Cardiovascular Alterations PDF

Cardiovascular Alterations PAT401 Week 1 Fall 2023 1  Disorders of the Pericardium Acute pericarditis Acute inflammation of the pericardium...

Cardiovascular Alterations PAT401 Week 1 Fall 2023 1  Disorders of the Pericardium Acute pericarditis Acute inflammation of the pericardium Clinical manifestations: fever, myalgias, and malaise, followed by the sudden onset of severe chest pain Treatment: rest, salicylates, and nonsteroidal antiinflammatory drugs; combined nonsteroidals and colchicine 2 Figure 32.14, Rogers, 2023, p. 1085 Disorders of the Pericardium (cont.) Constrictive (restrictive) pericarditis Fibrous scarring with occasional calcification of the pericardium causes the visceral and parietal pericardial layers to adhere Clinical manifestations: exercise intolerance, dyspnea on exertion, fatigue, and anorexia Treatment: dietary sodium restriction and diuretics to improve cardiac output Antiinflammatory drugs If these treatments are not successful, then surgical excision is performed. Figure 32.15, Rogers, 2023, p. 1086 3   Pericardial effusion Disorders of the Accumulation of fluid in the pericardial cavity Pericardium Tamponade Treatment: pericardiocentesis (cont.) 4  Disorders of the Myocardium: Cardiomyopathies Effects of neurohumoral responses to ischemic heart disease or hypertension on the heart muscle cause remodeling Many cases of cardiomyopathy are idiopathic 5 Figure 32.16, Rogers, 2023, p. 1086  Disorders of the Myocardium: Cardiomyopathies (cont.) Dilated cardiomyopathy Impaired systolic function, leading to increases in intracardiac volume, ventricular dilation, and systolic heart failure Causes: ischemic heart disease; valvular disease; diabetes; alcohol; drug toxicity; renal failure; hyperthyroidism, diabetes; deficiencies of niacin, vitamin D, and selenium; infection Clinical manifestations: dyspnea, fatigue, pedal edema Treatment: reduce blood volume, increase contractility, reverse underlying disorder 6 Figure 32.17, Rogers, 2023, p. 1087 Disorders of the Myocardium: Cardiomyopathies (cont.) Hypertrophic cardiomyopathy Hypertrophic obstructive cardiomyopathy Hypertensive or valvular hypertrophic cardiomyopathy Figure 32.18, Rogers, 2023, p. 1087 7  Hypertrophic obstructive cardiomyopathy Common inherited heart defect of a thick septal wall Clinical manifestations: angina, syncope, palpitations, symptoms of Disorders of the MI, symptoms of left heart failure Myocardium: Treatment Beta blockers or ACE inhibitors Cardiomyopathies Surgical resection of the (cont.) hypertrophied myocardium Septal ablation Prophylactic placement of an implantable cardioverter- defibrillators in high-risk individuals 8  Hypertensive or valvular hypertrophic Disorders of the cardiomyopathy Myocardium: Hypertrophy of the myocytes: attempts to compensate for increased myocardial workload Cardiomyopathies Clinical manifestations: asymptomatic or may (cont.) complain of angina, syncope, dyspnea on exertion, and palpitations 9  Disorders of the Restrictive cardiomyopathy Myocardium: Myocardium becomes rigid and noncompliant, impeding ventricular filling and raising filling pressures Cardiomyopathies during diastole. (cont.) Clinical manifestations: right heart failure occurs with systemic venous congestion Treatment: correct the underlying cause 10  Valvular dysfunction Stimulates chamber dilation and/or myocardial hypertrophy Disorders of Manifestations of cardiac valve disease vary the Depends on valve involved, form of dysfunction, Endocardium: and severity and rate of onset of dysfunction Valvular Heart Treatment Disease Careful fluid management Valvular repair or valve replacement with a prosthetic valve, followed by long-term anticoagulation therapy and life-long antibiotic prophylaxis before invasive procedures 11 Valvular Heart Disease Normal valves maintain normal If they do not close properly they can allow backflow (regurgitation) If the valve does not fully open or is narrowed (stenosed), then the raised direction of blood flow through resistance impedes blood movement on its normal route and extra the heart’s chambers propulsive force must be applied by the myocardium Abnormalities of valvular Acquired valvular disease is by far the most common and is most prevalent in the elderly structure and/or function can Congenital valvular defects arise from disrupted heart development, about either be congenital or acquired 50 percent of which involve the valves Valves exposed to high blood Makes them particularly susceptible to other risk factors that promote flow and pressures valvular damage Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. 