deck_16255153 Flashcards
ch 20
..
how many times heart beats each day
100000
35 million beats in a year and about 2.5 billion times in an average lifetime
how much blood pump each day
14,000 L
average mass of heart
250g female
300g male
roughly same size as
closed fist
cardiology
scientific study of heart and diseases
where does heart rest
thoracic cavity
directly behind sternum
in mediastinum
about mediastinum
mass of CT
cushions/protects heart
where mediastinum, from where to where
sternum to vertebral column
first rib to diaphragm
& between lungs
parts of mediastinum (physically divided)
anterior, middle, posterior mediastinum
superior, inferior mediastinum
inferior mediastinum consists of anterior/middle/posterior “
what landmark divides superior/inferior mediastinum
angle of louis (manubrial angle)
position of heart
2/3 on left of midline
apex of heart, formed by
tip of left ventricle
rests on diaphragm
points anterior, inferior, lateral (left)
@ 5th intercostal space
the base of heart
formed by atria
mostly left atrium
points, posterior, superior, lateral (RIGHT)
@ 3rd costal cartilage
heart sides – anterior surface
anterior surface
(deep to sternum, ribs)
inferior surface of heart
inferior surface
(BETWEEN APEX and RIGHT BORDER)
RESTS ON DIAPHRAGM
right border
Faces the right lung
left border
AKA pulmonary border
Faces LEFT LUNG
pericardium
Membrane that surrounds and protects the heart
Maintains the position of the heart within the mediastinum but also allows movement
a. fibrous pericardium
b. serous pericardium
(parietal serous pericardium
visceral serous pericardium )
fibrous pericardium
superficial, tough, strong, inelastic, dense irregular connective tissue
Anchor the heart in the mediastinum
Prevents overstretching of the heart
Provides protection
ATTACHES TO PARIETAL PERICARDIUM (serous)
serous pericardium
deep, thinner, delicate layer
parietal – outer layer
—> fused to the fibrous pericardium
visceral – inner layer
aka epicardium
—> One of the layers of the heart wall and adheres to the surface of the heart
Pericardial Cavity
the space between the parietal & visceral layers of the serous pericardium
pericardial fluid
pericardial fluid
viscous fluid that helps reduce friction between the layers during heart contractions
serous pericardium analogy
waterballoon
where does fibrous pericardium also attach
tunica adventitia of great vessels
pericarditis
inflammation of the pericardium
cardiac tamponade
excess accumulation of pericardial fluid
tamponade
“closure or blockage (as of a wound or body cavity) by or as if by a tampon, especially to stop bleeding”
“It’s from tampon, a stoppage/plug/etc. With -ade added to make it a new noun.”
layers of heart
a. Epicardium
b. Myocardium
c. Endocardium
epicaridium
External layer
Aka visceral layer of the serous pericardium
Gives the heart it’s smooth, slippery texture
myocardium
middle layer that makes up 95% of the heart
cardiac muscle tissue; striated & involuntary
Responsible for the hearts pumping action
endocardium
innermost layer
Thin layer of endothelium overlying a thin layer of connective tissue
Provides a smooth lining for the chambers of the heart and covers the heart valves
Continuous with the endothelial lining of the blood vessels attached to the heart
Minimizes friction of blood as it passes through the heart
heart chambers
there are 4 chambers altogether
2 atria – superior receiving chambers
2 ventricles – inferior pumping chambers
atria
the 2 superior chambers (right & left)
has auricles – “little ears”
where auricles
atriaw
which part
located on the anterior surface of each atrium, wrinkled pouch-like structure
what do
helps increase the capacity/volume of the heart
septu,m, septa
fibrous connective tissue that separates chambers
ventricles = interventricular septum
atrium = interatrial septum
sulci
small grooves on cardiac surface that hold blood vessels & fat
Mark the external boundary between two chambers of the heart
coronary sulcus
i. coronary sulcus - encircles the heart and separates the atrium from the ventricles
anterior interventricular sulcus
separates the 2 ventricles on the anterior side
posterior interventricular sulcus
separates the 2 ventricles on the posterior side
where blood go /come from each chamber
..
RA
Right atrium receives blood from systemic circuit
RV
Right ventricle pumps blood into pulmonary circuit
LA
Left atrium receives blood from pulmonary circuit
LV
Left ventricle pumps blood into systemic circuit
RA and right border of heart
Forms the right border of the heart
where receive de-O2 blood from?
superior vena cava
inferior vena cava
coronary sinus
anterior wall of RA
Rough due to pectinate muscles
pectinate muscles of RA
Muscular ridge that extend into the auricle
contribute to forceful atrial contractions.
valve between RA and RV
Blood passes from RA to RV through the Right atrioventricular valve (AV valve)
aka tricuspid valve
LA, vs base of heart
Forms most of the base of the heart
where receive blood (LA)
Receives oxygenated blood from the lungs through 4 pulmonary veins
LA anteiror wall
Smooth
“Embryologically, the left atrium is also derived from the sinus venosus and a primitive auricle. Similar to the RA, the sinus venosus provides a smooth back wall to the atrium, but, unlike the RA, almost the entire atrial wall is baldly smooth.”
LA auricle
Rough due to pectinate muscles
blood from LA to LV via
Blood passes from the LA to the LV through the bi-cuspid (mitral) valve
aka Left AV- valve
fossa ovalis
Oval depression in the interatrial septum
Remnant of the foramen ovale, an opening in the interatrial septum of the fetal heart
foramen ovale (of heart)
some blood skips pulmonary circuit
goes RA to LA
–> babies lungs don’t oxygenate blood
ligamentum arteriosum
remnant of ductus arteriosus in the fetal heart
Connects pulmonary trunk with aorta
ductus arteriosus
connect pulmonary trunk (artery) to aorta
some blood skips pulmonary circuit
–> babies lungs don’t oxygenate blood
RV, anterior surface
Forms most of the anterior surface of the heart
RV, receives from
Receives de-oxygenated blood from the right atrium
trabeculae carnae
Series of ridges formed by raised bundles of cardiac muscle fibers
Some help with cardiac conduction system, other are mechanical
chordae tendinae
Tendon-like cords
attach to the cusps of the tricuspid valve and to cone-shaped trabecular carneae called papillary muscles
help stabilize and strengthen the cusps and preventing them from everting during forceful ventricle contraction
trabeculae carneae etymology
Word origin: Latin columnae (column) + carneae (flesh) Synonyms: trabeculae carneae. fleshy beams.
