FAILURE

© The cardiac output is low. This is caused by elevated arterial pressure due to hypertension.

© Heart failure has two groups: diastolic dysfunction and systolic dysfunction.

© These two groups trigger arterial baroreceptors reflexes. This leads to pulmonary edema.

© Increased total peripheral resistance.

© Symphatic nerves to arterioles.

© Angiotensin 11 and vasopressin.

VENTRICULAR END-DIASTOLIC VOLUME (FRANK - STARLING)

RISK FACOTORS FOR CORONARY ARTERY DISEASE

© Smoking - Homocysteine

© Cholesterol - Hypertension

© Diabetes - Obesity

© Stress

DECREASING CORONARY ARTERY DISEASE

© Nutrition – decrease intake of saturated fats.

© Supplements – folic acid reduces blood concentration of amino acid (HOMOCYSTEINE).

© Alcohol – red wine in moderation has the power to help reduce rush of heart attack.

© Metabolized methionine and cysteine which is in high amounts has pro atherosclerosis effects.

EXCERISE PROTECTS AGAINST HEART ATTACK

© Decreased myocardial oxygen demand.

© Increase coronary arteries diameter.

© Decrease effect of hypertension and obesity.

© Decrease total plasma concentration.

© Decrease of blood clot and improving the ability to dissolve them.

EXCERISE PROTECTS AGAINST HEART ATTACK

CORONARY ARTERY DISEASE

© Changes in coronary artery cause insufficient blood flow (ischemia) and myocardial damage can exist.

© Myocardial infraction/heart attack – inadequate coronary blood flow in exertion or emotional tension.

© Symptoms – prolonged chest pain (more persistent in left arm)- nausea, vomiting, sweating, weakness, shortness of breath

© This can be diagnosed by an ECG which measures certain protein in plasma that leak into the blood when muscle is damaged.


© Sudden cardiac death during myocardial infraction is due to ventricular fibrillation where myocardial cells are damaged and causes abnormal conductive when the ventricular contraction are uncoordinated.

© Only a small amount of people can be saved by CPR.

© Cardiopulmonary resuscitation- allows small amounts of oxygenated blood to vital organs after which a more precise treatment is used. Electric current pass through heart to stop the abnormal electrical activity.

© Artificial fibrillation causes minor cardiac problems.


ARTHEROSCLEROSIS

© Caused by plaque.

© Cells lining the blood vessels get damaged from high LDL cholesterol

© eg. Smoking high levels.

© increase penetrability of blood vessel walls.

© achieve inflammatory response.

© Immune System sends macrophages.

© Smooth muscle cells in artery try to repair damage.


ARTHEROSCLEROSIS

© LDL particles trapped in blood vessel walls.

© Free radicals oxidize LDL cholesterol.

© Macrophages engulf oxidize LDL and swell forming plaque..

© Statins interferes with an enzyme involve in liver synthesis of Cholesterol which helps control atherosclerosis.

STAGES IN PLAQUE PROGRESSION


CORONARY THROMBOSIS

© Blood Clot.

© Try reducing clotting with Aspirin®

© Statins drug interfere with a critical enzyme involved in liver synthesis of cholesterol.

© ACE inhibitors, prevents the angiotensin converting enzyme ACE which is an enzyme that converts angiotensin1 to angiotensin 11. This lowers blood pressure by dilating arteries.

© Types of drugs:© Enalapril© Lisinopril© ramipril

DRUGS WHICH TREAT HYPERTENSION

© This helps kidney eliminate excess salt and water from body tissues and blood.

© Drugs: bumetamide, furosemide, microzide, acetazalamide diamox

DIURETICS (WATER PILLS)

© Reduces cardiac output it slows heart rate reducing stress on heart and arteries. This prevents the effect of adrenaline.

© Drugs: lopressor, blocadren,normodye, carteolol

BETA BLOKERS (ADRENERGIC RECEPTOR

© Reduce calcium in smooth muscle cells.

© Lower peripheral resistance.

© Blood pressure is reduced by the dilation of arteries.

© Drugs: amlodipine(norvasc), feladipine, nifedipine

(adalat)

CALCIUM CHANNEL BLOCKERS

© This also dilate arteries.

© Drugs: candesartar, losartan, valsartan.

ANGROTENSIN 11 RECEPTOR BLOCKER (ARB)

© Diuretics.© Cardiac inotropic drugs ( digitalis)© This makes heart beat stronger.© Dobutamine helps to use norepinephrine.© Dopamine increase amount of norepinephrine in body.

© Aspirin (acetyl salicylic acid ASA).This prevents platelets in blood from clotting which is forms in atherosclerosis.

DRUGS USED IN TREATING HEART FAILURE

© Lowers peripheral blood resistance whereby heart work less to pump blood.

© ACE inhibitor are used as vasodilators.

CALCIUM CHANNEL BLOCKERS:

© used in heart failure, if it is due to high blood pressure. It is used if patient is not responding to ACE or ARB inhibitors.

VASODILATERS

© Blocks the action of norepinephrine on heart muscles improving systolic function of the left ventricle.

© Influence the RAS system in kidney.

© Drugs: celiprotol, sotalol, labetalol

BETA ADRENERGIC RECEPTOR BLOCKERS / BETA BLOCKERS

Cardiovascular phsiology

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