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60 year old woman experienced a myocardial infarction (Heart Attack- death…
60 year old woman experienced a myocardial infarction
Background
anatomy
heart
transport system pump
pulmonary circuit
right side
receives deoxygenated blood
right atrium
pumps it right ventricle
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systematic circuit
left side
receives oxygenated blood
left atrium
pumps it to left ventricle
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size and location
size of of fist, hollow cone shape, 250 to 350 grams
superior to diaphragm, anterior to vertebral column and posterior to sternum
coverings of the heart
fibrous pericardium
superficial sac
dense connective tissue
protects the heart
anchors it to surrounding structures
prevents overfilling of the heart with blood
serious pericardium
deep to fibrous pericardium
two layers of serous membranes
parietal layer
lines internal surface of fibrous pericardium
visceral layer (epicardium)
over external heart surface
layers of heart
epicardium
superficial
(visceral layer)
myocardium
middle layer
composed of cardiac muscles
contracts
endocardium
inner most
layers of squamous epithelium and connective tissue
chambers and vessels
4 chambers
2 atria
interatrial spetum
separates both atria
right atria
pectinate muscles
inside right atria
(entrance to heart) veins
superior vena cava
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inferior vena cave
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coronary sinus
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left atria
pulmoonary veins
transports blood from lungs to heart
2 ventricles
interventricular septum
separates both ventricles
left ventricle (posterior)
pumps blood into aorta
for the body
more powerful than the right one
right ventricle (anterior)
pumps blood into pulmonary trunk
gas exchange
muscles
trabeculae carneae
irregular ridges of muscle
papillary muscles
help with valve function
Valves
artrioventricular Valves (AV)
prevent back flow of blood into atria
Tricuspid Valve (right)
Mitral Valve (left) or bicuspid valve
semilunar valves (SL)
Aortic semilunar valve
pulmonary semilunar valves
coronary arteries and veins
coronary Arteries
left coronary artery
runs toward left side of heart
circumflex artery
anterior interventricular artery
right coronary artery
courses to the right side of the heart
right marginal artery
posterior interventricular artery
coronary veins
coronary sinus
cardiac veins
middle cardiac vein
small cardiac vein
anterior cardiac vein
cardiac muscles muscles
structure
striated, short, branched, 1-2 nuclei per cell
has gap junctions between cells
fewer and wider T tubules
contract as a unit
functional syncytium
source of Ca
sarcoplasmic reticulum
extracellular fluid
physiology
Action potentials through the heart
pacemaker cells
pacemaker potential
ion channels, membrane interior becomes less and less negative. (more positive)
instrinsic conduction system
unstable resting potential
Depolarization
Ca channels open, Ca enters pacemaker cell causing action potential
Repolarization
Ca channels inactivate
instrinsic cardiac conduction system
SA node generates impulses
the impulses pause 0.1 sec at the AV node
AV bundle connects the atria to the ventricles
the bundle branches conduct impulses through the inter ventricular septum
Subendocardial conducting network depolarizes the contractile cells of both ventricles
contractile cardiac muscle cells
Depolarization, Na influx and positive feedback opens many Na channels, reversing membrane potential
Plateau phase,Ca influx, keeps cells depolarized because most K channels are closed
Repolarization, Ca channels inactivating and K channels opening. brings membrane potential back to its resting point.
