Heart and vessles

Pericardium

double-walled sac that encloses the heart
• Allows heart to beat without friction, provides room to expand, yet resists excessive expansion
• Anchored to diaphragm inferiorly and sternum anteriorly

Fibrous pericardium

outer wall, not attached to heart

Serous pericardium

•Parietal layer—lines fibrous pericardium
• Visceral layer (epicardium)—covering heart surface

Pericardial cavity

space between parietal and visceral layers of serous pericardium, filled with 5 to 30 mL of pericardial fluid

Pericarditis

painful inflammation of the membranes

Epicardium (external layer)

• Visceral layer of serous pericardium
• Smooth, slippery texture to outermost surface

Myocardium (contractile and conductile cells)

• 95% of heart is cardiac muscle

Endocardium (inner layer)

• Smooth lining for chambers of heart, valves and continuous with lining of large blood vessels

Atria

•Receiving chambers
•Right and left atria
•Auricles increase capacity

Ventricles

•Right and left ventricles
•Pumping chambers

Sulci

•Grooves on the surface of the heart
•Contain coronary blood vessels
•Coronary sulcus
•Anterior interventricular sulcus

Interatrial septum

wall that separates atria

Pectinate muscles

internal ridges of myocardium in right atrium and both auricles

Interventricular septum

muscular wall that separates ventricles

Trabeculae carneae

internal ridges in both ventricles; may prevent ventricle walls from sticking together after contraction

Cardiac muscle tissue

•Compared to skeletal muscle tissue
1. Small cell size with mitochondria that are larger and more numerous than in skeletal muscle
2. Striations
3. Single (sometimes two), centrally located nucleus
4. Branching interconnections
5. Specialized intercellular connections

Intercalated discs

• Desmosomes - cell adhesion structures
• Gap junctions
• Allow ions and molecules to move directly between cells
• Create direct electrical connection so an action potential can pass directly between cells

Metabolism of Cardiac Muscle

• Cardiac muscle depends almost exclusively on aerobic respiration to make ATP
• Rich in myoglobin and glycogen
• Huge mitochondria: fill 25% of cell
• Adaptable to different organic fuels
• Fatty acids (60%); glucose (35%); ketones, lactate, and amino acids (5%)
• More vulnerable to oxygen deficiency than lack of a specific fuel
• Fatigue resistant because it makes little use of anaerobic fermentation or oxygen debt mechanisms; does not fatigue for a lifetime

Autorhythmic Fibers

•Specialized cardiac muscle fibers (myocardial conducting cells - 1% of cardiac muscle cells)
• Self-excitable - have Na+ channels that never fully close - so the sodium slowly enters cell and then causes channels to open quickly and fully -spontaneous depolarization
• Repeatedly generate action potentials that trigger heart contractions
• Function• Act as pacemaker• Form conduction system

Myocardial Thickness

Thin-walled atria deliver blood under less pressure to ventricles

Right ventricle

pumps blood to lungs
• Shorter distance, lower pressure, less resistance

Left ventricle

pumps blood to body
• Longer distance, higher pressure, more resistance
•Left ventricle works harder to maintain same rate of blood flow as right ventricle

Atrioventricular valves

•Tricuspid and bicuspid valves
•When atria contract and ventricles are relaxed
• AV valves open, cusps project into ventricles
• In ventricles, papillary muscles are relaxed and chordae tendinae are slack
•When atria relax and ventricles contract
• Pressure drives cusps upward until edges meet and close opening
• Papillary muscles contract tightening chordae tendinae
• Prevents regurgitation

Semilunar Valves

•Aortic and pulmonary valves
•Valves open when pressure in ventricle exceeds pressure in arteries
•As ventricles relax, some backflow permitted but blood fills valve cusps closing them tightly
•No valves guarding entrance to atria
•As atria contract, they compress and nearly collapse the venous entry points

