The Cardiovascular System:

Heart Location

• The heart is located in the center of the chest in an area called the mediastinum.

Heart Wall• Fibrous Pericardium –

outer most layer.– tough and prevents heart

from overfilling.• Epicardium – Outermost

layer– visceral layer of the

serous pericardium– They are separated by

the fluid-filled pericardial cavity

• Myocardium – cardiac muscle layer forming the bulk of the heart.

• Endocardium – endothelial layer of the inner myocardial surface. – Deepest layer that is

continuous with the lumen of the heart and arteries.

Atria of the Heart

• Atria are the receiving chambers of the heart

• Blood enters right atria– Superior vena cava – inferior vena cava – coronary sinus

• Blood enters left atria via pulmonary veins

Ventricles of the Heart

• Ventricles eject blood from the heart– Right ventricle

pumps blood into the pulmonary trunk which will go to the lungs.

• Left ventricle pumps blood into the aorta which will go to the rest of the body

Atrioventricular Heart Valves

• Heart valves ensure unidirectional blood flow through the heart

• Atrioventricular (AV) valves lie between the atria and the ventricles

– Tricuspid Right – Bicuspid (Mitral) Left

• AV valves prevent backflow of blood into the atria when ventricles contract

• Chordae tendineae anchor AV valves to papillary muscles

– First heart sound (LUB) when valves close

• During diastole there is less pressure in the in ventricle. AV Valves open and filling the ventricle.

• During systole the AV valves prevent the back flow of blood into the atrium. – Failure to prevent the blood from going back into the atria (systolic heart

murmur)

Semilunar Heart Valves

• Aortic semilunar valve lies between the left ventricle and the aorta.

• Pulmonary semilunar valve lies between the right ventricle and pulmonary trunk– Semilunar valves prevent backflow of blood

into the ventricles.

• Second heart sound (DUB) when valves close.

Figure 19.9b

• During ventricular systole the semilunar valves allow blood to be ejected from the ventricles into the aorta and pulmonary trunk.

• During diastole they prevent the back flow of blood back into the ventricles.– Failure to prevent the backflow of blood into the ventricles (diastolic

murmur)

• Cardiac muscle is short and striated.• Ability to beat independent of

stimulation from the nervous system.– ANS

• Functional syncytium:– intercalated discs connect

cardiac cells which allow free passage of ions.

– This allows the spread of action potentials from one myocyte to another.

• The result is a coordinated contraction that moves the blood out of the heart.

Cardiac Muscle Cell Metabolism

• Aerobic respiration– Large mitochondria

Rich in myoglobin and glycogen

• Organic fuels:– fatty acids,

glucose, ketones

• Fatigue resistant

Intrinsic Conduction System• Autorhythmic cells: cells that spontaneously generating action

potentials without any influence from the CNS.• Main pacemaker of the heart is the (SA node) • Sinoatrial node (SA node) sets cardiac heart rate. • Atrioventricular node (AV node) leads into Bundle of His

which splits into branch bundles• Purkinjie fibers carry the impulse to the ventricular myocardium

Sequence of Cardiac Excitation

• Note bundle branch and Purkinje fibers connection to both the ventricular myocardium and papillary muscles– This is important when considering how the ventricular

myocardium and AV valves can function in a coordinated fashion.

Action Potential of Myocyte

Cardiac Cycle

• Cardiac cycle refers to all events associated with blood flow through the heart– Systole – contraction of heart muscle

• Forces blood out of the ventricles • This is felt when you take someone’s pulse

– Diastole – relaxation of heart muscle• Ventricles relax allowing the heart to fill with blood

Blood Flow Through The Heart

Phases of the Cardiac Cycle

• Ventricular filling – mid-to-late diastole– At the beginning of the cycle, the semilunar valves are

closed and the entire heart is in diastole.– Pressure in the heart blood is lower than in the vena

cavas and pulmonary veins resulting in the movement of blood into the atria

– As pressure in the atria now exceed ventricular pressure the AV valves are open allow blood to flow from the atria into the ventricles.

• Atria systole occurs (SA) node initiates depolarization of both atria

– Represented by the P-wave on an EKG– Both atrium contract forcing atrial blood into already

filled ventricles. (End Diastolic Volume)

Phases of the Cardiac Cycle• Ventricular systole

• Atria relax( repolarization) • There is a slight delay prior to the initiation of the AV node.

– (pr-segment)

• This allows atrial blood time to enter the ventricles• AV node sends action potential → to the bundle of His → branch

bundles → perkinje fibers depolarizing both ventricles leading to the ventricle myocardium to contract.

