Ch. 19 - Heart Flashcards
Structure of Cardiac Muscle Cells
short, branched, have 1 or 2 central nuclei. Extensive blood supply and numerous mitochondria.
endomysium
wispy layer of areolar connective tissue that supports cardiac cells
sarcoplasmic reticulum
surrounds bundles of myofilaments
Sarcomeres
bundle of myofilaments.
Sarcolemma
plasma membrane with invaginations. In cardiac they are folded at connections between cells to facilitate communication and stability.
Intercalated discs
structural formations that have desmosomes and gap junctions. Allows for quick
desmosomes
mechanically join cells with protein filaments to give extra support/strength.
functional syncytium
a mass of cells in the heart wall that have merged by gap junctions so that when one is stimulated all connected ones are as well. each heart chamber is a functional syncytium because they act as one.
gap junction
electrically join cells (allow ion flow) to make each heart chamber a functional unit
myoglobin
helps cardiac cell metabolism and energy needs. It binds to oxygen when muscle is at rest.
creatinine kinase
helps supply heart with energy. It catalyzes the transfer of Pi from creatinine phosphate to ADP, making ATP
Fuel molecules heart can use
fatty acids, glucose, lactic acid, amino acids, ketone bodies.
What type of metabolism does the heart use?
aerobic (relies on oxygen for energy). Makes heart susceptible to failure when ischemic
ischemic
when oxygen is low
Sinoatrial node anatomy
pacemaker, located high in posterior wall of right atrium
Atrioventricular node anatomy
located in floor of right atrium
Atrioventricular bundle anatomy
extends from av node through interventricular septum. Divides into right and left bundles.
Purkinje fibers
extends from left and right bundles to hearts apex through walls of ventricles. larger in diameter than other cardiac fibers, making action pot. extremely rapid to ensure ventricles contract at same time
Cardiac center
part of medulla oblongata, contains cardioacceleratory and cardioinhibitory centers.. Modifies rate and force of cardiac activity by sending signals via sympathetic and parasympathetic pathways.
Parasympathetic innervation
decreases heart rate. Starts at medullas cardioinhibitory center and relayed via vagus nerve (right vagus innervates SA node, left innervates AV)
Right vagus innervates
SA node
Left vagus innervates
AV node
Sympathetic innervation
increases hr and force of contraction. Starts at medulla’s cardioacceleratory center. relayed via neurons from t1-t5 segments of spinal cord… Extends to sa, av nodes, myocardium, and coronary arteries. Increases coronary vessel dilation.
Heart stimulation
heart contraction involves 2 events. The conduction system and cardiac muscle cells contraction
Nodal cells
nodal cells in SA nodes initiate heartbeat. They spontaneously depolarized and generate action potentials. Have common membrane proteins such as Na/k pumps and leak channels.
Resting membrane potential of Nodal cells
-60mV, but these cells do not have stable RMP
Specific voltage-gated channels unique to cardiac system
slow voltage-gated Na
Fast voltage-gated Ca
Voltage-gated K
autorhythmicity
spontaneous firing; exhibited by SA node cells
Initiation of Action Potential at SA node
- Reaching threshold: slow voltage Na open and Na flow in. Membrane goes from -60 to -40 (threshold)
- Depolarization: fast voltage Ca channels open and Ca flows in. Membrane potential goes from -40 to 0 mV.
- Repolarization: fast voltage ca channels close and K open, so k flows out. Membrane potential returns to -60 and slow voltage Na channels open, starting the process again.
How often does SA node action potential fire?
about every 0.8 seconds or about 75 bpm. Inherently the SA node would fire at 110, but it is kept slower parasympathetic.
Vagal tone
keeps the heart rate slower than 110. it is parasympathetic activity relayed by vagus nerve.
Pacemaker potential (of nodal cells)
ability to reach threshold without stimulation.
Conduction system
Starts at SA node –> action potential distributed through atria and reaches AV node –> Action potential delayed at AV but goes to AV bundle branches –> Purkinje fibers and through ventricles
Why is Action Potential delayed at AV node
smaller diameter and fewer gap junctions. Allows ventricles to fill before they contract. Insulation of fibrous skeleton means AV node is bottleneck (only path)
Papillary muscles
anchor chordae tendineae of AV cusps and pull just prior to increase in pressure in ventricles.
