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Cardiac muscle contains two types of cell junctions, know the purpose of each.
→ Desmosomes: Prevents cells separating during contraction
→ Gap Junctions: Allows for easy ion transport
By what method does cardiac muscle produce its ATP?
→ Aerobic respiration
Can cardiac muscle exhibit tetanus?
no, due to long refractory period
autorhythmicity
→ Cardiac muscle sets its own rhythm (rate of contraction)
What role do pacemaker cells play in the heart?
→ Spontaneously generate action potentials (pacemaker potentials)
Triggers action potentials in contractile cells
pacemaker potential:What 3 ion channels are involved?
→ HCN channels, voltage-gated calcium channels, voltage-gated potassium channels
pacemaker potential:What type of ion channel is responsible for the slow initial depolarization?
HCN channels
pacemaker potential:What causes that channel to open?
→ Hyperpolarization
pacemaker potenital:What is threshold for the conducting cells?
→ –40 mV
pacemaker potential:What ion channel opens for full depolarization? What ion enters/exits?
→ Voltage-gated Ca²⁺ channels open; Ca²⁺ enters
pacemaker potential:What allows these cells to repolarize?
→ Voltage-gated K⁺ channels open
pacemaker potential:What is the minimum potential phase?
→ K⁺ continues to exit, and membrane hyperpolarizes
pacemaker potential:What ion movement allows for the minimum potential phase?
→ K⁺ exits
What is the main pacemaker in the conducting system?
→ Sinoatrial (SA) node
What is the intrinsic rate of depolarization in the SA node?
→ 60–70 bpm on its own
Where is the AV node located?
→ Near tricuspid valve
What is the intrinsic rate of depolarization for the AV node?
→ 40–50 bpm on its own (usually overwritten by SA node)
What is the purpose of the AV node delay?
→ Brief delay in signal (allows atria to contract before ventricles)
Trace the pathway of the conducting system through the heart.
1. SA node (upper right atrium)
2. AV node (near tricuspid valve)
3. AV bundle (inferior interatrial septum and upper interventricular septum)
4. Left and right bundle branches (in interventricular septum)
5. Purkinje fibers (in outer walls of ventricles)
Ap in contractile cells:What ion channel and ion movement causes the depolarization?
→ Voltage-gated Na⁺ channels open; Na⁺ enters
Ap in contractile cells:What ion channel and ion movement causes the initial repolarization?
→ Voltage-gated Na⁺ channels inactivate; selected K⁺ channels open and some K⁺ exits
Ap in contractile cells:What two ions are entering/exiting during the plateau phase?
Ca²⁺ enters, K⁺ exits
Ap in contractile cells:What allows for the final repolarization?
→ Voltage-gated Ca²⁺ channels close; most voltage-gated K⁺ channels open and K⁺ exits
What is the purpose of an EKG?
→ Records the changes in electrical activity in the contractile cells
Know what each of the EKG waves represents.
→ P wave: Atrial depolarization
→ QRS complex: Ventricles depolarizing
→ T wave: Ventricle repolarization
Know what the EKG intervals correspond to
→ R–R interval: Entire duration of cardiac action potential
→ P–R interval: Time it takes for depolarization from SA node to spread through atria to the ventricles
→ Q–T interval: Entire duration of ventricular AP
What causes the two heart sounds?
1st sound: Closing of AV valves (loudest)
→ 2nd sound: Closing of semilunar valves (more quiet)
What (in general) causes heart failure?
→ Enlargement of the myocardium; heart does not pump efficiently
What symptoms result from left sided heart failure?
→ Blood backs up into lungs
Increased pressure in pulmonary veins causing pulmonary edema (fluid in the lungs)
What symptoms result from right sided heart failure?
→ Edema in extremities, enlarging liver and spleen
cardiac cycle:In which phase do the AV valves open? When do they close?
→ Open during passive ventricular filling (diastole); close during isovolumetric contraction
cardiac cycle:In which phase do the semilunar valves open? When do they close?
→ Open during ventricular ejection; close during isovolumetric relaxation
cardiac cycle:When do we do most of our ventricular filling?
→ Passive ventricular filling
cardiac cycle:What allows the two semilunar valves to open?
→ Pressure in ventricles increases
cardiac cycle:. In which phases does blood volume not change in the ventricles? Why doesn’t it change?
→ Isovolumetric contraction and isovolumetric relaxation — all four valves are closed
How does the sympathetic nervous system increase heart rate?
→ N.Epi released
Causes reduced repolarization of conducting cells
Increases HR
Cardioacceleratory centers
How does the parasympathetic nervous system decrease heart rate?
→ ACh released
Causes hyperpolarization of conducting cells
Decreases HR
Cardioinhibitory centers
when increasing Stroke volume:Does preload increase or decrease?
→ Increase
when increasing Stroke volume:Will afterload increase or decrease?
→ Decrease
when increasing Stroke volume:How will contractility change?
→ Increase
when decrease stroke volume:Does preload increase or decrease
→ Decrease
when decrease stroke volume:Will afterload increase or decrease?
→ Increase
when decrease stroke volume:How will contractility change?
→ Decrease
Understand the relationship between EDV and stroke volume, for example if EDV decreases, how does stroke volume change?
→ Decrease EDV = decrease stroke volume
Also understand the relationship between ESV and stroke volume.
→ Increase ESV = decrease stroke volume
Decrease ESV = increase stroke volume
afterload
→ Pressure ventricles must overcome to open SL valves and eject blood
arrythmia
→ Any variation in the rhythm and sequence in the excitation of the heart
Atrial Fibrillation
→ Atrial — atria beat out of sequence with ventricles
Can lead to formation of blood clots (increase risk of stroke)
Bradycardia
→ Slow HR (<60 bpm)
Cardiac Output
→ Volume of blood pumped per minute
CO = HR × SV
Contractility
→ Force of contraction of the heart
Diastole
→ Relaxation of the heart
Ectopic Pacemaker
→ Other pacemaker cells attempt to pace the heart
Results in irregular rhythms
Ejection Fraction
→ EF = (SV / EDV) × 100
End Diastolic Volume
→ Volume of blood in your ventricles once done with filling
Average is around 120–130 mL
End Systolic Volume
→ Volume of blood after ejection
Average is 50–60 mL
Heart Block
→ Blockages in conducting system
Heart Murmur
→ Abnormal sound heard when listening to heart sounds
Often a defective valve
Preload
→ Amount of stretch in cardiac muscle
Determined by EDV
Sinus Rhythms
→ Electrical rhythms set by the SA node
Stroke Volume
→ Volume of blood pumped per heartbeat
SV = EDV – ESV
Systole
→ Contraction of the heart
Tachycardia
→ High HR (>100 bpm)
Venous Return
→ Volume of blood returning to right atrium from systemic circuit
Ventricular Fibrillation
→ Immediately life-threatening
Electrical activity malfunctions