Coronary Circulation

• Myocardium has its own network of blood vessels
• Coronary arteries branch from ascending aorta
• Anastomoses provide alternate routes or collateral circuits
• Allows heart muscle to receive sufficient
oxygen even if an artery is partially blocked
• Coronary capillaries
• Coronary veins

Coronary veins

• Collect in coronary sinus
• Empty into right atrium

Arterial Supply

• Flow through coronary arteries is greatest when heart relaxes
• Contraction of the myocardium compresses the coronary arteries and obstructs blood flow
• Opening of the aortic valve flap during ventricular systole covers the openings of the coronary arteries blocking blood flow into them
• During ventricular diastole, blood in the aorta surges back toward the heart and into the openings of the coronary arteries

Right coronary artery

right atrium, portions of both ventricles and conduction system of heart

Marginal arteries

right ventricle surface

Posterior interventricular artery

interventricular septum and adjacent ventricular portions

Left coronary artery

left ventricle, left atrium, and interventricular septum

Circumflex artery

from left coronary artery, follows coronary sulcus to meet right coronary artery branches

Anterior interventricular artery

interventricular sulcus

Great cardiac vein

drains area supplied by anterior interventricular artery, empties into coronary sinus on posterior

Anterior cardiac veins

drains anterior surface of right ventricle, empties into right atrium

Coronary sinus

expanded vein, empties into right atrium

Posterior cardiac vein

drains area supplied by circumflex artery

Angina pectoris

chest pain from partial obstruction of coronary blood flow
• Pain caused by ischemia of cardiac muscle
• Obstruction partially blocks blood flow
• Myocardium shifts to anaerobic fermentation, producing lactate and thus stimulating pain

Myocardial infarction (MI)

sudden death of a patch of myocardium resulting from long-term obstruction of coronary circulation
• Cardiac muscle downstream of the blockage dies
• Heavy pressure or squeezing pain radiating into the left arm
• Some painless heart attacks may disrupt electrical conduction pathways, leading to fibrillation and cardiac arrest
• Silent heart attacks occur in diabetics and the elderly
• MI responsible for about 27% of all deaths in the U.S

Conduction System

• Begins in sinoatrial (SA) node (pacemaker) in right atrial wall
• Propagates through atria via gap junctions
• Atria contact
• Reaches atrioventricular (AV) node in interatrial septum
• Enters atrioventricular (AV) bundle (Bundle of His)
• Enters right and left bundle branches which extend through interventricular septum toward apex
• Large diameter Purkinje fibers conduct action potential to remainder of ventricular myocardium
• Ventricles contract

Pacemaker Physiology

• SA node does not have a stable resting membrane potential
• Starts at −60 mV and drifts upward due to slow Na+ inflow
• Gradual depolarization is called pacemaker potential
• When it reaches threshold of −40 mV, voltage-gated fast Ca2+and Na+ channels open
• Faster depolarization occurs peaking at 0 mV
• K+ channels then open and K+ leaves the cell
• Causing repolarization
• Once K+ channels close, pacemaker potential starts over
• When SA node fires, it sets off heartbeat
• As the internal pacemaker, it typically fires every 0.8 seconds, setting the resting rate at 75 bpm
• Ventricular myocardium electrical behavior - resting voltage of -90mV

Stages of action potential

• When stimulated --depolarization (brief) - Na+ channels open rapid rush of Na+ into the cell (+30mV)
• Plateau - Ca2+ moves into cytosol \-- contraction
• Repolarization- K+ channels open and K+ moves out

Refractory period

time interval during which second contraction cannot be triggered
•Lasts longer than contraction itself
•Tetanus (maintained contraction) cannot occur

ECG or EKG

• Composite record of action potentials produced by all the heart muscle fibers
• Compare tracings from different leads with one another and with normal records
• 3 recognizable waves:
• P, QRS, and T

