Cardiovascular System - Heart

Responsible for:

• Transport of materials:

  • Gases

  • Nutrients

  • Waste

  • Communication

  • Defense against pathogens

  • Temperature homeostasis

• Heart Pump:

  • Atria receives blood returning to heart

  • Ventricles pump blood out

  • Septum divides left and right halves

  • Left - oxygenated blood

  • Right - de-oxygenated blood

• Blood Vessels:

  • Veins, arteries, and capillaries

  • Pulmonary and systemic circulation

  • Portal system joins two capillary beds in series

• Blood:

  • Cells and plasma

The heart is composed mostly of myocardium

Two sets of heart valves ensures one-way flow

• Atrioventricular Valves

  • Between atria and ventricles

  • Tricuspid valve on the right side

  • Bicuspid (mitral) valve on the left side

• Semi-lunar Valves

  • Between ventricles and arteries

  • Aortic valve

  • Pulmonary valve

Structure of the heart:

• Encased within a membranous fluid-filled sac, the pericardium

Electrical Conduction

• Sinoatrial (SA) Node - Sets the pace of the heartbeat at 70 bpm

• Under certain conditions, the following may also act as pacemakers:

  • Atrioventricular (AV) Node - 50 bpm

  • Purkinje fibers - 25-40 bpm

• Inter-nodal pathway from SA to AV node

  • Routes the direction of electrical signals so the heart contracts from apex to base

  • AV node delay is accomplished by slower conductional signals through nodal cells

• Purkinje fibers

  • Transmits electric signals down the atrioventricular bundle (bundle of His) to left and right bundle branches

• The Conducting System of the Heart

  • SA node - depolarizes →

  • Internodal pathways - electrical activity rushes through to →

  • AV node - depolarization spreads more slowly across the atria (conduction slows through AV) →

  • Bundle branches - depolarization rushes through the ventricular conducting system to the apex of the heart →

  • Purkinje fibers - depolarization wave spreads upward from the apex

• SA Node

  • Cells within the sinoatrial node are the primary pacemaker site within the heart

  • Cells are characterized as having no true resting potential (voltage across cell membrane at rest) but instead generate regular, spontaneous action potentials

  • Unlike non-pacemaker action potentials in the heart, and most

    other cells that elicit action potentials (e.g., nerve cells, muscle

    cells), the depolarizing current is carried into the cell primarily

    by relatively slow Ca++ currents instead of by fast Na+

    currents.

  • There are, in fact, no fast Na+ channels and currents operating

    in SA nodal cells. This results in slower action potentials in

    terms of how rapidly they depolarize

  • Divided into three phases

    • Phase 4 is the spontaneous depolarization (pacemaker potential) that triggers the action potential once the membrane potential reaches a threshold between -40 and -30 mV

    • Phase 0 is the depolarization phase of the action potential

    • Followed by Phase 3, repolarization. Once the cell is completely repolarized at about -60 mV, the cycle is spontaneously repeated

Myocardial Action Potentials Vary

• Contractile Cells

  • depolarization due to Na+ entry

  • repolarization due to K+ exit

  • Long action potential (plateau) due to ca2+ entry in the cell prevents tetanus

• Autorhythmic Cells

  • unstable membrane potential called pacemaker potential

  • depolarization is due to Ca2+ channels opening

  • Phases of Cardiac contractile cell

    • 0 - Na+ channels open

    • 1 - Na+ channels close

    • 2 - Ca2+ channels open; fast K+ channels close

    • 3 - Ca2+ channels close; slow K+ channels open

    • 4 - Resting potential

The Waves of Electrocardiogram (ECG)

• Waves and segments are two major components of an ECG

• Three Waves Five Segments (P, Q, R, S, T)

  • P wave - depolarization of the atria

  • P-R segment - conduction through AV node and AV bundle

  • QRS complex: wave of ventricular depolarization

  • T wave - repolarization of the ventricle

  • Atrial repolarization is part of the QRS

Electrical Events of the Cardiac Cycle

• Mechanical events lag behind electrical events

  • ECG begins with atrial depolarization, atrial contraction at the end of P wave.

  • Q wave end - ventricular contraction begins and continues through T wave

• Analysis:

  • Heartrate - time between two P waves or two Q waves

  • Rhythm - regular pattern

  • Waves analysis - presence and shape

  • Segment length constant

Cardiac Muscle

• Contractile cells

  • striated fibers organized in sarcomeres

• Autorhythmic cells (pacemakers)

  • signal for contraction

  • smaller and fewer contractile fibers compared to contractile cells

• Myocardial muscle cells are branched, have a single nucleus, and are attached to each other by specialized junctions known as intercalated disks

• Intercalated disks contain desmosomes that transfer force form cell to cell and gap junctions that allow electrical signals to pass rapidly from cell to cell

