Exam 2 Study Guide PDF

Exam 2 - Study guide1 Neuro 1. Symptoms associated with headaches a. PPT#5 SLIDE 15 b. Neurological deficits c. Fever d. Photophobia e. Nausea, vomiting f. Excessive tearing or redness of the eye g. Sweating h. Nuch...

Exam 2 - Study guide1 Neuro 1. Symptoms associated with headaches a. PPT#5 SLIDE 15 b. Neurological deficits c. Fever d. Photophobia e. Nausea, vomiting f. Excessive tearing or redness of the eye g. Sweating h. Nuchal rigidity i. Nuchal rigidity refers to neck stiffness caused by bacterial meningitis and other serious medical conditions 2. s/s CVA a. SLIDE #16 b. Sudden, severe headache c. Numbness, weakness, or loss of motor function on one side of the body d. Visual difficulties e. Dysphagia 3. Cranial Nerves – what are they and how to assess for them a. SLIDE#19 b. Olfactory nerve (CN I) c. Optic nerve (CN II) d. Oculomotor nerve (CN III) e. Trochlear nerve (CN IV) f. Trigeminal nerve (CN V) g. Abducens nerve (CN VI) h. ​Facial nerve (CN VII) i. Vestibulocochlear nerve (CN VIII) j. Glossopharyngeal nerve (CN IX) k. Vagus nerve (CN X) l. Spinal accessory nerve (CN XI) m. Hypoglossal nerve (CN XII) 1 Exam 2 - Study guide2 2 Exam 2 - Study guide3 3 Exam 2 - Study guide4 4. Assessing Gait and Balance a. SLIDE#21 b. Muscles i. Observe size and contour of muscles ii. Note involuntary movements iii. Palpate muscles 1. If tenderness or spasm suggested 2. If muscles seem atrophic or hypertrophic c. Cerebellar function i. Assess balance, gait, and coordination 5. Assessing Coordination 4 Exam 2 - Study guide5 (Stereognosis tests the individual's ability to perceive and integrate a variety of sensory modalities and to interpret the stimuli to identify small objects placed in the hand. Expected findings - The individual can successfully identify 90-100% of all objects placed in his/her hand within 2-3 seconds of placement.) 6. Assessing Sensory Function a. SLIDE #22 b. Assess exteroceptive sensation i. Light touch, superficial pain, temperature c. Assess proprioceptive sensation i. Motion and position sense, vibratory sense 5 Exam 2 - Study guide6 d. Assess cortical sensation i. Stereognosis, graphesthesia, two-point discrimination, and extinction 7. Deep Tendon Reflexes, grading a. slide #23 b. Assess deep tendon reflexes (DTRs) i. Biceps, brachioradialis, triceps, patellar reflex, Achilles reflex c. Grading i. 5+ Clonus ii. 4+ Hyperactive iii. 3+ More brisk than normal iv. 2+ Normal v. 1+ Diminished vi. 0 Absent 8. Neonatal Reflexes a. Slide#30 b. Palmar and plantar grasp c. Babinski d. Sucking e. Rooting f. Tonic neck g. Startling (Moro reflex) h. Placing i. Stepping 9. Blood Brain Barrier a. PPT#2 SLIDE2 b. Maintains homeostasis within the CNS i. Microvascular capillary that strictly controls the passage of substances into and out of the CNS. ii. Complex ,continuous tight junctions iii. Tight barrier for water soluble molecules iv. These brain structures receive neurosecretory products from the blood and therefore lack a BBB. (circumventricular organs), include the area postrema, pituitary gland 6 Exam 2 - Study guide7 (specifically the posterior lobe), pineal gland, choroid plexus, and portions of the hypothalamus. c. Incompletely developed in the newborn. d. High vascular content of bile in jaundiced newborns may enter the basal ganglia, producing kernicterus. e. Disrupted by traumatic head injury, subarachnoid or intracerebral hemorrhage, or cerebral ischemia. f. Disrupted in several disease processes: multiple sclerosis, stroke, and brain tumors. g. Intentional intracarotid injection of a hyperosmolar solution shrinks the endothelial cells, opens tight junctions, and disrupts the BBB. (allows for the delivery of chemotherapeutic drugs through the BBB for the treatment of neural malignancy). h. (Osmotically active substances may penetrate the brain or spinal cord after BBB disruption.) 10. Lobes of the brain, which does what a. PPT#2 SLIDE 4 b. Frontal lobe - essential for motor control, c. Parietal lobe - senses of pain and touch. d. Cerebral cortex - nearly 50 structurally distinct areas called Brodmann areas e. Temporal lobe contains the auditory cortex f. Occipital lobe - the visual centers. 11. Meninges – meningeal layers a. Slide#6 b. Meninges_Connective sheaths that suspend and protect the brain inside the skull c. Slide#27-28 d. Migraine vs Cluster e. Cluster headaches i. are characterized by excruciating pain that is usually felt around one eye or on one side of the head. ii. The pain is often described as burning, piercing, or throbbing and can last anywhere from 15 minutes to 3 hours. iii. These headaches are relatively rare, affecting about 0.1% of the population, and are more commonly seen in men. f. Triggers for cluster headaches include 7 Exam 2 - Study guide8 i. alcohol consumption, strong odors, and changes in sleep patterns. g. Cluster headaches often occur in clusters or cycles, with multiple attacks happening over a period of weeks or months. h. On the other hand, migraines i. typically cause a throbbing pain that is felt on one or both sides of the head, often accompanied by nausea, vomiting, and sensitivity to light and sound. ii. Migraines can last anywhere from 4 to 72 hours and are more common, affecting about 12% of the population, and are more commonly seen in women. i. Triggers for migraines can include: i. hormonal changes, certain foods, stress, and changes in weather. j. Migraines can occur less frequently but with longer durations. k. PPT #2 slide 10 l. Brain and spinal cord are enveloped by three meningeal layers: i. dura mater - thickest of the meningeal layers, overlies the cerebral hemispheres and brainstem ii. arachnoid mater - thin, avascular membrane joining the dura mater iii. pia mater - thin avascular membrane adherent to the brain and spinal cord m. Subdural space, a potential space between the dura mater and the arachnoid mater. i. Unintentional injection of a local anesthetic during spinal anesthesia into the subdural space produces patchy, asymmetric block. ii. Injury to a blood vessel in the subdural space can create bleeding (subdural hematoma), requiring surgical intervention. n. The subarachnoid space lies between the arachnoid mater and the pia mater. i. Injury to the vascular structures may produce subarachnoid hemorrhage (SAH) and hematoma. o. The epidural space contains a venous plexus and epidural fat 12. Cerebrospinal Fluid a. PPT#2 Slide#12-13 b. Total volume of cranial and spinal CSF in the adult is approximately 150 mL. c. Specific gravity varies from 1.002 to 1.009, d. pH is 7.32. e. CSF bathes the brain and spinal cord, cushioning these delicate structures, and controls and maintains the extracellular milieu for neurons and glial cells. f. Entire CSF volume is replaced every 3 to 4 hours. g. Normal CSF pressure is between 5 and 15 mm Hg h. Spinal Cord i. Thirty-one pairs of spinal nerves carry motor and sensory information: 1. 8 cervical, 2. 12 thoracic, 8 Exam 2 - Study guide9 3. 5 lumbar, 4. 5 sacral, and 5. 1 coccygeal. ii. The first pair of cervical nerves exits the spinal cord between the base of the skull and the first cervical vertebra (atlas), and the remaining 30 pairs exit between adjacent vertebrae. iii. All exiting spinal nerves are covered with pia mater. iv. Because the spinal cord is approximately 25 cm shorter than the vertebral canal in adults, the lumbar and sacral nerves have relatively long roots (the cauda equina). 13. Sympathetic Nervous System a. PPT#2 slide 15 b. β-receptor stimulation produces an increased heart rate (positive chronotropic effect), an increase in conduction (positive dromotropic effect), and an increase in myocardial contractility (positive inotropic effect). c. Coronary artery α-receptor stimulation produces vasoconstriction. d. Bronchial dilation follows β2-receptor stimulation, and mild bronchoconstriction follows α-receptor stimulation. e. Activates liver glycogenolysis and gluconeogenesis, decreases secretions from pancreatic acinar cells and β-cells, initiates lipolysis, decreases the tone and motility of the gastrointestinal tract, contracts gastrointestinal sphincters, relaxes urinary smooth muscle, and increases renin secretion from the kidney. 