12 https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0. Disorders of the Endocardium: Valvular Heart Disease The acquired forms are more Worldwide, the most common common in adults and result cause of acquired valvular from dysfunction is degeneration or Either congenital or acquired Inflammatory, ischemic, traumatic, inflammation of the degenerative, or infectious alterations of valvular structure and function endocardium secondary to rheumatic heart disease Structural alterations of heart valves are caused by Previously undiagnosed, mild The prevalence of undiagnosed remodeling changes in the valvular heart disease is present moderate or severe valvular valvular extracellular matrix in approximately 1/2 of heart disease may be as high as and lead to stenosis, individuals ≥65 years of age 6.4% incompetence, or both 13  Age Risk Gender Factors Tobacco use Hypercholesterolemia Rheumatic heart disease HTN Type 2 diabetes Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. 14 https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0. Pathophysiology of Valvular Disease Presence of other factors such as hyperlipidemia, The constant stress of facing high flow and pressure hypertension, and inflammation accelerate this over thirty to forty million cardiac contractions a year process and promote the deposition of a form of is not without its consequences calcium phosphate Most common valvular disorder is calcification that Aortic and mitral valves are more prone to comes with “wear-and-tear” and aging calcification due to the pressure they face Most common pattern of calcification in aortic valve is mounded masses within cusps of the valve that eventually fuse and stop the valve from opening fully Calcification in the mitral valve tends to start in the fibrous annulus, which does not impact valvular function to the same extent, but in exceptional cases can cause regurgitation or stenosis, or even arrhythmias as calcium deposits impinge on atrioventricular conduction system Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0. 15  Valvular stenosis Valve orifice is constricted and narrowed Aortic Disorders of the Mitral Endocardium: Valvular regurgitation Valvular Heart Disease (cont.) Valve fails to shut completely. Is also called insufficiency or incompetence Aortic Mitral Tricuspid Characteristic heart sounds, cardiac murmurs, and systemic complaints: assist in determining which valve is abnormal Mitral valve prolapse syndrome https://my.clevelandclinic.org/health/articles/17067-heart-valves 16  Disorders of the Endocardium: Valvular Heart Disease (cont.) Aortic stenosis Orifice of the aortic semilunar valve narrows, causing diminished blood flow from the left ventricle into the aorta Clinical manifestations: angina, syncope, and heart failure Treatment Most require valve repair or replacement with a prosthetic valve, followed by long-term anticoagulation therapy Transcatheter aortic valve implantation 17 Figure 32.19, Rogers, 2023, p. 1089 Pathophysiology of Aortic Stenosis Algorithm 32.5, Rogers, 2023, p. 1090  Disorders of the Endocardium: Valvular Heart Disease (cont.) Mitral stenosis Impairment of blood flow from the left atrium to the left ventricle Most common cause: acute rheumatic fever Clinical manifestation: opening snap Treatment: surgical repair; may require valve replacement Figure 32.20, Rogers, 2023, p. 1090 19 Pathophysiology of Mitral Stenosis Algorithm 32.6, Rogers, 2023, p. 1091 20 Disorders of the Endocardium: Valvular Heart Disease (cont.) Aortic regurgitation Inability of the aortic valve leaflets to close properly during diastole Clinical manifestations: widened pulse