Cardiac A&P Review - BMH/Tele

Cardiovascular Review Natalie Bermudez, RN, BSN, MS Clinical Educator for Cardiac Telemetry Telemetry Course

The Human Heart Layers (3) Atria (2) Ventricles (2) Valves (4) Veins Arteries

Layers of the Heart 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 Myocardium P Cells Pacemaker cells Responsible for generation of action potentials electrical activity Cardiomyocytes Myocardial Cells Contractile cells that generate force Mechanical activity

Myocardial Cardiac Cell Types Fibroblasts Cells residing in the extracellular mix Endotehlial & 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 Structures Help 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 S 1 S 2 AV Valve Closes AV Valve 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 Mechanism In the intact heart, this means that the force of contractions will increase as 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!!

Preload Increased Preload Occurs With: Increased circulating volume Venous constriction (decreases venous pooling and increases venous return to the heart) Drugs: Vasoconstrictors

Preload Decreased 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)

Contractility Increased Contractility Occurs With: Drugs: Positive inotropic agents digoxin, milrinone, epinephrine, dobutamine Increased heart rate Bowditch’s phenomenon Sympathetic stimulation via ß 1 -receptors

Contractility Decreased 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)

Afterload Increased Afterload Occurs With: Aortic stenosis Peripheral arteriolar vasoconstriction Hypertension Polycythemia Drugs: Arterial vasoconstrictors

Afterload Decreased Afterload Occurs With: Hypovolemia Sepsis Drugs: Arterial vasodilators

Heart Rate Influenced By Many Factors: Blood volume status Sympathetic & Parasympathetic Tone Drugs Temperature Respiration Dysrhythmias Peripheral Vascular Tone Emotions Metabolic Status (includes hyperthyroidism)

Heart Rate Determinant of Myocardial O 2 Supply & Demand: Increased heart rates increase myocardial oxygen demand Fast heart rates (> 150 bpm) decrease diastolic coronary blood flow (shorter diastole)

Pumping Action of the Heart Systemic 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 Heart Systemic 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 Heart Systemic 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 Heart Systemic Vascular Resistance Conditions that cause an increase in SVR: Hypothermia Hypovolemia Pheochromocytoma Stress response Syndromes of low CO

Pumping Action of the Heart Systemic Vascular Resistance Conditions 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

Arterioles Autonomic 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

Arterioles Autonomic Nervous System Cholinergic (Inhibitory) System 1 Neurotransmitter Acetylcholine: Decreases heart rate; releases nitric oxide causing vasodilation

Capillaries Microscopic Walls are composed of only a single layer of endothelial cells

Capillaries Capillary pressure is extremely low to allow for exchange of nutrients, oxygen, and carbon dioxide with body cells

Sphincters At 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

Veins Valves prevent backflow Pooled 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 or vasoconstriction of the arterial vessels

Function of Blood Vessels What is the function of blood vessels??? Distribution of blood throughout the body Supplies all cells w/ O 2 & nutrients Removes metabolic waste & CO 2 Provides a conduit for hormones, cells of the immune system, & regulation of body temperature FYI – 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 afterload Arteriolar dilators reduce cardiac workload while causing cardiac output and tissue perfusion to increase

Blood Pressure Regulation Capacitance Vessels Dilation of veins (capacitance vessels) = reduced force of blood return to the heart thus decreasing preload Results 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. angiotensinogenase Converts angiotensinogen to angiotensin I

R-A-A-S Angiotensin I Has no biological activity Exists solely as a precursor to angiotensin II

R-A-A-S Angiotensin II Angiotensin I is converted into angiotensin II by the angiotensin-converting enzyme Potent vasoconstrictor Also acts on the adrenal cortex in releasing aldosterone

R-A-A-S Aldosterone Regulates sodium and potassium in the blood – retain sodium & excrete potassium Release triggered by increased levels of angiotensin II, ACTH, and potassium

References Comerford, 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, (11 th ed.). Philadelphia, PA: Lippincott Williams and Wilkins. Woods, S. L., Froelicher, E. S., Underhill Motzer, S., & Bridges, E. J. (2005). Cardiac nursing, (5 th ed.). Philadelphia, PA: Lippincott Williams & Wilkins.

Cardiac A&P Review - BMH/Tele

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