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    Cardiac A&P Review Cardiac A&P Review Presentation Transcript

    • Cardiovascular Review: There’sMore Than Just a Beating Heart Telemetry Course Natalie Bermudez, RN, BSN, MS Clinical Educator for Cardiac Telemetry
    • The Human Heart • Layers (3) • Atria (2) • Ventricles (2) • Valves (4) • Veins • Arteries
    • Layers of the Heart 2) Pericardium 2) Myocardium 3) Endocardium
    • The Pericardium• Double-walled serous sac surrounding the heart• Strengthened externally by a tough fibrous connective tissue layer
    • The Pericardium: Three Layers• Fibrous pericardium (outer) – Pericardiophrenic ligament • Blends with the outer fibrous layer or adventitia of all the great vessels except the IVC – Sternopericardial ligaments • Keeps heart in its place; attaches to the sternum
    • The Pericardium: Three Layers• Parietal Pericardium – Lines the inner surface of the fibrous pericardium• Visceral Pericardium – Aka epicardium – Serous fluid secreted by these cells forms a thin lubricating film in the pericardial cavity that provides a friction- free environment for the beating heart
    • Cardiac Tamponade• It is a potentially fatal condition that occurs when fluid rapidly accumulates in the pericardial cavity as a result of trauma, aortic aneurysm, or cardiac surgery.• The increased fluid causes external compression of the heart, which decreases venous return and CO.
    • The MyocardiumP Cells• Pacemaker cells – Responsible for generation of action potentials – electrical activityCardiomyocytes• Myocardial Cells – Contractile cells that generate force – Mechanical activity
    • Myocardial Cardiac Cell TypesFibroblasts• Cells residing in the extracellular mixEndotehlial & Smooth Muscle Cells• Cells found in the blood vessels
    • Atria & Ventricles Right Atrium Left Atrium Right Ventricle Left Ventricle
    • Heart Valves Right: Tricuspid Pulmonic Left: Bicuspid (Mitral) Aortic
    • Valvular Structures Leaflets AV Valves (2 or 3) Semilunar (3)
    • Additional Valvular StructuresHelp to keep A-V valves closed during ventricular systole
    • Blood Vessels Aorta (A & D) SVC IVC Pulmonary Artery Pulmonary Vein
    • Coronary Arteries Anterior View
    • Coronary Arteries Posterior View
    • Coronary Blood Flow Coronary filling occurs during ventricular Diastole
    • Coronary Blood Flow An increase in heart rate shortens diastole and can decrease myocardial perfusion
    • Coronary Blood Flow RCA Blood Supply: (a) Originates behind the right coronary cusp of the aortic valve (b) Supplies • Right atrium and Right ventricle • SA Node and AV node • Inferior-posterior wall of the LV (in 90% of hearts) • Inferior-posterior third of the intraventricular septum
    • Coronary Blood Flow LCA Blood Supply: Divides into the Anterior Descending Artery & Circumflex Artery • Left atrium • Most of the left ventricle • Most of the intraventricular septum
    • Coronary Blood Flow Cardiac veins lie superficially to the arteries The largest vein, the coronary sinus empties into to the right atrium
    • Coronary Blood Flow Most of the major cardiac veins empty into the coronary sinus However, the anterior cardiac veins empty into the right atrium
    • Pumping Action of the Heart Diastole: Atrial Contraction (ventricular muscle relaxation) Pressure Greater in the Atria A-V Valves Open Ventricles Fill
    • Pumping Action of the Heart Atrial Contraction → 10% to 20% left ventricular filling Pulmonary Veins passively fill left ventricle while mitral valve is open
    • Pumping Action of the Heart In elevated heart rates Atrial Contraction → 40% left ventricular filling A.K.A. Atrial Kick
    • Pumping Action of the Heart End-Diastolic Volume (EDV) Amount of blood in ventricular volume right before systole occurs Left Ventricular EDV is approximately 120 ml
    • Aortic Valve Opens Aortic Valve Closes AV AV Valve S1 S2 Valve Closes Opens
    • Pumping Action of the Heart Ventricular Contraction Systole: (relaxation of atrial muscles) Pressure Greater in Ventricles than Aortic & Pulmonic Blood Vessels Aortic & Pulmonic Valves Open Blood Ejected into Vessels
    • Pumping Action of the Heart Stroke Volume The amount of blood ejected by the left or right ventricle at each heartbeat.The amount varies with age, sex, and exercise but averages 60 to 80 ml. EDV = LVEDV - LVESV (Taber’s Medical On-line Dictionary)
    • Pumping Action of the Heart Cardiac Output The amount of blood discharged from the left or right ventricle per minute. (Taber’s Medical On-line Dictionary)
    • Pumping Action of the Heart Ejection Fraction The percentage of the blood emptied from the ventricle during systole The left ventricular ejection fraction averages 60% to 70% in healthy hearts (Taber’s Medical On-line Dictionary) Normal LV EF = 50% to 75% EF = Ventricular EDV/EDV x 100
    • Pumping Action of the Heart Cardiac Output is determined by: Preload Contractility Afterload Heart Rate (Core Curriculum for Progressive Care Nurses, p. 138)
    • Pumping Action of the Heart Preload Stretching of the muscle fibers in the ventricle. Results from blood volume in the ventricles at diastole (EDV). (Comerford & Mayer, 2007, p. 15)…Refers to the degree of stretch of the cardiac muscle fibers at the end of diastole (Smeltzer et al, 2008, p. 786)
    • Frank-Starling Mechanism Preload is described by the Frank-Starling Mechanism A.K.A.Frank-Starling Law of the Heart or Starling’s Law
    • Frank-Starling MechanismIn the intact heart, this means thatthe force of contractions will increaseas the heart is filled with more blood and is a direct consequence of the effect of an increasing load on a single muscle fiber.
