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conduction of the heart
consists of specialized cardiac muscle cells that generate and transmit electrical impulses to ensure a coordinated heartbeat. This system is autorhythmic meaning it can initiate its own electrical signals without input from the nervous system, which only serves to modify the heart rate.
electrical impulse traveling through the heart first step
sinoatrial (SA) node
electrical impulse traveling through the heart second step
Atrioventricular (AV) node
electrical impulse traveling through the heart third step
Atrioventricular (AV) Bundle of His
electrical impulse traveling through the heart fourth step
right and left bundle branches
electrical impulse traveling through the heart fifth step
Purkinjie fibers
SA node
the pacemaker initiating the electrical impulse across the atria
AV node
receives the signal from the SA node and delays it for about 0.1seconds to allow the atria to finish contracting and pushing blood into the ventricles before the ventricles contract
AV Bundle of His
is an electrical impulse between the atria and the ventricles and carries impulse from the AV node to the bundle branches
right and left bundle branches
conduct impulses through the interventricular septum to the Purkinjie fibers
Purkinjie fibers
rapidly distribute the electrical impulse, stimulating the ventricular muscle to contract in a coordinated, upward motion from the apex
SA node intrinsic rate
60-100 beats per min
AV node intrinsic rate
40-60 beats per min
Purkinjie fibers intrinsic rate
20-40 beats per min
cardiac plexus
branches of the autonomic nervous system located both superficial and deep to the aortic arch that supply the conduction system (SA and AV nodes), coronary vessels, and cardiac muscle cells
sympathetic innervation of the cardiac plexus
Cervical and upper thoracic ganglia travel as cardiac nerves in the cardiac plexus
Sympathetic activation increases the rate and force of contraction
T1-T5 sympathetic nerves that travel back to the spinal cord are responsible for angina
parsympathetic innervation of the cardiac plexus
Parasympathetic fibers travel in the vagus nerve, leave cardiac branches, and synapse in the cardiac plexus and heart
Parasympathetic activation decreases the rate and force of contraction
Sensory fibers traveling with the vagus nerve back to the brain stem mediate cardiac reflexes
day 19 of cardiovascular embryonic development
heart development begins with the formation of a pair of lateral endocardial tubes which will soon fuse to form the primitive heart tube
day 22 of cardiovascular embryonic development
the primitive heart tube begins to beat
day 23 of cardiovascular embryonic development
the tube starts to fold and loop, displacing the future chambers into their general adult positions
day 24 of cardiovascular embryonic development
the heart begins to circulate blood
sinus venosus
develops into the smooth-walled part of the right atrium, the coronary sinus, and the SA node
primitive atrium
gives rise to the muscular, ridged parts of the right and left atria, known as the pectinate muscles
primitive ventricle
becomes trabeculated (muscular, ridged)portions of the right and left ventricles. It is the strongest pumping chamber of the developing heart
bulbus cordis
the lower part differentiates into the smooth outflow tracts of both ventricles
truncus arteriosus
this cranial extension of the bulbus cordis ultimately forms the ascending aorta and the pulmonary trunk
atrial separation embryonic development of the heart
two septa, the septum primum and the septum secundum, grow from the roof of the primitive atrium to divide it into right and left chambers
foramen ovale embryonic development of the heart
an opening that allows for the continued shunting of blood from the right atrium to the left atrium and at birth, the rise in left atrium pressure forces this shut
ventricular and outflow tract separation embryonic development of the heart
divides into the ascending aorta and the pulmonary trunk by a pair of spiraling truncoconal septa which grow downwards to complete the interventricular septum
valve formation embryonic development of the heart
the AV valves and their supporting chordae tendinae and papillary muscles are sculpted from surrounding myocardium between weeks 5-8. By the end of week 8, a heart with all its definitive structures is functioning
the pathway of fetal blood flow
Oxygen from the placenta
first shunt (ductus venosus)
Oxygenated blood mixes with deoxygenated blood in the IVC before entering RA
Second shunt (foramen ovale)
Third shunt (ductus arteriosus)
Return to placenta for re-oxygenation via two umbilical arteries
fetal blood flow transition at birth
lungs inflate causing a drop in pulmonary resistance and allowing blood to flow into the pulmonry circulation
pressure in LA rises above RA functionally closing the foramen ovale
increased blood oxygen triggers the constriction of the ductus arteriosus and closes within days
the ductus venosus also closes forcing blood to pass through the liver
cardiac cycle
the sequence of mechanical and electrical events that occur during a single heartbeat. It is compromised of 2 principle phases: systole and diastole. (0.8 seconds)
diastole
the period of ventricular relaxation and filling
systole
the period of ventricular contraction and ejection
phases of the cardiac cycle
isovolumetric relaxation
ventricular filling
atrial systole
isovolumetric contraction
ventricular ejection
Isovolumetric relaxation
the initial phase of diastole immediately following ventricular ejection. The semilunar valves close producing the second heart sound (S2). All cardiac valves are closed. The ventricular myocardium relaxes, leading to rapid decline in intraventricular pressure.
