The Heart

The Heart

Anatomy and Physiology

Cardiovascular System (Overview) Heart beats over 100,000 times a

each day Pumps a total of 8000 liters of blood Closed System Pulmonary Circuit/ Systemic Circuit Works with the respiratory system

and blood for the delivery of oxygen and nutrients and removal of waste

Vessels Arteries (Efferent): Blood Away

Most cases oxygen rich Veins (Afferent): Blood Toward

Most cases oxygen poor Capillaries: vessels in between/

exchange vessels. Gas exchange: Semi-permeable

membrane

Anatomy of the Heart Four Chambers Upper Chambers

Atrium (Atria) Lower Chambers

Ventricles• Position within the thorax

Thoracic Location Anterior Chest/ Posterior to the

sternum Lies slightly to the left of the midline Sits at an angle Rotated toward the left side Surrounded by the pericardial cavity

Pericardium Fist into the center of a balloon Subdivided: Visceral and Parietal Pericardial Sac: 10-20 ml of

pericardial fluid Secreted by the pericardial

membranes Lubricant Pericarditis

Superficial Anatomy of the Heart Atria, the top chambers: Auricle Grooves

Coronary Sulcus Anterior interventricular sulcus Posterior interventricular sulcus Fat Deposits for cushion Base and Apex

Internal Anatomy Interatrial Septum Interventricular Septum Atrioventricular Valves

Right Atrium Blood Received from Superior Vena

Cava (SVC) and Inferior Vena Cava (IVC)

Coronary Sinus also returns blood to the heart

Foramen Ovale: Oval window that connects atria during the time when fetus in the uterus. Closes after birth

Right Ventricle Cusps (Tricuspid): An AV Valve Connected by the Chordae Tendineae to

the papillary muscles Allows for the doors to swing open, but

only in one direction Pulmonary Trunk, Pulmonary Semi-Lunar

valves. Into Pulmonary Arteries (left and right)

Left Atrium Blood returning from the lungs Four Pulmonary Veins Pools in the atria Through the Mitral Valve (bicuspid)

AV Valve

Left Ventricle Pumps at great pressure, systemic

circulation Aortic Semi-Lunar Valve Aortic Arch Descending Aorta Pulmonary Trunk is attached to the Aortic

Arch by the Ligamentum Arteriosum Aortic Rupture/Aortic Stenosis

Structural Difference Left Ventricle Large, must push

harder Six to seven times

as much force Thicker wall When it pumps it

bulges into the right ventricle

Right Ventricle Smaller, less

pressure Assisted by the left

ventricle as both ventricles pump at the same time

Closer Look at the Valves AV Valves

Prevents backflow into atria During vent relax, loose, valves open Vents contract, valves close

Semi-Lunar Valves Prevents backflow into vents Support each other like legs of a tripod MVP Rheumatic Fever

The Heart Wall Three Layers

Epicardium Myocardium Endocardium

Cardiac Muscle Tissue Muscle cells are intercalated discs Calcium plays a role Automaticity Smaller than typical skeletal muscle

cell

Blood Supply to Heart Myocardium needs blood Sensitive to low blood supply Coronary Circulation Right Coronary Artery

Rt Atrium Portions of both vent SA and AV nodes Posterior interventricular branch

Blood supply (cont) Left Coronary Artery

Lt atrium, Lt vent, Intervent septum Gives rise to circumflex branch and

anterior interventricular branch Cardiac Veins

Coronary Sinus Posterior and middle cardiac veins Small cardiac veins, anterior cardiac

veins

Innervation of the Heart Cardiac centers of the medulla Cardioacceleratory Center Cardioinhibitory Center Vagus Nerve Baroreceptors and Chemoreceptors

Conduction System Sinoatrial Node (SA) Atrioventricular Node (AV) Internodal pathways (Bundle