“small beam”
trabeculae carnae, papillary muscles
Each ventricle features large cone-shaped trabeculae carneae known as papillary muscles
(these are a specific type of trabeculae carneae)
pulmonary (semilunar) valve
Blood passes from the RV to the Pulmonary trunk via the pulmonary valve (aka Pulmonary semilunar valve)
pulmonary trunk in turn becomes the right and left pulmonary arteries
LV, apex of heart
Forms the apex of the heart
largest, strongest
The largest & strongest of the 4 chambers
Its myocardium is the thickest and therefore generates the most amount of force during contraction
why strongest
The left ventricle is the strongest because it has to pump blood out to the entire body.
trabeculae carneae, chordae tendinae
also has
Trabecular carneae and Chordae tendinae
anchor down the mitral (BICUSPID, left AV) valve to papillary muscles
where go from LV
Blood passes from the LV to the ascending aorta through the aortic valve (aka aortic semilunar valve)
where coronary arteries branch from
Coronary arteries branch from the ascending aorta to feed the heart muscle
Blood from ascending aorta to the arch of the aorta and thoracic and abdominal aorta then throughout the body
fibrous skeleton of heart
4 dense CT rings that surround the valves of the heart
fuse with one another and merge with the interventricular septum
Prevent overstretching of valves
Point of insertion for bundles of cardiac muscle fibers
Acts as an electrical insulator between atria and ventricles (CONTRACT INDEPENDENTLY)
electrical insulator
fibrous skeleton/septa
overstretching valves?
Prevent overstretching of valves (CT rings of fibrous skeleton
cardiac mjscles insertion
fibrous skeleton/setpa/CT rings
cardiac pathologies
..
myocarditis
inflammation of the muscles of the heart
myocarditis why
Usually due to viral infections, rheumatic fever, or chemical or pharmacological agents (drugs)
endocarditis
inflammation of the endocardium usually due to bacterial infections and typically involved the heart valves
dangerous, can be fatal
pericarditis
inflammation of the pericardium usually due to viral infections
m/c is acute pericarditis that begins suddenly
(ACUTE?) pericarditis mistaken for
Can be mistaken for a heart attack due to left shoulder and arm pain as a result of irritation to the pericardium
pericardial friction rub
Can have pericardial friction rub
“A pericardial friction rub, also pericardial rub, is an audible medical sign used in the diagnosis of pericarditis. Upon auscultation, this sign is an extra heart sound of to-and-fro character, typically with three components, two systolic and one diastolic.”
chronic pericarditis
Gradually and long lasting
Build up of pericardial fluid – leads to cardiac tamponade
chronic pericarditis risk factors
May be caused by cancer, TB
heart valves
All 4 valves ensure the one-way flow of blood (note trabeculae carneae and chordae tendinae)
Valves open and close in response to pressure changes as the heart contracts and relaxes
AV valves
Allow only one-way blood flow from atrium into ventricle
semilunar valves
at exit from each ventricle; allow only one-way blood flow from ventricle out into
aorta or pulmonary trunk
AV valve structure
Each has three (tricuspid) or two (mitral/bicuspid) cusps
Cusps attach to tendon-like connective tissue bands = chordae tendineae
Chordae tendineae anchored to thickened cone-shaped papillary muscles
AV valves when open?
When pressure is higher in atria than ventricle, AV valves open
rounded ends of the cusps project into the ventricle
Ventricles relaxed
Papillary muscles relaxed, chordae tendineae slack
is ventricles relaxed when atria contract?
Yes
including papillary muscles / chordae tendinae
when AV valves closed?
When pressure is higher in ventricle than atria, AV valves close
Cusps up
Ventricles Contracted
Pressure of blood in ventricles drives the cusps upwards
Papillary muscles contract, chordae tendineae tight
—> (Prevents everting of valves)
semilunar valves (pulmonary/aortic)
Composed of 3 crescent moon-shaped cusps
Each cusp is attached to the arterial wall by its convex outer margin
The free border of each cusp project into the lumen of the artery
when semilunar valves open
Ventricles contract
Pressure builds up within the ventricles
Valves open when pressure in the ventricles exceeds the pressure in the arteries
why doesn’t blood go back into atria when pressure in ventricles exceed atria/arteries?
because chordae tendinae & papillary muscles (special trabeculae carnae) contract the cusps of the tricuspid/bicuspid valves to prevent these valves from EVERTING
when semilunar valves closed?
Ventricles relax
pressure gradient changes again
stenosis
A narrowing of a heart valve opening, artery, or other structure (?) that restricts blood flow
stenosis risk factors, causes
Congenital heart defect
Aortic valve calcification
Rheumatic fever
High blood pressure
rheumatic fever, stenosis
The most common cause of mitral stenosis is rheumatic fever — a complication of strep throat.
This infection can scar the mitral valve, causing it to thicken with scar tissue and narrow
While rheumatic fever is now rare in the United States, it is still common in developing countries.
aortic valve calcification, stenosis
related to the presence of cardiovascular risk factors such as male sex, arterial hypertension, diabetes mellitus, dyslipidemia, and smoking, sharing many similarities with the process that regulates atherosclerosis
dyslipidemia
Dyslipidemia refers to abnormal levels of lipids in the bloodstream, which poses a significant risk factor for cardiovascular (CV) diseases.
Dysregulation in these lipid levels, whether due to genetic predispositions or lifestyle factors, can lead to atherosclerosis and other CV complications.
symptoms of stenosis
An irregular heart sound (heart murmur), palpitations
Chest pain (angina) or tightness with activity
SOB, faintness, dizziness, fatigue
irregular heartbeat stenosis?
recall that heart beating sound is blood opening valves, and valves making contact with structures (E.g. Aorta)
with stenotic valves (narrowing that restricts blood blow) that sound may be weaker (?) or with different pattern from usual (?)
angina (?), stenosis
a type of chest pain caused by reduced blood flow to the heart. Angina is a symptom of coronary artery disease.
reduced opening (narrowing) of valves = reduced blood flow to heart
valve insufficiency or incompetance
Failure of a valve to close completely
valve insufficiency can be caused by
Mitral Valve Prolapse (eversion) –> I.e. papillary muscles and chordae tendinae not functioning appropriately
valve insufficiency, mitral valve prolapse
backflow of blood from LV to LA
MOST COMMON VALVE DISORDER
what percentage of population affected by mitral valve prolapse?
m/c valvular disorder, affects 30% of the population
symptoms of valve insufficiency (E.g. Mitral valve prolapse)
A racing or irregular heartbeat (arrhythmia)
Dizziness or lightheadedness
shortness of breath, fatigue
rheumatic fever..
Infectious disease that can damage or destroy heart valves
Acute systemic inflammatory disease
Usually occurs after a streptococcal infection of the throat
AB’s attack connective tissue of joints, valves and other organs
Most often damage is to the mitral and aortic valves
rheumatic fever in North America (?)
