Chapter 9 Flashcards
Components of the Circulatory System
-heart: pump
-blood vessels: passageways
-blood: transports dissolved materials
Cardiac Muscle
-striated
-branched
-intercalculated discs: desmosomes + gap junctions
-consist of myosin, actin, troponin, tropomyosin
-have well developed SR and large T-tubules
-SR and ECF are the source of calcium
-deep red colour results from high oxygen blood and myoglobin
-high amounts of mitochondria for energy
Pulmonary Circulation
-closed loop of vessels carrying blood between heart and lungs
-low pressure and low resistance system
Systemic Circulation
-circuit of vessels carrying blood between heart and other body systems
-high pressure and high resistance system
Embryonic Development of the Heart
-day 25 is a single tube
-day 28 it forms a duct/sac like structure
-by birth it is fully functioning with 4 compartments
Base
part at the tip that tapers to a tip
Apex
-bottom of the heart
-directed to left side of the chest
The pump
-right and left sides of the heart function as two separate pumps even though they make up one organ
Atria
-divided into right and left halves
-superior chambers of the heart
Right Atrium
-where venous blood enters from superior and inferior vena cava (systemic veins)
Left Atrium
-where blood reenters heart via pulmonary veins after being reoxygenated in the lungs
Ventricles
-divided into right and left halves
-inferior portion
Right Ventricle
-blood flows here from right atrium and then goes to lungs via pulmonary arteries
Left Ventricle
-blood flows here from left atrium then heads to rest of the body via aorta then systemic arteries
Septum
-continuous muscular partition that prevents mixture of blood from the two sides of the heart
Lungs
-contain pulmonary capillaries that exchange nutrients (O2) and waste (CO2)
Veins
-carry blood from tissues to the atria
-not necessarily only carry deoxygenated blood
Arteries
-carry blood away from ventricles to tissues
-not necessarily only carry oxygenated blood
Which side of the heart is stronger?
-the left side
-pumps at a higher pressure into a longer system
Valves
-ensure blood flows in a linear/uni direction
-laminar flow
-blood can’t come backwards (turbulent flow)
Right Atrioventricular (AV) Valve
-aka tricuspid valve (has 3 regions)
-from right atrium to right ventricle
Left Atrioventricular (AV) Valve
-aka bicuspid/mitral valve (has 2 regions)
-between left atrium and left ventricle
Mitral Stenosis
-hardened/not working valve
Semilunar valves
-have 3 cusps/half moons
-Aortic SL Valve: from left ventricle to aorta
-Pulmonary SL Valve: from right ventricle to R and L pulmonary arteries
Chordae Tendinae
-though thin fibrous/tendon tissues that fasten the AV Valve leaflets
-prevent valves from being everted
Papillary Muscles
-extensions of the chordae tendinae cusp
-nipple shaped
-pull down chordae tendinae when ventricles contract
-keep valve tightly sealed
-anchor; prevent back flow
Heart Wall
-consists of 3 layers
Endocardium
-an extension of the endothelium that lines the entire circulatory system
-the thinner inner layer
-prone to endocarditis (infection)
Myocardium
-the cardiac muscle layer
-constitutes the bulk of the heart
-middle layer arrangement of spiral cardiac muscle
Epicardium
-thin external layer that covers heart
Action Potentials
-some cardiac cells can initiate own action potentials
-electrical impulse spread by gap junctions
-allow cells to contract as a single functional syncytium (atria and ventricles contract as separate units within this system)
Pericardium
-encloses heart
-2 layer outer sac:
1. tough, fibrous covering
2. secretory lining; secretes pericardial fluid that lubricates and prevents friction
Pericarditis
-results in a painful friction rub between the two layers when there is an infection
Autorhythmicity
-the heart contracts rhythmically as a result of action potentials that is generates itself
Contractile Cells
-constitute 99% of cardiac muscle cells
-do mechanical work of pumping
-normally do not initiate own action potentials
Autorhythmic Cells
~1% of cardiac muscle cells
-do not contract
-specialized for initiating and conducting action potentials responsible for contraction of working cells
Non-contractile Cell Locations
-SA node
-AV node
-Bundle of His
-Purkinje Fibres
Sinoatrial (SA) Node
-located in the right atrial wall near superior vena cava opening
-the normal pacemaker
-70-80 action potentials/minute
Atrioventricular (AV) Node
-located at the base of the right atrium near the septum
-40-60 action potentials/minute
Bundle of His
-originated at the AV node and enters the interventricular septum
-divides to form L and bundle branches which travel down the septum then curve up at the tip of the ventricles towards atria
-20-40 action potentials/minute w/ purkinje fibres
Purkinje Fibres
-spread through the ventricles
-extend from bundle of his
-twigs from the tree branch
-20-40 action potentials/minute w/ Bundle of His
Internodal Pathway
-from SA node to AV node
-100 milliseconds?