Electrocariography
Electrocardiogram (ECG)
electrical currents generated and transmitted through the heart
sequence
Atrial depolarization, initiated by SA node, causes the P wave
with atrial depolarization complete the impulse is delayed at the AV node
Ventricular depolarization begins at the Apex, causing QRS complex. Atrial depolarization occurs
Ventricualr depolarization is complete
Ventricular depolarization begins at apex, causing the T wave
Ventricular depolarization is complete
Cardiac Cycle
pressures and Valves
AV valves close when the ventricular pressure exceeds the atrial pressure
SL valves open when the ventricular pressure exceeds the aortic pressure
SL valves close when ventricular pressure drops below aortic pressure
AV valves open when the ventricular pressure drops below the atrial pressure
heart sounds
lub- dup
the second heart sound is caused by the SL valves closing
the first heart sound is caused by the AV valves closing
Blood Flow
ventricular filling phase
passive and atrial contraction
isovolumetric contraction phase
ventricular ejection phase
isovolumetric relaxation phase
Systole and Diastole
systole
occurs between the first and second heart sounds
diastole
occurs between the second heart sound and the first heart sound of next cycle
Blood flow through the heart
Poor oxygenated blood return to the heart through the Superior and inferior Vena Cava
enters Right Atrium
Goes through the Tricuspid valve into the Right Ventricle
Right Ventricle contract and blood flow through Pulmonary semilunar valve into the Pulmonary Trunk
oxygen poor blood is carried to pulmonary arteries to the lungs, gas exchange in the pulmonary capillaries
oxygen rich blood returns to the heart through the pulmonary veins
oxygenated blood enters the left atrium
Blood goes through the mitral valve into the left ventricle
Left ventricle contract and blood flow through the Aortic semilunar valve
oxygenated blood is delivered to the body tissues
stroke volume and heart rate
Cardiac output
amount of blood pumped out by each ventricle in 1 min
stroke volume
volume of blood pumped out by one ventricle with each beat
70ml/ beat
difference between EDV and ESV
Preload
cardiac muscle cells are stretched before they contract
controls Stroke Volume
Afterload
pressure that the ventricle must overcome to eject blood
Contractility
the contractile strength achieved at a given muscle length
heart rate
75 beats/min
when SV drops HR increases to maintain CO
factors
positive chronotropic factors
increase HR
negative chronotripic factors
decrease HR
blood volume
5 liters
Heart Attack- death of heart muscle
direct causes
diabetes type 2
increase development of heart disease
hardening of coronary arteries
obesity
changes structure and function of heart
more weight more blood needed
heart has to work harder to pump the extra blood
indirect causes
risk factors
high levels of blood cholesterol
blood vessels
fatty deposits
block blood flow
narrow passage in arteries
break and cause clot
atherosclerosis
arteries become hardened and narrow
heart has to work harder
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low levels of good cholesterol HDL
removes other forms of cholesterol
bloodstream
take it back to liver
high blood pressure
damages arteries inner lining
artery burst
heart attack
family history
inherited
artery disease
lead to heart attack
cigarette smoking
chemicals
increase formation of plaque
blood thickens
form clots
physical inactivity
heart muscle
not exercise
weakens and atrophy
symptoms
chest pain
crushing
squeezing
pressing
heavy
stabbing or burning
weakness
sweating
nausea
breathlessness
Downstream
effects of heart attact
permanent damage
papillary muscles left ventricle
failure of mitral valve to close
effects
allow blood to flow backwards
blood can not move from heart to body efficiently
feel tired and out of breath
treatment
heart surgery
replace valve
untreated
heart failure
heart arrhythmias
symptoms
abnormal heart sound
shortness of breath
fatigue
heart palpitations
swollen feet or ankles
circulatory problems
other systems
respiratory
pulmonary hypertension
caused by increase pressure in left atrium
pulmonary edema
buildup of fluid in lungs
caused
heart attack
leaking heart valves
high blood pressure
urinary
pressure to build
vein connected to kidneys
blockage and reduced supply of oxygen rich blood to kidneys
nervous system
abnormal activation of SNS
worsens heart failure
complications
immediate
arrhymias
irregular heart beats
cardiogenic shock
blood pressure drop
insufficient blood supply
hypoxemia
low levels of oxygen in blood
pulmonary edema
fluid in and around lungs
DVT
veins in legs and pelvis
develop clots
block blood flow
myocardial rupture
damage wall of heart
increase risk
heart wall rupture
ventricular aneurysm
ventricle forms a bulge
later complications
aneurysm
scar tissue
heart walls
blood clots
low blood pressure
abnormal heart rhythms
angina
chest pain
congestive heart failure
weak heart
exhausted
breathless
edema
fluid accumulation
legs
ankles
pericarditis
lining of heart inflamed
chest pain