Cardiac excitation-contraction coupling


00:00 / 00:00



Cardiac excitation-contraction coupling

Cardiovascular system

Anatomy and physiology

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

Cardiac output

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 and pressure-volume loops

Cardiac cycle

Cardiac work

Pressure-volume loops

Changes in pressure-volume loops

Cardiovascular physiological responses

Physiological changes during exercise

Cardiovascular changes during hemorrhage

Cardiovascular changes during postural change

Auscultation of the heart

Normal heart sounds

Abnormal heart sounds

Myocyte electrophysiology

Action potentials in myocytes

Action potentials in pacemaker cells

Excitability and refractory periods

Cardiac excitation-contraction coupling


Electrical conduction in the heart

Cardiac conduction velocity

ECG basics

ECG normal sinus rhythm

ECG intervals

ECG QRS transition

ECG axis

ECG rate and rhythm

ECG cardiac infarction and ischemia

ECG cardiac hypertrophy and enlargement

Blood pressure regulation



Renin-angiotensin-aldosterone system


Cardiac excitation-contraction coupling


0 / 10 complete

High Yield Notes

7 pages


Cardiac excitation-contraction coupling

of complete

External Links


Content Reviewers

Rishi Desai, MD, MPH


Evan Debevec-McKenney

Tanner Marshall, MS

Justin Ling, MD, MS

Cardiac excitation-contraction coupling is the relationship between electrical signals in the form of action potentials, and mechanical changes in the heart muscle cells, called cardiomyocytes, that causes them to contract.

Let’s start by looking at the structure of a cardiomyocyte. Cardiomyocytes have branches, and have intercalated disks along their edges which have small holes called gap junctions that allow ions to flow from one cardiomyocyte to the next. When a cardiomyocyte depolarizes, ions like calcium move from that cell into a neighboring cell, and these ions trigger depolarization to happen in that cell. This is what makes cardiomyocytes part of a “functional syncytium,” they’re like a little community of cells intimately working together. In addition, cardiomyocytes stay physically attached to one another through proteins called desmosomes, which are like staples that hold the cells together when they’re contracting. Another feature of cardiomyocytes are passageways called transverse tubules, or T-tubules. T-tubules are extensions of the outside environment. They increase the surface area of the cardiomyocyte and they look like the letter T, so it’s easy to remember their name. Think of a large walk-through aquarium: you can walk through tunnels and look at the sea creatures all around you, but you’re not in the water with them. Finally, there’s the sarcoplasmic reticulum, which is an organelle that stores intracellular calcium, the calcium that is sequestered inside the cell.

When a depolarization wavefront hits a cardiomyocyte, a few calcium ions flow through gap junctions, and if a threshold membrane potential is reached, then sodium channels start to open up. If there’s a depolarization, then ions start to move across the cell membrane, and that’s where the T-tubules play a key role. During the part of the cardiomyocyte action potential when calcium ions flow into the cell, the presence of T-tubules helps bring calcium deep into the cell. Once this extracellular calcium gets inside, it binds to the ryanodine receptors on the sarcoplasmic reticulum, which releases even more calcium into the cell - a process called calcium-induced calcium release. The calcium helps activate two contractile proteins, actin and myosin, which are called myofilaments, and are ultimately responsible for cell contraction, and that’s the key moment when the chemical signal is converted into a mechanical signal.


Cardiac excitation-contraction coupling is the process by which an electrical signal generated by the sinoatrial node (the heart's natural pacemaker) is converted into a mechanical force that makes the heart contract. It occurs in a series of events that include:

Excitation: The process by which an electrical signal causes calcium ions to enter the cell.

Calcium is released from the sarcoplasmic reticulum.

Myofilament activation: The released calcium ions bind to troponin C, which causes tropomyosin to move out of the way and expose binding sites on actin for myosin heads. With the help of ATP, the myosin heads then attach to the actin filaments and slide them past each other, shortening the sarcomere (the basic unit of muscle contraction) and leading to cardiac muscle contraction.

Relaxation: The calcium ions are removed from the cytosol by the sarcoplasmic reticulum, and tropomyosin returns to its position blocking the binding sites on actin. This prevents further interaction between myosin and actin, and the muscle relaxes.


  1. "Medical Physiology" Elsevier (2016)
  2. "Physiology" Elsevier (2017)
  3. "Human Anatomy & Physiology" Pearson (2017)
  4. "Principles of Anatomy and Physiology" Wiley (2014)
  5. "Cardiac T-Tubule Microanatomy and Function" Physiological Reviews (2017)

Copyright © 2023 Elsevier, except certain content provided by third parties

Cookies are used by this site.

USMLE® is a joint program of the Federation of State Medical Boards (FSMB) and the National Board of Medical Examiners (NBME). COMLEX-USA® is a registered trademark of The National Board of Osteopathic Medical Examiners, Inc. NCLEX-RN® is a registered trademark of the National Council of State Boards of Nursing, Inc. Test names and other trademarks are the property of the respective trademark holders. None of the trademark holders are endorsed by nor affiliated with Osmosis or this website.