Worldwide, incidence ranges from 8 to 51/100,000 (1), with lowest rates (< 10/100,000) in North America and Western Europe
Rheumatic fever is rare in Canada, the United States, and Europe. But it was fairly common until the 1950s. Widespread use of antibiotics to treat strep throat has greatly lowered the number of new cases of rheumatic fever.
pulmonary and systemic circulation
Systemic circulation
the system that brings blood to/from the rest of the body
Pulmonary circulation
the system that brings blood to/from the lungs
coronary circuit (?)
arteries
Arteries (carry blood away from the heart)
Also called efferent vessels
arterioles
Arterioles
small arteries, very little BP (pulse)
capillaries
exchange substances between blood and tissues
Interconnect smallest arteries and smallest veins
venules
small veins, low pressure, NO pulse
veins
Veins (carry blood to the heart)
Also called afferent vessels
Very low pressure, no pulse
aorta
largest artery, highest amount of BP, oxygenated blood
4 parts of aorta
Ascending Aorta
Aortic Arch
*Descending Thoracic Aorta
*Descending Abdominal Aorta
*sometimes/generally referred together as the descending aorta
systemic arteries
branches or extensions of the aorta
noticeable pulse & BP
major systemic arteries:
Carotid
Vertebral
iliac
Femoral
radial
ulnar
systemic capillaries
smallest of the blood vessels, NO pulse, NO BP
site where O2 & CO2 exchange
major veins
Inferior Vena Cava (from lower body)
Superior Vena Cava (from upper body, head, brain)
Pulmonary veins (from lungs ,*oxygenated)
coronary sinus (?)
pulmonary circuit
Right Atrium
Right Ventricle
Pulmonary Arteries
Pulmonary Arterioles
Pulmonary Capillaries
Pulmonary Venules
Pulmonary Veins
Left Atrium
Left Ventricle
systemic circuit
Left Atrium
Left Ventricle
Systemic Arteries (via Aorta)
Systemic Arterioles
Systemic Capillaries
Systemic Venules
Systemic Veins
Right Atrium
Right Ventricle
coronary circuit
Continuously supplies cardiac muscle (myocardium)
with oxygen/nutrients
Left and right coronary arteries
arise from ascending aorta;
fill when ventricles are
relaxed (diastole)
Myocardial blood
flow may increase
to 9 times the resting
level during maximal
exertion
why do coronary arteries fill when ventricle relaxed?
POSSIBLE THEORY:
pressure inside LV exceeds pressure of Aorta
causesaortic semilunar valve to open and fills aorta with blood
valve stays open until pressure gradient switches back
when pressure gradient switches back Left ventricle (ventricles in general) relaxes
at that point pressure inside aorta rises and causes blood to flow from area of higher pressure to area of lower pressure (Which includes coronary arteries
(Left and right coronary arteries from ascending aorta)
left coronary artery
Passes inferior to the left auricle and divides into:
A) anterior interventricular branch
B) circumflex branch
A) anterior interventricular branch
(aka. LAD – left anterior descending)
Passes in the anterior interventricular sulcus
supplies blood to both ventricles
B) circumflex branch
lies in coronary sulcus
supplies blood to left atrium & ventricles
RIGHT coronary artery
Supplies small branches to the right atrium and continues inferiorly to the right auricle and divides into:
A) posterior interventricular branch
B) marginal branch
circumflex define
bending around something else; curved.
A) posterior interventricular branch
(Posterior descending artery)
follows the posterior interventricular sulcus
supplies blood to both ventricles
B) Marginal branch
lies in the coronary sulcus
supplies blood to the right ventricle
coronary sinus
Deoxygenated blood from the myocardium drains into this large vascular sinus located in the coronary sulcus on the posterior surface of the heart
Empties directly into the right atrium
where cornary sinus
coronary sulcus on the posterior surface of the heart
coronary sinus receives blood from
Great Cardiac Vein
Middle Cardiac Vein
Small Cardiac Vein
Anterior cardiac Vein
great cardiac vein
Lies in the anterior interventricular sulcus
(with left anterior descending)
Drains the areas of the heart supplied by they left coronary artery (LV,RV,LA)
–> circumflex and LAD branch
Middle Cardiac Vein
Lies in the posterior interventricular sulcus
Drains the areas of the heart supplied by the posterior interventricular branch of the RCA (LV,RV)
(posterior descending artery)
Small Cardiac Vein
Lies in coronary sulcus
Drains RA and RV
Anterior Cardiac Vein
Drains RV and opens directly into RA (??)
myocardial ischemia
ischemia is the lack of blood supply due to partial obstruction of a vessel
causes hypoxia or anoxia
myocardial ischemia e..g
angina pectoris
myocardial infarction (MI, heart attack)
angina pectoris
Inadequate blood supply to the heart
mild to severe, crushing chest pain associated with myocardial ischemia
usually this pain pattern is referred to the neck, chin, left arm down to elbow
myocardial infarction
complete obstruction of coronary artery resulting in death of cells & tissue (infarction)
MI signs
chest pain or discomfort
uncomfortable, squeezing pressure over the chest
radiating pain to the jaw and over neck region
pain in epigastric region
nausea or vomiting
sweating
dizziness
shortness of breath
MI in women
Chest pain in only 30%
Unusual fatigue or weakness
Sleep Disturbances
Indigestion
shortness of breath
Anxiety
Cold sweats
Discomfort/pain between shoulder blades
Dizziness
silent heart attack
You may not even know you’ve had a silent heart attack until weeks or months after it happens. It’s best to know what’s normal for your body and get help when something doesn’t feel right. Knowing the subtle signs of a silent heart attack can help you identify one.
Studies differ, but some suggest that silent heart attacks are more common in women than in men. Women and their physicians may also be more likely to chalk up symptoms of a silent heart attack to stress or anxiety and dismiss them.
coronary angioplasty
a minimally invasive endovascular procedure used to widen narrowed or obstructed arteries or veins, typically to treat arterial atherosclerosis.
Angioplasty and Stent Placement for the Heart
coronary artery bypass grafting
CABG
vein graft sewn to bypass blockage
cardiac muscle tissue
..
cardiac vs skeletal ituse
..
length
Shorter in length (card
transvers seciton
Less circular in transverse sections
branching
Exhibit branching
cardiac nucleus
One centrally located nucleus (usually)
cardiac conection
Specialized intercellular connections
Intercalated discs = branching interconnections between cells
mitochondria
Larger and more numerous Mitochondria (cadiac)
tv tubules
transverse tubules are wider and less abundant
SR
Smaller sarcoplasmic reticulum
straitions
hows striations
alternating bands of light and dark
Same striations as skeletal muscle
Same arrangement of actin and myosin
Same bands, zones, Z discs
volun invol
considered involuntary
no conscious willful control
intecalated cdiskc
Intercalated discs
Connect neighboring cardiac muscle fibers
contain
i. desmosomes
ii. gap junctions
desmsomes
tight cell to cell junctions for lots of stability
hold the fibers together
gap juucnto
tubular shaped cell to cell junctions that allow for transmission of substances and/or signals between adjacent cells
allow muscle action potentials to conduct from one muscle fiber to its neighbor allowing the cardiac muscles to contract in coordinated fashion
cardiac conduciotn
Autorhythmicity = cardiac muscle’s ability to contract at its own pace independent of neural or hormonal stimulation
autorhymtmicity
Autorhythmicity = cardiac muscle’s ability to contract at its own pace independent of neural or hormonal stimulation
specialized cardiac fibres,
autorhythmic fibres
These specialized cardiac muscle fibers, called autorhythmic fibers, are self-excitable
can generate their own action potentials even without nerve attachments.
what percent of cardiac muscle fibreso are self exciatble
Only about 1% of the cardiac muscle fibers are autorhythmic fibers
conducting system
(PACEMAKER/conducting cells)
Conducting system = network of specialized cardiac muscle cells (pacemaker and conducting cells) that initiate/distribute a stimulus to contract
components of conducting system
A) Sinoatrial node (SA node)
B) Internodal pathways
C) Atrioventricular node (AV node)
D) AV bundle and bundle branches
E) Purkinje fibers
pacemaker (cells)
concentration of cells that “set the rhythm” for contraction through electrical excitation
Under normal functioning conditions, the SA node is the pacemaker
what part of conducting systme is pacemaker?
