NURS 8022 Exam 3 Study Guide: Cardiac

STRUCTURE AND FUNCTION OF THE CV AND LYMPHATIC SYSTEMS 1. Understand the basics of cardiac muscle contraction Cross-bridge cycling -Attachment of actin to myosin at the cross bridge -Myosin head molecule undergoes a position change -Causes thin filaments to slide past thick filaments (contraction) Calcium -Is stored in the tubule system and the sarcoplasmic reticulum -Enters the myocardial cell from the interstitial fluid after electrical excitation, which increases membrane permeability to calcium -Diffuses toward the myofibrils, where it binds with troponin Excitation contraction coupling - Is the process by which an action potential triggers the cycle of events, leading to cross-bridge activity and contraction - Requires calcium - Calcium-troponin complex facilitates the contraction process Myocardial relaxation - Is vital to optimal cardiac function as is contraction - Calcium, troponin, and tropomyosin also facilitate relaxation Troponin release of calcium begins myocardial relaxation. 2. Understand cardiac cycle and what each part represents Cardiac cycle -One contraction and one relaxation -Makes up one heartbeat Diastole (D=R) -Relaxation: Ventricles fill Systole (S=C) -Contraction: Blood leaves the ventricles `Phases of the cardiac cycle Phase 1: Atrial systole or ventricular diastole Phase 2: Isovolumetric ventricular systole Phase 3: Ventricular ejection (semilunar valves open) Phase 4: Isovolumetric ventricular relaxation (aortic valve closes) Phase 5: Passive ventricular filling (mitral and tricuspid valves open) • Atrial contraction – deoxygenated blood travels from the atria (top) to the ventricles through the AV valves (triscupid & mitral) • Isovolumetric contraction – pressure from the outside of the heart squeezes, closes the valves • Ventricular ejection – cont pressure makes the deoxygenated blood get pumped out form the right side of heart to the pulmonary veins to the lungs to get them oxygenated • Isovolumetric relaxation – release of the blood to the lungs • Atrial filling – oxygenated blood fills the atria • Ventricular filling, AV valves open, allowing oxygenated blood to enter the heart, L side pumps it all to the body Right Heart Function Left Heart Function Pumps blood through the lungs *pulmonary circulation Pumps oxygenated blood through the systemic circulation Delivers blood to the lungs for oxygenation Delivers metabolic waste products to the lungs, kidneys, & liver Is a LOW pressure system Is a HIGH pressure system 3. Understand EKG basics, waves, and intervals Normal electrocardiogram (ECG) -Sum of all cardiac action potentials P wave: Atrial depolarization (atrial contraction) PR interval: Time from the onset of atrial activation to the onset of ventricular activation (0.12-0.20 sec) QRS complex: Sum of all ventricular depolarizations ST interval: Ventricular myocardium depolarized, represents period between depolarization and depolarization of ventricles QT interval: “Electrical systole” of the ventricles - Varies inversely with the heart rate - Approximates time of ventricular contraction HR can be determined with reciprocal of time interval between each heartbeat - R-R interval 4. Remember the basic of the sequence of blood through the pulmonary system, heart, and systemic circulation, (superior vena cava, to RA, through tricuspid valve, into RV, and so on). As well as were there is oxygenated and unoxygenated blood Unoxygenated (venous) blood from systemic circulation to right atrium (RA) via superior & inferior vena cava RA through right AV (tricuspid) valve to right ventricle (RV) RV through pulmonic semilunar valve (pulmonary valve) to pulmonary artery, to lungs for oxygenation Oxygenated blood enters the left atrium (LA) through the 4 pulmonary veins (two from the left lung and two from the right) LA through the left AV valve (mitral valve) into the left ventricle (LV) LV through the aortic semilunar valve (aortic valve) into the aorta, which delivers it to the entire body 5. Function of atria and ventricle Atria act as primer pumps 80 percent of blood flows directly into ventricle from atria before atrial systole Atrial contraction causes additional 20 percent Normally heart can pump 3-4 times as much blood as is needed Therefore if atria fail, not normally symptomatic patient, unless under stress; ex: exercise 6. Understand volumes, EF, Cardiac output, preload, and afterload Cardiac output Is the volume of blood flowing through either the systemic or the pulmonary circuit Is expressed in liters per minute (L/min) Is calculated: CO = HR x SV Normal adult cardiac output at rest is 5 L/min Factors that affect CO: Preload Afterload Frank Starling Law of the heart Laplace’s Law Ejection fraction Is the