HN220 Final

3 components of the cardiovascular system

heart, blood vessels, blood

Main function of the cardiovascular system

transport of substances- oxygen and nutrients to cells, waste from cells to liver/kidney, hormones, immune cells, clotting proteins to target cells

Pulmonary circuit

supplied by the right heart, permits gas exchange in the lungs

Systemic circuit

supplied by left heart, transports blood to and from all tissues except the lungs

How does blood travel to systemic tissues?

arteries-->arterioles-->capillaries

How does blood travel back to the heart from the systemic tissues?

venules-->veins-->vena cava-->right heart

Epicardium

outer layer of the heart, has visceral pericardium that covers the heart

Myocardium

middle, muscular wall of the heart with concentric layers of cardiac muscle tissues

Endocardium

inner epithelial lining of the heart, provides protection for valves and heart chambers

Why is muscular layer on the right side of the heart thinner than on the left?

the right side doesn't have to generate as much force when contracting since it only needs to travel to the lungs

what drives blood flow?

Pressure gradients

Purpose of valves in the heart

prevent backward flow

AV valves

tricuspid and mitral (bicuspid), connected to myocardium by chordae tendinae and papillary muscle

Contractile cells

99% of all cardio myocytes, generate the pumping action of the myocardium

Autorhythmic cells

generate/spread action potentials spontaneously, can be pacemaker cells that initiate APs and set rhythm, or conduction fibers that transmit/spread APs

Characteristics of contractile myocardial cells

small, bifurcate, single central nucleus, aerobic-high in myoglobin, mitochondria, extensive blood supply. Involuntary but contract similar to skeletal muscle

How are contractile cardio myocytes cells similar to skeletal muscle?

are striated, have sarcomeres

How are contractile cardio myocytes different from skeletal muscle?

have short and wide T tubules, less SR with no terminal cisternae, under SNS and PNS control, single nucleus, have intercalated discs to connect cells

Gap junctions in intercalated discs

electrically connect adjacent cardiocytes, direct connection

Desmosomes in intercalated discs

the 'glue' that holds the cells together, links proteins binding adjacent cells, allow chemical communication

Sinoatrial node

pacemaker of the heart

Atrioventricular node

delays the conduction from atria to ventricle

Conduction fibers of the myocardium

spread APs via internodal pathways in the atria, Bundle of His in the ventricles, and Purkinje fibers in the ventricles

Pathway that APs spread throughout the cardiomyocytes

start at sinoatrial node through atrial muscle via interatrial pathways, to AV nodes via internodal pathway, delay at AV node, to atrioventricular bundle (bundle of His), splits into left and right bundle branches, to Purkinje fibers

Why does the SA node set the pace?

its the fastest to depolarize

P wave

movement of depolarization through the atria, atrial contraction

QRS complex

ventricular depolarization and contraction

T wave

ventricular repolarization

Why don't you see atrial repolarization on an ECG?

because it's masked by ventricular contraction

Funny channels

depolarize the cell from resting to threshold potential, leak K+ out and Na+ in

Transient calcium channels

open for a small amount of time after the funny channels to bring the membrane to threshold (-55mv-->-50mv)

Long lasting Calcium channels

open after the transient channels, bring membrane from threshold to peak (+10)

Phase 0 of electrical activity in cardiac contractile cells

increased permeability to Na+

Phase 1 of electrical activity in cardiac contractile cells

decreased permeability to Na+

Phase 2 of electrical activity in cardiac contractile cells

increased permeability to Ca2+, decreased permeability to K+

Purpose of phase 1 and 2 of electrical activity in cardiac contractile cells

to prolong action potentials

Phase 3 of electrical activity in cardiac contractile cells

increased permeability to K+, decreased permeability to Ca2+

Phase 4 of electrical activity in cardiac contractile cells

resting membrane potential

Duration of contractile cell action potential

250-300msec (compared to 1-2msec in skeletal muscle)

Resting potential for contractile cardiomyocytes

-90mv (K+ equilibrium potential)

Myocardial action potential duration

around 200msec, with a long absolute refractory period so that tetanus is impossible (don't want your heart to be tetanic)

Phase 1 of excitation contraction coupling in cardiac muscle

current spreads through gap junctions to contractile cell

Phase 2 of excitation contraction coupling in cardiac muscle

action potentials travel along plasma membrane and T tubules

Phase 3 of excitation contraction coupling in cardiac muscle

Ca2+ channels open in plasma membrane and SR

Phase 4 of excitation contraction coupling in cardiac muscle

Ca2+ induces Ca2+ release from SR

Phase 5 of excitation contraction coupling in cardiac muscle

Ca2+ binds troponin, exposing myosin-binding sites

Phase 6 of excitation contraction coupling in cardiac muscle

crossbridge cycle begins (contraction)

Phase 7 of excitation contraction coupling in cardiac muscle

Ca2+ is actively transported back into SR and ECF

Phase 8 of excitation contraction coupling in cardiac muscle

Tropomyosin blocks myosin-binding sites (relaxation)

Systole

ventricular contraction

Diastole

ventricular relaxation

When do atrioventricular valves open?

when atrial pressure is greater than ventricular pressure

When do semilunar valves open?

when ventricular pressure is greater than arterial pressure

How long does a typical cardiac cycle last?