14. Parasympathetic Nervous System a. PPT#2 SLIDE 16 b. Acetylcholine - secreted by both parasympathetic preganglionic and postganglionic fibers. c. Innervate the bronchioles, heart, coronary arteries, stomach, and large intestine up to the left colic flexure. d. Descending colon and the genitourinary systems are supplied by parasympathetic fibers from sacral segments of the spinal cord. e. Stimulation of the Vagus nerve accounts for approximately 75% of parasympathetic nervous system activity. 9 Exam 2 - Study guide10 GU 1. Causes of testicular pain a. slide #9 b. Testicular pain i. Epididymitis*, orchitis, and testicular torsion Testicular torsion* Epididymitis 2. Tests for diagnosing GU disorders a. slide #21 b. Blood tests 10 Exam 2 - Study guide11 c. Routine urinalysis d. Urine for culture and sensitivity e. 24-hour collection for protein and creatinine f. Intravenous pyelography (IVP) g. Fractional excretion of Na+ (FeNa+) level i. Fractional excretion of sodium is the amount of salt (sodium) that leaves the body through urine compared to the amount filtered and reabsorbed by the kidney. Fractional excretion of sodium (FENa) is not a test h. Glomerular filtration rate (GFR) i. Prostate-specific antigen test i. There is no specific normal or abnormal level of PSA in the blood. In the past, PSA levels of 4.0 ng/mL and lower were considered normal. However, some individuals with PSA levels below 4.0 ng/mL have prostate cancer and many with higher PSA levels between 4 and 10 ng/mL do not have prostate cancer 3. Function of the Kidney/Nephron/Tubule(s) a. Slide #23 - 35 b. Kidney i. Due to hepatic displacement, the right kidney’s position is slightly lower than the left kidney. ii. The renal pelvis is the major reservoir for urine. iii. Ureters connect the renal pelvis to the bladder. iv. Highly vascular v. Receiving 1100 to 1200 mL of blood per minute, or 20% to 25% of the cardiac output. vi. Blood reaches these organs through the renal arteries. vii. Filtration, reabsorption, and concentration of urine. viii. Blood returns to the central circulation via the renal veins. ix. Renal vein empties into the inferior vena cava. c. Nephron i. Functional unit of the kidney ii. Approximately 1,250,000 of these units reside in each kidney. iii. Filtered blood flows through the nephrons, which, in turn, retain iv. filtered fluid known as filtrate. v. End products of metabolism are excreted, and metabolically important substances such as water and electrolytes are reabsorbed as needed. vi. Formation of urine begins with the nephron viii. Tubular reabsorption permits conservation of water glucose, amino acids, and electrolytes 11 Exam 2 - Study guide12 ix. water and sodium absorbed throughout the nephron. Glucose completely reabsorbed when concentrations are low iix. Reabsorption maximal value - after the value is reached, excess material is excreted regardless of plasma concentration d. Tubule (s) i. Transport Mechanisms through tubular membrane 1. Active transport - the net movement of particles across a membrane against an electrochemical gradient, generally at the cost of metabolic energy. 2. Passive transport - involves the movement of substances across membranes and relies on either concentration gradients or chemical gradients. ii. Proximal Tubule 1. 60% to 70% of filtered sodium and water 2. 50% of urea 3. potassium, calcium, phosphate, uric acid, and the bicarbonate (HCO3) form of carbon dioxide (CO2) have been reabsorbed. 4. Glucose, proteins, amino acids, acetoacetate ions, and vitamins are completely or almost completely reabsorbed by active processes. 5. Protein molecules are too large to be reabsorbed by normal mechanisms, a special mechanism called pinocytosis is used to save proteins. In this process, the tubular membrane engulfs the protein and internalizes it. iii. Loop of Henle 1. Primary function -establish a hyperosmotic state 2. Conserve salt and water. 3. Involve a countercurrent exchange system - - uses a concentration gradient causing fluid to be exchanged across parallel pathways. iv. Late Distal Tubule 1. Sodium, under the influence of aldosterone, is reabsorbed. 2. Potassium is secreted into the lumen in exchange for sodium. It is mainly by this means that the potassium concentration is controlled in the extracellular fluids of the body. 3. Secretes hydrogen against a concentration gradient - a role in acid-base balance and determines the final degree of urine acidification. 4. Reabsorbs 10% of filtered water. 5. Permeable to water only in the presence of antidiuretic hormone (ADH). v. Collecting Duct 1. Permeability to water is controlled by ADH plasma levels, which determine urine concentration. 2. Can also secrete hydrogen, and therefore, has a role in acid-base balance. 12 Exam 2 - Study guide13 vi. Renal Secretion 1. In addition to renin, hydrogen, and potassium, the kidneys release erythropoietin - a glycoprotein stimulating red blood cell production in the bone marrow. 2. Any condition that causes the quantity of oxygen transported to the tissues to decrease stimulates the release of erythropoietin, production of red blood cells, and correction of hypoxia. 3. Anemia emerges when both kidneys are destroyed by renal disease. vii. Renal Fraction 1. The cardiac output portion that passes through the kidney. 2. Cardiac output in a 70-kg adult is approximately 5 - 6 L/min, and blood flow through both kidneys is approximately 1 - 1.2 L/min, making the normal renal fraction of cardiac output between 20% and 25%. 4. Regulation of renal blood flow a. slide #36 b. Determined by the arteriovenous pressure difference across the vascular bed and is given by the following relationship: c. RPF is the renal plasma flow, and HCT is the hematocrit. d. Renal blood flow is regulated by intrinsic autoregulation and neural regulation. e. Autoregulation implies that blood flow remains normal despite a considerable change in pressure. f. With a mean arterial pressure (MAP) between 50 and 180 mmHg, renal blood flow to both kidneys remains 1000 mL/min. g. If mean systemic blood pressure falls below 50 mm Hg, filtration ceases. h. Afferent arteriole vasodilation and myogenic mechanisms are responsible for autoregulation i. Direct relationship between renal blood flow and glomerular filtration. When renal blood flow decreases, glomerular filtration is reduced. j. Myogenic mechanisms -When arterial pressure rises, the arterial wall is stretched, the vessel constricts, and blood flow remains normal. When arterial pressure decreases, the opposite effect occurs. Therefore, renal blood flow remains constant over a wide range of pressure changes. 13 Exam 2 - Study guide14 k. Neural regulation. Sympathetic nervous system innervates the afferent and efferent arterioles. Autoregulation will override the adrenergic system with mild stimulation; acute sympathetic stimulation and associated vasoconstriction can decrease renal blood flow substantially. l. Parasympathetic nervous system not physiologically significant in relationship to renal blood flow. 5. Glomerular Filtration a. slide #39 b. ​Dependent on the following physiologic factors: i. The pressure inside the glomerular capillaries ii. The pressure in the Bowman capsule iii. The colloid osmotic pressure of the plasma proteins c. Selective Process (some substances are filtered and some are not) d. Several factors can alter GFR. Increased renal blood flow, dilation of the afferent arteriole, and increased resistance in the efferent arteriole increase GFR. e. Decreased glomerular filtration causes overabsorption of sodium ions (Na+) and chloride ions (Cl − ) in the ascending limb of the loop of Henle f. Decreases in sodium and chloride concentrations cause afferent arterioles to dilate, thus increasing renal blood flow and GFR. 6. GFR autoregulation a. slide #40 b. Renin clears angiotensinogen from the liver to form angiotensin I. c. In the lung, angiotensin I is changed into angiotensin II under the influence of a converting enzyme, known as angiotensin-converting enzyme (ACE). d. In addition to having a generalized vasoconstricting effect, angiotensin II causes efferent arteriole constriction. e. This causes the pressure in the glomerulus to increase and the GFR to return to normal. f. In this manner, the renal system autoregulates blood flow, and GFR remains relatively unchanged despite changes in systemic blood pressure. 