SA NODE
(under normal conitions)
1) SA node
Natural pacemaker: sets the fundamental rhythm
Nerve impulses from the ANS and blood borne hormones (epinephrine) modify the timing and strength of each heart beat
what modifies timing and strength of each heart beat
nerve singals from ANS (vagus nerve?)
hormones (e.g. epinephrine)
SA node, AP
Each heartbeat begins
with action potential
generated here
In posterior wall of
right atrium, near
superior vena cava
Impulse is initiated here
and spreads through adjacent cells
Average 60–100 bpm
where is SA node
In posterior wall of
right atrium, near
superior vena cava
graded potential of heartbeat?
“Pacemaker potential” (?)
2) internodal pathways
Formed by
conducting cells
Distribute signal
through both atria
3) AV node
At junction between
atria and ventricles
Relays signals from
atria to ventricles
Has pacemaker cells
that can take over
pacing if SA node fails
AV pacing is slower—40 to 60 bpm
where is AV node
junction between
atria and ventricles
where does AV node send/transmit signals
Relays signals from
atria to ventricles
which part of conducting system can take over if SINOATRIAL node malfunctions?
AV node
what is AV pace
40 to 60 bpm
what is SA pace
60-100 bpm
4) AV bundle
Conducting cells
transmit signal from
AV node down through interventricular septum
Usually only
electrical connection
between atria/
ventricles
which structure does AV budnle run along
transmit signal from
AV node down through interventricular septum
IV SEPTUM
5) AV bundle branches
Right and left
branches
Left bundle branch
larger
Conducting cells
transmit signal to
apex of heart, then
spreading out in
ventricular walls
6) purkinje fibres
Radiate upward
through ventricular
walls
Propagate action
potentials as fast as
myelinated neurons
Stimulate ventricular
myocardium and trigger contraction
what is diameter of purkinje fibre cells
large
which structure’s speed do they match?
neurons with mylenated axons
which part of mycardium do purkinje cells stimulate
Stimulate ventricular
myocardium and trigger contraction
pathology
artificial pacemakers
If the SA node becomes damaged or diseased an artificial pacemaker may be inserted
which structure’s function does artificial pacemaker replace
SA node
artificial pacemaker about
Runs on a battery w/ leads into the right atrium, this simulates the firing of the SA node which in turn propagates a signal down the normal conduction system.
what is a feature of new artificial pacemakers
New - activity adjusted pacemakers
Automatically speed up during exercises
skeletal muscle vs cardiac muscle contraction
..
AP
Brief action potential
(skeletal)
Long action potential
(cardiac)
Ca2+ speed
(SKELETAL)
Contraction ends when sarcoplasmic reticulum reclaims Ca2+
(CARDIAC)
Ca2+ enters cells over prolonged period
–>Long contraction
(~250 msec)
refractory period
(SKELETAL)
Short refractory period ends before peak tension develops
(CARDIAC)
Refractory period continues into relaxation
wave summation / tetany
(SKELETAL)
Twitches can summate; tetanus can occur
(CARDIAC)
No tetanic contractions occur (otherwise heart couldn’t pump blood)
important note about AP, contraction, and refractory period
by the time cardiac muscle relative refractory period ends, heart muscle is close to fully relaxed
by the time absolute refractory period ends, heart muscle is partially relaxed
FOR SKELETAL MUSCLE, RELATIVE REFRACTORY PERIOD ENDS BEFORE MUSCLE FIBRE EVEN REACHES MAXIMUM TENSION
ABSOLUTE REFRACTORY FOR SKELETAL MUSCLE ENDS ALMOST BEFORE MUSCLE FIBRE EVEN BEGINS CONTRACTING (?)
repolarization of membrane potential in cardiac muscle
in skeletal muscle, repolarization occurs @ end of ABSOLUTE REFRATORY PERIOD
in cardiac muscle, full repolarization occurs @ end of relative refractory period
partial repolarization in cardiac muscle occurs @ end of absolute refractory period
3 stages of cardiac muscle AP
Rapid depolarization
Plateau
Repolarization
1) rapid depolarization
similar to that in skeletal muscle
At threshold, voltage-gated fast sodium channels open
Massive, rapid Na+ influx
Channels
open quickly
and very
briefly
2) Plateau
from -90 RMP, to +30 after rapid depolarization
leading into PLATEAU is quick dip from +30 to 0mV (where it stays for plateau period)
why stay @ 0mV for plateau phase
Fast sodium channels close as potential nears +30 mV, Cell actively pumps Na+ out
K+ channels outflow into interstitial fluid
Voltage-gated slow calcium channels open— Ca2+ influx
Opening of slow Ca2+ channels in sarcolemma increasing Ca2+ in cytosol and triggering a contraction (calcium induced calcium release)
****
So, because Ca2+ positive charge offset Na+ leaving cell (?)
note subtances that alter flow of Ca2+ through slow Ca2+ channels
–> how do they influence strength of heart contractions??
Substances that alter the movement of Ca2+ through slow Ca2+ channels influence the strength of heart contractions (contractility)
E.g.
Epinephrine: increases Ca2+ = increases contraction force
3) repolarizaiton
Slow calcium channels close
Slow potassium channels remain open; K+ rushes out; causes rapid repolarization and restores resting potential
cardiac muscle ATP produciton
Produces little ATP by anaerobic cellular respiration
(same as all cells, relatively, but more so here)
Relies on aerobic cellular respiration in its numerous mitochondria
what do cardiac muscle fibres use for energy during aerobic repsiration?
AT REST:
Oxidation of fatty acids (60%) and glucose (35%)
what do they use during exercise?
Use lactic acid
heart also uses
creatine phosphate
note creatine phosphate vs creatine kinase
what does creatine kinase do?
Creatine Kinase is the enzyme that catalyzes transfer of a phosphate group from CP to ADP to make ATP
what is the creatine kinase test?
normally is contained in the muscle tissue but will be released in any cardiomyopathy
CK is the 1st enzyme in blood they test for in heart attacks.
ECG
a recording of the electrical currents generated by action potentials propagating through the heart.
what does ECG determine
1) If the conduction pathway is abnormal (i.e.. arrhythmias)
2) If the heart is enlarged (?)
3) If certain regions of the heart are damaged (i.e.. MI)
4) Causes of chest pain
how ECG show enlarged heart?
An electrocardiogram (ECG) can show if the heart is beating too fast or too slow. A health care provider can look at signal patterns for signs of a thickened heart muscle (hypertrophy).
ECG, MI
The most frequently used electrocardiographic criterion for identifying acute myocardial infarction is ST segment elevation in two or more anatomically contiguous leads.
