Heart Anatomy & Conduction (LAB PRACTICAL) Flashcards
Apex & Base of Heart
-Apex: Inferior portion
-Base: Superior portion
Veins
Carry blood to the heart
Arteries
Carry blood away from the heart
Atria
Receive blood from the vena cavae and pulmonary vein
Ventricles
Receive blood from atria, pumps blood into aorta & pulmonary artery
Interatrial septum
Separates atria into left atrium and right atrium
Interventricular septum
Separates ventricles into the left and right ventricles
Four heart valves
-Pulmonary semilunar valve
-Aortic semilunar valve
-Tricuspid valve
-Bicuspid/Mitral valve
Semilunar valves
-Located at openings TO the arteries after ventricles
-Consists of 3 moon-shaped cusps/flaps
-Pushed flat against artery wall during ventricular contraction
-Prevent back flow of blood into the ventricles as ventricles relax
Atrioventricular valves
2 valves located between atria and ventricles
Right atrioventricular valves
Tricuspid: 3 cusps/flaps of endocardium
Left atrioventricular valve
Bicuspid/Mitral Valve
Function of atrioventricular valves
-During diastole, blood flows through valves from atria into ventricles
-During systole, AV valve closes passively as pressure builds in ventricle to prevent back flow into atria
Chordae tendinea
Cords that prevent the inversion of AV valves. Like an umbrella flipping inside out in the wind
Papillary muscle
Anchors the chordae tendineae
Lub sound of heart
Closure of the AV valves at the start of ventricular systole after blood enters ventricles
Dub sound
Closure of the semilunar valves at the end of ventricular systole
Pericardium
Double walled sac of the heart
Systole
Contraction
Diastole
Relaxation
Outer wall of pericardium
Fibrous pericardium
Inner wall of pericardium
Serous pericardium (Double layered)
Parietal pericardium
Outer layer of inner wall that lines the fibrous pericardium
Visceral pericardium
Inner layer of inner wall that forms the outermost layer of the heart wall called the epicardium
Myocardium
-Middle layer of cardiac muscle
-Striated with intercalated discs under involuntary control
-Fibrous skeleton composed of a dense network of fibrous connective tissue that supports the cardiac muscle fibers and heart valves
Epicardium
-Outermost layer of the heart wall
-Visceral pericardium
Endocardium
-Innermost layer of heart muscle
-Made of simple squamous epithelium
Systemic circulation
Carries blood to all tissues for nourishment, then transports deoxygenated blood back to the heart
Pathway of systemic circulation
-Left ventricle
-Aorta
-Arteries
-Arterioles
-Capillaries
-Venules
-Veins
-Vena Cavae
-Right atrium
Pulmonary circulation
Carries deoxygenated blood to the lungs for gas exchange, then brings oxygenated blood back to the heart
Pulmonary circulation pathway
-Right ventricle
-Pulmonary trunk
-Pulmonary arteries
-Capillaries in the lungs
-Left atrium
Intrinsic conduction of the heart
-Composed of noncontractile cardiac pacemaker cells that generate electrical impulses
-Induces myocardium to contract
-Impulse begins at SA node in right atrium
-Change in electric potential (Depolarization) and the generation of action potential results in muscle contraction
-Cardiac muscle cells are connected through gap junctions which allow for the spread action potential
Mechanism of heart contraction
- Sinoatrial node generates impulse
- Impulses pause for 0.1 seconds at the atrioventricular nodes
- Atrioventricular bundle conducts the impulses to the bundle branches
- Bundle branches conduct the impulses through the interventricular septum
- The sub-endocardial conducting network (Purkinje fibers) depolarizrs the contractile cells of both ventricles
Sinoatrial node
-Located in the superior portion of the right atrium
-Sets the depolarization rate (Pacemaker)
-Stimulus travels through atria to cause atrial contraction
-Stimulus reaches AV node
Bundle branches
Conducting nerves in the interventricular septum
Atrioventricular node
-Node located in the inferior atrial septum of the right atrium
-Allows for atrial contraction to be completed before ventricular depolarization begins in order to prevent premature closure of the AV valves
AV Bundle/Bundle of His
Located in interventricular septum
Subendocardial conducting network (Purkinje Fibers)
Found in muscles of the ventricular walls and denser in left ventricle.
Sympathetic nervous system role in heart conduction
Accelerates heart rate
Parasympathetic nervous system role in heart conduction
Decelerates heart rate
Four peak signals of depolarization in electrical conductions
- Depolarization of SA node
- Depolarization and contraction of atrial muscle
- Depolarization of AV node
- Depolarization and contraction of ventricular muscle
P wave
Depolarization of the atria immediately prior to atrial contraction
QRS complex
-Depolarization of ventricles, immediately prior to ventricular contraction.
-Atrial repolarization also happens during ventricular contraction
T wave
Repolarization of ventricles
PR interval
Signal travels from SA node to AV node
PR interval greater than .2 seconds
May indicate partial heart block
prolonged QRS complex
May indicate partial blockage of right or left bundle branch
QT interval
From ventricular depolarization to repolarization
QT interval during increased heart rate
Shorter QT interval
Consequence of prolonged QT interval
Greater risk of ventricular arrhythmia
Junctional Rhythm
-P wave absent
-Signifies SA node is not acting as the pacemaker leading to the AV node to pace the heart
Second degree heart block
-Not all P waves are followed by a QRS complex
-Indicates damage to the AV node
Ventricular fibrillation
-Impulses generated in the atria do not pace ventricular contractions
-Uncoordinated contractions of the myocardium
-Typical in acute myocardial infarction
Bradycardia
A heart rate <60 bpm
Tachycardia
Heart rate >100 bpm
Fibrillation
Rapid uncoordinated contractions
Atherosclerosis
Arteries blocked by fat and cholesterol deposits, reducing blood flow
Cardiac muscle immediately following myocardial infarction
-Loss of striations
-Loss of nuclei
Cardiac muscle 1-2 days after myocardial infarction when healing
-Necrosis of cardiac tissue
-Invasion of neutrophils to phagocytize debris
Cardiac muscle 6+ months after myocardial infraction
-Extensive collagen deposits (scarring)
-Scar tissue is noncontranctile
