Action potentials in pacemaker cells

47,575views

Action potentials in pacemaker cells

ETP CVS

ETP CVS

Introduction to the cardiovascular system
Anatomy of the heart
Anatomy of the coronary circulation
Anatomy clinical correlates: Heart
Anatomy of the superior mediastinum
Anatomy of the inferior mediastinum
Anatomy clinical correlates: Mediastinum
Development of the cardiovascular system
Fetal circulation
Cardiac muscle histology
Artery and vein histology
Arteriole, venule and capillary histology
Cardiovascular system anatomy and physiology
Lymphatic system anatomy and physiology
Coronary circulation
Blood pressure, blood flow, and resistance
Pressures in the cardiovascular system
Laminar flow and Reynolds number
Resistance to blood flow
Compliance of blood vessels
Control of blood flow circulation
Microcirculation and Starling forces
Measuring cardiac output (Fick principle)
Stroke volume, ejection fraction, and cardiac output
Cardiac contractility
Frank-Starling relationship
Cardiac preload
Cardiac afterload
Law of Laplace
Cardiac and vascular function curves
Altering cardiac and vascular function curves
Cardiac cycle
Cardiac work
Pressure-volume loops
Changes in pressure-volume loops
Physiological changes during exercise
Cardiovascular changes during hemorrhage
Cardiovascular changes during postural change
Normal heart sounds
Abnormal heart sounds
Action potentials in myocytes
Action potentials in pacemaker cells
Excitability and refractory periods
Cardiac excitation-contraction coupling
Cardiac conduction system
Cardiac conduction velocity
ECG basics
ECG rate and rhythm
ECG intervals
ECG QRS transition
ECG axis
ECG normal sinus rhythm
ECG cardiac infarction and ischemia
ECG cardiac hypertrophy and enlargement
Baroreceptors
Chemoreceptors
Renin-angiotensin-aldosterone system
Arterial disease
Angina pectoris
Stable angina
Unstable angina
Myocardial infarction
Prinzmetal angina
Coronary steal syndrome
Peripheral artery disease
Subclavian steal syndrome
Aneurysms
Aortic dissection
Vasculitis
Hypertension
Hypertensive emergency
Conn syndrome
Hypotension
Orthostatic hypotension
Abetalipoproteinemia
Familial hypercholesterolemia
Hypertriglyceridemia
Hyperlipidemia
Chronic venous insufficiency
Thrombophlebitis
Deep vein thrombosis
Lymphedema
Lymphangioma
Shock
Vascular tumors
Human herpesvirus 8 (Kaposi sarcoma)
Angiosarcomas
Persistent truncus arteriosus
Transposition of the great vessels
Total anomalous pulmonary venous return
Hypoplastic left heart syndrome
Atrial septal defect
Coarctation of the aorta
Patent ductus arteriosus
Tetralogy of Fallot
Ventricular septal defect
Atrial flutter
Atrial fibrillation
Premature atrial contraction
Atrioventricular nodal reentrant tachycardia (AVNRT)
Wolff-Parkinson-White syndrome
Ventricular tachycardia
Brugada syndrome
Premature ventricular contraction
Long QT syndrome and Torsade de pointes
Ventricular fibrillation
Atrioventricular block
Bundle branch block
Pulseless electrical activity
Tricuspid valve disease
Pulmonary valve disease
Mitral valve disease
Aortic valve disease
Dilated cardiomyopathy
Restrictive cardiomyopathy
Hypertrophic cardiomyopathy
Heart failure
Cor pulmonale
Endocarditis
Myocarditis
Rheumatic heart disease
Pericarditis and pericardial effusion
Cardiac tamponade
Dressler syndrome
Cardiac tumors
Acyanotic congenital heart defects: Pathology review
Cyanotic congenital heart defects: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Coronary artery disease: Pathology review
Peripheral artery disease: Pathology review
Valvular heart disease: Pathology review
Cardiomyopathies: Pathology review
Heart failure: Pathology review
Supraventricular arrhythmias: Pathology review
Ventricular arrhythmias: Pathology review
Heart blocks: Pathology review
Aortic dissections and aneurysms: Pathology review
Pericardial disease: Pathology review
Endocarditis: Pathology review
Hypertension: Pathology review
Shock: Pathology review
Vasculitis: Pathology review
Cardiac and vascular tumors: Pathology review
Dyslipidemias: Pathology review
Sympatholytics: Alpha-2 agonists
Adrenergic antagonists: Presynaptic
Adrenergic antagonists: Alpha blockers
Adrenergic antagonists: Beta blockers
ACE inhibitors, ARBs and direct renin inhibitors
Thiazide and thiazide-like diuretics
Calcium channel blockers
cGMP mediated smooth muscle vasodilators
Class I antiarrhythmics: Sodium channel blockers
Class II antiarrhythmics: Beta blockers
Class III antiarrhythmics: Potassium channel blockers
Class IV antiarrhythmics: Calcium channel blockers and others
Lipid-lowering medications: Statins
Lipid-lowering medications: Fibrates
Miscellaneous lipid-lowering medications
Positive inotropic medications
Cardiomyopathies: Clinical
Congenital heart defects: Clinical
Valvular heart disease: Clinical
Infective endocarditis: Clinical
Pericardial disease: Clinical
Chest trauma: Clinical
Hypertension: Clinical
Pulmonary hypertension
Aortic aneurysms and dissections: Clinical
Raynaud phenomenon
Peripheral vascular disease: Clinical
Heart failure: Clinical
Coronary artery disease: Clinical
Deep vein thrombosis and pulmonary embolism: Pathology review
Fascia, vessels and nerves of the upper limb
Vessels and nerves of the forearm
Vessels and nerves of the hand
Anatomy of the abdominal viscera: Blood supply of the foregut, midgut and hindgut
Fascia, vessels and nerves of the lower limb
Vessels and nerves of the gluteal region and posterior thigh
Anatomy of the popliteal fossa
Ventilation
Ventilation-perfusion ratios and V/Q mismatch
Gas exchange in the lungs, blood and tissues
Oxygen binding capacity and oxygen content
Oxygen-hemoglobin dissociation curve
Carbon dioxide transport in blood
Trypanosoma cruzi (Chagas disease)
Yellow fever virus
Rickettsia rickettsii (Rocky Mountain spotted fever) and other Rickettsia species
Arteriovenous malformation
Cerebral circulation