12 LEAD ECG
10 electrodes placed in specific positions
By comparing electrodes, 12 different trackings are produced (12 leads)
12 leads ?
6 limb leads
6 precordial (chest) leads
precordial
in front of the heart; involving the precordium.
from English precordium ((anatomy) The region of the body over the heart and thorax.)
6 limb leads
I, II, III, aVR, aVL, aVF
Measure vertical vectors or electrical conduction
6 precordial leads
V1-V6
Measure horizontal vectors of electrical conduction
note movement of ELECTRIC VECTOR towards/away positive pole, and corresponding positive/negative inflection on ECG
Movement towards positive pole gives positive inflection on ECG
Movement away from positive pole gives negative inflection on ECG
random facts, leads
The electrical axis of the heart is most similar to lead II
Therefore, lead II is often used as reference for basic ECG
ECG,
P, QRS, T
P wave
QRS complex
T wave
P wave =
ATRIAL DEPOLARIZATION
QRS complex =
VENTRICULAR DEPOLARIZATION
ATRIAL repolarization occurs @ same time as Ventricular depolarization (so it’s hidden under QRS complex)
T wave =
ventricular repolarization
more about P wave
P wave = atrial depolarization
Atria begin contracting ~25 msec after P wave starts
more about QRS complex
QRS complex = ventricular depolarization
Larger wave due to larger ventricle muscle mass
Ventricles begin contracting shortly after R wave peak
Atrial repolarization also occurs now but is masked by QRS
why QRS complex wave larger?
Larger wave due to larger ventricle muscle mass
when do ventricles begin contracting?
begin contracting shortly after R wave peak
INTERVALS/SEGMENTS
P-Q interval
(sometimes called P-R interval)
Q–T interval
S–T segment
PQ interval (or PR interval)
Period from start of atrial depolarization to start of ventricular depolarization
what does a PQ interval greater than 200ms indiciate?
> 200 msec may mean damage to conducting pathways or AV node
Possibly from scar tissue d/t previous MI
QT interval
beginning of the QRS complex to the end of the T-wave.
This represents the time from start of ventricular depolarization to the end of ventricular repolarization.
QT interval is from
from BEGINNING of ventricular depolarization
to END of ventricular repolarization
what causes lengthened QT interval?
May be lengthened by
electrolyte disturbances,
medications,
conduction problems (conduction system/NODES/pacemaker cells),
coronary ischemia,
myocardial damage
ST segment
end of the QRS complex to the beginning of the T-wave. This represents the interval between ventricular depolarization and repolarization
ST segment is from
from END of DEPOLARIZATION
to BEGINNING of REPOLARIZATION
(interval where there is neither depolarization, nor repolarization – PLATEAU phase)
note ST segment vs PLATEAU phase
The ST segment corresponds to the plateau phase of the ventricular transmembrane action potential.
(NEITHER depolarization, nor repolarization)
–> actually technically, it is depolarized, and in a continuous state of “
why elevated ST segment (length?)
Can see and elevated ST segment in acute MI
ECGs and arrythmias
ECGs valuable for detecting/and diagnosing arrhythmias
cardiac arrhythmias
abnormal patterns of cardiac electrical activity
what percentage of healthy people experience a few abnormal heartbeats each day?
About 5% of healthy people experience a few abnormal heartbeats each day
Not a clinical problem unless pumping efficiency is reduced
ECG and average heartrate
Average heart rate is between 60 - 100 bpm
Tachycardia = fast heart rate (>100 bpm)
Bradycardia = slow heart rate (<60 bpm)
note bradycardia not necessarily pathological
some athletes can have lower than 60bpm resting heartbeat
PREMATURE ATRIAL CONTRACTIONS (PACs)
Often occur in healthy people
Normal atrial rhythm momentarily interrupted by “surprise” atrial contraction
I.e.
SOONER THAN EXPECTED
Increased incidences caused by stress, caffeine, various drugs that increase permeability of the SA pacemakers
Normal ventricular contraction follows the atrial beat
Paroxysmal atrial tachycardia (PAT)
Premature atrial contraction triggers flurry of atrial activity
Ventricles keep pace
Heart rate jumps to about 180 bpm
ATRIAL FIBRILLATION
Impulses move over atrial surface at up to 500 bpm
Atria quiver—not organized contraction
Ventricular rate cannot follow, may remain fairly normal
Atria nonfunctional, but ventricles still fill passively
Person may not realize there is an arrhythmia
arrhythmias affecting ATRIA
Premature atrial contractions (PACs)
Paroxysmal atrial tachycardia (PAT)
Atrial fibrillation
arrythmias affecting VENTRICLES
Premature ventricular contractions (PVCs)
Ventricular tachycardia
Ventricular fibrillation
Premature ventricular contractions (PVCs)
Purkinje cell or ventricular myocardial cell depolarizes; triggers premature contraction
Cell responsible called an ectopic pacemaker (pacemaker other than the SA node)
Single PVCs common, not dangerous
Frequency increased by epinephrine, stimulatory drugs, or ionic changes that depolarize cardiac
muscle cells
Ectopic pacemaker cells
An ectopic pacemaker, also known as ectopic focus or ectopic foci, is an excitable group of cells that causes a premature heart beat outside the normally functioning SA node of the heart.
It is thus a cardiac pacemaker that is ectopic, producing an ectopic beat.
ectopic define
in an abnormal place or position.
ektopos: out of place
ectopia: present of tissue, cells, etc. in an abnormal place
ectopia
a situation in which an organ or body part is in the wrong position, either from birth or because of an injury
ventricular tachycardia
Also known as VT or V-tach
Defined as four or more PVCs without intervening normal beats
Multiple PVCs and V-tach may indicate serious cardiac problems
Ventricular fibrillation
Also known as VF or V-fib
Responsible for condition known as cardiac arrest
Rapidly fatal because ventricles quiver, but cannot pump any blood
note ECGs and exercise stress test
Exercise Stress test
Continuous ambulatory electrocardiographs
Holter monitor
Holter monitor
A Holter monitor is a small, wearable device that records the heart’s rhythm, usually for 1 to 2 days.
It’s used to spot irregular heartbeats, also called arrhythmias.
A Holter monitor test may be done if a traditional electrocardiogram (ECG or EKG) doesn’t provide enough details about the heart’s condition.
INTRO TO CARDIAC CYCLE
Two phases:
Contraction (systole)—blood leaves the chamber
Relaxation (diastole)—chamber refills
contraction sequence (Atria contract)
Atria contract together first (atrial systole)
Push blood into the ventricles
Ventricles are relaxed (diastole) and filling
contraction sequence (Ventricles contract)
Ventricles contract together next (ventricular systole)
Push blood into the pulmonary and systemic circuits
Atria are relaxed (diastole) and filling
how long does cardiac cycle last?
