Cardiac cycle

29,120views

Cardiac cycle

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

Transcript

Watch video only

A cardiac cycle is the sequence of mechanical and electrical events that occurs with every heartbeat. Now, the heart is shaped like a cone and it contains two upper chambers, called atria; and two lower chambers, called ventricles.

Now, the left atrium receives oxygenated blood from the lungs via the pulmonary veins; while the right atrium receives deoxygenated blood from all of our organs and tissues via the superior and inferior vena cava.

From the atria, the blood flows into the lower chambers of the heart: the left ventricle, which pumps oxygenated blood to all our organs and tissues via the aorta; and the right ventricle, which pumps the deoxygenated blood back to the lungs via the pulmonary arteries.

Alright, so each heartbeat consists of two phases: systole, which is when the heart contracts and pumps blood out of the ventricles; and diastole, which is when the heart relaxes and ventricles fill with blood. Now, the cardiac cycle graph is used to express events during one cardiac cycle.

Along the y-axis are aortic pressure, left atrial pressure, and left ventricular pressure, heart sounds, ventricular volume, right atrial pressure curve, and ECG; while along the x-axis is time.

But, before we continue, here’s something to keep in mind: since there are no valves separating the right atrium from the superior vena cava and the jugular veins, the jugular venous pulse will follow the same pressure changes as the ones that arise in the right atrium.

In other words, an increase in the atrial pressure will result in an increased jugular venous pulse, and vice versa. Therefore, below the right atrial pressure curve let’s write JVP for jugular venous pulse.

And right above the graph, we’ll write the seven phases of the cardiac cycle. The first phase is the atrial contraction, which lasts about 0.1 seconds.

Next, isovolumetric ventricular contraction, rapid ventricular ejection, reduced ventricular ejection, are phases of ventricular systole and together they last about 0.3 seconds.

The last three phases, isovolumetric ventricular relaxation, rapid ventricular filling, and finally, reduced ventricular filling, also known as diastasis, are phases of ventricular diastole and together they last about 0.4 seconds.

Now, the first phase of the cardiac cycle, atrial contraction, starts with the firing of the sinoatrial, or SA node, which sends an electrical signal that propagates outward through the walls of the heart and depolarizes the atria.

On the ECG, this corresponds to the P wave. Now, atrial depolarization is followed by the contraction of the right and left atrium, and as the atria contract, the pressure within the left atrium increases.

Now, as the atria pumps blood into the ventricle, the ventricular volume increases and therefore the ventricular pressure slightly increases.

At the same time, as the right atrium contracts, an increase in the right atrial pressure will be noted as the a wave on the right atrial pressure curve.

In some conditions, such as ventricular hypertrophy, during this phase, the fourth heart sound (S4) can be heard.

This sound is caused by vibration of the stiffened ventricular wall as the blood is pushed from the atria into the ventricles. The next phase of the cardiac cycle is the isovolumetric contraction.

On the ECG, this phase begins with the appearance of the QRS complex, which represents ventricular depolarization. Ventricular depolarization is followed by ventricular contraction.

But, prior to ventricular contraction, when the pressure within the ventricle exceeds the atrial pressure, atrioventricular valves close, producing the first heart sound (S1).

At this point, both the atrioventricular and aortic and pulmonary valves are closed, so the blood volume within the ventricles remain the same - hence the term “isovolumetric”.

But the ventricles contract, so ventricular pressure increases rapidly. However, in the left ventricle, the pressure doesn’t exceed aortic pressure, so the aortic valve is still closed.

At the same time, there’s a slight increase in the left and right atrial pressure because the increasing ventricular pressure makes the atrioventricular valves bulge into the atria.

This increase in the atrial pressure is registered as the C wave, on both left and right atrial pressure curves.

By the end of isovolumetric contraction, the pressure within the ventricles becomes higher than the pressure within the aorta and pulmonary arteries, so the aortic and pulmonary valves open.

This event marks the start of the next phase - rapid ventricular ejection. This phase is called rapid ventricular ejection due to a sudden ejection of a large amount of blood from the ventricles.

Now, as the left ventricle ejects the blood, the pressure from the left ventricle is equally transmitted to the aorta. In other words, both, ventricular and aortic pressures reach their maximum. At the same time, the volume of blood within the left ventricle decreases sharply.

On the ECG, this phase matches the ST segment - the flat section of the ECG between the end of QRS complex and the beginning of the T wave, which represents the period between ventricular depolarization and ventricular repolarization.

Key Takeaways

The cardiac cycle is a repeating process by which the heart pumps blood into circulation. It consists of two phases: the diastole (relaxation) phase and the systole (contraction) phase.

During diastole, major events include isovolumetric ventricular relaxation and ventricular filling, which enables the heart to relax and ventricles to get filled with blood. During systole, the main events are isovolumetric ventricular contraction and systolic ejection, meaning the heart contracts and pumps the blood out of the ventricles.