Correlation of ECG Waves and Systole

•Systole \= contraction and diastole \= relaxation
• Cardiac action potential arises in SA node
• P wave appears
• Atrial contraction (atrial systole)
• Action potential enters AV bundle and out over ventricles
• QRS complex
• Masks atrial repolarization
• Contraction of ventricles (ventricular systole)
• Begins shortly after QRS complex appears and continues during S-T segment
• Repolarization of ventricular fibers
• T wave
• Ventricular relaxation (diastole)

Sinus rhythm

normal heartbeat triggered by the SA node
• Adult at rest is typically 70 to 80 bpm (vagal tone)

Ectopic focus

a region of spontaneous firing other than the SA node
• May govern heart rhythm if SA node is damaged

Nodal rhythm

if SA node is damaged, heart rate is set by AV node, 40 to 50 bpm
• Other ectopic focal rhythms are 20 to 40 bpm and too slow to sustain life

Normal heart rate

70-100 bpm

Tachycardia

(fast) over 100 bpm

Bradycardia

(slow) less than 60 bpm

Junctional (nodal) rhythm

40-50 bpm

Ventricular tachycardia

100-200bpm

Ventricular fibrillation

quivering of ventricles (Hallmark of heart attack (MI)

Serious arrhythmia

caused by electrical signals traveling randomly
• Heart cannot pump blood; no coronary perfusion
• Kills quickly if not stopped

Defibrillation

strong electrical shock with intent to depolarize entire myocardium and reset heart to sinus rhythm
• Not a cure for artery disease, but may allow time for other corrective action

Atrial fibrillation

quivering of atria

Cardiac Cycle

• All events associated with one heartbeat
• Systole and diastole of atria and ventricles
• In each cycle, atria and ventricles alternately contract and relax
• During atrial systole, ventricles are relaxed
• During ventricle systole, atria are relaxed
• Forces blood from higher pressure to lower pressure
• During relaxation period, both atria and ventricles are relaxed
• The faster the heart beats, the shorter the relaxation period
• Systole and diastole lengths shorten slightly

Heart Sounds

• Auscultation
• Sound of heartbeat comes primarily from blood turbulence caused by closing of heart valves
• 4 heart sounds in each cardiac cycle - only 2 loud enough to be heard
• Lubb - AV valves close
• Dupp - SL valves close

Cardiac Output (CO)

• CO \= volume of blood ejected from left (or right)ventricle into aorta (or pulmonary trunk) each minute
• CO \= stroke volume- volume per pump (SV) x heart rate(HR)
• In typical resting male: 5.25L/min \= 70mL/beat x 75 beats/min
• Entire blood volume flows through pulmonary and systemic circuits each minute

Cardiac reserve

difference between maximum CO and CO at rest
• Average cardiac reserve 4-5 times resting value

Phases of the Cardiac Cycle

• Ventricular filling (during diastole)
• Isovolumetric contraction (during systole)
• Ventricular ejection (during systole)
• Isovolumetric relaxation (during diastole)
• The entire cardiac cycle (all four of these phases) is completed in less than 1 second

Ventricular filling

Ventricles expand and their pressure drops below that of the atria
• AV valves open and blood flows into the ventricles
• Filling occurs in three phases:
• Rapid ventricular filling: first one-third
• Diastasis: second one-third; slower filling
• P wave occurs at the end of diastasis
• Atrial systole: final one-third; atria contract
• End-diastolic volume (EDV) achieved in each ventricle (about 130 mL of blood)

Isovolumetric contraction

• Atria repolarize, relax and remain in diastole for rest of cardiac cycle
• Ventricles depolarize, causing QRS complex, and begin to contract
• AV valves close as ventricular blood surges back against the cusps• Heart sound S1 occurs at the beginning of this phase
• "Isovolumetric" because although ventricles contract, they do not eject blood
• Pressures in aorta and pulmonary trunk are still greater than those in the ventricles
• Cardiomyocytes exert force, but with all four valves closed, the blood cannot go anywhere