Typical cardiac cycle lasts 800 msec (0.8 secs)
60s / 0.8 = 75 (BPM)
cardiac cycle
..
what is cardiac cycle
period between start of one heartbeat and the next (a complete round of systole and diastole)
2 phases of cariac cycle
Contraction (systole)—blood leaves the chamber
Relaxation (diastole)—chamber refills
sequence of contractions
Atria contract together first (atrial systole)
Ventricles contract together next (ventricular systole)
Typical cardiac cycle lasts 800 msec (0.8 secs)
atria push…
ventricles are…
Push blood into the ventricles
Ventricles are relaxed (diastole) and filling
ventricles push…
atria are…
Push blood into the pulmonary and systemic circuits
Atria are relaxed (diastole) and filling
assuming 800msec cardiac cycle
heart rate 75 bpm
phases for 75bpm
1)
Cardiac cycle begins—all four chambers are
relaxed (diastole; ventricles are passively refilling)
2)
Atrial systole (100 msec)—atria contract; finish filling ventricles
3)
Atrial diastole (270 msec)—continues until start of next cardiac cycle (through ventricular systole)
4)
Ventricular systole—first phase. Contracting ventricles push AV valves closed but not enough pressure to open semilunar valves
(= isovolumetric
contraction—no
volume change)
5)
Ventricular systole—second phase. Increasing pressure opens semilunar valves; blood leaves ventricle (= ventricular ejection)
6)
Ventricular diastole—early. Ventricles relax
and their pressure drops; blood in aorta and
pulmonary trunk backflows, closes semilunar valves
7)
Isovolumetric relaxation. All valves closed; no volume change; blood passively filling atria
8)
Ventricular diastole—late. All chambers relaxed; AV valves open; ventricles fill passively to ~70%
note about atrial systole
SA node fires, causing both atria to contract (atrial systole)
Increases pressure within atrium, pressure remains low in ventricles
Blood is ejected thru AV valve (tricuspid & mitral) from atrium to ventricles
Contributes 25mL to an already 105mL in each ventricle = total of 130mL in the ventricles at the end of atrial systole/ventricle diastole
Called the end diastolic volume (EDV)
what causes atria to contract?
SA nodes
what does atrial contracting add to ventricles
25mL to 105mL that was already in ventricles
105 from passively filling
what is amount in ventricles called AFTER atria contract?
END DIASTOLIC VOLUME
“diastolic” referring to the end of diastole for the ventricles, before they contract
I.e.
after atria finish contracting, then immediately ventricles are @ end of diastole
I.e.
ventricular systole begins exactly when atrial systole ends
when does first 105mL fill?
during period when both atria and ventricles are in diastole (second phase of ventricular diastole)
—> (about half the entire Cardiac Cycle)
(filling passively)
about ventricular systole
During ventricular systole the atria are relaxed (atrial diastole)
(atrial diastole begins precisely when ventricular systole begins)
what is a significant feature of the EARLY VENTRICULAR CONTRACTION
BOTH SEMILUNAR AND AV valves are CLOSED
I.e.
Isovolumetric contraction
(Iso- “same” – volume)
I.e.
volume of ventricle doesn’t change during early ventricular contraction
UNTIL the pressure in the chamber is enough to EXCEED the pressure in the pulmonary trunk & Aorta (pressure of the semilunar valves).
After this pressure is reached, the valves open and blood enters the pulmonary/systemic circuit.
WHAT IS THE pressure required to open the semilunar valves
LV pressure > 80mmHg (continue to rise to 120mmHg)
RV pressure > 20mmHg (continue to rise to 25-30mmHg)
how long does ventricle ejection last?
I.e. how long ventricular systole last (?)
250-270msec (?)
notes say 250msec
diagram shows 270msec for ventricle systole
WHAT IS THE VOLUME at the END of ventricular systole
END SYSTOLIC VOLUME
In our example of 130mL End diastolic volume, how much of that blood can be expected to be ejected via ventricular systole?
about 70mL
end systolic volume would be 60mL in this example
what portion of the cardiac cycle are BOTH atria+ventricles RELAXED
about 1/2 cardiac cycle
400msec in example of 800msec cycle
what portion of cardiac cycle are ventricles relaxed
about 500msec / 800
what portion of cycle are atria relaxed
about 700msec / 800
more about ventricular diastole
Ventricle pressure decreases and blood in the aorta and pulmonary trunk flows back toward the low pressure ventricles = closing the semilunar valves
Aortic valves close at 100mmHg
why aorta valves close at 100mmHg, when they initially opened at 80mmHg
because as blood from LV flows into aorta, pressure increases from 80 –> 120 (in this example)
???
therefore, when LV pressure decreases to 100, there is not enough pressure to continue flowing into aorta, and backflow closes aortic semilunar valve
Why?
both pressure simultaneously decrease to 100mmHg, until decrease in LV exceeds decrease in aorta @ 100mmHg, and backflow closes SL valve (?)
when do ventricles begin filling again?
Ventricle pressure drops below atrial pressure and the AV valves open and ventricle filling begins
(PASSIVE FOR MAJORITY OF FILLING)
recall:
passively filling for about 400msec / 800
(entire heart diastole) –NOT QUITE –> they fill during SECOND phase of Ventricular DIASTOLE, not the entire duration
= 105 / 130 mL
last 25mL via atrial systole
note again, pressure changes in aorta
Increase in pressure with opening of aortic valve
Drop in pressure with closing of aortic valve (because blood moves along aorta and away from the initial segment, causing pressure to decrease gradually
NOTE DICROTIC NOTCH
even though pressure gradually decreases with aortic semilunar valve closing,
there is a short pressure rise in aorta as ELASTIC WALLS RECOIL
phenomenon known as DICROTIC NOTCH in pressure tracing
dicrotic
(dúo, “two”) + κρότος (krótos, “beat”)
cardiac cycle and heart sounds
Auscultation – the process of listening to sounds in the body (heart, GI, lungs)
performed with a stethoscope
heart sounds
The sounds of the heartbeat come from blood turbulence created by closing valves
S1 ( “lubb”)—when AV valves close; marks start of ventricular contraction
S2 (“dupp”)—when semilunar valves close
S3 - —very faint; rarely heard in adults
blood flowing into ventricles
S4—almost always pathologic (?)
heart murmers
abnormal sounds (whooshing or swishing) that is heard before, between or after normal heart sounds.
They may also mask normal heart sounds
Tends to be common in children due to developing cardiac structures, but abnormal in adults
2-4 years old
Innocent or functional heart murmurs
vs.
Congenital heart murmurs
what age innocent/functional heart murmers
2-4 years old
what can heart murmers do to normal heart sounds
They may mask normal heart sounds
when can heart murmers be heard relative to normal heart sounds
heard before, between or after normal heart sounds
what can the noise of heart murmers resemble
abnormal sounds (whooshing or swishing)
what about heart murmers in adults
Not always indicative of heart problems (innocent)
May indicate valve disorder
E.g.
Stenosis or valvular insufficiency
cardiac output
the amount/volume of blood that is ejected from the left ventricle each minute
Measured in mL/min
how to calculate Cardiac outpute
Cardiac Output = HR × SV
heart rate stroke volume
HR SV
Heart rate (HR) = # contractions/minute (beats per minute)
Stroke volume = volume of blood pumped out of ventricle per contraction
how is CO changed
By changing either or both HR and SV, cardiac output is precisely controlled to meet changing needs of tissues.