– QRS complex on EKG

• This results in rising ventricular pressure causing the closing of AV valves (LUB) 1st heart sound

• Isovolumetric contraction phase • (The ventricles are contracting with all 4 valves closed )• This allows ventricular pressure to increase rapidly.

Phases of the Cardiac Cycle• Ventricular ejection phase: semilunar valves open once

pressure in the ventricles exceed the pressure in the aorta and the pulmonary trunk. – Blood will now flow out of the heart.( Stroke Volume)– ST segment on EKG

• Isovolumetric relaxation – early diastole– Ventricles relax represented by the T-wave on the EKG– Backflow of blood in aorta and pulmonary trunk closes

semilunar valves making the second heart sound ( Dub)– This marks the end systolic volume (ESV)

Cardiac Output

• The cardiac output is a measure of cardiac function.• Cardiac functions changes based on the demands that are

placed on it. • The heart must:

– Deliver vital nutrients such as O2, hormones and all the fuels sources body as quickly as they are used.

– Remove CO2, urea, lactic acid… from the cells of the body as quickly as they are produced.

– Vigorous activities will increases systemic and cardiac O2

demands while producing more CO2 that will need to be expired.

– During strenuous activities the bodies cardiac output will increase dramatically to meet these demands.

Cardiac Output (CO)

• HR= is the number of heart beats per minute• EDV = amount of blood collected in a ventricle during

diastole.• ESV = amount of blood remaining in a ventricle after

contraction• SV = is the amount of blood pumped out by a ventricle

with each beat– SV = end diastolic volume (EDV) minus end systolic volume

(ESV)

• CO is the amount of blood pumped by each ventricle in one minute– CO is the product of heart rate (HR) and stroke volume (SV)

Cardiac Output

• Normal Cardiac Output– CO (ml/min) = HR (75 beats/min) x SV (70

ml/beat)– CO = 5250 ml/min (5.25 L/min)

• Exercise CO can increase 7 fold – HR (160 beats/min) x SV (220 ml/beat)– CO = 35200 ml/min (35.25 L/min)

• Sympathetic nervous system (SNS) stimulation is activated by stress, anxiety, excitement, or exercise (Fight and Flight) increase both heart rate and force of contraction.

• Parasympathetic nervous system (PNS) stimulation is mediated by acetylcholine and opposes the SNS which reduces the heart rate and force. (rest and restoration)

External Regulation of Heart Rate: Autonomic Nervous System

Extrinsic Innervation of the Heart

Regulation of HR

• The sympathetic cardiac nerve originating from the cardioacceleratory center in the medulla of the brain releases the neurotransmitter norepinepherine (adrenergic agent) onto the cells of the SA node – causes an increase in the frequency of action

potentials in the SA node leading to an increase in HR.

• What gates would you open to increase the frequency of action potentials?

– Force of contraction is also increased because of the increased uptake of extra cellular calcium.

Regulation of HR

• Parasympathetic: Stimulation via (Vagus) nerve originating from the cardio inhibitory center in the medulla.

• This center releases the neurotransmitter acetylcholine (cholinergic agent) onto the cells of the SA node – causes a decrease in the frequency of action

potentials in the SA node leading to a decrease in HR• What gates would you open to decrease the frequency of

action potentials?

Frank-Starling Law of the Heart

• Preload : degree of myocardial stretch is related to the volume of blood in the ventricles .The greater the stretch on the ventricular walls, the greater the force the myocardium will contract thus increasing stroke volume.– Slower heart rate increase

ventricular filling time (venous return) increasing SV

• How will blood loss effect heart rate and stroke volume?

Factors Affecting Stroke Volume• Afterload – back pressure exerted

by blood in the large arteries leaving the heart– The greater the afterload the

harder the heart has to work to eject blood.

• During diastole the coronary arteries fill with blood as blood recoils off the aortic semilunar valves.

• Patients with chest pain (angina) are not getting enough blood to meet myocardial demand.

Blood Vessels

• Blood is carried in a closed system of vessels that begins and ends at the heart

• The three major, and types of vessels are:– arteries, capillaries, veins

• Arteries carry blood away from the heart, veins carry blood toward the heart

• Veins transport blood back to the heart– 65% of blood is located in the veins

• Capillaries contact tissue cells and directly serve as site for gas exchange

Arteries

• Blood exits the ventricle into an artery– Aorta: blood exits the left ventricle which delivers

blood into systemic circulation.– Pulmonary trunk: de-oxygenated blood is carried to

the lungs (pulmonary circulation) • Arteries become more numerous and smaller in

diameter as the get further from the heart.– As the arteries become smaller in diameter they

become arterioles• Arterioles flow into capillaries

Capillaries • Capillaries are location for exchange of materials

between the blood and the cells of the body.• These vessels are the smallest diameter and are the

most numerous.