Ventricle stimulation starts at
apex to ensure blood is efficiently ejected towards arterial trunks
Ectopic pacemaker
when pacemaker fails, something else must take over that can spontaneously depolarize. AV is default pacemaker with a rhythm of 40-50 bpm; enough to sustain life. If both fail; cardiac muscles set a rhythm of 20-40 bpm (too slow to survive)
Cardiac Muscle Cells RMP
-90mV. Maintained by fast Na, slow Ca and K. VOLTAGE GATED CHANNELS ARE CLOSED WHEN CELL IS AT REST
Cardiac Muscle Action Potential steps
- depolarization: gap junctions open fast voltage gated Na changing -90 to +30
- plateau: depolarization opens voltage k and opens slow Ca channels. K leaves and Ca enters so membrane remains depolarized
- Repolarization: slow Ca channels close and k remains open, back to -90mV
Crossbridge cycling
Ca enters sarcoplasm from interstitial fluid and sarcoplasmic reticulum. binds to troponin, crossbridge formation, powerstroke, release of myosin head, reset myosin. Ca channels close and pumps move Ca out so relaxation occurs.
Why cant cardiac muscles exhibit tetany
unlike skeletal muscle, cardiac cells have long refractory period. Cells cant fire new impulse during refractory. In cardiac cells, period is 250ms. Must relax before contracting again.
Electrocardiogram (ECG/EKG)
skin electrodes detect electrical signals of cardiac muscle cells, common diagnostic tool.
P wave
part of ekg that reflects electrical changes of atrial depolarization originating in SA node.
QRS complex
electrical changes associated with ventricular depolarization, atria also simultaneously repolarizing.
T wave
electrical change associated with ventricular repolarization.
PQ segment
associated with atrial cells’ plateau (atria are contracting)
ST segment
associated w/ ventricular plateau (ventricles contraction)
P-R interval
time from beginning of P wave to beginning of QRS deflection. from atrial depolarization to beginning of vent. depolarization. Time required to transmit action potential through entire conduction system.
Q-T interval
time from beginning of QRS to end of T wave; reflects the time of ventricular action potentials and length depends on Hr. Changes may result in tachyarrhythmia (rapid, irregular hr)
Cardiac Arrhythmia
any abnormality in hearts electrical activity. May be a result of heart blocks, premature vent. contractions, or fibrillation.
heart block
impaired conduction that may result in light-headedness, fainting, irregular heartbeat, and chest palpitations.
First-degree AV block: PR prolongation- slow conduction between atria and ventricles.
Second-degree AV block- failure of some atrial action potentials to reach ventricles.
Third-degree AV block: complete block- failure of all action potentials to reach ventricles.
Premature ventricular contractions
result from stress, stimulants, or sleep deprivation. Abnormal action potentials within AV node or ventricles. Not detrimental unless they occur in large numbers
Atrial fibrillation
chaotic timing of atrial action potentials
Ventricular fibrillation
chaotic electrical activity in ventricles. uncoordinated contraction and pump failure that leads to death of heart cells. Treated with automated external defibrillator (AED)
systole
contraction; highest pressure
diastole
relaxation; lowest pressure
Overview of Cardiac cycle
blood moves down pressure gradient and ventricular activity is most important driving force
Ventricular contraction raises
ventricular pressure. AV valves and closed and semilunar are pushed open.
Atrial contraction and Ventricular filling
first step in cardiac cycle. The SA node starts atrial excitation and push blood into ventricles. Ventricles are filled to end-diastolic volume (EDV) and atria remains relaxed.
Isovolumetric contraction
Second step in Cardiac cycle; purkinje fibers initiate ventricular excitation. Ventricles contract, pressure rises, and AV valves are pushed closed. Vent. pressure is still lower than Arterial truck pressure, so semilunar stay closed.