IMPORTANT NOTE ABOUT SV
Right ventricle SV = left ventricle SV
Stroke volume depends on the relationship between end-diastolic volume and end-systolic volume
calculate stroke volume
SV = EDV – ESV
assuming SV 70mL and HR 75bpm, what is CO
70*75
= a bit over 5000mL
I.e. entire volume of blood is pumped through entire circuit(s) in 1 minute
how increase CO
any factor icnreasing SV or HR
CARDIAC RESERVE
the difference between the maximum CO & CO at rest
average person cardiac RESERVE
Average person has a CR of 4 to 5 times resting value
certain athletes cardiac reserve
Athletes have reserves up 7-8 times their resting Cardiac Output (CO)
what about cardiac reserve of people with heart disease (esp severe)
almost no reserves
= limited ADLs
regulation of heart rate
which TWO factors?
Important in short-term control of CO and BP
Most important regulators of heart rate are:
1) the ANS
2) hormones released by the adrenal medulla
note that ANS signals to adrenal medulla, so it’s really just the ANS that regulates HR
resting heart rate facts
Varies with age, general health, physical conditioning
Normal range is 60–100 bpm
Bradycardia
Heart rate slower than normal (<60 bpm)
Tachycardia
Heart rate faster than normal (>100 bpm)
*note that certain athletes may have lower than 60bpm but still normal
note about SA node and heart rate regulation
Pacemaker potential in SA node cells occurs 80–100 times/min
Establishes heart rate
SA node brings AV nodal cells to threshold before they reach it on their own, thus SA node paces the heart
SA node pacemaker potential rate
80–100 times/min
autonomic regulation of heart rate is @
@
cardiovascular center of the medulla oblongata
(anterior to cerebellum)
where does (cardiovascular centre of) medulla oblongata get signal from
input from sensory receptors and higher brain centers
higher brain centres =
limbic system, cerebral cortex
what does CV centre of medulla oblongata do with signal from higher brain centres and sensory receptors?
directs the divisions of the ANS to increase or decrease frequency of nerve impulses
what 3 sensory receptors give feedback to CV centre @ medulla?
A)
baroreceptors – pressure changes (aorta, carotid aa)
B)
chemoreceptors – chemical changes in blood
C)
proprioceptors – sensory from the limbs & extremities
note baroreceptor of carotid
when pressing on carotid, can change BP, activate sensory feedback of baroceptor
–> change heartbeat (?) or change BP (?)
recall two divisions of ANS
sympathetic, parasympathetic
CV centres of medulla
–> two parts
Cardioinhibitory center
Cardioacceleratory center
Cardioinhibitory center
Controls parasympathetic neurons; slows heart rate
Parasympathetic supply to heart via vagus nerve (X); synapse in cardiac plexus
Postganglionic fibers to SA/AV nodes, atrial musculature
which nerve gives parasympathetic signals to HEART?
where does it send those signals?
vagus nerve (CN X)
to Cardiac Plexus
where do the nerves ultimately synapse?
(???)
Postganglionic fibers to SA/AV nodes, ultimately atrial musculature
2) Cardioacceleratory center
Controls sympathetic neurons; increases heart rate
Sympathetic innervation to heart via postganglionic fibers in cardiac nerves; innervate nodes, conducting system (nodes/branches/bundles), atrial and ventricular myocardium
how do sympathetic signals travel?
via which structure(s)?
sympathetics travel thru CARDIAC ACCELERATORY NERVES in the thoracic region of the spinal cord
what NT is released via sympathetic signal of CARDIAC ACCELERATORY NERVES?
Releases norepinephrine:
—> Speeds the rate of spontaneous depolarization
—> Enhances calcium entry – increasing contractility
what other variable is altered via norepinephrine release?
Enhances calcium entry – increasing contractility
how do parasympathetic signals travel?
via which structure(s)?
parasympathetics travel thru the right and left Vagus Nerve (CN X)
what NT is released via parasympathetic signal of VAGUS NERVES?
Release acetylcholine:
—> Decreases rate of spontaneous depolarization
more about sympathetic influence
Sympathetic stimulation increases heart rate
(norepinephrine can also increase BP)
Binding of norepinephrine to beta-1 receptors opens ion channels:
—> Increases rate of depolarization
—> Decreases repolarization
key thing to note:
“Binding of norepinephrine to beta-1 receptors opens ion channels” (increase depolarization)
But what else does norepinephrine do to beta receptors?
NOTE BETA BLOCKERS mechanism:
(sympathetic response also affect BP)
Beta blockers are medicines that lower blood pressure. They also may be called beta-adrenergic blocking agents.
The medicines block the effects of the hormone epinephrine, also known as adrenaline.
Beta blockers cause the heart to beat more slowly and with less force. This lowers blood pressure.
more about parasympathetic influence
Parasympathetic stimulation decreases heart rate
ACh from parasympathetic neurons:
A) Opens K+ channels in plasma membrane
B) Hyperpolarizes membrane (K+ outflow?)
C) Slows rate of spontaneous depolarization
D) Lengthens repolarization
note chemical factors affecting HR
Electrolyte Imbalances:
Ca2+: elevated interstitial levels ↑ strength of contraction and speeds heart rate
K+: elevated blood levels will decrease/block AP, thus decreases ↓ muscle contraction and HR
other chemical factors affecting HR
Hormones:
(REMEMBER SAME SUBSTANCE CAN BE CONSIDERED EITHER NT OR HORMONE DEPENDING ON HOW IT IS RELEASED. RELEASE FROM GLAND = HORMONE, FROM NEURON = NT)
Hormones:
epinephrine & norepinephrine will ↑ HR and contractility
—> (From adrenal medulla)
other hormones affecting HR
Thyroid hormones:
Increase cardiac contraction and increase HR
other miscellaneous factors affecting HR
Age
Gender
Physical fitness
Body temperature
REGULATION OF STROKE VOLUME (SV)
recall that there is always 40-50% of blood volume that remains in the ventricles after full ventricular systole (approx 60 mls)
which 3 factors regulate SV
Preload
Contractility
Afterload
1) Preload
The degree of stretch on the heart before it contracts, proportional to the END DIASTOLIC VOLUME
note Frank-Starling Law
akin to a rubber band, the more you stretch it, the more force it will snap back with.
Thus, the more blood enters the ventricles, the higher the volume, the more stretch or load on the muscle tissues the greater the contraction.
(NOTE THAT TOO MUCH STRESS CAN STILL DECREASE CONTRACTILITY, just like with Skeletal muscle)
which two factors determine End Diastolic Volume?
The duration of ventricle diastole
Venous return
(passively filling ventricles)
2) CONTRACTILITY
the strength of contraction of muscle tissue/fibers
which substances affect contractility
positive inotropic agents increase contraction
negative inotropic agents decrease contraction
inotropic define
“modifying the force or speed of contraction of muscles.”
