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Heart pt.2

A&P II Chapter 20

QuestionAnswer
Systole Depolarization, squeeze, positive, Higher BP number (120mmHg is Ideal) contraction
Diastole Repolarization, relax, resting, lower BP
membrane potential polarity (1/1000 of a volt)
Cardiac Cycle Relies on Electricity, measured on ECG/EKG Excitation = contraction of monocytes Higher BP causes Valves to open and close
Heartbeat single cardiac contraction all heart chambers contract in series 1st atria 2nd ventricles
route of electrical conduction through myocardium
Rhythmicity regular heartbeat
Automaticity heart makes its own electricity through ATP Spontaneously pump via pacemaker cells (generators)
Cardiac Myocytes connected by intercalated discs (only in cardiac) and gap junctions small size, will sync with each other, 1 central nucleus branching interconnections between cells
Intercalated Discs connect cardiac contractive discs secured by desmosomes (spot welds) linked by gap junctions for ion movement convey force of contraction make ATP (electricity)
Two types of Cardiac Myocytes 1. Conductive Cells 2. Contractile Cells
Conductive Cells nodes and electrical branches of autorhythmric cells Modified cardiac myocytes distribute action potentials (electric messages)
Contractile Cells systole cardiac muscle cells, produce contractions calcium dependent
Cardiac Action Potential Phases Phase 0. Depolarization Phase 1. Brief (early) Repolarization Phase 2. Plateau Phase 3. Repolarization Phase 4. Diastole/Rest Absolute Refractory Period Relative Refractory Period
Conduction Pathway of Electricity Sinoatrial node, internodal tracts & Brachman's Bundle, Atrioventricular Node, Atrioventricular bundle of His, Left and Right Bundle Brackets, Purkinje Fibers
Sinoatrial Node always firing an action potential highest rate of spontaneous depolarization and sets the pace in post wall of R. atrium near entrance of superior Vena Cava
Sinus Rhythm normal electrical pattern established by SA node
Pacemaker prepotential/ SA node nodes are always in state of slow depolarization SA & AV nodes dont have a stable resting membrane potential Action potential results to spontaneous depolarization of SA node
Approaching threshold in nodes Constant and slow influx of Na, causes nodes to try and approach threshold Ca2+ channels open (Na+ Close) is leaving the cell
"funny currents" control beginning of depolarization of SA node
AV node delays 100ms, due to small diameter of AV cells allows atria to contract before ventricle contract -spreads to ventricular myocardium so ventricles can begin contraction MAX AP limit = 230/min, higher= damage
AV Bundle of His connects atria to the ventricles electrically
Left and Right Bundle Branches extend towards apex & fan out to reach Purkinje Fibers, send impulse through moderator band to papillary muscles of R Ventricle
Purkinje Fibers fast conductors that reach all ventricular myocytes
Cardiac Cycle start of one heartbeat to the start of another one all chambers in the heart experience alternate periods of contraction and relaxation
5 phases of Systole and Diastole 1. Atrial Systole (Atrial depol. & contract) 2. Early Ventricular Systole (Vent. depol,) 3. Late Ventricular systole (ventricular ejection) 4. Early ventricular diastole( vent. repol) 5. Late Ventricular diastole (passive vent. filling)
Early Ventricular Systole Ventricular depolarization, Iso volumetric ventricular contraction, S1-lub
Early Ventricular Diastole Ventricular repolarization, Iso volumetric ventricular S2- dub
Blood Pressure and Flow BP in each chamber: rises during systole falls during diastole blood flows high to low pressure -controlled by timing of contractions directed by one- way valves
Cardiac Output amount of blood the heart pumps out in 1 min indicates blood flow through peripheral tissues =health of ventricles HRxSV=CO
Stroke Volume amount of blood pumped out of ventricle during each contraction SV= EDV-ESV
End diastolic Volume (EDV) amount of blood in each ventricle @ end of vent diastole
End Sytolic Volume (ESV0 amount of blood in each ventricle @ end of vent systole
Ejection Fraction percentage of EDV during contraction (60-80% usually)
Factors effecting stroke volume 1.Preload (tension/stretch) due to filling of blood in vent= more volume=more preload 2. Contractility- force of ventricular contraction 3. Afterload- obstacles like pressure that vent must overcome to force semilunar valves open & eject blood
High BP bad bc resistance
Normal HR young adult females- 72-80bpm young adult male- 64-72bpm
Ecoptic Pacemaker abnormal cells generate high rate of APs bypasses conducting system disrupts timing of ventricular contractions
Neurotransmitters change cardiac output Norepinephrine- used by SNS -speeds up HR (more O2) Acetylcholine- used by PNS -slows HR via Vagus nerve
Intropic agents affect contractility of the heart + factors strengthen heart contraction (more Ca2+) - factors weaken heart contraction (less Ca2+)
Chrontropic agents influence HR + increase HR - decrease HR affect electrical conduction system of the heart by affecting nodes
Right Sided Heart Failure R. Ventricular Fail -vena cava backup and swelling Systemic edema (esp; legs and feet), enlarged liver and spleen, JVD, ascites
Left Sided Heart Failure L. ventricular fail pulmonary backup and drown SOB, pulmonary edema, coughing
Created by: treylowrey1
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