Ventricular ejection
ventricles continue to contract until vent. pressure is > arterial pressure. Semilunar valves open and blood moves to arterial trunks.
stroke volume
amount of blood ejected by ventricle. influenced by venous return, inotropic agents, and afterload.
end systolic volume (ESV)
amount of blood remaining in ventricle after contraction.
ESV equation
ESV = EDV - SV
end diastolic volume ESV
amount of blood in ventricle after atria emptying.
Isovolumetric relaxation
4th stage in cardiac cycle. ventricles relax and expand, lowering pressure. Arterial pressure is greater than ventricular so semilunar valves close and AV valves remain open. When all valves close, blood neither enters nor leaves and the time is called isovolumetric.
Atrial relaxation and Ventricular filling
all chambers are relaxed and atrial bp forces AV valves open and blood flows into ventricles starting the cardiac cycle over.
Ventricular balance
equal amounts of blood are pumped by left and right sides of the heart. left heart pumps blood farther so it must be thicker and stronger. Must remain same or edema can occur
edema
swelling in tissue
Cardiac Output (CO)
amount of blood pumped by a single ventricle in one minute, measures effectiveness of cardiovascular system. Increases in healthy people during exercise
Equation to determine cardiac output
HR X SV (amnt. ejected per beat. liters per minute
Resting Cardiac output
CO must meet tissue needs, so people with smaller hearts have a smaller SV and faster HR (children)
Cardiac reserve
capacity to increase cardiac output above resting level. HR accelerates and SV increases during exercise. CO can increase 4 fold in healthy people and 8 fold in athletes.
Equation for Cardiac reserve
CO w/ exercise - CO at rest
Chronotropic agents
change hr by altering activity of nodal cells. often work via ANS or hormones.
Positive Chronotropic agents
increase Hr. Sympathetic nerve stimulation that causes norepinephrine and EPI to be released. NE and EPI bind to nodal cells beta-one adrenergic receptors and increase their firing rate. Ca channels opening so cell fires sooner
Thyroid hormone
pos. chronotropic agent that increase # of beta-one adrenergic receptors on nodal cells
Caffeine
positive chronotropic agent that inhibits breakdown of cAMP.
Nicotine
pos. chronotropic agent that increases release of norepinephrine
Cocaine
pos. chronotropic agent that inhibits reuptake of norepinephrine.
Negative chronotropic agents
decrease heartrate; stimulate parasympathetic activity. Parasympathetic axons release ACh onto nodal cells which binds to muscarinic receptors and opens K cells. Takes longer for nodal cells to reach threshold.
beta-blocker drugs
interfere w/ EPI and NE binding; used to treat high bp.
Autonomic reflexes
baroreceptors (pressure) and chemoreceptors send signals to cardiac center to influence SNS and parasympathetic NS as needed.
Atrial reflex (Bainbridge reflex)
protects heart from overfilling. Baroreceptors in atrial walls stimulated by increased venous return. Increased nerve signals to cardioacceleratory center to increase excitation of sympathetic axons to heart. Increased hr to decrease atrial stretch.
Venous return
directly related to SV. determines amount of ventricular blood prior to contraction or the EDV. Volume determines preload
preload
pressure stretching heart wall before shortening.
Inotropic agents
change stroke volume by altering contractility (force of contraction). Generally due to changes in Ca available in sarcoplasm, which directly relates to number of crossbridges formed.
Positive inotropic agents
increase available Ca. EPI and NE work via beta1 adrenergic receptors to increase Ca. TH increases # of B1 receptors and certain drugs (digitalis) boost cardiac output by increasing contractility.
Negative inotropic agents
decrease available Ca and lower contractility. Electrolyte imbalances such as increased K or H and certain drugs that block Ca such as bp drugs are neg. inotropic agents.
Afterload
resistance in arteries to ejection of blood by ventricles. It is the pressure that must be exceeded before blood ejection.
Atherosclerosis
plaque within vessel lining seen in aging. Increases afterload and decreases SV.
Variables that influence Cardiac Output
heart rate, stroke volume
Frank-Starling law
the stroke volume of the left ventricle will increase as the left ventricular volume increases due to the myocyte stretch causing a more forceful systolic contraction. Causes a balanced ventricular output.