From Ancient Greek ἴς (ís, “sinew, tendon; strength, force”) + -tropic (“affecting, changing”)
positive inotropic agents E.g.
sympathetic nervous system (CARDIAC ACCELERATORY NERVES),
digitalis (drug),
epinephrine (from adrenal medulla?),
anything that increases Ca2+ inflow (?)
negative inotropic agents E.g.
parasympathetics (E.g. via Vagus Nerves),
anoxia,
drugs,
anything that blocks or inhibits Ca2+ inflow (calcium channel blockers)
3) AFTERLOAD
the pressure that must be overcome before the semilunar valves (aortic & pulmonary) can open.
what happens to SV if afterload INCREASES
Factors that increase the afterload will decrease the SV
what can increase AFTERLOAD?
increase BP (hypertension) in systemic arteries
ex. via Atherosclerosis, Weight gain (??)
so to increase SV, what happens to 3 variables
increased PRELOAD
increased CONTRACTILITY
decreased AFTERLOAD
ultimately?
increased SV –> increased CO
Congestive Heart Failure (CHF)
A loss of pumping efficiency by the heart
cause?
CAD,
congenital defects,
high BP,
MI,
valve disorders
what happens during CHF
(A positive feedback loop)
Pumping becomes less effective
—> increase in EDV (preload)
—> heart becomes overstretched
—> contract less forcefully
during CHF, which side usually fails before the other?
Left Ventricle more common, leads to pulmonary edema
Right Ventricle, leads to peripheral edema
CARDIAC PATHOLOGIES
..
arrythmias
Abnormal rhythm of the heart as a result of a defect in the conduction system of the heart
Leads to asynchronous contractions & therefore abnormal blood pumping
arrythmias refects in
conduction system
recall conduction system
nodes, branches, bundles, fibres, etc
primary feature of arrythmias (dysrhythmias)
leads to asynchronous contractions & therefore abnormal blood pumping
symptoms..
chest pain, shortness of breath, lightheadedness, dizziness, fainting
potential risk factors for arryhtmias
stress, caffeine, alcohol, cocaine, nicotine, CAD, MI, HTN (many)
HTN = hypertension (?)
E.g. arrythmia
Bradycardia (below 50beats/min) (60?)
Tachycardia (above 100beat/min)
Fibrillation (rapid, uncoordinated heartbeats)
coronary artery disease (CAD)
Results from the effects of the accumulation of atherosclerotic plaques in coronary arteries, which leads to a reduction in blood flow to the myocardium
primary cause
accumulation of atherosclerotic plaques in coronary arteries
risk factors, CAD
Smoking, high BP, DM, high cholesterol, obesity, sedentary lifestyle, family Hx
Males > females, > after 70 years of age
signs symtpoms, CAD
dependent on severity (chest pain, dyspnea, etc.)
can have complications:
angina pectoris
MI
leading cause of death
Cardiovascular disease is the leading cause of death
athersclerotic plaques
arteriosclerosis vs atherosclerosis
athero - meaning gruel or paste and sclerosis meaning hardness
Arteriosclerosis: Thickening of artery walls and loss of elasticity
Atherosclerosis
One form of arteriosclerosis
about atherosclerosis
Progressive disease characterized by the formation of lesions called atherosclerotic plaques in the walls of large and medium sized arteries
These plaques are cholesterol or fatty acid molecules that accumulate too much, too fast, too often
Congenital heart defects, E.g.
Coarctation of the aorta
Patent ductus arteriosus
Septal defect (patent foramen ovale)
Tetralogy of Fallot
Coarctation of the aorta
A segment of the aorta is narrowed
Resulting in reduced oxygenated blood flow
Sx: Depend on severity
Pale, sweating, dyspnea
Tx: catheterization and low BP medications
Patent Ductus Arteriosus
The ductus arteriosus remains open rather than closing shortly after birth
Aortic blood flows into the lower pressure pulmonary trunk
Tx depends on severity, some are never recognized
patent define
MEDICINE
(of a vessel, duct, or aperture) open and unobstructed; failing to close.
Septal Defect
(E.g.? patent foramen ovale)
Atrial:
The fetal foramen ovale fails to close (patent foramen ovale)
Ventricular:
Incomplete development of the septum
Oxygenated and deoxygenated blood mix
Tetralogy of Fallot
Combination of 4 defects:
1) Ventricular septal defect
2) Aorta that emerges from both ventricles (overriding aorta)
3) Pulmonary valve stenosis
4) Right ventricular hypertrophy
(note that if pulmonary SL valve is stenosed, RV requires more force to push blood into pulmonary circuit –> i.e. RV hypertrophy)
tetralogy define
MEDICINE
a set of four related symptoms or abnormalities frequently occurring together.
tetralogy of fallot can result in
Results in a decreased blood flow to lungs and a mixing of oxygenated and deoxygenated blood
can lead to cyanosis, “blue baby”
overriding aorta
“An overriding aorta is a congenital heart defect where the aorta is positioned directly over a ventricular septal defect, instead of over the left ventricle”
I.e. septal defect is directly related to overriding aorta
cardiac arrest
A clinical term meaning cessation of an effective heartbeat
Can be spontaneous (SCA) or due to trauma (TCA)
Causes:
Arrhythmia
Coronary artery disease
Cardiomyopathy or CHF
Penetrating wound or blunt trauma (commotio cordis)
commotio cordis
Penetrating wound or blunt trauma
sudden arrhythmic death caused by a low/mild chest wall impact
About 59% of people who experience it survive. You’re most likely to survive if you receive CPR right away.
commotio cordis – how common?
With commotio cordis (Latin for “agitation of the heart”), the impulse from the object disrupts the normal heart rhythm and leads to sudden cardiac arrest. How common is commotio cordis? Cases of commotio cordis are extremely rare. There are fewer than 30 cases each year.
“struck in the chest at a specific time in the heart rhythm cycle”
Paroxysmal tachycardia
A period of rapid heartbeats that begins and ends suddenly
Cardiomegaly (Heart enlargement)
SSx: dyspnea, arrhythmia, edema
Causes: MI, valve disease, cardiomyopathy, hypertension, anemia, etc.
Cor Pulmonale (CP)
A term referring to right-sided heart failure from disorders that bring about HTN into the pulmonary circulation
Causes: Left-sided heart failure, COPD, cystic fibrosis, and more
development of heart
The heart is the first functional organ
One of the first systems to form in an embryo
(heart and brain)
Begins its development from mesoderm on day 18/19 following fertilization
Develops from a group of mesodermal cells called the cardiogenic area
Most development occurs between weeks 5 and 9
CPR
a rescue technique in which an unconscious, pulseless person is assisted in maintaining heart rate (cardio) and breathing (pulmonary)
CPR keeps oxygenated blood circulating until the heart can be restarted
what to do when in doubt (CPR) ?
When in doubt – chest compressions, chest compressions, chest compressions
2007 Japanese study found that in lay-person rescue, chest compressions alone are equally as effective as traditional CPR with ventilation
Place the heel of your hand on the centre of the person’s chest, then place the palm of your other hand on top and press down by 5 to 6cm (2 to 2.5 inches) at a steady rate of100 to 120 compressions a minute.