    • Frank-Starling Mechanism The Rubber Band Effect The farther a rubber band is stretched, the farther it will go!!
    • PreloadIncreased Preload Occurs With:• Increased circulating volume• Venous constriction (decreases venous pooling and increases venous return to the heart)• Drugs: Vasoconstrictors
    • PreloadDecreased Preload Occurs With:• Hypovolemia• Mitral stenosis• Drugs: Vasodilators• Cardiac Tamponade• Constrictive Pericarditis
    • Pumping Action of the Heart Contractility Refers to the inherent ability of the myocardium to contract normally It is directly influenced by preload The greater the stretch, the more forceful the contraction (Comerford & Mayer, 2007, p. 15)
    • ContractilityIncreased Contractility Occurs With:• Drugs: Positive inotropic agents – digoxin, milrinone, epinephrine, dobutamine• Increased heart rate – Bowditch’s phenomenon• Sympathetic stimulation – via ß1-receptors
    • ContractilityDecreased Contractility Occurs With:• Drugs: Negative inotropic agents – Type 1A antiarrhythmics, ß-Blockers, CCBs, barbituates• Hypoxia• Hypercapnia• Myocardial ischemia• Metabolic acidosis
    • Pumping Action of the Heart Afterload Refers to the pressure that the ventricular muscles must generate to overcome the higher pressure of the aorta to the blood out of the heart (Comerford & Mayer, 2007, p. 15)
    • AfterloadIncreased Afterload Occurs With:• Aortic stenosis• Peripheral arteriolar vasoconstriction• Hypertension• Polycythemia• Drugs: Arterial vasoconstrictors
    • AfterloadDecreased Afterload Occurs With:• Hypovolemia• Sepsis• Drugs: Arterial vasodilators
    • Heart RateInfluenced By Many Factors:• Blood volume status• Sympathetic & Parasympathetic Tone• Drugs• Temperature• Respiration• Dysrhythmias• Peripheral Vascular Tone• Emotions• Metabolic Status (includes hyperthyroidism)
    • Heart RateDeterminant of Myocardial O2 Supply & Demand:• Increased heart rates increase myocardial oxygen demand• Fast heart rates (> 150 bpm) decrease diastolic coronary blood flow (shorter diastole)
    • Ventricular Function Curve
    • Pumping Action of the HeartSystemic Vascular Resistance Also affects cardiac output… The resistance against which the left ventricle must pump to move blood throughout systemic circulation (Comerford & Mayer, 2007, p.13)
    • Pumping Action of the HeartSystemic Vascular Resistance Can be affected by:• Tone and diameter of the blood vessels • Viscosity of the blood• Resistance from the inner lining of the blood vessels (Comerford & Mayer, 2007, p.13)
    • Pumping Action of the HeartSystemic Vascular Resistance SVR has an inverse relationship to CO If SVR decreases, CO increases If SVR increases, CO decreases SVR = mean arterial pressure – central venous pressure x 80 cardiac output (Comerford & Mayer, 2007)
    • Pumping Action of the HeartSystemic Vascular ResistanceConditions that cause an increase in SVR: • Hypothermia • Hypovolemia • Pheochromocytoma • Stress response • Syndromes of low CO
    • Pumping Action of the HeartSystemic Vascular ResistanceConditions that cause a decrease in SVR: • Anaphylactic and neurogenic shock • Anemia • Cirrhosis • Vasodilation
    • Blood Vessels • About 60,000 miles of arteries, aterioles, capillaries, venules, and veins keep blood circulating to and from every functioning cell in the body! • There is approximately 5 liters of total circulating blood volume in the adult body
    • Blood Vessels Five Types: Arteries Arterioles Capillaries Venules Veins
    • Arteries• Strong, compliant elastic-walled vessels that branch off the aorta, carry blood away from the heart, and distribute it to capillary beds throughout the body• A high-pressure circuit• Able to stretch during systole and recoil during diastole because of the elastic fibers in the arterial walls
    • Arterial Baroreceptors • These are receptors that are sensitive to arterial wall stretching • Located in the aortic arch and near the carotid sinuses • Responsible for modulation of vascular resistance and heart rate in order to maintain appropriate BP • Keep MAP constant
    • Arterial Baroreceptors Vasomotor Center: • In high blood pressures, the aortic arch and carotid sinus stretch • When stretching is sensed, a message is sent via the vagus nerve (aortic arch) and the glossopharyngeal nerve (carotid sinus)
