Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
SIUE Cardiac Muscle
Cardiac Muscle
| Question | Answer |
|---|---|
| What is the resting potential of cardiac muscle? | -85mV |
| Cardiac muscle depolarization timing compared to skeletal muscle | cardiac muscle is depolarized for 15x longer than skeletal muscle |
| How AP is reached in cardiac Muscle | 1.Fast Na+ channels open quickly-rapid upstroke of AP 2. Slow Ca++ channels open slowly and stay open-plateau 3.When AP is reached K+ perm decreases 5-fold, so K+ is not forced out of the cell. 4. When slow Ca++ chan close K+ leaves the cell = repolarize. |
| Absolute Refractory Period of ventricles | Lasts .25-.30 sec; occurs during plateau phase; cell cannot depolarized again |
| Absolute refractory period of Atria | .15 sec; cell cannot depolarize again |
| Relative Refractory Period | .05 sec; very difficult, but not impossible to excite the cell; occurs when cell is almost repolarized |
| Contraction of Cardiac Muscle | AP spread across membrane to T-Tubule; T-Tubule stimulates SR to release Ca++; T-Tubule contain negatively charged particles that attract Ca++; Ca++ in T-Tubule diffuse into sarcoplasm during AP; Ca++ binds to T-TM complex allowing contraction to occur |
| Relaxation of Cardiac Muscle | Ca++ pump on SR resequesters some Ca++ (ATP required); Ca++/Na+ exchanger removes the rest of the Ca++; Additional Na+ is removed by the Na+/K+ Pump; When Ca++ is out of the cell relaxation occurs |
| Intrinsic Rate of SA node | 100-115, but it is acutually less due to parasympathetic stimulation |
| Location of SA Node | Posterolateral Wall of right Atrium |
| Resting Potential of SA Node | -55 - -60; caused by increased permeability to Ca++ and Na+; Fast Na+ gates are inactivated at this resting potential |
| Make-up of SA Node | Very Short Myofilalments causing almost no contraction to occur; connected to surrounding atrial fibers so AP created by SA node spreads immediately to atrial muscle wall |
| Ion involved with SA node Depolarization | Ca++ |
| AV Node Location | Posterior wall of R atrium immediately behind the tricuspid valve |
| Where does the AV node receive stimulation from? | Small bands that extend from the SA node and from the atrial muscle fibers |
| Intrinsic Rate of AV node | 40-60 |
| Purkinje System | Extends from AV node to AV bundles and the rest of the ventricles |
| Purkinje Fibers | Transmit AP very quickly due to highly permeable gap junctions between the purkinje cells; |
| Direction of AP in Purkinje fibers | From AV node to ventricles, but not backwards. |
| Purkinje Fiber Branches | Right and left side of ventricular septum and extend towards apex and around the sides of the heart back toward the base; terminate 1/3 of the way into the cardiac muscle mass and become continuous with cardiac muscle fibers; very fast transmission |
| Vagal Stimulation of Cardiac Muscle | Parasympathetic response that leads to the release of ACh = decreased heart rate |
| Sympathetic stimulation of Cardiac Muscle | NE is released and binds with beta-1 receptors causing an increase in heart rate |
| What type of muscles are cardiac muscles? | striated |
| Function of Striated muscles | They are interlinked in a laticework arrangement that allow AP to travel quickly through muscles |
| Intercalated discs | Allow ions to move along longitudinal axis of muscle fibers; allows for depolarization of several muscles from one impulse |
| Ryanodine Receptors | Found on SR and are activated by Ca++ that enters the sarcoplasm from the ECF; When the receptors are ativated they cause the SR to release additional Ca++; Responsible for contractile strength |
| Ions associated with phase 0 of Cardiac AP | Na+ enters cell through fast sodium channels |
| Ions associated with phase 1 of Cardiac AP | K+ and Cl- move out of cell |
| Ions associated with phase 2 of Cardiac AP | Ca++ enters cell through slow channels and K+ slowly moves out (permeability to K+ is decreased 5-fold) |
| Ions associated with phase 3 of Cardiac AP | Ca++ and Na+ channels close and K+ membrane potential returns to normal allowing K+ to rush out of cell |
| Phase 4 of Cardiac AP | Resting Potential |
| Cardiac Output =? | SV X HR |
| Stroke Volume | Amount of Blood ejected from the ventricles with each beat. Regulated by Frank-Starling Law |
| Frank-Starling Law | Increased preload = Increased Contraction Strength |
