Cardiovascular system

Dr Longa Kaluba Banda

 Cardiovascular | Structures and Layers of the Heart

Heart
- YouTube

+Four chamber muscular organ

+Comparable to the size of a closed fist
+Located in the mediastinum
+Behind sternum
+Between 2nd and 6th ribs
+Between T5-T8
+Apex – base of heart
+Located at the 5th intercostal space
Coverings of the Heart
+Pericardium – loose fitting sac surrounding
the heart
+Fibrous pericardium – tough, loose-fitting,
inelastic
+Serous pericardium
+ Parietal layer: lines the inside of the fibrous
pericardium
+ Visceral layer: adheres to outside of the heart
+Pericardial space: between parietal and visceral
layer
+ Filled with 10-15mL of pericardial fluid
+ Decreases friction
Walls of the Heart
+Epicardium – outer layer
+Epicardium = serous pericardium
+Myocardium – thick, contractile layer composed of
cardiac muscle cells
+Intercalated disks contain many gap junctions
+Allow cardiac muscle cells to function as a single unit 
syncytium
+Endocaridium – interior of cardiac wall
+Endothelial tissue
+Covers projections of myocardial tissue called trabeculae
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Chambers of the Heart

+Atria – two superior chambers
+“Receiving chambers”
+Blood from veins enters atria
+Ventricles – two inferior chambers
+“pumping chambers”
+Thick muscular walls to increase force of pumping action
+ Left > right
+Separated by interventricular septum
Valves of the Heart
+Atrioventricular valves +Semilunar (SL valves)
(AV valves) +Pulmonary semilunar valve
+Tricuspid valve + Btwn R ventricle and
+ Btwn R atrium and ventricle pulmonary trunk
+ 3 flaps of endocardium +Aorta semilunar valve
+ Connected to ventricular
papillary muscle via chordae + Btwn L ventricle and aorta
tendinae
+Bicuspid valve
+ Btwn L atrium and ventricle
+ Also called mitral valve
+ Two flaps of endocardium
Chambers & Valves

Trace the blood flow through the heart

Blood vessels
+ Arteries and veins have a tunica externa,
tunica media, and tunica interna.
(a)Arteries have thicker muscle layers in
proportion to their diameters than do
veins because arteries must withstand
a higher blood pressure.
(b)Veins have venous valves that direct
blood to the heart when the veins are
compressed by the skeletal muscle
pumps.
+ Capillaries are composed of endothelial
cells only. They are the basic functional
units of the circulatory system.
Types of Blood Vessels
+Artery – carries oxygenated blood away from the heart
+“distributors”
+Arteriole: small artery
+Precapillary sphincters: regulate the blood flow into capillaries
+Vein – carries unoxygenated blood towards the heart
+Great ability to stretch (capacitance)
+Function as reservoirs: blood pools in the valves then is
pushed forward from the pumping pressure
+Venules: small vein
Types of Blood Vessels Contd.
+Capillaries – arterial system
switches to venous system
+“primary exchange vessels”
+Transport materials to and
from the cells
+Speed of blood flow decreases
to increase contact time
+Microcirculation: blood flow
between arterioles, capillaries
and venules
Electrical activity of the heart
and the
Electrocardiogram(ECG)
Introduction
+Heart beats in the absence of any nervous connections
because the electrical activity that generates the
heartbeat (pacemaker) resides within the heart itself
+After initiation, action potential spreads throughout the
heart, reaching every cardiac cell rapidly with the
correct timing
+Contraction of heart muscle is initiated by AP spread
Conducting system of the heart
+Consists of specialized myocardial cells that generate
and conduct action potentials within the heart
+ Sino atrial (SA) node
+ Internodal atrial pathways
+ Atrioventricular(AV) node
+ Atrioventricular bundle(Bundle of His) and its branches(left
and right)
+ Purkinje fibers
 Conduction system of the
SA node  heart
Atrial muscle
Internodal fibers
AV node 
AV bundle 
right and left
bundle branches
Purkinje fibers→
Ventricular muscle
Normal impulse generation rate and
conduction velocities
TISSUE BEATS PER IMPULSE
MINUTE CONDUCTION
VELOCITY(m/s)
SA NODE 60 -100 0.05
ATRIAL - 1
PATHWAYS
AV NODE 40 - 60 0.05

BUNDLE OF HIS - 1
PUKINJE 15 - 30 4
SYSTEM
VENTRICULAR - 1
MUSCLE
Action potentials in heart muscle
+Two types of action potentials take place in the heart ;
i. Fast response action potentials→ Occurs in normal
atrial, ventricular muscles and purkinje fibers
ii. Slow response action potentials→ Occurs in the SA
node(pacemaker) of heart and Atrioventricular node
Fast-response action potential
+Myocardial cells have a stable resting membrane potential
of -90mV
+Their action potential duration is longer than that of
neuron or skeletal muscle (250 msec) and has five phases:
+ Phase 0 (rapid depolarization)
+ Phase 1 (early rapid repolarization)
+ Phase 2 (Plateau)
+ Phase 3 (Late repolarization)
+ Phase 4 (Resting membrane potential)
Ionic basis of fast-response action
potential
i. Phase 0 : Caused by Na⁺ influx through rapidly opening
voltage-gated Na⁺ channels
ii. Phase 1: Caused by inactivation of Na⁺ channels and
transient K+ efflux
iii. Phase 2: Caused by Ca²⁺ influx through slowly opening
Ca²⁺(L-type) channels
iv. Phase 3: Caused by net K⁺ efflux through delayed rectifier
K⁺ channels
v. Phase 4: Caused by efflux of K+ through K+ leaky channels
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Myocardial Physiology
Contractile Cells

