Physiology of the Cardiovascular System

Chapter 19

Heart’s Role in Maintaining Homeostatis

• Circulation (pumping action) varies based on needs of the body

• Hemodynamics - Describes a collection of mechanisms that influence the active and changing circulation of blood throughout the body – Increase activity = increased blood flow

Heart as a Pump

• 4 Chambers of the heart create two pumps– Right side pulmonary circulation– Left side systemic circulation

Conduction System of the Heart

• 4 structures composed of specialized cardiac muscle make up the conduction system of the heart:– SA Node, AV Node, AV bundle (Bundle of

His), Purkinje Fibers– Non contractile– Permit generation or rapid conduction of

an action potential

SA Node

• Pacemaker of the heart• R atrium at base of superior vena

cava• Specialized cells within the node

produce an intrinsic rhythm– Produce impulses without stimulation

from any other body system

• Fires or discharges 70-75 times/minutes

Conduction Route

Impulse generated in SA node interatrial bundle allows conduction of

impulse to L atrium internodal bundles carry impulse to AV node

**conduction slows through AV node to allow complete contraction of atria**

Conduction increases after passing though AV node R/L branches of AV bundle purkinje fibers ventricular muscles simultaneous ventricular

contraction

Conduction Route

• Ectopic pacemakers– If SA node loses ability to generate

impulses, the AV node or Purkinje fibers will take over

– HR will be slower

Artificial Pacemakers

• Surgically inserted device which stimulates the heart at a set rhythm

• Stimulate a set rhythm or fire when HR drops below a set minimum

• Transvenous approach– Incision above R clavicle– Electrode threaded into jugular vein– Advanced to apex of R ventricle– Power pack is attached to subcutaneous

tissue

Artificial Pacemakers

Electrocardiogram (ECG)

• Conduction through the heart creates electrical currents that spread to the surface of the body

• ECG is a graphic record of the electrical activity of the heart

• Electrodes of a electrocardiograph attached to a person’s skin can record changes in the heart’s electrical activity– Observed as deflections

Cardiac muscle @ rest – no difference in charge btwn electrodes

Action potential reaches first electrode. External surface becomes relatively negative. Upward deflection on ECG.

AP reaches 2nd electrode. No difference in charge. Deflection returns to zero.

End of AP reaches the 1st electrode. Sarcolemma is slightly positive creating a downward deflection.

End of AP reaches the 2nd electrode. No difference in charges. Deflection returns to zero.

Summary

• Depolarization – deflection representing cardiac muscle moving away from resting membrane potential

• Repolarization – deflection in the opposite direction; cardiac muscle moving back towards resting membrane potential

Analyzing ECGs• Series of deflection

waves and intervals

• Represents net change in polarity– Ex: ventricles are

depolarizing while atria are repolarizing

Analyzing ECGs

• P wave– Depolarization of the atria– Electrical impulse passes from SA node

to R/L atria• QRS complex

– Depolarization of the ventricles– Repolarization of the atria

• Voltage fluctuation overshadowed by the depolarization of the ventricles

• First to depolarize, first to repolarize

Analyzing ECGs

• T wave– Repolarization of the ventricles

• First to depolarize, last to repolarize

**ECG is a record of the electrical activity of the heart, NOT of the heart’s contraction. Contraction occurs after depolarization**

Cardiac Dysrhythmias

• Abnormal rhythm of the heart• Heart Block

– Conducted blocked after AV node– Ventricles contract slowly– Wide spaces between P waves and QRS

complex– Complete Heart Block – multiple P wave

per QRS complex

Cardiac Dysrhythmias• Bradycardia

– Slow HR (< 60bpm)– ECG will show spread out waves– Causes:

• Damaged SA node• Abnormal autonomic nervous control

• Tachycardia– Increased HR (>100bpm)– ECG will show condensed waves– Causes:

• Abnormal autonomic nervous control• Blood loss/shock• Drugs• Fever

Cardiac Dysrhythmias• Atrial fibrillation (“A-fib”)