Branches: Bundle of His) Purkinje Fibers

SA Node Pacemaker Cells 50 msec from SA to AV Stimulates rt and lt atria Action spreads through cell to cell

contact

AV Node Less efficient pathways 100 msec Junction as a pausing location Important so that the atria

depolarize before the ventricles

AV Bundle and Bundle Branches Only electrical connection between

atria and ventricles Left bundle branch serves left

ventricle Conduct the impulse to the purkinje

fibers Purkinje rapidly fire

ECG or EKG P wave QRS Complex T wave P-R Interval (no more than .2 sec) Q-T Interval Rate/Rhythm ST Segment

Heart Attacks Myocardial Infarction (MI) Coronary Thrombosis Cardiac Enzymes

Lactate Dehydrogenase (LDH) Serum Glutamic Transaminase (SGOT) Creatine Phosphokinase (CPK) CPK-MB: Special CPK in cardiac muscle

Cardiac Cycle The period between start of one heart

beat and the next is a single cardiac cycle Contractions/Relaxations Systole (Contraction) Pump Diastole (Relaxation) Fill Fluid moves from high to low pressure Atrial and ventricular systole not at same

time

Phases Atrial Systole (Beginning) 100 msec Blood pushed through AV valves Ventricles already 70% full, Atria tops off

(70% is passive from previous cardiac cycle)

At end of Atrial Systole, vents have max blood: End Diastolic Volume (130ml)

Phases (Cont) Ventricular Systole 270 msec Vent contract at first it is isovolumetric

contraction all heart valves closed, no blood flow yet

As pressure increases, semilunar valves open (ventricular ejection)

Pressures slowly decline, before the valves close, blood returns to vents

Stroke volume 80 ml (60%) of EDV End-Systolic pressure 50 ml 40% of EDV

Phases (Cont) Ventricular Diastole 430 msec All valves close Vent myocardium resting Vent pressure is higher than atrial blood

cannot flow to vents This is isovolumetric relaxation Vent pressures drop, event atrial pressure

is higher, the AV valves open

Heart Sounds Ausculation Four Sounds (S1-S4) S1 Lubb: Start of Vent contraction,

AV valves close S2: Dupp: vent filling, semi-lunar

valves close S3-S4 harder to hear: Blood flowing

into vents and atrial contraction

Cardiodynamics Movements and forces generated

during cardiac contractions EDV, ESV, SV, and Ejection Fraction

(which is percentage of the EDV represented by SV)

SV most important CO (Cardiac Ouput) CO= SV x HR (80 ml x 75= 6 l/m)

Factors controlling SV EDV (filling time and venous return) ESV three factors

Preload degree of stretching during vent diastole: stretching of muscle: At rest not a lot, during exercise it increases• More in More Out: Frank-Starling Principle

Factors controlling SV (cont) ESV Factor two

Contractility: amount of force at contraction. Some cause increase contractility (CA entry for example) Some cause decrease (CA blocking)

Generally three things control it Autonomic Activity (epi and norepi, or Ach decreasing SA and AV nodes) Hormones: Epi/Norepi/ Glucagon (+), Thyroid (+) Ions: Calcium (hyper +/hypo -), Potassium (hyper weak contractions/hypo rate decreases)

Factors controlling SV (Cont) ESV Factor Three

Afterload: amount of tension the contracting ventricle must produce to force open semilunar valves

As afterload increases, stroke volume decreases

Heart failure and increase in PVR

Factors Affecting HR What can affect this? Brady and Tachy Autonomic Innervation: Ach and NE Ach for example opens K channels slows

rate of depolarization, decline in HR NE release increase rate by open CA

channels All happening at the SA

Factors Affecting HR (Cont) Hormones Epi, Norepi, Thyroid increase

contractility thus increase HR Changes in Ions (earlier discussed) Changes in Body Temp: decrease

temp, decrease HR, Increase temp, increase HR

Open Heart Surgery, chilly room

HR and B/P Palpated where arteries are close to

bones: Radial, Brachial, Carotid, Femoral

B/P Systolic/Diastolic 120/80 Measured in mm of Hg B/P Cuff/ Placement Lab