7. Atrial Natriuretic Factor a. slide #43 b. ​Peptide hormone synthesized, stored, and secreted by the cardiac atria. c. Acts on the kidney to increase urine flow and sodium excretion, d. May enhance renal blood flow and GFR e. Antagonizes both the release and end-organ effects of renin, aldosterone, and ADH. f. The stimulus for ANF release is atrial distention, stretch, or pressure. g. ANF is one of the most potent diuretics known. h. Inhibition of plasma renin, angiotensin, and aldosterone can produce a dose-dependent decrease in blood pressure. i. (Natriuretic peptides drugs used for treating heart failure (Nesiritide) j. The heart produces different types of natriuretic peptides found in low levels in the bloodstream. k. High levels of natriuretic peptides may indicate that the heart is not functioning efficiently. (BNP)) 8. s/s dysfunction of the kidney 14 Exam 2 - Study guide15 a. Common Chief Complaints Related to the Male Genitourinary System (1 of 2) i. Dysuria ii. Urinary frequency or urgency iii. Polyuria iv. Hematuria v. Nocturia vi. Urinary incontinence vii. Penile discharge viii. Pain in the genital region ix. Lesions b. Common Female Genitourinary Chief Complaints i. Pelvic pain ii. Abnormal vaginal bleeding iii. Discharge iv. Lesions v. Dysuria vi. Hematuria vii. Frequency or urgency viii. Incontinence 9. General anesthesia considerations r/t renal considerations a. slide #46 b. Temporary depression of renal blood flow, GFR, urinary flow, and electrolyte excretion. c. Magnitude tends to parallel the degree of sympathetic block and cardiovascular depression. d. Attributed to several factors i. Type and duration of surgical procedure, physical status of the patient, volume and electrolyte status, depth of anesthesia, and choice of agent e. High levels of spinal or epidural anesthesia can impair venous return, diminish cardiac output, and reduce renal perfusion. f. All anesthetics have the potential to alter the physiologic state, usually depressing the cardiovascular system and affecting renal blood flow, GFR, and urinary output. g. Although systolic arterial blood pressure may not fall below 80 to 90 mm Hg, renal blood flow may be decreased by 30% to 40% after the administration of various anesthetics. This suggests impairment of autoregulation. 10. s/s renal injury a. Intravascular volume depletion i. Hemorrhage—trauma, surgery, postpartum, gastrointestinal ii. Gastrointestinal losses—diarrhea, vomiting, nasogastric tube loss iii. Renal losses—diuretic use, osmotic diuresis, diabetes insipidus iv. Skin and mucous membrane losses—burns, hyperthermia v. Nephrotic syndrome vi. Cirrhosis vii. Capillary leak b. Reduced cardiac output i. Cardiogenic shock ii. Pericardial diseases—restrictive, constrictive, tamponade 15 Exam 2 - Study guide16 iii. Congestive heart failure iv. Valvular diseases v. Pulmonary diseases—pulmonary hypertension, pulmonary embolism vi. Sepsis c. Systemic vasodilation i. Sepsis ii. Cirrhosis iii. Anaphylaxis iv. Drugs d. Renal vasoconstriction i. Early sepsis ii. Hepatorenal syndrome iii. Acute hypercalcemia iv. Drugs—norepinephrine, vasopressin, nonsteroidal antiinflammatory drugs, angiotensin-converting enzyme inhibitors, calcineurin inhibitors v. Iodinated contrast agents vi. Increased Intraabdominal Pressure 1. Abdominal compartment syndrome 11. Creatine clearance a. slide #53 b. Current Classification: Serum creatinine clearance and urinary output as markers for severity of injury: i. Acute Dialysis Quality Initiative’s RIFLE (risk of renal dysfunction, injury to the kidney, failure of kidney function, loss of kidney function, and end-stage renal disease [ESRD]) or the Acute Kidney Injury Network’s (AKIN) stages 1 through 3. ii. Both classifications demonstrate that serum creatinine clearance is a sensitive marker for AKI, as opposed to urine output. iii. Additional markers, such as urine creatinine levels, angiotensinogen, or presence of proteinuria can be used in conjunction with RIFLE or AKIN classifications to aid in diagnosing the severity of AKI. iv. Use of diuretics must be factored in before using these additional biomarkers. 12. CKD a. slide #55 b. Slow, progressive, irreversible condition characterized by diminished functioning of nephrons and a decrease in renal blood flow, GFR, tubular function, and reabsorptive capacity. c. GFR is less than 60 mL/min/1.73 m2 for 3 months or more. d. Primary causes include glomerulonephritis, pyelonephritis, diabetes mellitus, hyperlipidemia, autoimmune disease, obesity, vascular or hypertensive insults, and congenital defects. e. Normal aging processes reduce nephron function by 10% for each decade of life - renal insufficiency is common in the geriatric population. f. The general course of progressive CKD can be divided into five stages.*** i. Stage 1: Kidney damage with normal or increased GFR ii. Stage 2: GFR 60 to 89 mL/min/1.73 m2 with evidence of kidney damage iii. Stage 3: GFR 30 to 59 mL/min/1.73 m2 iv. Stage 4: GFR 15 to 29 mL/min/1.73 m2 v. Stage 5: End-stage renal failure with GFR less than 15 mL/min/1.73 m2 16 Exam 2 - Study guide17 Cardiac 1. Chambers of the heart- Slide#4-#8 a. Upper two chambers (right and left atria) i. Thin-walled, low-pressure chambers ii. Receive blood from the venae cava and pulmonary arteries iii. Pump blood into the respective ventricle iv. Right Atrium 1. RA acts as a reservoir for the RV 2. Thickness of approximately 2 mm. 3. RA receives blood from the superior vena cava, the inferior vena cava, and the coronary sinus. 4. RA consists of an anterior, thin-walled trabeculated portion and a posterior, 5. smooth-walled portion called the sinus venarum. 6. Superior vena cava - blood from the upper body. 7. Inferior vena cava - blood from the lower body. 8. Entrance of the inferior vena cava into the RA is protected by a rudimentary valve called the eust 9. Entrance from the coronary sinus is protected in part by a rudimentary valve of the coronary sinu v. Left Atrium 1. Reservoir for the oxygenated blood 2. Receives blood from the four pulmonary veins 3. Serves as a pump during atrial systole. 4. Provides a 20% to 30% increase in left ventricular end-diastolic volume (LVEDV), which is known 5. Located superiorly and posteriorly to the other chambers. 6. Walls of the LA are slightly thicker (3 mm) as compared to the RA. 7. Connects to the LV through mitral valve. b. Lower two chambers (right and left ventricles) i. Thick, muscular-walled chambers ii. Pump blood from the atria to the lungs and throughout the body via the aorta iii. Right Ventricle 1. Ejects blood into the pulmonary artery 2. Communicates with RA -tricuspid valve. 3. Communicates with the pulmonary tract - pulmonic valve. 4. Walls much thicker (4−5 mm) than those of the RA 5. Superior portion conical appearance -s called the conus arteriosus or infundibulum. 6. Inner wall of the conus is smooth, but the remainder of the right ventricular wall has a rough app carneae. 7. One of the trabeculae carneae (the moderator band) crosses the cavity of the ventricles and carr 8. Papillary muscles have attachments to the ventricular walls and to the chordae tendineae. 9. Chordae tendineae are attached to the cusps of the tricuspid valve; together with the papillary m iv. Left Ventricle 1. Receives blood from the LA and ejects it into the aorta. 2. Wall thickness is approximately 8 to 15 mm, or two to three times the thickness of the RV. 3. Must overcome systemic vascular resistance (SVR), or afterload, and to maintain stroke volume ( 4. Two-thirds of the septum and the rest of the ventricular wall are covered with trabeculae carnea 5. Two large papillary muscles 6. Chordae tendineae of each muscle is attached to the cusps of the mitral valve and prevents ever 17 Exam 2 - Study guide18 2. Pericardium a. Slide #12 b. Fibrous, double-walled sac -envelops the heart and the roots of the great vessels. c. Visceral portion – Epicardium d. Outer parietal portion adheres to the fibrous pericardium e. The visceral pericardium and parietal pericardium are separated by a thin potential space known as the pericardial cavity. -normally contains approximately 10 to 25 mL of serous fluid, which provides lubrication for the free movement of the heart within the mediastinum. 