ventricular filling
when intraventricular pressure falls below the pressure within the atria, the atrioventricular valves (mitral and tricuspid) open. This allows blood that has accumulated in the atria to flow passively into the ventricles.
atrial systole (atrial kick)
to complete ventricular filling, the atria contract, actively ejecting the final 20-30% of blood into the ventricles. The stretch on these ventricular muscle fibers is defined as preload.
isovolumetric contraction
ventricles begin to contract, increases intraventricular pressure, AV valves close and produces the first heart sound (S1). For a brief interval, all valves remain closed and ventricular pressure rises sharply but ventricular volume remains constant.
ventricular ejection
once intraventricular pressure surpasses the pressure in the aorta and pulmonary artery, the semilunar valves are forced open and ventricular ejection begins
when is S1 sound heard
isovolumetric contraction
when is S2 sound heard
isovolumetric relaxation
afterload
the resistance the ventricles must overcome to eject blood
stroke volume
the volume of blood ejected from a ventricle during a single contraction
ejection fraction
the proportion of blood ejected from the ventricle relative to its end-diastolic volume (55-70%)
preload
the stretching of the cardiac muscle fibers at the end of diastole just before contraction- it is determined by the volume of blood in the ventricles at the end of this phase.
contractility
the intrinsic ability of the heart muscle to pump blood with a given force
cardiac output
the total blood volume pumped by the heart per minute (CO= SV * HR)
Frank Starling Mechanism
the rule that the heart pumps out more blood if more blood fills it up (more in, more out)
blood pressure
=cardiac output * total peripheral resistance
total peripheral resistance (TPR)
is determined primarily by the diameter of the arterioles
vasoconstriction
raises TPR and blood pressure
vasodilation
lowers TPR and blood pressure
baroreceptor reflex
when baroreceptors found in the carotid sinus and the aortic arch continuously sense arterial wall stretch to signal an increase or decrease in sympathetic/parasympathetic activity to control heart rate and blood vessels to increase/decrease blood pressure
baroreceptor reflex pathway example
decrease VP → decrease baroreceptor firing→ increase sympathetic activity → increase HR, contractility, vasoconstriction
baroreceptor reflex importance
this reflex is the body’s primary rapid mechanisms for stabilizing blod pressure, such as with postural changes or exertion
basic pathophysiology principle of the baroreceptor reflex
Because BP and perfusion both depend on CO and TPR, a change in any single input (heart rate, contractility, preload, afterload, or vessel diameter) can shift blood pressure or reduce downstream tissue perfusion even when the other inputs are normal
heart sounds
Normal is “lub-dub.” The presence of abnormal sounds, such as murmurs or gallops can indicate valvular heart disease, heart failure, or other structural defects
ECG/EKG
a test recording the electrical activity of the heart
ECG/EKG importance
It detects arrhythmias, myocardial infarction, and other cardiac abnormalities by analyzing the heart’s electrical signals
cardiac biomarkers
are proteins and enzymes released into the blood when the heart muscle is damaged, stressed, or lacking oxygen
troponin levels
elevated levels are a key marker for diagnosing MI and assessing the extent of heart damage
lipid profile
high levels of LDL and triglycerides increase the risk of atherosclerosis and heart disease
beta blockers
decrease heart rate and contractility by blocking sympathetic B1 effects on the SA node and the myocardium. This leads to decreased cardiac output, decreased myocardial O2 demand, decreased heart rate, increase EDV, increase preload, and decreasing afterload.
calcium channel blockers
relax smooth muscle which leads to a decrease in TPR/afterload, some agents decrease HR and contractility and have little to no effect on preload.
ACE inhibitors/ARBs
block angiotensin II formation or action which leads to vasodilation (decreasing afterload) and aldosterone-driven fluid retention (decreasing preload) making it easier for the heart to pump blood.
diuretics
decrease the circulating blood volume which results in a decrease in preload and a decrease in venous return.