– Premature contractions– Absence of P waves– Chambers do not pump efficiently– Treated with digoxin (digitalis) or defibrilation– Causes:

• Mitral stenosis• Rheumatic heart disease• Myocardial infarction

Cardiac Dysrhythmias

• Ventricular fibrillation (“v-fib”)– Ventricular contraction/pumping stops– Life threatening situation– Treated with defibrillation

Cardiac Cycle

• One complete heart beat• Consists of one contraction (systole)

and one relaxation (diastole) of both the atria and ventricles

1. Atria contract simultaneously2. Ventricles contract; atria relax3. Ventricles relax; atria remain relaxed

Atrial Systole

• Atria contracted• AV valves open• Ventricles filling with blood• Semilunar valves closed• Begins with P wave of the ECG

Isometric Ventricular Contraction

• “having the same measured volume”• Time between ventricular systole and

opening of SL valves• Volume is constant; pressure

increases• Ventricular systole coincides with the

R wave & the first heart sound

Ejection

• Ejection occurs when pressure in the ventricles exceeds pulmonary artery & aorta

• Rapid ejection – initial, shorter phase• Reduced ejection – coincides with T

wave• Residual volume – blood that remains

in the ventricles after ejection– Increases in ppl with heart failure– Ejection fraction

Isovolumetric Ventricular Relaxation

• Begins with ventricular diastole• SL valves close; AV valves remain

closed• Volume is constant; pressure

decreases• Second heart sound

Passive Ventricular Filling

• Atria filling increases intraatrial pressure

• AV valves are forced open

Heart Sounds• “Lubb-Dubb”• “Lubb” – systolic sound

– contraction of the ventricules and closing of the AV valves

– Longer, lower

• “Dubb” – diastolic sound– Closure of the SL valves – Shorter, sharper

• Heart murmur – abnormal heart sounds– Incomplete closing of the valves

• Valvular insufficiency or stenosis

Primary Principle of Circulation

Arterial Blood Pressure

• Maintaining arterial pressure is necessary to maintain circulation

• Arterial blood pressure is directly proportional to arterial blood volume

• Cardiac output and peripheral resistance influence arterial volume

• Stroke volume x Heart Rate = Cardiac output

(SV x HR = CO)• Stroke volume: volume of blood

pumped out of the ventricles by each heart beat

• Increase speed or strength of contraction = increase arterial volume = increase arterial pressure

Cardiac Output

Factors Affecting Stroke Volume

• Starling’s Law of the Heart– Longer muscle

fibers prior to contraction = stronger contraction• Increased blood

return to the heart per minute = longer muscle fibers

Factors Affecting Heart Rate

• Aortic baroreceptors and carotid barorecetors are located near the heart and are sensitive to changes in pressure– Carry sensory information to cardiac

center in medulla oblongata – If HR above a set point, a signal is sent to

the SA node via efferent parasympathetic pathways of the vagal nerve

– Achtylcholine is released to decrease firing of SA node

– Negative feedback loop

Factors Affecting Heart Rate

• Sympathetic nervous system can increase heart rate– Release of epinephrine and

norepinephrine – Exercise, fight or flight response, pain,

fever

Peripheral Resistance• Resistance to blood flow due to friction

between blood and arterial walls• Friction due to:

– 1) viscosity• Red blood cell count• Blood protein concentration

– 2) diameter of arterioles and capillaries• “arteriole runoff” = amount of blood that runs

out of the arteries into the arterioles• Greater resistance = less runoff = increased

blood volume in arteries = increased arterial pressure

Peripheral Resistance

• Aortic and carotid baroreceptors also exhibit vasomotor control– Increase in arterial pressure inhibits

vasoconstrictor center in medulla oblongata• Impulses sent via parasympathetic fibers to slow

