EvCC 3rd Qtr Cardiac Exam
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| What are the 3 structures of the heart? | Pericardium, myocardium, and endocardium
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| Describe the pericardium | double walled sac: parietal & visceral layers
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| What is the name for the outer most layer of the heart? | Pericardium
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| What is the name for the middle layer of the heart? | Myocardium
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| What is the name for the inner layer of the heart? | Endocardium
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| Which layer is the muscular layer? | Myocardium (middle layer)
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| Describe the Endothelium layer of the heart | Vascular layer that is 1 cell thick, contributes to hemostatic process and can regenerate, repair, and remodel itself.
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| Which chemicals cause local vasodilation? | nitric oxide & prostacyclin
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| Which checmicals cause local vasoconstriction? | endothelin, serotonin & angiotensin II
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| What is the hemostatic process? | blood clotting
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| What is collateral recirculation? | process of regerating, repairing, and remodeling of the endothelium
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| Which layer contain the "nodes?" | Myocardium
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| What is automaticity? | Ability of specialized cells in the conduction system to spontaneously initiate an impulse
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| What is excitability? | Ability of cardiac cells to respond to an electrical impulse-->action potential
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| What is conductivity? | Ability of excited cardiac cells to transmit an electrical impulse to the next cardiac cell
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| What does polarized mean? | Cell is at REST. No electrical activity. INSIDE of cell is more negative than outside of cell. More POTASSIUM concentrated INSIDE the cell and more SODIUM concentrated OUTSIDE the cell
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| What is depolarization? | Allows electrical impulse to spread throughout myocardial tissue. Sodium rushes INTO the cell and makes it more POSITIVE on the inside
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| What is repolarization? | Returns cells to resting or relaxed state. The cell CTOPS the flow of sodium into the cell so that the INSIDE of the cell is more NEGATIVE than the outside.
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| What is the role of calcium? | During DEPOLARIZATION, the cell membrane allows calcium to ENTER. Important for cardiac muscle contraction
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| When are the heart cells at REST? | When the heart is polarized
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| When are the heart cells actively sending electrical impulses throughout the myocardial tissues? | During depolarization
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| When is the OUTSIDE of the cell more POSITIVE? | polarized
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| When is sodium more concentrated on the OUTSIDE of the cell? | polarized
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| When does sodium rush INTO the cell? | during depolarization
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| During which phase does the cell stop the flow of sodium into the cell? | During repolarization
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| In which phase is the cell more permeabile to potassium? | During repolarization
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| Which node is located in the right upper atrium? | SA node (pacemaker)
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| How fast does the SA node fire? | 60-100 times/min
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| Which node is located in the floor of the right atrium above the TRICUSPID valve? | AV node/junction
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| How fast does the AV node/junction fire? | 40-60 times/min
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| What slows/delays the impulse between atria & ventricles to allow time for the atria to empty? | AV node/junction
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| What is the Bundle of His? | It receives impulses from the AV node and relays it to the right & left bundle branches
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| Where is the Bundle of His located? | Top portion of interventricular septum
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| What are the purkinje fibers? | Distal/terminal branches of the right bundle branch (RBB) and left bundle branch (LBB)
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| How fast do the purkinje fibers fire? | 20-40 times/min
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| What is the funciton of the purkinje fibers? | They are multiple brances to provide electrical excitation to both ventricles
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| What is the path of electrical impulses? | SA node-->AV node-->Bundle of His-->Purkinje transmission
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| Where do the superior/inferior vena cava flow? | Into the right atrium
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| Which chamber leads to the aorta? | Left ventrical
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| What is the re-entry phenomenon? | absolute refractory period that ensures the cardiac muscle is completely relaxed before another action potential can be initiated
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| Which absolute refractory period is shorter? | The atria is shorter
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| Why is the absolute refractory period of the atria shorter? | To allow the atrial contraction to be faster than the ventricular contractions
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| When is the relative refractory period? | It follows the absolute refractory period near the END of repolarization
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| When is it possible for cardiac muscle cells to be depolarized again, but ONLY by a greater than normal stimulus? (BEAR) | During the RELATIVE refractory period
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| What are sarcomeres? | Actin & myosin filaments parallel to each other
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| What causes shortening & contraction of myofibril? | Cross bridges of myosin pulls actin towards the center of the sarcomere
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| What inhibits the ability of actin to connect with myosin? | Troponin & Tropomyosin
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| Which sound is systole? | S1
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| Which sound is diastole? | S2
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| Which phase is systole? | Contraction of the muscles
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| Which phase is diastole? | Resting period between contractions
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| What causes the sound of S1 (the beginning of systole)? | When the increase in intraventricular pressure during a contraction exceeds the pressure in the atria, causing the AV vales to close
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| What causes the sound of S2 (the end of systole)? | The ventricles begin to relax causing the pressure within the heart to be less than that of the aorta & pulmonary arteries which closes the semilunar valves
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| Where is S1 heard best? | At the location of the mitral(apex) and tricuspic valves (Left 5th intercostal space)
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| Where is S2 heard best? | At the aortic & pulmonic valve area (L/R 2nd intercostal space)
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| Where are S3 & S4 murmurs heard best? | At the mitral area (apex)
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| What is the definition of cardiac output? | The amount of blood pumped from the left ventricle per minute
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| What is the definition of stroke volume? | The volume of blood ejected from left ventricle with each contraction
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| What is a normal 150 lb adult cardiac output (CO)? | 5-6 Liters per minute
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| What is preload? | The degree of muscle fiber stretch that occurs as a result of load or tension placed on the muscle of the left ventricle before contraction.