Ventricular ejection

• Begins when ventricular pressure exceeds arterial pressure and semilunar valves open
• Pressure peaks in left ventricle at about 120 mm Hg and 25 mm Hg in the right
• First: rapid ejection—blood spurts out of ventricles quickly
• Then: reduced ejection—slower flow with lower pressure
• Ejection lasts about 200 to 250 ms - corresponds to plateau phase of cardiac action potential
• T wave of ECG occurs late in this phase
• Stroke volume (SV) is about 70 mL
• Ejection fraction is about 54% of EDV (130 mL)
• 60 mL remaining blood is end-systolic volume (ESV) \= EDV − SV

isovolumetric relaxation

• T wave ends and ventricles begin to expand
• Blood from aorta and pulmonary trunk briefly flows backward filling cusps and closing semilunar valves
• Creates pressure rebound that appears as dicrotic notch in graph of artery pressure
• Heart sound S2 occurs
• "Isovolumetric" because semilunar valves are closed and AV valves have not yet opened
• Ventricles are therefore taking in no blood
• When AV valves open, ventricular filling begins again

Congestive heart failure (CHF)

results from the failure of either ventricle to eject blood effectively
• Usually due to a heart weakened by myocardial infarction, chronic hypertension, valvular insufficiency, or congenital defects in heart structure

Left ventricular failure

blood backs up into the lungs causing pulmonary edema
• Shortness of breath or sense of suffocation

Right ventricular failure

blood backs up in the vena cava causing systemic or generalized edema
• Enlargement of the liver, ascites (pooling of fluid in abdominal cavity), distension of jugular veins, swelling of the fingers, ankles, and feet
• Eventually leads to total heart failure

Regulation of Stroke Volume

Factors that ensure left and right ventricles pump equal volumes of blood
•Preload - effect of stretching
•Contractility
•Afterload - force to be overcome
• Degree of stretch on the heart before it contracts
• Greater preload increases the force of contraction
• Frank-Starling law of the heart - the more the heart fills with blood during diastole, the greater the force of contraction during systole

Factors that determine EDV

• Duration of ventricular diastole
• Venous return - volume of blood returning to right ventricle
•Strength of contraction at any given preload
•Positive agents increase contractility
• Often promote Ca2+ inflow during cardiac action potential
• Increase stroke volume
• Epinephrine, norepinephrine, digitalis
•Negative agents decrease contractility
• Anoxia, acidosis, some anesthetics, and increased K+ in interstitial fluid
• Beta blockers - interfere with norepinephrine
• Calcium channel blockers - interfere with entry of Ca2

•Pressure that must be overcome before a semilunar valve can open•
Increase in afterload causes stroke volume to decrease
• Blood remains in ventricle at the end of systole
•Hypertension and atherosclerosis increase afterload

Total peripheral resistance

•(resistance of entire cardiovascular system affects afterload)
• Must be overcome by sufficient pressure from the heart
• Depends on three factors
1. Vascular resistance - diameter and length
2. Viscosity - dissolved solutes and formed elements
3. Turbulence - irregularity of vessel walls

Arterial pressure is variable

• Rising during ventricular systole (systolic pressure)
• Declining during ventricular diastole (diastolic pressure)
• Commonly written with a "/" between pressures
• Example: 120/90

Pulse pressure

(difference between systolic and diastolic)
• Example: 120 - 90 \= 30 mm Hg

Mean arterial pressure (MAP)

• Adding 1/3 of pulse pressure to diastolic pressure
• Example: 90 + (120 - 90)/3 \= 100 mm Hg

Arteries

transport blood away from heart

Veins

Transport blood to the heart

Capillaries

exchange substances between blood and tissues
• Interconnect smallest arteries and smallest veins

Tunica intima (tunica interna)

• Innermost layer of arteries and veins
• Endothelial cells with connective tissue with elastic fibers
• In arteries, outer margin has layer of elastic fibers(internal elastic membrane)

