Heart and Vascular Systems

Overview of Heart and Vascular System

* partly a transport system that takes necessary substances to specific places and removes waste materials


* diffusion is slow
* responsible for movement of O2 and CO2, nutrients and hormones
* tightly linked to other systems such as urinary and respiratory system
* two circulatory divisions

Pulmonary Division

* takes deoxygenated blood from heart to lungs and delivers oxygenated blood back

Systemic Division

* delivers oxygenated blood from heart to rest of body and takes deoxygenated blood back

Nervous Control

* cardiac muscle must contract in highly synchronized manner, first both atria then both ventricles
* heart controls its own contraction, doesn’t rely on nervous system but can be altered by it
* myogenic vs neurogenic
* two types of specialized muscle cells, pacemaker cells and conduction fibers

Pacemaker Cells

* unlike typical nerve cells, these continuously depolarize to generate regular action potentials
* these stimulate muscle to contract rhythmically, determining the pace at which the heart beats
* found mainly in two regions

Sinoatrial Node

* located in superior vena cava
* rate of about 75 beats per minute
* impulses are generated here, they are the fastest and drive the beating of the heart

Atrioventricular Node

* interatrial septa superior to ventricles
* 50 beats/min

Conduction Fibers

* specialized to conduct quickly the action potentials generated by the pacemaker cells
* innervate cardiac muscle cells of myocardium, purkinje fibers help conduct electrical stimulus in the ventricular walls
* larger in diameter and can conduct impulses faster

What causes the atrial muscle to contract?

* sinoatrial node generates impulses

What causes the ventricular muscle to contract?

* the generated impulse triggers the atrioventricular node
* there is a brief delay between contraction of atria and ventricles

Artificial Pacemakers

* implanted to regulate irregular heart contractions
* most frequently used to increase heart rates
* are also used to slow heart rate in some cases

Electrocardiogram (ECG or EKG)

* electrical activity is carried to the skin and can be recorded by surface electrodes
* 6 electrodes are attached to arms and legs and 6 are attached to the chest
* has 3 parts

P wave

* depolarization of atria

QRS complex

* depolarization of ventricles
* repolarization of atria (hidden)

T wave

* ventricle repolarization

Where does the impulse generate from?

* from the sinoatrial node into the walls of the atria causing the atria to contract (P wave)

Where does the impulse move to from the sinoatrial node?

* after a delay, it moves into the atrioventricular node into the heart apex where the signal spreads and the ventricle contracts (QRS complex)

Heart Arrhythmia

* caused by defects during the electrical heart process
* is an irregular beating of the heart

Fibrilation

* very rapid, out-of-phase contractions
* defibrillation is shocking the heart

Systole

* first part of the cardiac cycle
* ventricular contraction

Diastole

* second part of the cardiac cycle
* ventricular relaxation

Lub

* closing of the mitral valve
* ventricles contract at the start of systole

Dub

* closing of the semilunar valve
* ventricles relax at the beginning of diastole

Phonocardiogram

* detects and records heart sounds, four sounds are usually produced by the heart
* only two are ordinarily audible, can hear four with a stethoscope lub dub

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Electrocardiogram and Heart Cycle Steps

1. Ventricles fill up
2. Mitral valve closes, ventricles contract
3. Ventricle eject blood
4. Aortic valve closes, ventricles relax
5. Blood returns to heart
6. Ventricles fill up

Vascular Physiology

* at the basic level, there are three types of blood vessels, arteries, capillaries, veins

Artery Inner Layers

* tunica interna, tunica media and tunica externa

Vein Inner Layers

* tunica intima, tunica media and tunica adventitia

Elastic Artery

* more elastic and close to the heart

Muscular Artery

* more muscle and further from the heart

Hemodynamics

* flow of blood through vascular system
* F=P/R
* F= flow rate (volume of blood passing through/unit of time)
* P= pressure
* R= resistance

Pressure Gradient

* difference in pressure between the beginning and end of a blood vessel
* the contraction of the heart provides pressure which decreases as blood flows vessels due to resistance