Veins

• After leaving the capillaries, blood flows into venules• As the blood continues to move towards the heart; the

venules converge into larger diameter vessels called veins

• The veins merge into a single vein which returns the blood back to the atria of the heart– Superior Vena Cava above the diaphragm.– Inferior Vena Cava below the diaphragm.

Structure of Blood Vessels

• Arteries and veins are composed of three tunics:– tunica interna, tunica media, and tunica

externa

• Lumen – central blood-containing space in the center of the vessel

• Capillaries only have an endothelium layer necessary for exchange of gases and nutrients.

Generalized Structure of Blood Vessels

Tunics

• Tunica interna (tunica intima)– Endothelial layer that lines the lumen of all vessels (inner

most layer)• Tunica media (middle layer)

– Smooth muscle and elastic fiber layer, regulated by sympathetic nervous system

– Smaller vessels have a more muscular layer than larger vessels

• SNS causes vasoconstriction.– (no stimulation ) results in vasodilatation of vessels

– This will affect blood pressure and distribution)• Tunica externa (tunica adventitia)

– Collagen fibers that protect and reinforce vessels– Larger vessels like the aorta have more to allow them to

deal with higher pressures

Blood Flow Through Capillary Beds

• There are 5-6 liters of blood and 60 thousand miles of vessels in the circulatory system.

Capillary Beds

• Precapillary sphincter shunt blood to where it is need.

• Blood flow is regulated primarily by the SNS

• If all the precapillary sphincters were to open simultaneously what would happen? – The answer will SHOCK

you!!.

Blood Flow in Response to Needs

• Arterioles shift blood flow with changing priorities

Systemic Blood Pressure• The pumping action of the heart generates blood

flow through the vessels along a pressure gradient, always moving from higher- to lower-pressure areas

• Pressure results when flow is opposed by resistance

• Systemic pressure:– Is highest in the aorta– Declines throughout the length of the pathway– Is 0 mm Hg in the right atrium

• The steepest change in blood pressure occurs in the arterioles

Systemic Blood Pressure

Velocity of Blood Flow

Arterial Blood Pressure

• Systolic pressure – pressure exerted on arterial walls during ventricular contraction

• Diastolic pressure – lowest level of arterial pressure during a ventricular cycle– Pulse pressure – the difference between systolic

and diastolic pressure

• Increased blood pressure stimulates the cardioinhibitory center to stimulate the vagus nerve to:– Decrease heart rate, cardiac output, vasodilatation of

major vessels. • The result is reduced peripheral resistance, and a lower BP

• Low blood pressure also stimulates the cardioacceleratory center to:– stimulates the SNS to constrict blood vessels

• Increase blood pressure, increase cardiac output and peripheral resistance

Baroreceptor regulation of BP

Baroreceptor Reflexes

Capillary Blood Pressure

• Capillary BP ranges from 20 to 40 mm Hg

• Lower capillary pressure is desirable because high BP would rupture fragile, thin-walled capillaries.

• Low BP is sufficient to force filtrate out into interstitial space and distribute nutrients, gases, and hormones between blood and tissues.

• The artery has a much thicker tunica media and a large lumen

• The vein is much thinner and tends to collapse

Mechanisms of Venous Return• Several factors affect venous pressure

gradient and venous return.– Gravity drains blood from head and neck– Skeletal muscle pump in the limbs– Thoracic pump

• inhalation - thoracic cavity expands (pressure ) abdominal pressure , forcing blood upward

• central venous pressure fluctuates– 2mmHg- inhalation, 6mmHg-exhalation– blood flows faster with inhalation

Muscle Pump

Figure 20.19a

Valves Prevent Back Flow

Capillary Exchange - Filtration and Reabsorption

• Hydrostatic pressure– physical force exerted against a surface by a liquid,

(BP is an example)

• blood (hydrostatic) pressure drives fluid out of capillary

• high on arterial end of capillary, low on venous end

– colloid osmotic pressure (COP) draws fluid into capillary

• results from plasma proteins (albumin)- are maintained in the vessel drawing fluid back into the blood via osmosis

• oncotic pressure = net COP (blood COP - tissue COP)

Hypotension• Orthostatic hypotension – temporary low BP and

dizziness when suddenly rising from a sitting or reclining position

• Chronic hypotension – – poor nutrition: low protein diet = low albumin levels

• Insufficient osmotic gradient to draw water back into circulatory system

– warning sign for Addison’s disease• Decreased Aldosterone production

• Acute hypotension – important sign of circulatory shock– Threat to patients undergoing surgery and those in

intensive care units

Hypertension• Hypertension can increase both cardiac preload and

afterload. Hypertension maybe transient or persistent Chronic hypertension (140/90 mmHg) damages the arterial walls promoting atherosclerosis and increases energy requirements of the heart.