HR and dilate arterioles

– Decrease in arterial pressure stimulates vasoconstrictor center in medulla oblongata• Impulses send via sympathetic fibers to increase

vasoconstriction

Venous Return to the Heart

• Venous Pumps– Inspiration increases pressure gradient

between peripheral and central veins (vena cava)• Contraction of the diaphragm increases

thoracic cavity therefore decreasing pressure within those blood vessels (vena cava and atria)

Venous Return to the Heart• Venous pumps

– Skeletal muscle contractions squeeze surrounding veins and help “milk” blood back to heart

Venous Return to the Heart• Total Blood Volume

– Increase blood volume = increased blood return to the heart

– Capillary Exchange: exchange of material between plasma and interstitial fluid in tissues• Osmotic and hydrostatic pressure create

inward and outward directed forces at arterial and venous ends

• No net loss of blood volume• Fig 19-18, page 614

Capillary Exchange

Venous Return to the Heart• Changes in Total Blood Volume

– Antidiuretic Hormone (ADH)• Secreted from posterior pituitary • Increases water absorption in kidneys• Increase water absorption = increase blood

plasma volume

– Renin-angiotensin mechanism• Renin is secreted from kidneys when blood

pressure is low• Triggers series of events leading to secretion

of aldosterone from adrenal glands• Aldosterone causes sodium retention in

kidneys; water follows Na+ = blood volume increases

Venous Return to the Heart

• Changes in Total Blood Volume– ANH mechanism (atrial natriuretic

hormone)• Released from cells of the atrial wall in

response to overstretching (abnormally high venous return)

• Increases sodium loss in urine; water follows

Measuring Arterial Blood Pressure

• Measured using a sphygmomanometer

• Measured in mmHg– How high (in mm) air pressure raises a

column of mercury (Hg)• Procedure:

– Cuff wrapped around brachial artery (upper arm)

– Pump cuff full of air until the air pressure exceeds blood pressure (compresses the artery)

Measuring Arterial Blood Pressure

– Place stethoscope of brachial artery at bend of elbow

– Slowly release air from cuff and listen for Korotkoff sounds

– First sound will be heard when air pressure = blood pressure Systolic Blood Pressure• Force against arterial wall when ventricles are

contracting

– Second sound Diastolic Blood Pressure• Force against arterial wall when ventricles are

relaxed

Measuring Arterial Blood Pressure

• Difference between systolic and diastolic blood pressure = pulse pressure

SBP – DBP = PP– Increased in patients with arteriosclerosis

and aortic valve insufficiency– Bruits (“vascular murmur”): abnormal

blowing sounds heard in the carotid arteries• Present in patients with increased pulse

pressure and/or arteriosclerosis

Measuring Arterial Blood Pressure

• Continuous Blood Pressure Monitoring – Arterial blood pressure

Pulse

• Expansion and recoil of an artery• Based on 2 factors:

– 1) Intermittent ejections of blood from the ventricles into the aorta

– 2) Elasticity of the arterial walls allows for stretch and recoil

Hypertension

• High blood pressure exceeding 140/90• Causes:

– Idiopathic, kidney disease, oral contraceptives, pregnancy

• S/S:– Headache, fainting, dizziness

• Complications:– Ischemic heart disease, heart failure,

kidney failure, stroke

Circulatory Shock

• Failure of circulatory system to deliver oxygen to tissues– Cardiogenic shock: results from heart

failure• MI, heart infection, etc• Heart can no long act as efficient pump

– Hypovolemic shock: loss of blood volume• Hemorrhage is common cause• Loss of interstitial fluid (ex: diarrhea,

vomiting, dehydration, extensive burns)

Circulatory Shock– Neurogenic shock: systemic dilation of

blood vessels• Results from abnormal autonomic control• Decreased blood pressure = decreased blood

flow

– Anaphylactic shock: acute allergic reaction called anaphylaxis• Causes systemic vasodilation

– Septic shock: complication of septicemia• Toxins in bloodstream cause vasodilation• Toxins also damage tissues• Ex: toxic shock syndrome (TSS) results from

staphylococcal infection