3. Cardiac Tamponade a. Slide #13 b. In disease states, the pericardial space can fill with blood and or serosanguinous fluid, compress the heart, and decrease cardiac output (CO). c. In acute cardiac tamponade, the volume rapidly increases, producing myocardial dysfunction. d. In chronic cardiac tamponade, the degree of pressure exerted on the heart increases slowly because the pericardial sac stretches over time to accommodate the blood that accumulates. The pressure may eventually increase as much as 10-fold before symptoms associated with cardiac tamponade occur. e. The pericardium receives its arterial blood supply from the branches of the internal thoracic arteries and through the bronchial, esophageal, and superior phrenic arteries. f. Venous drainage from the pericardium occurs through the azygos system and the pericardiophrenic veins, which anastomose with the internal thoracic veins. g. Nervous innervation to the pericardium is derived from the vagus nerve, the phrenic nerves, and the sympathetic trunks. 4. Assessing function of cardiac valves a. Slide #18-22 b. The cardiac valves increase the heart’s efficiency by ensuring unidirectional flow of blood through the circuit. c. They open and close in response to pressure gradients that exist above (atrium) or below (ventricles) the valves. d. These valves may be categorized as: i. Atrioventricular valves (AV), which exist between the atria and ventricle, or ii. semilunar (pulmonary artery or aorta). e. Cardiac Valves i. Most accurate ways to determine valvular pathology is by calculating the valvular area. Best done during cardiac catheterization. ii. Echocardiography is a noninvasive method of determining valvular area and it is used to estimate the presence and degree of valvular heart disease. iii. Valvular gradients can be determined by Gorlin formula or its correction, which can provide information regarding the degree of pathology that exists: iv. where K is a hydraulic pressure constant, heart rate (HR) (beats per minute), systolic ejection period (SEP) expressed in seconds, and square root of mean valve gradient 18 Exam 2 - Study guide19 expressed in mm Hg. 9 f. Tricuspid Valve i. Three leaflets attached to the chordae tendineae, which are anchored to the papillary muscles. ii. This structure prevents eversion of the valve leaflets into the RA during ventricular systole. iii. Normal tricuspid valve area is approximately 7 cm2. iv. Symptoms associated with tricuspid valve stenosis typically occur when the valve area is less than 1.5 cm2. g. Mitral Valve i. Two major leaflets - connected by commissural tissue. ii. The normal mitral valve area is 4 to 6 cm2. iii. When the surface area of the valve is decreased by half, clinical symptoms may appear. iv. Like the tricuspid valve, the mitral valve has papillary muscles and chordae tendineae attached to the leaflets to prevent eversion of the valve during ventricular systole. h. Semilunar Valve i. Each valve is composed of three cusps. ii. Above the aortic valve is a dilation known as the sinus of Valsalva, which allows the valve to open efficiently without occluding the coronary ostia or openings that communicate with the coronary arteries. iii. Eddy currents form behind the valve leaflets and prevent contact between the valve leaflets and the walls of the aorta. iv. Normal aortic valve area is 2.5 to 3.5 cm2. Reduction of the valve area by one-third to one-half is associated with an increase in the symptoms caused by aortic stenosis. 5. Cardiac Innervation – terms a. Slide #27 b. Chronotropic – increase heart rate (sympathetic activity) c. Inotropic – force of myocardial contraction d. Dromotropic – rate of AV discharge e. Increased distribution of sympathetic nerves that innervate the ventricles. Some also join with the parasympathetic fibers. f. Parasympathetic nervous system - primarily slows the HR and decreases contractility – Acetylcholine g. Suppression/blockade of this thoracic portion of the spinal cord by regional anesthesia causes bradycardia and hypotension (inhibition of the sympathetic ganglia = parasympathetic nervous system predominance). h. maximal vagal nerve (parasympathetic) stimulation reduces contractility by only 30%, whereas maximal sympathetic stimulation increases contractility by 100%. 6. Factors that affect myocardial O2 supply a. slide # 37 b. Myocardial O2 supply i. At rest, 4% to 5% of CO, (225 mL/min) passes through the coronary vasculature. ii. Greater coronary blood flow occurs during diastole. iii. Myocardial O2 supply determined by arterial blood content, diastolic blood pressure (DBP), diastolic time as determined by HR, oxygen extraction, and coronary blood flow. iv. Demand is determined by preload, afterload, contractility, and HR. 19 Exam 2 - Study guide20 7. Coronary Artery Autoregulation a. slide # 38 b. MAP range of 60 to 140 mm Hg. c. When arterial blood pressure is less than or exceeds these pressure limits, coronary blood flow becomes pressure dependent. d. During hypotension, when the coronary arteries are maximally dilated, coronary blood flow is determined by the MAP minus the right atrial pressure. e. Cardiac pathology (including untreated hypertension), coronary artery disease, and cardiomyopathies cause the normal autoregulatory curve to shift to the right necessitating a MAP greater than 60 mm Hg to maintain adequate myocardial perfusion. 8. Coronary Perfusion Pressure a. slide #39 b. CPP estimate - calculated by subtracting LVEDP from DBP (i.e., CPP = DBP – LVEDP). c. Under normal conditions, LVEDP (10 mm Hg) is significantly less than DBP (80 mm Hg). d. Therefore the major determinant of CPP is DBP. e. Coronary vascular reserve is the difference between the maximal flow and the autoregulated flow. f. The closer these two values are, the lower the coronary reserve of the patient. g. Factors that increase myocardial oxygen demand and limit supply decrease coronary reserve flow and can result in myocardial dysfunction. h. (Coronary flow reserve is the maximum increase in blood flow through the coronary arteries above the normal resting volume.) 9. Coronary Steal a. slide #40 b. Vasodilation associated with the use of medications such as adenosine, nitroglycerin, and isoflurane. c. When stenosis of a coronary artery exists (atherosclerotic plaque), this region of the coronary artery is maximally dilated to meet the metabolic demands of the myocardium. d. If vasodilator treatment is administered to a patient who has both an ischemic area of the heart that is supplied by a stenotic vessel with collateral flow and another area that has an intact autoregulated vessel, only the autoregulated vessel dilates further and has the ability to increase its flow. e. Therefore only the areas of the heart with intact autoregulation respond to vasodilators and receive preferential flow over the stenotic area. f. Lastly, by dilating the coronary arterial system, flow in the region of stenosis can decrease causing myocardial ischemia. g. A second factor that could result in this phenomenon is coronary steal–prone anatomy. This has been defined as complete occlusion of one coronary artery and at least 50% occlusion of a second coronary artery that supplies collateral blood flow to the area in which the complete occlusion exists. h. Evidence suggests that the inhaled anesthetics isoflurane, desflurane, and sevoflurane produce myocardial protection during periods of ischemia in humans by decreasing the formation of free radicals, preserving myocardial ATP stores, and inhibiting intracellular calcium. i. This phenomena is referred to as anesthetic preconditioning. 20 Exam 2 - Study guide21 10. Ejection Fraction a. slide #42 b. Percentage of the EDV ejected during systole. c. Normal EF is 60% to 65%. d. EF of less than 40% is associated with significant left ventricular impairment. e. Factors that alter the normal loop include increases and decreases in LV preload, LV afterload, and LV contractility. f. These factors can be acute and transient, such as during the administration of vasoactive medications, or chronic because of myocardial compensation caused by valvular heart disease (stenosis vs regurgitation). 11. Valsalva maneuver a. slide #44 b. Valsalva maneuver occurs as a result of forced expiration against a closed glottis. c. Mimics many normal activities, (defecation, blowing up a balloon, or playing the saxophone). d. Performing the Valsalva maneuver causes an increase in intrathoracic pressure, leading to a reduction in preload to the heart. e. Cardiovascular changes occur during and after this maneuver due to baroreflex and other compensatory reflex mechanisms that are initiated by decreased preload. 