Download 17. CV II - EKG-mechanical.doc

January 15, 2018 | Author: Anonymous | Category: , Science, Health Science, Cardiology
Share Embed

Short Description

Download Download 17. CV II - EKG-mechanical.doc...



Cardiac Muscle: • autorhythmic tissue with branched fibers interconnected by special lowresistance junctions (= intercalated discs = gap junctions) (fig. 18 - 11) • synchronized electrical activity spreads instantaneously as if no intervening cell membranes existed (functional syncytium); wave of electrical activity occurs independently of nervous system and causes the contractile activity of the heart • Action Potential of Cardiac Muscle: spontaneous depolarization with state of prolonged refractoriness; eliminates tetanic contractions (figs. 18 - 12 & 18 - 13) 4.

Pacemaker and Conducting System (fig. 18 - 14): • tissue with fastest rhythm sets the pace of the entire myocardium; heart's electrical system has specialized fibers serving as pacemaker and conducting system: a. Sinoatrial (SA) Node: located in back wall of right atrium; initiates atrial depolarization/repolarization sequence b. Atrioventricular (AV) Node: located in right atrium near interatrial septum and atrioventricular junction; serves as only path for electrical conduction to ventricular myocardium; relays signal after delay of approx. one-tenth second (ensures atrial contraction precedes ventricular contraction) c. Conducting System: AV node conveys signal directly to AV bundle (bundle of His), onward to bundle branches and ultimately to network of Purkinje fibers (distribute signal throughout ventricular myocardium) 5.

Electrocardiography (ECG) (figs. 18 - 16 & 18 - 17): • non-invasive monitoring of heart’s electrical activity; possible due to electrolytic properties of body fluids • typical electrocardiogram features standard deflections: P Wave: signifying atrial depolarization (discharge of pacemaker) QRS Wave or Complex: caused by depolarization of ventricles (atrial repolarization masked by this) T Wave: caused by repolarization of ventricles PR Interval: time elapsed between start of P wave and R wave (period of delay at AV node) (called PQ interval in text) • ECG Leads (12 combinations of electrode placements routinely used) a. 6 limb leads (3 bipolar: I, II, III; 3 unipolar: aVL, aVR, aVF) b. 6 chest leads (all unipolar: V1 - V6) • ECG normal pattern = sinus rhythm • digressions from normal pattern (arrhythmias) signify various disorders: tachycardia (elevated heart rate), bradycardia (depressed heart rate), flutter (rapid rate in a particular chamber), & fibrillation (loss of coordination) • Depressed ST Segment: usually coronary ischemia with angina pectoris

Bio 108/508

lec. 17 - p. 2

• Elevated ST Segment (sometimes accompanied by inverted T wave): usually signifies heart attack (myocardial infarction) • Prolonged PR Interval: various types of heart block • QT Interval: duration of ventricular electrical signal

Bio 108/508

lec. 17 - p. 3


Cardiac Blood Flow : • blood flow is one-way due to operation of valves (AV valves and SL valves) (figs. 18 - 8 to 18 - 10): right atrium --(tricuspid valve)--> right ventricle --(pulmonary valve)--> pulmonary trunk --> lungs --> pulmonary veins --> left atrium--(mitral valve)--> left ventricle --(aortic valve)--> aorta --> body tissues --> venae cavae --> right atrium • valve operation is passive (no muscle tissue); respond to external pressures: a. AV valves open when atrial pressure > ventricular pressure b. AV valves close when atrial pressure < ventricular pressure c. SL valves open when arterial pressure < ventricular pressure d. SL valves close when arterial pressure > ventricular pressure • Pressure Considerations: • pressure rises in a chamber when blood is entering it or the chamber is contracting or recoiling • pressure falls in a chamber when. blood is leaving it or chamber is relaxing 7.


Cardiac Cycle (fig. 18 - 20): a. Systole: contraction of ventricles - ventricular P rises: AV valves close isovolumetric contraction (IVC) - both sets of valves closed ventricular ejection - ventricular P exceeds arterial P and opens SL valves b. Diastole: relaxation of ventricles - ventricular P drops: SL valves close isovolumetric relaxation (IVR) - both sets of valves closed ventricular filling - ventricular P falls below atrial P: AV valves open again

Cardiac Output (fig. 18 - 22): • cardiac output (CO) = heart rate (HR) x stroke volume (SV) • Heart Rate regulated by: • Epinephrine: hormone with positive chronotropic effect • Autonomic Nervous System: sympathetic division (like epinephrine) • parasympathetic division has negative chronotropic effect • Stroke Volume regulated by: • Venous Return: amount of blood returned by veins (preload) • Contractility ( strength of contractions): a. Starling’s law of the heart b. Epinephrine: hormone with positive inotropic effect c. Autonomic Nervous System: sympathetic: positive inotropic effect • parasympathetic: negative inotropic effect • Afterload (factors which obstruct effectiveness of pumping): a. High Arterial Pressure: opposes opening of SL valves b. Enlarged Ventricle: once ventricular radius exceeds certain threshold value, wall tension falls off for a given contractile force c. Valve Disorders: stenosis (improper opening) stifles blood flow; insufficiency (improper closing) allows retrograde flow • detectable by presence of “heart murmur”

View more...


Copyright © 2017 HUGEPDF Inc.