+Initiation
+ Action potential via pacemaker cells
to conduction fibers
+Excitation-Contraction Coupling
1. Starts with CICR (Ca2+ induced Ca2+
release)
+ AP spreads along sarcolemma
+ T-tubules contain voltage gated L-type
Ca2+ channels which open upon
depolarization
+ Ca2+ entrance into myocardial cell and
opens RyR (ryanodine receptors) Ca2+
release channels
+ Release of Ca2+ from SR causes a Ca2+
“spark”
+ Multiple sparks form a Ca2+ signal
Myocardial Physiology
Contractile Cells

+ Excitation-Contraction Coupling cont…

2. Ca2+ signal (Ca2+ from SR and ECF) binds to troponin to
initiate myosin head attachment to actin
+ Contraction
+ Same as skeletal muscle, but…
+ Strength of contraction varies
+ Sarcomeres are not “all or none” as it is in skeletal muscle
+ The response is graded!
+ Low levels of cytosolic Ca2+ will not activate as many myosin/actin
interactions and the opposite is true
+ Length tension relationships exist
+ Strongest contraction generated when stretched between 80 & 100% of
maximum (physiological range)
+ What causes stretching?
+ The filling of chambers with blood
Myocardial Physiology
Contractile Cells

+ Relaxation
+ Ca2+ is transported back into the
SR and
+ Ca2+ is transported out of the cell
by a facilitated Na+/Ca2+
exchanger (NCX)
+ As ICF Ca2+ levels drop,
interactions between
myosin/actin are stopped
+ Sarcomere lengthens
Slow-response action potential
+Normally found in the sino atrial(SA) node and
atrioventricular(AV) node
+Their action potential control the heart rate
+They are characterized by an unstable resting
membrane potential(prepotential) or pacemaker
potential of between -55mV and -60mV(phase 4
depolarization)
Slow-response action potential
+The pacemaker cells have a lesser negative resting
membrane potential because they are leaky to sodium
and potassium
+The positive charges of leaking Na+ and K+ neutralizes
intracellular negativity
+At resting membrane potential of pacemaker cells fast
sodium channels are already inactivated
Slow-response action potential
+Comprised of three(3) phases;
i. Phase 0(Upstoke of action potential)
ii. Phase 3 (Repolarization)
iii. Phase 4 (Prepotential, pacemaker potential or
spontaneous depolarization)
+Phase 1 and phase 2 as are absent in pacemaker cell
action potentials
 Effect of sympathetic stimulation on
pace maker potential
• Altering Activity of Pacemaker Cells
– Sympathetic activity
• Norepinephrine increase If channel activity
– Binds to β1 adrenergic receptors which activate cAMP and
increase If channel open time -↑ opening L channels
– Causes more rapid pacemaker potential and faster rate of
action potentials

Sympathetic
Sympathetic Activity
Activity
Summary:
Summary:
increased
increased chronotropic
chronotropic
effects
effects
heart rate
heart rate
increased
increased dromotropic
dromotropic
effects
effects
conduction of
conduction of APs
APs
 Effects of parasympathetic
stimulation on pace maker potential
• Altering Activity of Pacemaker Cells
– Parasympathetic activity
• Acetylcholine binds to muscarinic(M₂) receptors
– Increases K+ permeability and decreases Ca2+
permeability = hyperpolarizing the membrane
» Longer time to threshold = slower rate of action
potentials

Parasympathetic
Parasympathetic Activity
Activity
Summary:
Summary:
decreased
decreased chronotropic
chronotropic
effects
effects
heart rate
heart rate
decreased
decreased dromotropic
dromotropic
effects
effects
 conduction
conduction of
of APs
APs
decreased
decreased inotropic
inotropic effects
effects
Blood flow(Q)
+Pattern of blood flow can either be laminar or turbulent
+Laminar flow is in a straight line and turbulent flow is not
+Reynold’s number predicts whether blood flow is turbulent
or laminar
+>3000 – turbulence
+<2000 - laminar
+When Reynold’s number is increased, there will be
turbulence and audible vibrations (bruits)
+Note Reynold’s number =(diameter * velocity * density)/viscosity
+Factors that increase Reynold’s number (promote
turbulent flow)
+Increasing tube diameter
+Increasing velocity
+Decreasing blood viscosity e.g anemia
+Vessel branching
+Narrow orifice (severe stenosis)
Wall tension
+Laplace relationship
+ Tension = pressure *radius/wall thickness
+ The aorta has the greatest wall tension

+Vessel compliance
+How easily a vessel is stretched
+ Easily stretched –very compliant
+ Not easily stretched – non compliant or stiff
+ Systemic veins are 20 times more compliant than systemic arteries; a
small change in the venous system causes a large change in venous
volume
+Factors affecting systolic pressure
+Increase in stroke volume
+Decrease in heart rate (via increased SV)
+Decrease in vessel compliance
+Factors affecting diastolic pressure
+Decrease in TPR, HR, SV and vessel compliance
+Factors affecting pulse pressure
+Increase in SV (systolic increases more than diastolic)
+Decrease in vessel compliance (systolic increases and diastolic
decreases)
Starling’s law of the capillaries
Cardiac Output- Fick principle
+Flow = O2 consumption/ arterial –venous oxygen
content concentration difference across the organ