800 msec, 300msec in systole and 500msec in diastole

Phase 1 of the cardiac cycle

ventricular filling- blood returning to the heart enters relaxed atria, passes AV valves and into ventricles, atria contract at the end of this phase. Semilunar valves are closed in this phase

Phase 2 of the cardiac cycle

isovolumetric contraction- ventricles contract, AV valves close, semilunar valves closed. Ends when ventricular pressure is more than aortic pressure

Phase 3 of the cardiac cycle

ventricular ejection- blood leaves ventricles, pressure reaches peak as contraction and blood continues to leave ventricles, ventricular volume decreases, blood ejected from ventricles until semilunar valves close when pressure in ventricle is lower than aorta

Phase 4 of the cardiac cycle

isovolumetric relaxation- heart is resting, some blood remains in ventricles, still some pressure, all valves are closed

What happens to aortic pressure in diastole?

aortic valves close, blood is still leaving aorta so pressure falls. Lowest point is measured

What happens to aortic pressure in systole?

aortic valve opens, pressure rises rapidly with ejection, aortic valve closes at the end. Highest point is measured

Why is blood flow continuous during the cardiac cycle?

aorta and large arteries are elastic, makes them a pressure reservoir that stores energy as walls stretch in systole, energy is released during diastole as walls recoil inwards. Aortic pressure maintains blood flow for the entire cycle

Cardiac output

heart rate x stroke volume or MAP/TPR

Average cardiac output

5L/min at rest

Average blood volume

5.5L

Average resting heart rate

70bpm

Average stroke volume

70 mL

EDV (end diastolic volume)

volume of blood in ventricle at the end of diastole

ESV (end systolic volume)

volume of blood in ventricle at the end of systole

SV (stroke volume)

volume of blood ejected from the ventricle each cycle. =EDV-ESV

Ejection fraction

fraction of end diastolic volume ejected during a heart beat. =SV/EDV

Intrinsic regulation of cardiac output

autoregulation

Extrinsic regulation of cardiac output

neural and hormonal, SNS and PNS (opposing effects)

Stroke volume regulation

ventricular myocardium is only innervated by the SNS, only SNS influences ventricular contraction

How does PNS activity decrease HR?

PNS postganglionic neurons release ACh. ACh binds to muscarinic cholinergic receptors on SA nodal cells, opening K+ channels and closing funny and T-type channels, slows depolarization and decreasing conduction speed of impulses

How does SNS activity increase HR above 100bpm?

increased SNS through nerves or epinephrine stimulate beta 1 receptors in the SA node, increases open state of funny and CA2+ channels, increases rate of spontaneous depolarization, increases heart rate

Hormonal control of HR

increases epi increases HR and conduction velocity; thyroid hormone, glucagon and insulin also increase HR

Epinephrine

released from renal medulla due to increased SNS activity, increases AP frequency in SA node and conduction velocity

Frank Starling law of the heart

increased EDV= increased force of contraction= increased SV

Why is there upper limitations to EDV?

ventricular expansion limited by connective tissue and pericardial sac, can only stretch so far (increased stretch=increased force of contraction)

Afterload

pressure in the arterial system after ventricular contraction begins, increase in arterial pressure will decrease SV

Key feature of arterioles

variable radius, allows regulation of BP and blood flow to tissues

Flow

change in pressure/resistance

Pressure gradients in the cardiovascular system

heart creates a pressure gradient for bulk flow of blood, must exist to maintain blood flow

change in pressure in the systemic circuit

pressure in aorta minus pressure in vena cava just before it empties into the right atrium (MAP-CVP)

Mean arterial pressure

pressure in aorta, around 85-90mmHg at rest

Central venous pressure

pressure in vena cava, 0mmHg at rest

Flow is ________ to pressure gradient

proportional

Why is the pressure gradient greater in the systemic circuit than the pulmonary circuit?

because there's a much greater distance to travel, so resistance is higher

What factors affect resistance to flow?

radius of vessel, length of vessel, viscosity of fluid

Poiseuille's Law

flow=(change in pressure x radius^4)/8nL. therefore change in radius will influence P the most

What is inversely proportional to resistance?

flow

Vasoconstriction effect on blood flow

decreased radius in vessels, increases resistance, decreases flow

Vasodilation effect on blood flow

increased radius in vessels, decreases resistance, increases flow

Total peripheral resistance (TPR)

combined resistance of all blood vessels within the systemic circuit

Vessels involved in microcirculation

arterioles, capillaries, venules

Tunica intima

inner layer of a blood vessel, made of endothelium, subendothelial layer, internal elastic membrane

Tunica media

middle layer of a blood vessel, smooth vessel and elastic fibers, external elastic membrane. Thicker in arteries

Tunica externa

collagen fibers, vasa vasorum

Valves in veins

keeps blood flow unidirectional

Lining of capillaries

single layer of epithelial cells