12. Relevance of baroreceptors a. slide #45 b. Baroreceptors sense a decreases in BP causing an increase in sympathetic tone, which results in increased myocardial performance and vasoconstriction. c. Acute hypertension causes the opposite cardiovascular response to occur. d. The baroreceptor response is inhibited by inhalation anesthetic agents in a dose-dependent manner and results in a decreased ability of the baroreceptors to respond to blood pressure changes when these agents are used. e. The responsiveness of the baroreceptor reflex also decreases as part of the normal aging process. 13. Celiac Reflex vs Atrial Stretch Reflex vs Cushing reflex vs Chemoreceptor reflex vs Bezold-Jarisch reflex a. Celiac reflex slide #46 i. Elicited by traction on the mesentery or the gallbladder or stimulation of the vagus nerve in other areas of the body, such as the thorax and abdominal cavity. ii. Stimulation of this reflex causes bradycardia, apnea, and hypotension. iii. Clinically, the celiac reflex can be initiated indirectly as a result of a air or gas in the peritoneal cavity. iv. Resolved by stopping the initiating stimulus. v. This vagal response to the heart can be antagonized by administration of an anticholinergic agent (atropine or glycopyrrolate). b. Bainbridge reflex (atrial stretch reflex) slide #47 i. Elicited as a result of an increased volume of blood in the heart – causing sympathetic nervous system stimulation. ii. Stretch receptors are located in the right atrium, junction of the vena cava, and pulmonary veins. iii. The SA node is also involved in this process and can increase heart rate by 10% to 15%. 21 Exam 2 - Study guide22 iv. Antidiuretic hormone secretion from the posterior pituitary gland is decreased, resulting in decreased circulating blood volume. v. Atrial natriuretic peptide is increased, which also promotes diuresis. c. Cushing reflex slide #48 i. Response to CNS ischemia caused by increased intracranial pressure. ii. Triggered as a result of an elevation of intracranial pressure to a value greater than the MAP, thereby decreasing cerebral perfusion and potentially causing cerebral ischemia. iii. An intense sympathetic nervous system response is initiated by the vasomotor center, resulting in intense vasoconstriction. These compensatory physiologic changes attempt to restore adequate cerebral perfusion. iv. However, if cerebral ischemia is not relieved, cerebral infarction results. v. When the vasomotor area becomes ischemic as a result ofhypotension (MAP 1 L). iv. Constrictive pericarditis and cardiac tamponade result in impaired diastolic filling, which results in decreased CO. e. Acute Pericarditis - Presentation i. Sudden onset chest pain. ii. Pain is differentiated by the inclusion of a pleural component, which includes increased discomfort associated with postural changes and relief on sitting or leaning forward. iii. Fever with a pericardial friction rub iv. Absence of elevation of cardiac enzymes levels v. Diffuse ST segment elevation in two or three limb leads and in most of the precordial leads. vi. Echocardiography is another reliable method for diagnosing pericarditis and pericardial effusion. f. Chronic Constrictive Pericarditis i. Results from pericardial thickening and fibrosis. ii. Most common cause is idiopathic in nature and can occur following cardiac surgery, neoplasia, uremia, radiation therapy, and rheumatoid arthritis. iii. Stiff, fibrous tissue encircles the heart and limits its ability to expand during diastole. iv. Chronic constrictive pericarditis is abnormal diastolic filling. v. Reduced myocardial compliance impairs filling of both ventricles. vi. Filling pressures increase, and as a result pulmonary and peripheral congestion occurs. 24 Exam 2 - Study guide25 vii. SV and CO can also be decreased. viii. Over time the underlying myocardial tissue may atrophy, and systolic function decreases. g. Chronic Constrictive Pericarditis-Presentation i. Increasing fatigue and dyspnea. ii. Increasing venous pressure and congestion 1. engorgement of neck veins, hepatomegaly, ascites, and peripheral edema. 2. In approximately 50% of patients, the fibrous enclosure becomes calcified and is visible on a chest radiograph. 3. 25% of patients have atrial dysrhythmias because of the involvement of atrial conduction pathways. 4. Diagnosis is confirmed by demonstration of pericardial thickening with echocardiography or computed tomography. iii. Pericardiotomy. May precipitate malignant cardiac dysrhythmias and massive bleeding. Consequently, pericardiotomy is associated with relatively high perioperative morbidity and mortality rates, ranging from 6% to 19%. 16. Cardiac Tamponade -presentation a. slide #61 b. Impairment of diastolic filling of the heart because of continual increases in intrapericardial pressure. c. Slow accumulation of fluid in the pericardial space initially causes minute increases in intrapericardial pressure. d. The causes of cardiac tamponade include: i. (1) trauma, including sharp or blunt trauma to the chest and dissecting aortic aneurysms; ii. (2) complications associated with cardiac surgery; iii. (3) malignancy within the mediastinum; and iv. (4) expansion of pericardial effusions after any form of pericarditis. e. Cardiac Tamponade- Pathophysiology i. Accumulation of pericardial fluid leads to an increase in intrapericardial pressure. ii. Diastolic expansion of the ventricles decreases. iii. Poor ventricular filling develops and leads to peripheral congestion and a decrease in SV and CO. iv. Decrease in SV decreases peripheral perfusion causing catecholamine release manifested as tachycardia, vasoconstriction, and increased venous pressure, which helps maintain CO. v. If these mechanisms fail, cardiac collapse can occur. f. Cardiac Tamponade - Presentation i. Cardiac distress ii. Beck triad: 1. hypotension, 2. jugular venous distention 3. muffled heart sounds. 25 Exam 2 - Study guide26 iii. Pulsus paradoxus - exaggerated decrease in systolic blood pressure (i.e., >10 mm Hg) that normally occurs with inspiration. iv. Chest radiography may show an enlarged cardiac silhouette. v. ECG - decrease in voltage across all leads or electrical alterations of either the P wave or the QRS complex. vi. Echocardiography is the most sensitive, noninvasive method for detection of pericardial effusion and exclusion of tamponade. vii. Pulmonary artery catheter may reveal equilibration of right and left atrial pressures and right ventricular end-diastolic filling pressures at approximately 20 mm Hg. g. Cardiac Tamponade - Treatment i. Pericardiocentesis, performed percutaneously by needle decompression, through a subxiphoid incision, or via thoracotomy or video-assisted thorascopic surgery to create a pericardial window. ii. In contrast to patients with constrictive pericarditis, immediate hemodynamic improvement occurs once the pericardium is opened and direct pressure exerted on the heart is relieved. iii. However, despite this fact, pulmonary edema, acute right and left ventricular dysfunction, and circulatory collapse can occur. 17. Cardiac sounds or extra sounds a. S1 - Lub - related to the closure of the mitral and tricuspid valves i. S1 result from closure of the mitral and tricuspid valves - Intensity is loudest over the mitral area or apex, and it is best heard with diaphragm of the stethoscope - intensity is increased by blood viscosity and mitral stenosis - intensity is decreased with obesity, pericardial effusion, pulmonary/systemic HTN, and calcification of the mitral valve - Splitting is possible from asynchronous contraction of the left and right ventricles b. S2 - Dub - closure of the aortic and pulmonary valve - physiological splitting is an expected, but can be abnormal and it is best heard during inspiration - physiological splitting - occurs during inspiration when the difference between the timing of aortic and pulmonic valve closure is accentuated c. S3 - results from the passive flow of blood from the atria - S3 results from passive flow of blood from the atria. The sound is low-pitched and is best heard with the bell of the stethoscope with the patient in the left lateral recumbent position. The rhythm resembles that of "Ken-tuc-ky." Although this sound is normal in children and young adults, it is an indicator of systolic dysfunction after age 40, representing abnormal early