amount of blood ejected per beat Normal is 55% or higher stroke volume divided by end-diastolic volume Is an indicator of ventricular function Cardiac Index Definition CO indexed against body size Formula- CI = CO/ BSA Normal value = 2.5-4.0 L/min/m2 Decreased CO/CI Increased CO/CI MI HTN Shock Dec vascular resistance Dec HR Pulmonary edema Dec SV Inc metabolic state Negative inotropes Positive inotropes Cardiac tamponade Hypovolemia Valvular heart disease High PEEP Preload: the pressure generated at the end of diastole also called left ventricular end-diastolic pressure (LVEDP) determined by 2 primary factors -Amount of venous return to the ventricle -Blood left in the ventricle after systole or end-systolic volume When preload exceeds physiologic range, further muscle stretching causes a decline in cardiac output Preload is assessed by measuring the filling pressure of each ventricle RV preload = CVP (central venous pressure) (3-8mmHg) LV preload = PAOP (pulmonary artery occlusion pressure) aka PCWP (2- 15mmHg) Clinical significance Represents fluid returning to the heart aka the “filling pressure” Increased preload represents increased myocardial oxygen consumption or (MVO2) Afterload: Is the resistance to ejection during systole Aortic systolic pressure is a good index of afterload for the left ventricle Decreased afterload: Heart contracts more rapidly Increased afterload: Slows contractions and increases work load Afterload is assessed by measuring the resistance in the ventricle during systolic ejection Right ventricle afterload = PVR (100 -250 dynes/sec/cm-5) Left ventricle afterload = SVR (800-1200dynes/sec/cm-5) Clinical significance: Increased afterload = increased work of the heart and increased oxygen demand Factors that increase afterload - Vasoconstriction - Valvular stenosis - Increased blood volume - Factors that decrease afterload: Vasodilation 7. Know different valves and which type they are Purpose of valves -Ensure one way blood flow Atrioventricular valves (AVs) One-way flow of blood from the atria to the ventricles Tricuspid valve: 3 leaflets or cusps Bicuspid (mitral) valve: 2 leaflets or cusps Semilunar valves One-way flow from the ventricles to either the pulmonary artery or to the aorta Pulmonic semilunar valve Aortic semilunar valve HEART SOUNDS No sound with opening of valves Heart sounds a result of valve closure and vibration of surrounding fluids under sudden pressure changes - 1st Heart Sound is low in pitch and long-lasting - Closure of the A-V valves - 2nd Heart Sound is a rapid snap - Closure of the semilunar valves - 3rd Heart Sound - Very low pitch - Caused by inrushing of blood into ventricles - 4th Heart Sound - Atrial contraction late in diastole - Hard to hear with stethoscope except in hypertensive patients with a thick left ventricle 8. Potassium and calcium do what to the heart Excess K+ decreases contractility - Cause heart to become dilated and flaccid, slows heart rate - Rise to just 2-3 times normal (8-12mEq/L) can lead to death Excess Ca++ causes spastic contraction, and low Ca++ causes cardiac dilation - Calcium abnormalities not as big of a concern as potassium because blood levels more regulated 9. Understand electrical pathway of the heart – basics. Know different nodes and what they do PATHWAY OF HEARTBEAT Begins in the sinoatrial (S-A) node Internodal pathway to atrioventricular (A-V) node Impulse delayed in A-V node and bundle (allows atria to contract before ventricles) A-V bundle takes impulse into ventricles Left and right bundles of Purkinje fibers take impulses to all parts of ventricles SA NODE Normal rate of discharge in sinus node is 60-100/min.; A-V node - 40-60/min.; Ventricular rate- 20-40/min. Sinus node is pacemaker because of its faster discharge rate Rhythmic beating of heart originates in the modified muscle fiber of SA node -Located in rt atrium near entry of superior vena cava Spontaneously depolarizes from 60-100bpm Impulses spread rapidly from SA node along individual atrial muscle cells to depolarize the right and left atria Causes atrial contraction A-V NODE Located in posterior wall of right atrium immediately behind tricuspid valve Delays cardiac impulse Most delay is in A-V node Designed so that impulse does not travel too quickly from atria to ventricle, allowing time for atria to empty blood into the ventricles, before ventricular contraction begins. A-V BUNDLES Normally one-way conduction through the bundles. Only conducting path between atria and ventricles is A-V node - A-V bundle Divides into left and right bundles Transmission time between A-V bundles and last of ventricular fibers is 0.06 second (QRS time) 10. Know sympathetic and parasympathetic effects on the heart Sympathetic Parasympathetic -causes increases HR and increases -decreases HR markedly and decreases contractility Norepinephrine and epinephrine Increases electrical conductivity and the strength of the myocardial contraction Releases norepinephrine at sympathetic ending Causes increased SA node discharge Increases rate of conduction of impulse Increases force of contraction in atria and ventricles contractility slightly. Vagal fibers go mainly to atria Acetylcholine Slows conduction of action potentials through the heart, and reduces the strength of contraction Parasympathetic (vagal) nerves, which release acetylcholine at their endings, innervate S-A node and A-V junctional fibers proximal to A-V node Causes hyperpolarization because of increased K+ permeability in response to acetylcholine This causes decreased transmission of impulses reducing HR, or temporarily stopping heart rate Cholinergic receptors NT = Acetylcholine -2 types 1. Muscarinic receptors 2.Nicotinic receptors -only involved in muscle contraction; NMJ Adrenergic receptor function: controls HR α- or β-adrenergic receptors Alpha 1 - direct response activity or muscle tone of cell is increased Located on all vascular smooth muscle; GI and urinary sphincters; dilator muscle of the iris; and arrestor pili muscles of the hair follicles Norepinephrine binds with alpha 1 receptors causing smooth muscle contraction and vasoconstriction of the peripheral arteries (direct or stimulating effect) Subtype of alpha 2 receptor, alpha 2a- located in sympathetic ganglia and nerve terminals Norepinephrine binding with these receptors inhibits release of more norepinephrine Promotes more vasodilation providing another “safety mechanism” to prevent excess blood pressure elevation Beta-1 normal heart (“1 Heart= Beta-1) Activation leads to increases in contractile force and heart rate Located on cardiac pacemaker, myocardium, salivary gland ducts, scribe and apocrine sweat glands Norepinephrine and Epinephrine Beta-2- vascular and nonvascular smooth muscle (“2 lungs = Beta-2) Regulatory; inverse response of cell (stimulation =decreased activity or muscle tone of the cell is decreased) Located on smooth muscle; GI tract, urinary bladder, skeletal muscle arteries, bronchial tree, and some coronary arteries Epinephrine mostly, only interacts with norepinephrine released from the adrenal gland not from nerve endings Activation leads to vascular and nonvascular smooth muscle relaxation β3 receptors Decrease myocardial contractility (negative inotropic effect) May provide a “safety mechanism” to prevent an overstimulation of the heart by the sympathetic nervous system. Stimulation of both the β1 and β2: Increases the heart rate (chronotropy) and force of the myocardial contraction (inotropy) If the heart rate is affected, then the effect is called chronotropy - Negative chronotropy: Decreases heart rate - Positive chronotropy: Increases heart rate If the heart contraction is affected, then the effect is called inotropy - Negative inotropy: Decreases force of contraction Acetylcholine released from the vagus nerve - Positive inotropy: Increases force of contraction Norepinephrine from the sympathetic nerves supplying the heart Epinephrine from the adrenal medulla. Thyroid hormone and dopamine **hypoxia dec contractility 11. Understand basics about capillary hydrostatic pressure, plasma oncotic/colloid pressure, interstitial pressure, and interstitial fluid oncotic/colloid pressure = Starling forces - Starling Forces 4: 1. Hydrostatic pressure in the capillary 2. Hydrostatic pressure in the interstitium 3. Oncotic pressure in the capillary 4. Oncotic pressure in the interstitium Frank-Starling Law Related to the volume of blood at the end of diastole/ preload and stretch placed on the ventricle *** More stretch = Increased force of contraction - Greater stretch during diastole = greater force of contraction = greater amt of blood pumped out Laplace’s law Contractile force within a chamber depends on the radius of the chamber and the thickness of its wall - Smaller chambers and thicker chamber walls equal increased contraction force - In ventricular dilation, the force needed to maintain ventricular pressure lessens available contractile force Poiseuille’s law o Greater the resistance, the lower the blood flow. Pressure o Force is exerted on a liquid per unit area. Resistance o Is the opposition to blood flow. o Diameter and length of the blood vessels contribute to resistance. o Vessel radius or diameter greatly affects resistance. Velocity o Is the distance blood travels in a unit of time. Viscosity o Thick fluids move more slowly and cause greater resistance to flow than thin fluids. o High hematocrit reduces the flow through the blood vessels. Laminar and Turbulent Flow