Cardiac vs Skeletal

• Smaller and have single nucleus per fiber

• Branch and join neighboring cells through intercalated disks

  • desmosomes allow force to be transferred

  • Gap junctions provide electrical connection

• T-tubules are larger and branch

• Sarcoplasmic reticulum is smaller

• Mitochondria occupy one-third of cell volume

Cardiac Muscle Contraction can be graded

• Action potential starts with the heart pacemaker cells

  • voltage-gated L- type Ca2+ channels in the cell membrane open (extra cellular calcium contributes 10%)

  • ryanodine receptors open in the sarcoplasmic reticulum (SR)

  • Calcium binds to troponin

  • Crossbridge cycle as in skeletal muscle

• Relaxation:

  • Calcium removed from cytoplasm

    • Back in the SR with Ca2+ ATPase and out of the cell through the Na+ - Ca2+ exchanger (NC)

• Force generated is proportional to # of active crossbridges

  • Determined by how much calcium is bound to troponin

• Sacromere length affects force of contraction

Electrocardio Coupling in Cardiac Muscle

• Action Potential enters from adj. cells

• Voltage-gated Ca2+ channels open allowing entry into cell

• Ca2+ induced Ca2+ release thru ryanodine receptor channels (RyR)

• Local release causes Ca2+ spark

• Summed Ca2+ sparks create a Ca2+ signal

• Ca2+ ion bind to troponin to initiate contractions

• Relaxation occurs when Ca2+ unbinds from troponin

• Ca2+ is pumped back into the SR for storage

• Ca2+ is exchanged with Na+ by the NCX antiporter

• Na+ - K+ ATPase

Heart Sounds

• First heart sound

  • Vibrations following closure of AV valves

  • “Lub”

• Second Heart Sounds

  • Vibrations created by closing of semi-lunar valve

  • “Dup”

• Auscultation is listening to the heart thru the chest wall w/ a stethoscope

Mechanical events of the Cardiac cycle

• Diastole - cardiac muscle relaxes

• Systole - cardiac muscles contract

• Beginning of the cycle - the heart is at rest; atrial and ventricular diastole

  • The atria are filling with blood from the vein

  • AV valves open → ventricles fill

• Atrial systole - atria contracts

  • Early ventricular contraction and AV valves close → first heart sound

• Atrial diastole - all valves shut, isometric contraction of the heart, atria relax and blood flows in the atria

• Ventricular systole - ventricles finish contracting, pushing smei-lunar valves open

• Ventricular diastole - ventricular relaxation and pressure drops, still higher than atrial pressure

  • Arterial blood flows back pushing semi-lunar valves shut → second heart sound

• Isovolumic ventricular relaxation, volume of blood in ventricles not changing

• AV valves open when ventricular pressure drops below atrial pressure

Summed Cardiac Cycle

• Late diastole - both sets of chambers are relaxed and ventricles fill passively

• Atrial systole - contraction forces a small amount of additional blood into ventricles

• Isovolumic ventricular contraction - 1st phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open SL valves

• Ventricular ejection - as pressure rises and exceeds pressure in the arteris, the SL valves open and blood is ejected

• Isovolumic ventricular relaxation - ventricles relax, pressure falls, blood flows back into cusps of semilunar valves and snaps them close

Stroke Volume and Cardiac Output

• end diastolic volume (EDV)

• end systolic volume (ESV)

• Stroke volume

  • amt of blood pumped by one ventricle during a contraction

  • Force of contraction is affected by:

    • length of muscle fiber - determined by volume of blood at beginning of contraction

    • contractility of heart

      • any chemical that affects contractility is an inotropic agent

        • epinephrine, norepinephrine, and digitalis have positive inotropic effects

      • chemicals w/ neg. effects decrease contractility

        • “beta-blockers?”

    • as stretch of the ventricular wall increases so does stroke volume

    • preload is the degree of myocardial stretch before contraction

  • Sympathetic activity speeds heartrate

    • β1-adrenergic receptors on the autorhythmic cells

  • Parasympathetic activity slows heart rate

  • volume of blood before contraction - volume of blood after contraction = stroke volume

  • EDV - ESV = stroke volume

  • Avg. = 70 mL

• cardiac output (CO)

  • Volume of blood pumped by one ventricle in a given period of time

  • Heartrate * stroke volume = cardiac output

  • Avg. 5 L/min

Heart Failure

• Hypertrophic

  • diastolic

  • stiff thick chambers

  • heart can’t fill

• Dilated

  • systolic

  • stretched and thin chambers

  • heart can’t pump

Myocardial Infarction (Heart Attack)

• Type 1

  • Plaque rupture/erosion w/ occlusive thrombus

  • plaque rupture/erosion w/ non-occlusive thrombus

• Type 2

  • Atherosclerosis and oxygen supply/demand imbalance

  • Vasopasm or coronary microvascular dysfunction

  • Non-atherosclerotic coronary dissection

  • Oxygen supply/demand imbalance alone