filling of the ventricles. d. S4 - late diastolic sound immediately preceding S1 - S4 is a late diastolic sound immediately preceding S1. It is best heard with the bell at the apex or mitral area with the patient in the left lateral recumbent position. The rhythm of the cardiac cycle with an audible S4 resembles that of "Tenn-es-see." An S4 sound is 26 Exam 2 - Study guide27 characteristic of diastolic dysfunction, representing a noncompliant ventricle that resists expansion. e. Extra cardiac sounds i. Mitral ejection - clicks are best heard at the apex and are the most common ejection sound. They are associated with mitral valve prolapse and mitral regurgitation. ii. Aortic ejection - clicks are heard at both the base and the apex and do not change with respiration. They are associated with ascending aortic aneurysm, coarctation of the aorta, hypertension with aortic dilation or aortic stenosis, and obstruction of the aorta. iii. Pulmonary ejection - licks are heard at the base in the pulmonic area and change markedly with respiration. They are associated with pulmonic stenosis, pulmonary hypertension, idiopathic dilation of the pulmonary artery, and hyperthyroidism. iv. The opening snap of the mitral valve - is best heard just inside the apex, radiates toward the base, and is sharper and higher-pitched than ventricular filling sounds. It is associated with mitral stenosis. v. The opening snap of the tricuspid valve - is difficult to differentiate from the louder opening snap of the mitral valve. It is occasionally heard with atrial septal defects, but otherwise has limited diagnostic value. vi. Pericardial friction rub - rub is best heard over the left sternal border in the upright position with the patient leaning slightly forward. It is high-pitched and scratchy and not eliminated by breath holding. It is associated with either uremic pericarditis with underlying hypertension and air in the mediastinum or myocardial infarction. vii. Mediastinal crunch - is a random crunching or grating sound, also referred to as Hamman’s sign. Cardiac surgery may cause it to occur. 18. Systolic Murmurs Location a. Slide#14 - cardiovascular system part II b. Mitral regurgitation: Holosystolic; best heard at the apex to left sternal border c. Tricuspid regurgitation: Holosystolic; best heard at the parasternal border at the third and fifth intercostal space d. Ventricular septal defect: Holosystolic; best heard at the left sternal border at the third to fifth ICS e. Aortic stenosis: Midsystolic; best heard at second ICS f. Pulmonary stenosis: Midsystolic; best heard at second left ICS 19. Grading of murmurs a. Slide #16 - cardiovascular system part II b. Grade I—very faint, not heard in all positions c. Grade II—soft but easily heard d. Grade III—moderately loud e. Grade IV—loud, may be associated with a thrill f. Grade V—very loud, may be heard with the stethoscope barely on the chest, associated with a thrill g. Grade VI—may be heard with the stethoscope off the chest, associated with a thrill 27 Exam 2 - Study guide28 h. Murmurs should be described according to grade (intensity), location, radiation, pitch (high, medium, low), quality (blowing, rumbling, harsh, musical), and where they occur in the cardiac cycle. 20. Consequence of each type of valve problem a. Slide #26, #37 b. Consequences of Mitral Stenosis i. Increase pressure between the LA and the LV. ii. Any marked increase in HR can increase in left atrial pressure, lead to increase in pulmonary artery pressures, potential fluid backup, and pulmonary edema. iii. Left atrial hypertrophy and distention iv. Atrial dysrhythmias, most commonly atrial fibrillation. v. Atrial systolic “kick” is lost during atrial fibrillation vi. Pulmonary congestion and eventually pulmonary edema. vii. In patients with chronic mitral stenosis, pulmonary hypertension develops c. Consequences of Aortic Stenosis i. The consequence of LVH in aortic stenosis is a decrease in ventricular compliance, hypertrophic remodeling, and an eventual decrease in the intrinsic contractility of the myocardium. 21. Pulmonary Capillary Wedge Pressure a. Pulmonary capillary wedge pressure is an integrated measurement of the compliance of the left side of the heart and the pulmonary circulation. 22. Differentiating Aortic Stenosis vs Mitral Stenosis vs Mitral Regurg vs Aortic Regurg vs Mitral Valve Prolapse a. Aortic stenosis i. Most common causes : ii. congenital defect resulting iii. rheumatic valvular heart disease. iv. Isolated aortic valvular dysfunction in patients with rheumatic heart disease is rare. Commonly, rheumatic valvular disease is associated with mitral valve involvement. v. During auscultation, a low-frequency systolic ejection murmur is characteristic of aortic stenosis. vi. Heard best in the second right intercostal space with the client leaning forward. 28 Exam 2 - Study guide29 vii. Murmur is harsh, loud, and often associated with a thrill. viii. May radiate to the neck, left sternal border, and, in some cases, to the apex. ix. Syncope, angina, and dyspnea (remembered with the acronym SAD) on exertion x. Angina may be present because of decreased perfusion of the left ventricle due to left ventricular hypertrophy (LVH) rather than CAD, but both exist in many cases. xi. Associated physical: an early ejection click, a diminished S2, a heave or sustained apical impulse with LVH, crackles at the lung bases with left ventricular failure, jugular venous distension, hepatomegaly, and peripheral edema that may be associated with right ventricular failure. Treatment includes medical and/or surgical intervention. xii. Normal aortic valve area of 2.5 to 3.5 cm2 xiii. Normal left ventricular systolic pressure of 100 to 130 mm Hg is sufficient to generate flow rates of 250 to 300 mL/sec. xiv. To ensure normal flow rates and CO the velocity of systolic ejection must increase. xv. Ventricular systolic pressure increases dramatically xvi. Results in LVH xvii. Aortic valve area of less than 1 cm2 produces a clinical triad of symptoms that includes angina (even in the absence of significant coronary artery disease), syncope, and congestive heart failure. xviii. Aortic valve area less than 1 cm2 represents severe aortic stenosis and should be a cause of concern during anesthetic management because of the associated increase in perioperative cardiac morbidity. xix. Aortic valve area less than 0.7 cm2 is associated with sudden death. xx. Left ventricular concentric hypertrophy -compensatory change associated with aortic stenosis. xxi. Several hemodynamic adaptations that are unique to aortic stenosis and present a challenge and a dilemma with regard to anesthesia management. xxii. The consequence of LVH in aortic stenosis is a decrease in ventricular compliance, hypertrophic remodeling, and an eventual decrease in the intrinsic contractility of the myocardium. xxiii. Reduction in ventricular compliance affects normal hemodynamics b. Mitral stenosis i. Progressively narrowed - Normal mitral valve area is 4 to 6 cm2 ii. Reduced flow from the LA into the LV during diastole. 29 Exam 2 - Study guide30 iii. To compensate - Pressure develops across the valve orifice. This creases more pressure with subsequent decrease in the opening. iv. Flow is restricted and left ventricular volume is decreased. v. RESULT 1. Pulmonary congestion, decreased CO, and potential RV overload/failure. vi. When narrows to 1.5 to 2.5 cm2, - increased HR and CO. vii. Less than 1 cm2, the prolonged diastolic filling time and elevated mean left atrial pressure are incapable of maintaining normal LVEDV, -symptoms that occur at rest viii. Pulmonary congestion occurs as a result of increases in left atrial pressure. ix. Decreased SV is caused by decreased left ventricular volume. x. Left ventricular filling is dependent on the length of diastole, the gradient between the LA and LV, and the surface area of the mitral valve. xi. Because mitral stenosis presents a fixed resistance to ventricular inflow, most of the pressure generated during atrial systole is used to overcome the resistance caused by the stenotic valve rather than used for producing forward flow. As the HR increases to greater than 90 bpm and diastolic time intervals are shortened, LVEDV is decreased. Blood flow through the mitral valve can be calculated by using the Gorlin formula, which has been described earlier. c. Mitral regurg i. A portion of systolic ventricular flow regurgitates back through the insufficient valve. ii. Degree of regurgitation, called regurgitant fraction, determined by four factors: 1. 