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| What is afterload? | The resistance to blood flow as it leaves the left ventricle
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| What is the Frank-Starling law? | The greater the stretch the stronger the contraction
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| What is cardiac reserve? | The ability of the heart to quickly adjust stroke volume and HR to meet increased demands placed upon it
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| What is contractility? | The ability of myocardium to contract in an organized and vigorous manner
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| How does the heart compensate for increased demands? | By quickly adjusting the stroke volume and HR
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| What is systolic pressure? | The amount of pressure exerted against aterial walls as the heart ejects blood out into systemic circulation
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| What is diastolic pressure? | The amount of pressure exerted against arterial walls as the heart relaxes
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| What is pulse pressure? | The difference between the systolic and diastolic pressures
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| What is mean arterial pressure? | The average amount of pressure exerted against ateries during one complete heartbeat (cardiac cycle)
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| What are baroreceptors? | Nerve endings sensitive to pressure changes in ateries.
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| Where are baroreceptors located? | in the aortic arch, carotid arteries & right atrium
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| How do the baroreceptors function? | When increased stretch in the arteries are sensed, an impulse is sent to the medulla to stimulate the parasympathetic NS, which decreases sympathetic activity
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| What are chemoreceptors? | Receptors located in the aortic arch & carotid bodies that are sensitive to the amount of CO2, O2, hydrogen ions in the blood.
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| What happens when the chemoreceptors sense and increase in CO2 or a decrease in O2 or pH? | The impulse is sent to the medulla to stimulate the sympathetic NS
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| What affect does the sympathetic NS have on the heart? | Stimulating effect
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| What affect does the parasympathetic NS have on the heart? | Inhibiting effect
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| What happens when the sympathetic NS is stimulated? | The nerve endings release norepinephrine which increases HR, increases the conduction through the AV node, increases atrial & ventricular contractions
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| What happens during Fight or flight? | Norepinephrine is released to increase HR and atrial & ventricular contractions
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| What does the chronotrophic stimulation cause? | increases HR
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| What does the inotropic stimulation cause? | increased myocardial contractions
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| Which nerve endings innervate the SA node, AV node and purkinje fibers? | Vagus nerve
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| When the parasympathetic NS is triggered, what is the effect? | It releases acetylcholine which decreases SA node discharge & conduction through atria, thus decreasing HR & strength of contractions
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| When the sympathetic nervous system stimulates the adrenal medulla, what is released? | Catecholamines (norepinephrine & epinephrine)that interact with adrenergic receptors to produce physiologic effects
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| How does the renin-angiotensin-aldosterone system (RAAS) work? | Renin converts angiotensinogen to angiotensin I
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| What converts angiotensin * to angiotensis II & III? | ACE
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| What does the activation of the RAAS lead to? | the release of aldosterone & ADH, reabsorption of sodium, increase in plasma volume, and vasoconstriction?