pressure as a result of increased stroke volume and diastolic backflow Treatment: valve replacement may be delayed for many years with the use of vasodilators and inotropic agents 21 Algorithm 32.7, Rogers, 2023, p. 1092 Disorders of the Endocardium: Valvular Heart Disease (cont.) Mitral regurgitation Most common causes: mitral valve prolapse, rheumatic heart disease, infective endocarditis, MI, connective tissue disease, dilated cardiomyopathy Permits backflow of blood from the left ventricle into the left atrium Treatment: surgical repair or valve replacement 22 Algorithm 32.8, Rogers, 2023, p. 1092 Disorders of the Tricuspid regurgitation Endocardium: Leads to volume overload in the right atrium Valvular Heart and ventricle, increased systemic venous blood pressure, and right heart failure Disease (cont.) 23 Disorders of the Endocardium: Valvular Heart Disease (cont.)  Mitral valve prolapse syndrome Anterior and posterior cusps of the mitral valve billow upward (prolapse) into the left atrium during systole Clinical manifestations: asymptomatic Treatment: none needed or beta blockers 24 Figure 32.21, Rogers, 2023, p. 1093  A client has a diagnosis of valvular regurgitation. What pathophysiologic process is the client experiencing? The valves: Use Your are constricted and narrowed, impeding the forward flow of blood Clinical fail to close completely, permitting the backflow of blood to continue have an inherited defect, such as Judgement! thickening of the septal wall cause acute pericarditis and filling of the pericardial sac CARDIOVASCULAR ALTERATIONS IN CHILDREN 26  Leading cause of death (except for prematurity) in the first year of life Cause is known in only 10% of defects Congenital Heart Disease Prenatal, environmental, and genetic risk factors Maternal: rubella, lupus, insulin-dependent diabetes, alcoholism, illicit drug use, age (> 40 years) phenylketonuria (PKU), and hypercalcemia Chromosomal aberrations 27  Based on blood flow Classification Lesions increasing pulmonary blood flow Defects that shunt from high-pressure left side of Congenital to low-pressure right side with pulmonary congestion; acyanotic Lesions decreasing pulmonary blood flow Heart Disease Generally complex with right-to-left shunt and cyanosis Obstructive lesions Right- or left-sided outflow tract obstructions that curtail or prohibit blood flow out of the heart; no shunting Mixing lesions Desaturated blood and saturated blood mix in the chambers or great arteries of the heart 28  Classification of Congenital Heart Disease (cont.) Shunting of blood flow from left heart into right heart called a left-to-right shunt Cause shunting of blood from the right side of heart directly Left-to-right shunt increases into left side of heart (right- Acyanotic volume in right side of heart Results in increased blood Cyanotic to-left shunt) Right-to-left shunt heart flow into the pulmonary circulation heart decreases blood flow through the pulmonary defects Because blood continues to flow through lungs defects system Causes less-than-normal before passing into oxygen delivery to tissues systemic circulation, there resulting in cyanosis is no decrease in tissue oxygenation or cyanosis 29 Classification of Most congenital heart defects are named to describe underlying defect (valvular abnormalities, abnormal openings in the septa, Congenital Heart malformation or abnormal placement of great vessels) Disease (cont.) Figure 33.1, Rogers, 2023, p. 1111 30 Shunting of Blood in Congenital Heart Disease Figure 33.2, Rogers, 2023, p. 1111 31 Defects With Increased Pulmonary Blood Flow 32  Failure of the ductus arteriosus to close Normally closes within first few hours of birth. PDA allows blood to shunt from the pulmonary artery to the Patent Ductus aorta. Arteriosus Clinical manifestation Continuous, machinery-type (PDA) murmur Bounding pulses, active precordium, thrill upon palpation, and signs and symptoms of pulmonary overcirculation. Treatment Surgical closure involving ligation by incision, catheter, or video-assisted thoracoscopy 33 Figure 33.3, Rogers, 2023, p. 1112  Atrial Septal Defect Abnormal communication between atria Blood