• Hypertension :risk factors in include diet, obesity, age, race, heredity, stress, smoking and identifiable disorders such as endocrine disorders.

• What hormones might contribute to hypertension?

Antihypertensive Therapy– Beta Blockers :Block sympathetic stimulation to Beta-1

receptors located on cardiac muscle. This lowers the heart rate and contractility reducing myocardial demand. Increases time in diastole which increases the perfusion time of the heart. Reduces cardiac afterload.

– Diuretics increase electrolytes elimination such as sodium in the urine. This reduces the blood volume which reduces blood returning to the heart. The result is a reduction in preload.

– Ca+ channel blockers: decrease the amount of intracellular Ca2+. The reduction in intracellular Ca2+ promotes relaxation of the myocardium and muscles within the artery walls. The result is decreased ventricular contractility, SV and arterial blood pressure. This will reduce the afterload thus reducing cardiac workload.

– Nitroglycerin: promotes rapid vasodilation which can reduce both preload and afterload. This is the drug of choice if someone is complaining of chest pain.

Which Medication Is This?

Healthy Vessel

Atherosclerosis

Arteriosclerosis

Markers for Atherosclerosis.

• Inflammation plays a major role in the pathophysiology of atherosclerosis.

• HDL/ LDL ratios and total triglycerides levels also give vital information on risk of developing atherosclerosis– Low HDL’s and high LDL and triglycerides are a

dangerous cholesterol profile • Markers of inflammation such as high-sensitivity C-

reactive protein are associated with sudden cardiac death.

Effects of Prolonged Hypertension

Angiogram

Myocardial Infarction • Progression of coronary

artery disease– Leads to reduced blood flow

to myocardium.• Angina will result

• Thrombus breaks off– Embolism travels until it

blocks the flow of blood distal to the clot.

– Acute damage to endothelium causes inflammatory response that occludes lumen.

• Lack of blood=lack of O2 (hypoxia)=myocardial muscle death

Angina and the Elderly

Congestive Heart Failure (CHF)

• Congestive heart failure (CHF) is caused by:– Coronary atherosclerosis, high blood

pressure, multiple myocardial infarcts– Look at the anatomy to figure out why you

have the symptoms and what part of your heart is involved.

– Can be:• Right sided • Left sided• Biventricular

Left Sided Heart Failure

• Left ventricle is not able to pump the blood out as fast as it returns from the lungs. Blood backs up to the lungs.– Presents as fatigue and SOB with minimal exertion

as the blood backing up to the lungs.– Orthopnea (need to be upright) Drowning in own

fluids while lying down – Crackles in the lung bases( water in lungs)– Cyanosis ( blue lips, and nail beds) results from

impaired pulmonary gas exchange from fluid overload in lungs.

– Tachycardia from heart working harder.• deliver less oxygen to tissues • rising levels carbon dioxide

Right Sided Heart Failure

When the right side is pump blood out as fast as it returns it will back up in both vena cavas. Clinically you will see :– Organomegoly: organs become swollen from blood

backing up into the inferior vena cava.– Abdominal ascites and rapid weight gain from the

veins that would normally drain the abdomen.– Pitting Edema usually in the both legs as blood backs

up the IVC.– Distention of jugular vein as SVC backs up into

jugular vein

Other Causes of Edema Capillary filtration from chronic capillary BP leads to

Capillary reabsorption.– Hypoproteinemia (oncotic pressure blood albumin)– Cirrhosis and famine may lead to reduced albumin

production – Hypertension results in excessive albumin lose in the

blood.

• Kidney failure: Not able reabsorb solutes needed to maintain proper osmotic balance in the blood.– Swelling will be bilaterally

• Obstructed lymphatic drainage: swelling is usually only on the affected side.

Cerebral Vascular AccidentCVA

• Ischemic Stroke: – Thrombus occludes

blood flow to specific areas of the brain causing tissue death.

• Hemorrhagic Stroke– Ruptured blood vessel

causes blood to pool in the cranium placing pressure on the brain.

Cardiovascular/RespiratoryScreen

• Shortness of breath • Chest ,back and L arm Pain • Heart palpitations• Syncope(Fainting)• Fatigue/ Weakness• Cough/ Sputum• Edema / weight gain• Cyanosis (lips,nails,skin)• Nausea• Dizziness• Changes in heart rate• Change in Respiratory Rate• Changes in distal pulses