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| Does the activation of RAAS cause vasoconstriction or vasodilation? | Vasoconstriction
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| What causes the arteries & aorta to become stiff and rigid as we age? | A decrease in elastic fibers and calcium deposits in the medial layer of arteries
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| How does aging affect the baroreceptors? | It decreases their sensitivity
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| What affect does aging have on the beta-adrenergic stimulation? | It decreases the response
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| What happens to the valves, endocardium & myocardium with aging? | The are thickened
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| Afterload | the force against which a ventricle contracts that is contributed to by the vascular resistance especially of the arteries and by the physical characteristics (as mass and viscosity) of the blood
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| Antiarrythmics | medications to counteract or prevent cardiac arrhythmias
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| arrythmia | an alteration in rhythm of the heartbeat either in time or force
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| Asystole | a condition of weakening or cessation of systole
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| Atrium | an anatomical cavity or passage; especially : a chamber of the heart that receives blood from the veins and forces it into a ventricle or ventricles
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| Atrial Fibrillation | very rapid uncoordinated contractions of the atria of the heart resulting in a lack of synchronism between heartbeat and pulse beat -- called also auricular fibrillation
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| Atrial Flutter | an irregularity of the heartbeat in which the contractions of the atrium exceed in number those of the ventricle -- called also auricular flutter
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| AV Node | small mass of tissue in the wall of the right atrium adjacent to the septum between atria, passes impulses from sinoatrial node to ventricles thru the bundle of His, and in some pathological states replaces the sinoatrial node as pacemaker of the heart
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| Baroreceptors | a sensory nerve ending especially in the walls of large arteries (as the carotid sinus and arch of the aorta) that is sensitive to changes in blood pressure -- called also pressoreceptor
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| beta adrenergic | of, relating to, or being a beta-receptor <a beta-adrenergic blocking agent>
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| bradycardia | relatively slow heart action whether physiological or pathological
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| bundle of His | modified cardiac muscle that passes from atrioventricular node in the right atrium to the right & left ventricles via the septum and that maintains the normal sequence of the heartbeat by conducting the wave of excitation from right atrium to ventricles
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| cardiac output | the volume of blood ejected from the left side of the heart in one minute -- called also minute volume
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| cardiomyopathy | disease of heart muscle marked by hypertrophy of cardiac muscle, enlarged heart, rigidity & loss of flexibility of the walls, or by narrowing of the ventricles not due to congenital dvlpmntl defect, coronary atherosclerosis, valve dysfunction, or HTN
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| cellulitis | diffuse and especially subcutaneous inflammation of connective tissue
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| chemoreceptors | a sense organ (as a taste bud) responding to chemical stimuli
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| Coronary Artery Disease (CAD) | a condition and especially one caused by atherosclerosis that reduces the blood flow through the coronary arteries to the heart muscle and typically results in chest pain or heart damage -- called also coronary disease, coronary heart disease
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| diuretics | an agent that increases the excretion of urine
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| dysrhythmia | an abnormal rhythm; especially : a disordered rhythm exhibited in a record of electrical activity of the brain or heart
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| edema | an abnormal excess accumulation of serous fluid in connective tissue or in a serous cavity
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| electrocardiography | an instrument for recording the changes of electrical potential occurring during the heartbeat used especially in diagnosing abnormalities of heart action
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| endocarditis | inflammation of the lining of the heart and its valves
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| endocardium | a thin serous membrane lining the cavities of the heart
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| heart failure | a condition in which the heart is unable to pump blood at an adequate rate or in adequate volume
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| infarction | an area of necrosis in a tissue or organ resulting from obstruction of the local circulation by a thrombus or embolus
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| ischemia | deficient supply of blood to a body part (as the heart or brain) that is due to obstruction of the inflow of arterial blood (as by the narrowing of arteries by spasm or disease)
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| mitral valve | valve guarding opening between left atrium & ventricle, prevents blood in ventricle from returning to atrium
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| stenosis | a narrowing or constriction of the diameter of a bodily passage or orifice
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| murmurs | an atypical sound of the heart typically indicating a functional or structural abnormality
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| myocardium | the middle muscular layer of the heart wall
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| P wave | a deflection in an electrocardiographic tracing that represents atrial activity of the heart
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| pericarditis | inflammation of the pericardium
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| peripheral resistance | vascular resistance to the flow of blood in peripheral arterial vessels that is typically a function of the internal vessel diameter, vessel length, and blood viscosity
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| PR interval | the interval between the beginning of the P wave and the beginning of the QRS complex of an electrocardiogram that represents the time between the beginning of the contraction of the atria and the beginning of the contraction of the ventricles
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| preload | the stretched condition of the heart muscle at the end of diastole just before contraction
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| pulse pressure | the pressure that is characteristic of the arterial pulse and represents the difference between diastolic and systolic blood pressures of the heart cycle
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| QRS complex | the series of deflections in an electrocardiogram that represent electrical activity generated by ventricular depolarization prior to contraction of the ventricles
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| sinus rhythm | the rhythm of the heart produced by impulses from the sinoatrial node
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| sinus bradycardia | abnormally slow sinus rhythm; specifically : sinus rhythm at a rate lower than 60 beats per minute
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| sinus tachycardia | abnormally rapid sinus rhythm; specifically : sinus rhythm at a rate greater than 100 beats per minute
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| stroke volume | the volume of blood pumped from a ventricle of the heart in one beat
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| syncope | loss of consciousness resulting from insufficient blood flow to the brain
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| valsalva maneuver | forceful attempt at expiration when airway is closed at some point; esp a conscious effort made while holding nostrils closed & keeping mouth shut for testing the patency of the eustachian tubes, adjusting middle ear pressure, or aborting tachycardia
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| vasodilator | an agent (as a parasympathetic nerve fiber or a drug) that induces or initiates vasodilation
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| ventricular tachycardia | tachycardia that is associated with the generation of electrical impulses within the ventricles and is characterized by an electrocardiogram having a broad QRS complex -- abbreviation VT, V-tach
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| ventricular fibrillation | very rapid uncoordinated fluttering contractions of the ventricles of the heart resulting in loss of synchronization between heartbeat and pulse beat -- abbreviation VF, V-fib
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