Chapter 19 - Heart Flashcards
Layers of Heart
Fibrous Pericardium, Parietal Serous Pericardium, Pericardial Cavity, Visceral Serous Pericardium (Epicardium), Myocardium, Endocardium, Heart Chamber
Pericarditis
Inflammation of the pericardium
Myocardium
Thick muscle layer around heart surrounded by Epicardium and Endocardium
Atria
receiving chambers, small thin walls, contribute little to propulsion of blood
Ventricles
most of volume of heart, thicker walls, actual pumps, especially the left
Functions of heart valves
unidirectional blood flow, open and close in response to pressure, 2 Atrioventricular Valves (Mitral -L and Tricuspid -R)and 2 Semilunar valves (aortic - L and Pulmonary - R)
Valve Open vs Closed
Open = Slack, relaxed; Closed = Taut, Contracted
Pulmonary Circuit
Right side = receives O2 poor blood from tissues and pumps to lungs to exchange CO2 for O2
Systemic Circuit
Left Side = Receives O2 rich blood from lungs and pumps to body tissues
Valve Problems
Incompetent Valve = Heart re-pumps same blood over and over; Valvular Stenosis = Stiff Flaps
Route of blood
Blood enters right atrium via tricuspid AV valve Right ventricle contracts forcing the opening of pulmonary semilunar valve and into pulmonary trunk, sent to lungs. Gets rid of Co2 and pick up 02. Back from lungs and into left atrium via pulmonary veins. Fills Atrium, mitral valve opens and blood fills left ventricle, mitral valve closes into left ventricle. Then through the aortic semilunar valve and into the aorta, aorta delivers 02 rich blood to tissues of body.
Circuit Differences
Pulmonary = low pressure, short and slow; Systemic = High pressure, long and strong
Ventricle Differences
Left side is 3x stronger than right
Angina Pectoris
Thoracic pain caused by fleeting deficiency in blood delivery to myocardium, cells weakened
Myocardial Infarction
Heart Attack, coronary blockages, areas of cell death repaired with scar tissue
Describe Cardiac Muscle
Striated, short branched, interconnected by intercalated discs containing desmosomes and gap junctions, 1 nuclei, many mitochondria,
2 intercellular junctions
Desmosomes - prevent cells from separating; Gap Junctions - allow pass through of ions and allow coordinated movement of single unit
Cardiac Veins
Collect blood from Capillary veins and ensure myocytes get oxygen as well
Cardiac Muscle Contraction
Don’t need nervous system stimulation, automatically, all cardiomyocytes contract as one unit, intercalated discs connected by desmosomes, many mitochondria for aerobic respiration
Autorhythmic Cells
Have unstable resting membrane potentials, pacemaker potentials, due to slow opening of Na+ channels ( Continuously depolarized)
Events of Cardiac Conduction
- Sinoatrial (SA) node (pacemaker) generates impulse. 2. The impulse pauses (.1sec) at the atrioventricular (AV) node 3. The AV Node connects to the AV bundle connects the atria to ventricle 4. The bundle branches conduct the impulses through the interventricular septum 5. The Subendocardial conducting network depolarized the contractile cells of both ventricles.
Arrhythmias
Irregular heart rhythms, uncoordinated atrial and ventricular contractions (defective nodes)
Fibrillation
rapid, irregular contractions; useless for pumping blood, brain death, defibrillation to treat
Defective SA Node
Ectopic focus: abnormal pacemaker; AV node may take over
Defective AV node
Few or no impulses reach ventricles, so heart beats too slow for life - need artificial pacemaker
P Wave
Atrial depolarization initiated by SA Node
Q
With Atrial depolarization complete, short delay
R
Ventricular depolarization begins at Apex, causing the QRS complex
S
Atrial repolarization
ST
Stall after ventricular depolarization is complete
T
Repolarization of ventricle begin at Apex creates T wave
P-R Interval
Beginning of atrial excitation to beginning of ventricular excitation
S-T Segment
Entire ventricular myocardium depolarization
Q-T Interval
Beginning of ventricular depolarization to ventricular repolarization
Lub Dub Sound
Valve closures; First: Bicuspid & Tricuspid, Second: Semilunar Valves, Pause: The filling of blood
Heart Murmurs
Inefficiencies in the valves
Systole
Contraction during cardiac cycle
Diastole
Relaxation during cardiac cycle
Cardiac Cycle
Ventricular Filling: AV valves are open, pressure low; 80% of blood passively flows into ventricles, atrial systole delivers remaining 20%. Ventricular Systole: Ventricles contract, rising ventricular pressure, closing AV Valves, Ejection phase - vent pressure exceeds pressure in large arteries so SL Valve opens. Isovolumetric Relaxation: Ventricules relax, atria relax and filled, backflow of blood in aorta and pulmonary trunk closes SL valves.
Calculation of Cardiac Output
CO = Heart Rate (BPM) x Stroke Volume ( volume of blood pumped out by 1 ventricle with each beat)
Calculation of Stroke Volume
SV = End Diastolic Volume x End Systolic Volume
3 factors to effect Stroke Volume
Preload, Contractibility, Afterload
Preload
Frank-Starling Law of Heart - degree of stretch of cardiac muscle cells before they contract, length-tension relationships. Most important factor in stretch is venous return
Contractibility
Contractile strength of given muscle length, independent of muscle stretch and EDV; increased by sympathetic and Ca2+ influx
Afterload
Pressure ventricles must overcome to eject blood, hypertension increases afterload, resulting in increased ESV and reduced SV
Atrial (Bainbridge) Reflex
Sympathetic reflex initiated by increased venous return and increased atrial filling, stretch receptors stimulates SA Node
Tachycardia
Abnormally fast heart rate, may lead to fibrillation - > 100 beat/min
Bradycardia
Heart rate slower than 60 beats/min; inadequate blood circulation but can also be due to endurance training
Congestive heart failure
progressive condition; CO2 low, circulation inadequate, weakened myocardium caused by atherosclerosis, high BP, myocardial infarction
Fetal Heart Structures
Foramen Ovale connects 2 atria, Arteriosus connects pulmonary trunk to aorta
Age related Changes to Heart
Sclerosis - thickening of flaps; Decline in cardiac reserve; Fibrosis of cardiac muscle; Atherosclerosis
End Diastolic Volume
Volume of blood in ventricles at end of ventricular diastole
End Systolic Volume
Blood in ventricles after systole
Dicrotic Notch
Brief rise in aortic pressure as blood rebounds off close valve.
Cardiac Output (image)