Interatrial Pathway
-from SA node to left atrium
-30 milliseconds?
Bundle of His/Purkinje Pathway
-30 milliseconds
Total Contraction time of the heart
160 milliseconds
AV Nodal Delay
Pacemaker Potential
-autorhythmic cells don’t have a defined resting membrane potential
-instead have pacemaker activity: membrane slowly depolarizes between action potentials until threshold is reached and ap is generated
Electrical Activity of the Heart
slides 24-31
Electrocardiogram (ECG)
-the sum of multiple action potentials
-records overall speed of activity throughout heart during depolarization and repolarization (not single action potential)
-has 3 major waves
-provides heart rate, rhythm, conduction of signals
-record at any given time represents the sum of electrical activity
-both electrodes are recording the same potential so no difference in potential is recorded
Leads
-ECG has 12 electrode system
-each pair of electrodes is called a lead; there are 6 between limbs and chest
P Wave
-represents atrial depolarization
QRS Complex
-represets ventricular depolarization
-atria is repolarizing simultaneously
T Wave
-ventricular repolarization
PR Segment
-AV Nodal Delay
ST Segment
-time during which ventricles are contracting and emptying
-not a record of contractile activity
TP Interval
-time during which ventricles are relaxing and filling
-heart is repolarized and at rest
Why is there no wave for SA nodal depolarization?
-not enough electrical activity is generated
-P wave is then the first to be recorded when wave of depolarization spreads across atria
Why is the P wave smaller than the QRS complex?
-atria have much smaller muscle mass than ventricles and generate less electrical activity
What ECG can measure?
-electrical activity triggers mechanical activity so abnormal electrical patterns are usually accompanied by abnormal contraction
-tells us about 3 main deviations:
1. abnormalities in rate
2. abnormalities in rhythm
3. cardiac myopathies
Abnormalities in Rate
-determined from the distance between two consecutive QRS complexes
Tachycardia (rate)
-rapid heart rate of more than 100bpm
Bradycardia (rate)
-slow heart rate of fewer than 60bpm
Arrhythmias (Abnormalities in Rhythm)
-variation from normal rhythm and sequence of excitation
Atrial Flutter (rhythm)
-rapid but regular sequence of atrial depolarizations
-200-380bpm
Atrial Fibrillation (A-Fib) (rhythm)
-rapid but irregular atrial depolarizations with no definite P waves
-QRS complexes occur sporadically
-no definite P waves
Ventricular Fibrillation (V-Fib) (rhythm)
-ventricular musculature exhibits uncoordinated, chaotic contractions
-emergency state
-saw edge reading
-need to shock heart to reset SA node
-brain won’t get enough blood and systems will start to fail
Heart Block (rhythm)
-defects in the cardiac conducting system
-only every second or third atrial impulse is passed to the ventricles
-2:1 or 3:1 block
-complete block: complete disassociation between atrial and ventricular activity
Cardiac Myopathies
-damage of the heart muscle
Myocardial Ischemia (myopathies)
-inadequate delivery of oxygenated blood to heart tissue
Necrosis (myopathies)
-actual death of hear muscle cells
Acute Myocardial Infarction (myopathies)
-occurs when supplying blood vessels becomes blocked or ruptured
-aka heart attack
Cardiac Cycle
-assumes SA node is normal
-consists of: contraction and emptying, relaxation and filling, changes in blood flow
-all brought about by rhythmic changes in electrical activity
Diastole
-relaxation and filling
Systole
-contraction and emptying