Resistance

* measure of hindrance to blood flow caused by friction between the moving fluid and the stationary walls
* depending on viscosity and vessel length/radius
* resistance is 16x greater in a tube that’s twice the diameter

Viscosity

* friction between molecules
* tends to be relatively constant in blood

Vessel Length/Radius

* friction between blood and vessel

Factors Affecting Blood Flow

* pressure, resistance and total area of the vessels affect the speed of blood flow throughout the circulatory system

Cardiac Output

* volume of blood pumped out of each ventricle/minute, average is 5.5L/min
* measured in ml/min
* calculated by cardiac rate (average resting is 70 beats/min) x stroke volume (average is 78-80 ml/beat)
* also equivalent to total blood volume of the body

Heart Rate and Stroke Volume Affecting Cardiac Output

* heart rate is influenced by nerves and hormones
* stroke volume is affected by blood volume and vascular resistance

Regulation of Cardiac Rate

* in the absence of neural stimulation, the heart will beat according to the SA node
* if the SA node was in complete control, the heart would always beat the same rate
* heart rate is modified by the autonomic nervous system and endocrine system

Increasing Heart Rate

* sympathetic system excretes norepinephrine
* adrenal glands excrete epinephrine

Decreasing Heart Rate

* parasympathetic system excretes acetylcholine

Regulation of Stroke Volume

1. Contractility- the strength of ventricular contraction
2. End Diastolic Volume- amount of blood in the ventricles just before they begin to contract
3. Afterload/ Total Peripheral Resistance- the pressure ventricles have to work against

Contractility

* any force that causes the ventricles to contract with much more force will increase stroke volume and in return increases cardiac output

Nervous Control Affecting Contractility

* ANS control of stroke volume is regulated almost entirely by the sympathetic nervous system
* epinephrine increases contraction strength

Hormonal Control Affecting Contracility

* ventricular conctracility increased by numerous hormones, insulin, glucagon and thyroid hormones

End Diastolic Volume

* force of ventricular contraction varies in response to stretching of ventricular wall
* sterlings law (simply increased blood volume leads to increased stretch of the myocardium which increases the force of blood pumping out)
* if the amount of blood that returns increases, cardiac muscle will contract more to compensate

Sterling’s Law

* when the rate at which blood flows into the heart from the veins (venous return) changes, stretching of the ventricular wall changes, causing the ventricle to contract with greater or lesser strength so that the stroke volume (output) matches the venous return (input)

Afterload

* stroke volume also depends on the amount of force opposing contraction
* increased arterial pressure causes stroke volume to decrease
* afterload is determined in the aorta after contraction starts
* increased resistance=increased pressure=increased afterload=decreased stroke volume

Blood Pressure

* regulated by blood volume (regulated by kidneys), peripheral resistance and cardiac rate
* any increase in one will increase bp
* in the sympathetic system, vasoconstriction increases TPR and promote cardiac output with both increase bp

Baroreceptors

* detect changes in blood pressure and counteract pressure changes
* stretch receptors located in the aortic arch and the carotid sinuses, increase in pressure causes wall to stretch
* signals travels through two cranial nerves to medulla oblongata

What do the kidneys do?

* play a vital role in regulating blood volume
* decrease in bp going into the kidney, the cells of the kidney release renin which increases angiotensin II

How does angiotensin II promote a rise in blood pressure?

1. increased resistance of blood vessels by acting directly on small arteries and arterioles (vasocontriction)
* also known as the renin-angiotensin-aldosterone system
2. Increased blood volume
* thirst centers in the hypothalamus are stimulated along with the adrenal glands which secrete aldosterone
* causes more salt and water to be retained by the kidneys

Circulatory Shock

* inadequate blood flow and/ or oxygen uptake by tissues
* can result from low blood volume or vasoconstriction in various organs such as skin
* results in low blood pressure, rapid pulse and clammy skin
* blood is diverted to the heart and brain

Septic Shock

* dangerously low blood pressure that results from sepsis (infection)
* high mortality rate (50-70%)
* bacterial action activates immune system which promotes vasodilation, leaks from blood vessels and blood pressure drops