1. Size of the valve orifice (surface area measured in cm2) 2. 2. Pressure between the LA and the LV 3. 3. Time available for regurgitation (systole 4. 4. Aortic outflow impedance SVR; Regurgitant fraction can be significantly influenced by changes in impedance to aortic blood flow. Increased afterload will decrease SV. iii. RESULTS IN: 1. Volume overload of the LA and LV. iv. Acute and chronic MR have substantially different pathophysiologic manifestations. v. If acute MR is caused by papillary muscle rupture, which can occur after an acute MI, the mortality rate aprox. 75% within 24 hours, 95% within 48 hours. 30 Exam 2 - Study guide31 vi. Chronic MR produces long-standing and gradual elevation of left atrial pressure - results in remodeling of LA causing LA dilation. Hypertrophic changes occur in response to a continual increased left ventricular volume by increasing the left ventricular chamber size. vii. This type of hypertrophic change is called eccentric hypertrophy. viii. Eccentric hypertrophic changes occur to compensate for increases in volume ix. Hypertrophic Left Atrium accommodates a larger regurgitant volume, which results in small increases in pressure. x. Dilated and compliant LA allows the pulmonary vascular circuit to be buffered from the excessive left atrial volume. xi. Chronic MR causes pulmonary venous congestion, which creates pulmonary vascular reactive changes that eventually result in pulmonary artery hypertension. xii. Distention of the Left Atrium may lead to atrial fibrillation xiii. Other s/s: Hoarseness due to compression of the left branch of the recurrent laryngeal nerve, partial paralysis of the left vocal cord could result in respiratory distress in those patients with respiratory disease. xiv. Pulmonary Vasculature and Right Ventricular Function 1. In acute MR -marked elevation of left atrial pressure - results in almost immediate development of pulmonary edema. 2. Creates an increased right ventricular workload. 3. Results in ventricular dilation and consequently may lead to right ventricular failure. 4. In chronic MR - more gradual-allows secondary pulmonary artery hypertension - inner layer of arteries become fibrous. 5. If coexisting mitral stenosis, pulmonary vascular resistance and right ventricular pressures may be excessively elevated. d. Aortic regurg i. Acute or chronic ii. Primary or secondary - depending on the cause. iii. Primary chronic - caused by rheumatic valvular disease and almost always involves the mitral valve to some degree. iv. Primary acute - is most commonly caused by infective endocarditis, which results in direct damage to the aortic valve cusps. 1. Acute secondary (functional) results from aortic root dissection caused either by trauma or aneurysm and results in a mechanical and functional impairment of functional aortic valve closure. 2. The major hemodynamic aberration related to AI occurs during diastole. 31 Exam 2 - Study guide32 3. Portion of the blood volume ejected from the LV into the aorta regurgitates back into the ventricle because of incomplete closure of the aortic valve. 4. Causes volume overload of the LV. 5. Chronic ventricular overload causes eccentric ventricular hypertrophy and chamber dilation. 6. Diastolic time and diastolic pressure can be manipulated during the course of anesthesia so that the amount of regurgitant flow is decreased and the amount of forward flow is increased. 7. A HR of 90 to 100 bpm decreases the diastolic time period, which reduces the time available for regurgitation. v. Chronic – may be asymptomatic 1. Except during times of stress, the clinical symptoms are usually not incapacitating. 2. End-stage - myocardial failure with decreased CO -with evidence of pulmonary congestion. 3. As long as ventricular hypertrophy and dilation do not affect the mitral valve, the pulmonary circulation is not affected by the pathophysiologic 4. Increased myocardial occurs because of the development of eccentric hypertrophy. e. Mitral valve prolapse i. 5% to 15% of the US population, is presently estimated at 1.6% to 2.4% of adults. ii. Familial predisposition exists iii. Women are three times more likely than men to develop MVP. iv. Other conditions frequently associated with MVP include pectus excavatum and kyphoscoliosis. v. Weakness, vi. Dizziness, vii. Syncope viii. Atypical chest pain ix. Palpitations. x. Atrial and ventricular dysrhythmias are common findings in asymptomatic patients. xi. Confirmed through echocardiography. xii. Medical therapy - β-blocking drugs, xiii. Most patients do not require medical or pharmacologic management xiv. Changes primarily affect the cusps and the chordae tendineae. -become pliable and long xv. Valve leaflets become supple and redundant – evert in LA during systole 32 Exam 2 - Study guide33 xvi. Undiagnosed in the majority of patients. xvii. Manifestation that commonly occurs in healthy patients who are receiving anesthesia is an unexpected dysrhythmia (e.g., premature ventricular contractions), many of which resolve spontaneously. xviii. β-blockers - best choice for control of dysrhythmias xix. Preoperative anxiety potentially increasing the degree of MVP and concomitant dysrhythmias. xx. Managing anxiety important. xxi. Anticholinergics can cause tachycardia and should therefore be omitted from the preoperative regimen. 23. Cardiomyopathy – recognize the different types, what are the risks /consequences a. slide #46 part 2 b. Cardiomyopathy i. Heart muscle disease - myocardium - chronic and frequently progressive in nature. ii. Result in fatal dysrhythmias, progressive cardiac disability, and sudden cardiac death. iii. All forms of cardiomyopathy can result in congestive heart failure and death. iv. Intrinsic cardiomyopathy cannot be attributed to a specific external causative factor. v. Extrinsic cardiomyopathy -directly attributed to a disease process or toxin (ischemia, chronic inflammation, congenital heart disease, metabolic diseases (e.g., hemochromatosis), and toxins (e.g., chronic alcohol intake, chemotherapeutic agents). vi. Patients with a severe cardiomyopathy frequently present for cardiac procedures such as pacemaker implantation or heart transplantation. vii. Thorough preoperative evaluation is essential viii. Analysis of the invasive and noninvasive cardiac studies, including TEE and the cardiologist’s impression of the patient’s cardiac status, is vital. c. Hypertrophic cardiomyopathy i. Genetically transmitted disorder ii. Myocardial dysfunction that can cause CAD, valvular dysfunction, ventricular remodeling, and hypertension. iii. 1 in 500 adult persons. iv. Obstructive HCM has previously been referred to as idiopathic hypertrophic subaortic stenosis. v. Currently, the preferred term used to describe this pathologic state is HCM with or without left ventricular outflow obstruction. vi. Signs/ symptoms 1. Most common cause of sudden death in the pediatric and young adult populations. 2. Major cardiac changes a. ventricular hypertrophy b. decreased ventricular chamber size c. increased ventricular wall thickness d. impaired ventricular relaxation. 3. Defect related to the contractile mechanism. 4. Increase in the density of calcium channels is one abnormality that appears to lead to myocardial hypertrophy. 5. Asymmetric hypertrophy of the interventricular septum of the LV occurs 33 Exam 2 - Study guide34 6. Asymmetric hypertrophy of the intraventricular septum causes a left outflow tract obstruction, and the hemodynamic consequences are similar to those that are characteristic of aortic stenosis. 7. Coronary arterial walls become narrowed because of the presence of collagen. 