Flashcards

Action potentials in pacemaker cells

0 of 15 complete

Questions

USMLE® Step 1 style questions USMLE

0 of 1 complete

During an evaluation of the action potential of the heart, some cells were identified to be responsible for the rate of the heart. These cells are located in the right atrium near the opening of the superior vena cava. The action potential of these cells is recorded and shown below. It was found that the slope of phase 4 (marked with the blue dot) determines the rate at which the heart contracts. Which of the following events occur during this phase?  

Transcript

Watch video only

Action potentials are the really rapid electrical changes that occur across the membrane of certain cells, and often propagates from one cell to an adjacent cell. Cells in the heart communicate this way. That signal’s gotta start somewhere, so some of these cells, called pacemaker cells, have the responsibility of setting the rhythm and the pace of the heartbeat. They’ve got this really important job, but they’re a relatively tiny group -- only about 1% of the heart cells -- and they’re able to continually generate new action potentials that get conducted to the rest of the heart -- the other 99% -- and that’s what tells the heart pump. Now, pacemaker cells also listen to which usually come from neighboring pacemaker cells. But if those don’t come, then a pacemaker cell will simply launch its own and that action potential will then spread around. This is called automaticity, and that’s easy to remember because it’s got “automatic” right in it.

So let’s start by mapping out those pacemaker cells. The first clump of pacemaker cells is tucked up here into the corner of the right atria, and that’s the sinoatrial node, which sometimes gets called the SA node. We’ve also got pacemaker cells in internodal tracts between nodes, in the atrioventricular, or AV node, the Bundle of His, and the Purkinje fibers, and that’s our electrical conduction system.

And all around these pacemaker cells are heart muscle cells or cardiomyocytes and they pick up the action potential too, but that happens just a tiny bit more slowly -- we can think of these bands of pacemaker cells as highways that carry the action potential to its destination super fast, and then the muscle cells are like little side roads where it’s slower. That’s important because we want all of the myocytes to pick up that action potential and contract at the same time. We call this whole system a functional syncytium, which means that the mechanical, chemical, and electrical connections between these cells allow them to act as one unit in some ways, and it’s the pacemaker cells that make that happen.

Okay, now let’s take a closer look at the chemistry that gets that action potential moving. Action potentials are initiated by depolarization, which is the opposite of polarization. Polarization is when there’s a higher negative charge inside the cell relative to outside the cell, and that difference in charge is called the membrane potential. So if the membrane potential is negative the inside of the cell is more negative than the outside, if it’s positive the inside is more positive than the outside, and if it’s 0mV, then the inside and outside have the same charge - there’s 0mV of difference. Ok -- so, the key here is understanding how the membrane potential changes, and it all comes down to the movement of ions. Specifically, two factors -- which ion wants to move across the membrane, and how permeable the membrane is to that ion. So, depolarization is when ions move across the membrane and the membrane potential becomes less negative or even slightly positive.

Think of a really pessimistic negative cell throwing his hands up and enjoying a moment of joy. When one cell depolarizes enough - it can cause some ions to flow into neighboring cells and trigger them to depolarize as well. If one cell after another depolarizes, then there’s a depolarization wave which you can imagine would look like a wave moving through a crowd at a football stadium. Each depolarization wave causes heart muscle contraction, so the rate at which depolarization waves ripple through the heart actually sets the heart rate. So if depolarization waves are going through about once per second, that means that your heart beats once per second, or sixty times in a minute.

Key Takeaways

Action potentials are voltage changes that propagate along the surface of cells. In the heart, they are generated by specialized cell structures called pacemaker cells, which use them to control the rhythmic contraction of muscles.

In cardiac pacemaker cells, action potentials occur when specialized channels in the cell membrane open and allow ions to flow into or out of the cell. This change in electric charge makes the cell more positive on the inside, which attracts more ions from neighboring cells and triggers a chain reaction that propagates the action potential along the heart muscle. This eventually leads to the contraction of the heart and pumps blood around our bodies.

Sources

  1. "Medical Physiology" Elsevier (2016)
  2. "Physiology" Elsevier (2017)
  3. "Human Anatomy & Physiology" Pearson (2017)
  4. "Principles of Anatomy and Physiology" Wiley (2014)
  5. "How does the shape of the cardiac action potential control calcium signaling and contraction in the heart?" Journal of Molecular and Cellular Cardiology (2010)
  6. "The Role of the Funny Current in Pacemaker Activity" Circulation Research (2010)
  7. "Impact of Sarcoplasmic Reticulum Calcium Release on Calcium Dynamics and Action Potential Morphology in Human Atrial Myocytes: A Computational Study" PLoS Computational Biology (2011)