Systole and Diastole
-refer to ventricle activity, unless otherwise stated
Mid Ventricular Diastole
-atrium is also still in diastole
-TP interval of ECG
-AV valves open
-passive filling (no pressure)
-volume slowly increases till full
Late Ventricular Diastole
-atrial contraction
-P wave
-80% full
-AV valves are about to close
End of Ventricular Diastole
-ends at the onset of contraction
-atrial contraction and ventricular filling have completed
-volume of blood in the ventricle at the end of diastole is called: End-Diastolic Volume (EDV) = maximum filling ~135mL
Onset of Ventricular Systole
-QRS complex = ventricular excitation, which induces contraction
-ventricular pressure sharply increases after QRS, signalling systole
-AV valve closes
Isovolumetric Ventricular Contraction
-ventricular pressure must continue to increase to open aortic valve
-constant volume cause both valves are closed
Ventricular Ejection
-ventricular pressure exceeds aortic pressure
-aortic valve is forced open and ejection of blood begins
Stroke Volume
-amount of blood pumped out each ventricle with each contraction
-usually 70mL
End of Ventricular Systole
-does not empty completely
-usually only half leaves
-amount of blood left is the ESV: end-systolic volume which is usually 65mL
Calculating stroke volume
EDV-ESV=SV
Relaxation
-aortic valve closes but AV valve has not yet opened
-no blood can enter ventricle from atrium
-all valves closed for a brief period
Heart Sounds
1st: low pitched, soft “lub”
2nd: higher pitch “dup”
Lub
-first
-slow
-low pitch
-end of diastole
-closure of AV valves
Dup
-second
-faster
-higher pitch
-end of systole
-closure of SL valves
Murmurs
-should be no extra sounds in healthy heart
Stenotic Valve (whistle)
-stiff/narrowed valve
-doesn’t open completely
-blood is squeezed out
-turbulence
-whistle sounds
Insufficient Valve (swish)
-leaky valve
-flaps don’t fit properly
-turbulence
-swish sound
Systolic Murmur Timing
-murmur happens between sounds
-ie. lub murmur dup
Diastolic Murmur Timing
-murmur occurs at end of cycle
-ie. lub dup murmur
Murmur Variations
-combination of type of murmur and timing
Lub-whistle-dup
-stenotic (whistle)
-systolic (middle)
-SL valve doesnt open completely
Lub-dup-whistle
-stenotic (whistle)
-diastolic (end)
-AV valve doesnt open
Lub-swish-dup
-insufficient (swish)
-systolic (middle)
-AV valve doesnt close
Lub-dup-swish
-insufficient (swish)
-diastolic (end)
-AV valve doesnt close
Rheumatic Fever
-caused by bacteria
-can cause heart infection
-usually mitral valve stenosis
-heart failure or death possible
Cardiac Output
-the amount of blood that comes out of each ventricle per minute
-determined by:
1.assuming SA node is setting hr
2. heart rate
3. stroke volume
Stroke Volume and Cardiac Output
-determined by the extent of the venous return and sympathetic activity
-influenced in intrinsic and extrinsic controls
-both factors increase sv by increasing the strength of heart contraction
Calculating Cardiac Output
-heart rate x stroke volume (EDV-ESV)
-ie. 70bpm x (135-65) = 4900 mL/minute
Cardiac Reserve
-difference between cardiac output at rest and at maximum exercise
Intrinsic and Extrinsic Control of Stroke Volume
-in the sympathetic nervous system
Intrinsic Control
-increase venous return, increase EDV, increase contraction, increase stroke volume
Extrinsic Control
-increase contraction, increase stroke volume
Innervation
-by sympathetic and parasympathetic nervous system
-controlled by medulla
Parasympathetic Stimulation
-will decrease heart rate
-controlled by vagus nerve (CN X)