8. Patients with HCM and sarcomere myofilament mutations have a greater degree of microvascular impairment, an increased incidence of myocardial fibrosis, and impaired myocardial remodeling. d. Hypertrophic cardiomyopathy i. Systolic and diastolic dysfunction. ii. Loss of diastolic compliance iii. Congestive heart failure may ensue as left atrial pressures continue to increase. iv. Maintenance of normal sinus rhythm is critical for adequate SV. v. Thickening of the internal lumen of the coronary arteries decreases myocardial perfusion, leading to ischemia. e. Dilated Cardiomyopathy i. Most common form of cardiomyopathy ii. Most often occurs in adults. iii. Genetic link - 20% and 30% autosomal dominant mutation iv. Also occur in patients as a result of autosomal recessive traits, such as in patients with Duchenne muscular dystrophy. v. Viral illness, increased inflammation from metabolic abnormalities, autoimmune mechanism, or toxins. vi. More often in men than in women vii. Risk factor for developing CHF viii. Eccentric hypertrophy affects both left and right ventricles. ix. Interstitial fibrosis and myocardial cell death, the ventricular chambers increase in size without an associated increase in the diameter of the ventricular walls or interventricular septum. x. Heart becomes an inefficient pump xi. Tension on the ventricular walls is increased due to the decreased size and increased diameter of the ventricular walls. xii. Impaired systolic function (decreased SV) occurs because of the loss of myocardium causing decreased contractility. xiii. Myocardial oxygen consumption is increased xiv. Does not cause direct damage to the atrioventricular valves. xv. As ventricular dilation occurs, changes in ventricular dimensions can cause mitral valve and/or tricuspid valve regurgitation potentially intensifying volume overload, decreased SV, and increased pulmonary congestion. xvi. As the EF decreases, decreased peripheral perfusion causes increased circulating catecholamines, cortisol excretion, and activation of the renin-angiotensin-aldosterone system, which causes vasoconstriction and increased renal absorption of fluid. xvii. Left-sided heart failure resulting in pulmonary venous congestion or biventricular failure leads to fulminant congestive heart failure. xviii. Increased risk of thromboembolism as a result of stasis of blood from inadequate ventricular emptying. f. Restrictive cardiomyopathy 34 Exam 2 - Study guide35 i. Genetic predisposition (e.g., familial cardiomyopathy), infiltrative disease (e.g., sarcoidosis), storage diseases (e.g., hemochromatosis), and endomyocardial dysfunction (e.g., endomyocardial fibrosis). ii. Can occur in the pediatric population; although rarest forms iii. High mortality rate once symptoms begin to develop. iv. Infiltration of fibrous tissue and deposition into the myocardium and/or endomyocardium v. one or both ventricles become stiff and noncompliant, which inhibits normal diastolic filling. vi. Restricted ventricular filling, SV is decreased. vii. Atria become dilated as a compensatory response to volume overload, and left- and/or right-sided heart failure can occur. g. Arrhythmogenic Right Ventricular Cardiomyopathy i. AKA: Arrhythmogenic right ventricular dysplasia - autosomal dominant genetic disorder. ii. Diagnosis is often made postmortem - sudden cardiac death is a common iii. Signs and symptoms can occur during childhood, but more often manifest during adolescence. iv. During sports-related exercise, severe intolerance caused by increasing myocardial oxygen demand can result in lightheadedness, syncope, and/or sudden death. v. Fibrous fatty infiltrates invade the right ventricular myocardium and cause myocyte dysfunction and death. vi. Right ventricular cardiac output - decreased. vii. Left ventricle undergoes this type of pathologic change in approximately half of patients and CHF sign of disease progression. viii. Ventricular dysrhythmias are common and range from premature ventricular contractions to ventricular fibrillation. ix. May be exquisitely sensitive to increased catecholamine levels, which may further provoke these dysrhythmias. h. Takotsubo Cardiomyopathy i. Transient cardiac syndrome that involves left ventricular apical akinesis. ii. Mimic acute coronary syndrome. iii. Also referred to as stress cardiomyopathy, transient LV ballooning syndrome, apical ballooning syndrome, and broken heart syndrome. iv. Complains of chest pain, develops ST segment elevation on ECG, and has elevated cardiac troponin levels consistent with an acute MI. v. Cardiac angiogram will reveal an absence of significant coronary artery disease and severe left ventricular apical enlargement or ballooning. vi. 1) akinesis or dyskinesis of LV wall motion abnormalities (ballooning), (2) chest pain, (3) electrocardiographic changes (ST segment elevation or T wave inversion), (4) absence of obstructive epicardial coronary artery disease, and (5) absence of pheochromocytoma or myocarditis. vii. Coronary artery vasospasm, altered myocardial fatty acid metabolism, and LV outflow tract obstruction have all been postulated. viii. Leading theory is that elevated endogenous catecholamine concentrations cause myocardial toxicity leading to myocardial inflammation and dysfunction. ix. Physiologic or psychological stress appears to be the trigger for the development of TCM x. Has occurred during general anesthesia. xi. Systolic function is significantly reduced, with the reported EF ranging from 20% to 49%. xii. Currently, the treatment is supportive. 35 Exam 2 - Study guide36 xiii. Majority of patients regain normal cardiac function within 4 to 8 weeks after onset of symptoms. 24. Pacemakers, general types, including leadless pacemakers a. Pacemakers i. Approximately the size of a quarter ii. Two main components: (1) a pulse generator that houses the battery, circuitry, and connectors, and (2) the insulated lead wires that conduct energy to and from the myocardium. iii. The pulse generator is usually implanted in the pectoral pocket on either the right or left side of the chest. iv. Implantation is accomplished while the patient receives a general anesthetic or local anesthetic with sedation v. A sensing circuit, located within the pulse generator, picks up signals transferred from the myocardium via the leads. vi. High amplitude is seen by the PM as intrinsic activity, and low amplitude is seen as interference commonly referred to as noise. vii. The low amplitude signals are filtered, and native cardiac signals are sensed. The PM can interpret intrinsic activity correctly, and pacing is initiated appropriately. viii. However, in the presence of EMI, this noise causes the PM to inaccurately sense intrinsic cardiac activity resulting in PM inhibition. ix. May contain up to three lead wires. x. The wires are imbedded into the right atrium, the right ventricle, both the right atrium and ventricle, or the right atrium and both ventricles. xi. Unipolar configuration - greater distance between the anode and cathode -places the PM at an increased risk for EMI. xii. Bipolar leads contain two electrodes. Less distance between the two poles, decreasing the chance of EMI and the potential for disruption xiii. Sensing and capturing responses that may be identifiable by the presence of spikes on the ECG. xiv. When the PM lead wire is placed in the right atrium there is a spike followed by a P wave on the ECG, representing atrial depolarization xv. When the lead is inserted in the right ventricle, a spike followed by a QRS complex on the ECG indicates ventricular depolarization xvi. If the device is a dual-chamber PM (a lead is inserted in both the right atrium and ventricle), there is a spike before the P wave and before the QRS complex followed by both atrial and ventricular depolarization xvii. If the pacing device is sensing the patient’s intrinsic rhythm and not providing a paced response due to inherent cardiac activity, only a sensing marker is visualized on the surface ECG. xviii. External pacemakers 1. External pacing, transcutaneous pacing pads are applied (a) anteriorly on the right upper chest and anteriorly on the left lower chest, or (b) anteriorly midchest and posteriorly between the scapulae. 2. In transvenous pacing, the pacing catheter is passed into the central circulation (usually via an introducer sheath) and into the appropriate cardiac chamber(s). The pacing lead is connected to an external pacemaker generator and is programmed as needed. 36 Exam 2 - Study guide37 3. Epicardial pacing leads are often inserted at the completion of cardiac surgery. These pacing wires are directly sewn, by the cardiac surgeon, onto the epicardium, passed through the skin, attached to an external pacing device, and programmed as dictated by the clinical situation. 4. Indications a. Ventricular tachycardia (VT) b. Ventricular fibrillation (VF) c. Postmyocardial infarction with an ejection fraction (EF)