Tunica media

• Middle layer
• Contains concentric sheets of smooth muscle
• Capable of vasoconstriction or vasodilation
• Collagen fibers connect tunica media to other layers

Tunica externa

• Outermost layer
• Connective tissue sheath with collagen and elastic fibers
• Generally thicker in veins
• Anchor vessel to surrounding tissues

Elastic arteries

large vessels close to the heart that stretch and recoil when heartbeats

Muscular arteries

medium-sized arteries, distribute blood to skeletal muscles and internal organs

Arterioles

Poorly defined tunica externa and tunica media only 1-2 smooth muscle cells thick

Venules

small veins lacking tunica media, collect blood from capillaries

Medium-sized veins

tunica media is thin but tunica externa is thick with longitudinal collagen and elastic fibers

Large veins

superior and inferior venae cavae and tributaries having thin tunica media

Continuous capillaries

• Endothelium is a complete lining
• Located throughout body in all tissues except epithelium and cartilage
• Permit diffusion of water, small solutes, and lipid-soluble materials
• Prevent loss of blood cells and plasma proteins

Fenestrated capillaries

• Contain windows or pores penetrating endothelium
• Permit rapid exchange of water and larger solutes
• Examples: capillaries in brain and endocrine organs, absorptive areas of GI tract, kidney filtration sites

Sinusoids

• Resemble fenestrated capillaries that are flattened and irregularly shaped
• Commonly have gaps between endothelial cells
• Basal lamina is thin or absent
• Permit more water and solute (plasma proteins) exchange
• Occur in liver, bone marrow, spleen, and many endocrine organs

Capillary beds

are networks of 10 to 100 capillaries
• Usually supplied by a single arteriole or metarteriole
• Drain into venule or distal end of metarteriole
• At any given time, 75% of body's capillaries are shut down
• Most control involves constriction of upstream arterioles
• Precapillary sphincters control flow in capillary beds supplied with metarterioles
• When sphincters are relaxed, capillaries are well perfused with blood
• When sphincters contract, they constrict the entry to the capillary and blood bypasses the capillary

Veins

•Veins are the capacitance vessels
• Thin-walled and flaccid
• Collapse when empty, expand easily
• Greater capacity for blood containment than arteries
• At rest, about 64% of blood is in veins, 15% in arteries
• Have steady blood flow (unlike pulses in arteries)
• Subjected to relatively low blood pressure
• Averages 10 mm Hg with little fluctuation
• Blood pressure in venules and medium veins is

Increasing venous blood flow

• Skeletal muscle contractions squeezing veins with valves
• Sympathetically controlled constriction of veins(venoconstriction)
• Venoconstriction can maintain arterial blood volume despite hemorrhaging

Capillary Exchange

two way movement of fluid across capillary walls
•The most important blood in the body is in the capillaries
•Only through capillary walls are exchanges made between the blood and surrounding tissues
•Water, oxygen, glucose, amino acids, lipids, minerals, antibodies, hormones, wastes, carbon dioxide, ammonia

Chemicals pass through the capillary wall by three routes

• Through endothelial cell cytoplasm
• Intercellular clefts between endothelial cells
• Filtration pores (fenestrations) of the fenestrated capillaries
•Mechanisms involved: Diffusion, transcytosis, filtration, and reabsorption

Diffusion

• Diffusion is the most important form of capillary exchange
• Glucose and oxygen, being more concentrated in blood, diffuse out of the blood
• Carbon dioxide and other waste, being more concentrated in tissue fluid, diffuse into the blood

Capillary diffusion can only occur if

• The solute can permeate the plasma membranes of the endothelial cell, or
• Find passages large enough to pass through
• Filtration pores and intracellular clefts

Lipid-soluble substances

Steroid hormones, O2 and CO2 diffuse easily through plasma membranes

Water-soluble substances

Glucose and electrolytes must pass through filtration pores and intercellular clefts