    • Arterial Baroreceptors • Inhibition of SNS outflow to the peripheral blood vessels & Stimulates the PNS • Blood Pressure Decrease by: – Vasodilation of peripheral vessels – Decrease in HR & contractility – Decrease SVR
    • Arterial Baroreceptors • Responsible for short-term adjustment of BP • Respond to abrupt fluctuations in BP (postural changes) • Less effective in long-term regulation of BP – Reset or become insensitive when subjected to prolonged elevated BP
    • Arterial Baroreceptors In low blood pressures: • SNS is stimulated & PNS is inhibited • Blood Pressure Increased by: – Increased HR & Contractility – Peripheral Arterial & Venous Constriction • Preserves blood flow to the brain & heart
    • Arterioles • Control systemic vascular resistance and thus arterial pressure • Lead directly into capillaries • Have strong smooth muscle walls innervated by the ANS
    • ArteriolesAutonomic Nervous System• Adrenergic (Stimulatory) System – 2 Neurotransmitters • Epinephrine: stimulates β-receptors which increases heart rate and contractility and causes arteriolar vasodilation • Norepinephrine: stimulates α-receptors which results in vasoconstriction
    • ArteriolesAutonomic Nervous System• Cholinergic (Inhibitory) System – 1 Neurotransmitter • Acetylcholine: Decreases heart rate; releases nitric oxide causing vasodilation
    • Capillaries MicroscopicWalls are composed of only a single layer of endothelial cells
    • CapillariesCapillary pressure is extremely low to allow for exchange of nutrients, oxygen, and carbon dioxide with body cells
    • SphinctersAt the ends of the arterioles and beginning of capillaries • Dilate to permit blood flow • Constrict to increase blood pressure • Close to shunt blood
    • Venules Gather blood from capillaries Walls are thinner than those of arterioles
    • Veins Thinner walls than arteries Large diameters because of the low blood pressure of venous return to the heart
    • VeinsValves prevent backflowPooled blood in each valve segment is moved toward the heart by pressure from the moving volume of blood in the previous valve segment
    • Veins Most veins return blood to the right atrium of the heart
    • Blood pressure regulation is maintained via vasodilation orvasoconstriction of the arterial vessels
    • Function of Blood VesselsWhat is the function of blood vessels???• Distribution of blood throughout the body – Supplies all cells w/ O2 & nutrients – Removes metabolic waste & CO2• Provides a conduit for hormones, cells of the immune system, & regulation of body temperatureFYI – The lymphatic system is a parallel circulatory system that functions to return excess interstitial fluid to the heart
    • Blood Pressure Regulation Resistance Vessels Dilation of arteries (resistance vessels) = decrease in cardiac afterloadArteriolar dilators reduce cardiac workload while causing cardiac output and tissue perfusion to increase
    • Blood Pressure Regulation Capacitance VesselsDilation of veins (capacitance vessels) = reduced force of blood return to the heart thus decreasing preloadResults in decreased force of ventricular contraction and oxygen consumption, decreased cardiac output and tissue perfusion
    • Renin-Angiotensin-Aldosterone System Blood Pressure Regulatory Mechanism
    • R-A-A-S Renin a.k.a. angiotensinogenaseConverts angiotensinogen to angiotensin I
    • R-A-A-S Angiotensin I Has no biological activityExists solely as a precursor to angiotensin II
    • R-A-A-S Angiotensin II Angiotensin I is converted intoangiotensin II by the angiotensin- converting enzyme Potent vasoconstrictorAlso acts on the adrenal cortex in releasing aldosterone
    • R-A-A-S AldosteroneRegulates sodium and potassium in the blood – retain sodium & excrete potassium Release triggered by increased levels of angiotensin II, ACTH, and potassium
    • ReferencesComerford, K.C., & Mayer, B.H. (Eds.). (2007). Hemodynamic monitoring made incredibly visual. Ambler, PA: Lippincott, Williams, and Wilkins.Donofrio, J., Haworth, K., Schaeffer, L., & Thompson, G. (Eds.). (2005). Cardiovascular care made incredibly easy. Ambler, PA: Lippincott, Williams, and Wilkins.Smeltzer et al. (2008). Brunner and suddarth’s textbook of medical-surgical nursing, (11th ed.). Philadelphia, PA: Lippincott Williams and Wilkins.Woods, S. L., Froelicher, E. S., Underhill Motzer, S., & Bridges, E. J. (2005). Cardiac nursing, (5th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.