| 3 factors that determine SV | Preload; Contractility; Afterload |
| When do coronary arteries receive blood? | During diastole |
| How do Coronary arteries receive blood? | Back flow of blood from the aorta caused by adequate SVR leads to blood supply of the coronary arteries |
| How do you increase colateral coronary circulation? | EXERCISE!! |
| Where do the cardiac center and the vasomotor center get their info from? | Baroreceptors and Chemoreceptors |
| What does the cadiact center regulate? | Cardiac output |
| What does the vasomotor center regulate? | Blood Pressure and vessel diameter |
| How Renin-Angiotesnsin-Aldosterone system works | Low BP detected by kidneys; renin is released; renin converts angiotensinogin to angiotensin I; Angiotensin I is converted to Angiotensin II by ACE in lungs; Angiotensin II contricts vessels and stimulates release of aldosterone from adrenal cortex |
| What effect does aldosterone have on blood pressure | Aldosterone causes Na+ retention and in turn draws more fluid into the vessels increasing BP |
| ADH effect on BP and where what secretes it | ADH increases BP by retaining fluids; it is secreted by the hypothalmus |
| ANP effect on BP and where it comes from | causes vasodilation and increased urine output; secreted by atria |
| Nitric oxide effect on BP and where it comes from | Causes vasodilation (it is the main controller of vasomotor tone); it is secreted by endothelial cells |
| Electrical Current | rate of charge flow past a given point; measured in amperes |
| Amperes | Coulombs per second |
| Coulomb | a unit of electrical charge |
| What does an EKG measure? | Change in electrical potentials |
| How the atria act as primers to the ventricles | 80% of blood flows directly from atria to ventricles before the atria contract; the final 20% of the blood is delivered to the ventricles during atrial contraction (atrial kick) |
| What happens during ventricular systole | The A-V valves close and the atria fill w/ blood; Ventricles contract and semilunar valves open and blood is ejected |
| What happens following ventricular systole? (pressure wise) | AV valves open due to relatively low ventricular diastolic pressure; 1st 1/3 of diastole - period of rapid filling; 2nd 1/3 of diastole - small amt of blood continues to fill ventricles; 3rd 1/3 of diastole - Atrial Kick |
| Isovolumetric Contraction during systole | Immediately following ventricular contraction there is an abrupt increase in ventricular pressure causing AV valves to close; pressure builds up causing semilunar valves to open (.02-.03 sec) |
| What causes S1 | Closing of AV valves |
| Isovolumetric Relaxation | at the end of systole the pressure in the ventricles decreases rapidly causing blood from the aorta/pulmonary arter to backflow which closes the semilunar valves; ventricles relax, but don't gain volume. |
| What causes S2? | Closing of the semilunar valves at the end of systole |
| End Diastolic Volume | Amount of blood in ventricles at the end of diastole (110-120 mL) |
| Normal Stroke volume | 70mL |
| End Systolic Volume | Volume of blood that remains in the ventricles following systole |
| Ejection fraction | stroke volume/EDV (usually about 60%) |
| How do you maximize stroke volume? | Increase EDV and Decrease ESV |
| Tricuspid Valve | Opens during diastolic filling of right ventricle and inhibits back flow of blood from RV to RA during systole |
| Mitral Valve | Bicuspid Valve; opens during diastolic filling of Left Ventricle & inhibits back flow of blood from LV to LA during systole |
| Aortic Valve | Opens during LV systole and closes during diastole to prevent backflow from the aorta to the LV |
| Pulmonary Valve | Opens during RV systole and closes during diastole to prevent backflow from pulmonary artery to RV |
| Function of papillary muscles | Pull on the AV valves to ensure that they stay closed during ventricular contraction (they prevent regurgitation) |
| Special facts about semilunar valves | The snap closed in respones to art pressure; increased velocity of blood through valves = increased mechanical abrasion; they are strong and pliable to withstand physical stress |
| R vagus nerve stimulates... | SA Node |
| L vagus nerve stimulates... | AV Node |
| What is th Nucleus Tractus Solitarius? | Recieves sensory input and sends PSNS and SNS stimulation to the heart. |
Created by:
SRNA84
Popular Nursing sets