-ACh is released to increase permeability of the SA node to K+ by slowly closing K+ channels
-rate at which action potentials are initiated is reduced
-ACh binds to muscanaric G Protein receptor and reduced cAMP activity
-leads to 4 outcomes to decrease cardiac output:
- SA Node (parasympathetic)
-increased permeability to K+
-gets hyperpolarized
-reduces If current
-decreased rate of threshold
-decreases heart rate
- AV Node (parasympathetic)
-decreases excitability
-increases AV Nodal delay
- Atrial Muscle (parasympathetic)
-decreases and weakens contraction
-depolarizes slowly
- Ventricular Muscle (parasympathetic)
-decreases and weakens contraction
-depolarizes slowly
Sympathetic Stimulation
-thoracolumbar branch
-intends to increase heart rate
-norepi and epi released and bind to adrenergic B1 receptor
-increases cAMP activity
-4 outcomes to increase cardiac output:
- SA Node (sympathetic)
-increases rate of depolarization to threshold
-increases heart rate
- AV Nodal Delay (sympathetic)
-increases excitability
-delay is decreased
- Atrial Muscle (sympathetic)
-increases and strengthens contraction
- Ventricles (sympathetic)
-increases and strengthens contraction
Frank-Starling Law
-states that “heart normally pumps out during systole the volume of blood returned to it during diastole”
-the greater the diastolic filling (muscles stretched) the larger the EDV
Heart Failure
-the inability of the cardiac output to keep pace with the bodys demands for supplies and removal of wastes
-inadequate cardiac output to reach brain and organs
Prime Defect
-a decrease in cardiac contractility
-weakened cardiac muscle contracts less effectively
-heart operates at a lower length-tension curve
-pumps out a smaller SV
Compensatory Measure
-sympathetic activity is increased for a limited time
-sympathetic nerves: increase SV and cardiac output
-kidneys: retain more salt, water follows, this increases plasma/blood volume, in turn sv and cardiac output are increased
Decompensated Heart Failure
-compensatory measures failed
-forward failure: heart can’t pump adequate blood to the tissues
-backward failure: lungs are backed up with blood
-congestive heart failure
Systolic Failure
-decrease in cardiac contraction (as previously described)
Diastolic Failure
-ventricles do not fill normally
-less blood pumped out with each contraction
Nourishing Heart Muscle
-supplied with blood and nutrients via coronary circulation
Coronary Circulation
-most blood received during diastole
-like a garden hose: during systole coronary vessels are compressed by the contracting muscle
Coronary Vessels
-branches off aorta to supply heart
Dicrotic Notch
-closure of the aortic valve produces a disturbance/ notch
Role of Adenosine
-adenosine is formed from ATP during cardiac metabolic activity
-when heart uses more ATP = more adenosine
-heart needs more oxygen
-adenosine vasodilates coronary vessels to increase O2
-important cause heart can’t get enough ATP through anaerobic metabolism
Coronary Artery Disease (CAD)
-blocking of the coronary vessels so oxygen isn’t supplied to the heart
-can lead to heart attack
-3 mechanisms:
- Vascular Spasm
-is reversible
-abnormal spastic contraction that narrows coronary vessels
-early stages of CAD
-not enough oxygen = endothelium releases platelet activating factor
- Atherosclerosis
-plaques form in heart vessels
-by oxidized cholesterol
Angina
-chest pain
-treated with nitrogylcerine (vasodilator)
Embolus
-floating plaque causes clot
-immediate death
Thromboembolism
-when a blood clot forms in a vein