shunted from left to right Clinical manifestations Often asymptomatic; diagnosed by murmur Three major types of defect Ostium primum Ostium secundum Sinus venosus Treatment Surgical closure before school age results in better health 34 Figure 33.4, Rogers, 2023, p. 1113  Ventricular Septal Defect Abnormal communication between ventricles Shunting from high-pressure left side to low-pressure right side Clinical manifestations Depends on age of child, size of defect, level of PVR Heart failure Poor weight gain Murmur and systolic thrill Treatment Minimal treatment to surgical repair Figure 33.5, Rogers, 2023, p. 1113 35  Use Your Clinical Judgement!  Atrioventricular Canal Defect Results from nonfusion of the endocardial cushions Abnormalities demonstrated in the atrial and ventricular septa and AV valves Complete, partial, and transitional AVC defects Clinical manifestations Presents with a murmur, heart failure, respiratory tract infections Treatment Complete repair between 3 and 6 months of life Figure 33.6, Rogers, 2023, p. 1114 37 Obstructive Defects 38  Coarctation of the Aorta Narrowing of the lumen of aorta that impedes blood flow 8% to 10% of defects Is almost always found in the juxtaductal position But can occur anywhere between origin of aortic arch and bifurcation of aorta in lower abdomen 39 Figure 33.7, Rogers, 2023, p. 1115 Coarctation Clinical manifestations: Newborns usually exhibit HF of the Aorta Once the ductus closes, rapid deterioration occurs from hypotension, acidosis, and shock (cont.) Clinical manifestations: Older children Hypertension in the upper extremities Decreased or absent pulses in the lower extremities Cool mottled skin Leg cramps during exercise Treatment Prostaglandin administration Mechanical ventilation Inotropic support Maintain cardiac output Surgery 40  A nurse is assessing a child with coarctation of Use Your the aorta. What will the nurse find? Clinical Squatting when short of breath Judgement! Hypercyanotic spells High blood pressure in the upper extremities with decreased pulses in feet Syncopal episodes with chest pain 41 Aortic Stenosis Narrowing of the aortic outflow tract (10% of defects) Caused by malformation or fusion of the cusps Causes an increased workload on the left ventricle Clinical manifestations Often asymptomatic Signs of exercise intolerance in preadolescence Syncopal episodes, epigastric pain, and exertional chest pain in more severe forms Murmur Treatment Commissurotomy; aortic valvotomy; Ross procedure 42 Figure 33.8, Rogers, 2023, p. 1116  Pulmonic Stenosis Narrowing of pulmonary outflow tract Abnormal thickening of valve leaflets Narrowing of valve Pulmonary atresia Severe form Clinical manifestations Often asymptomatic Exertional dyspnea, murmur, fatigue, thrill, cyanosis, HF Treatment Mild Not treated, closely observed Figure 33.9, Rogers, 2023, p. 1117 Severe Balloon angioplasty; pulmonary valvotomy 43 Defects With Decreased Pulmonary Blood Flow 44  Tetralogy of Fallot Syndrome represented by four defects Large ventricular septal defect Overriding aorta straddles the ventricular septal defect Pulmonary stenosis Right ventricle hypertrophy Cyanosis, hypoxia, and clubbing, feeding difficulty, dyspnea, restlessness, squatting Hypercyanotic spell or a “tet spell” that generally occurs with crying and exertion Most cases corrected surgically in early infancy before 1 year of age; Blalock-Taussig shunt, transcatheter pulmonary valve replacement, patch Figure 33.10, Rogers, 2023, p. 1118 45  Tricuspid Atresia Imperforate tricuspid valve No communication between the right atrium and the right ventricle Additional defects Septal defect Hypoplastic or absent right ventricle Enlarged mitral valve and left ventricle Pulmonic stenosis 46 Figure 33.11, Rogers, 2023, p. 1118 Tricuspid atresia (cont.) Central cyanosis and growth failure Clinical manifestations Exertional dyspnea, tachypnea, and hypoxemia Polycythemia, clubbing, hepatomegaly Prostaglandin administration Blalock-Taussig shunt Rashkind procedure: balloon atrial Treatment septostomy PA band Closure of septal defects 47 Mixing Defects 48  Transposition of the Great Arteries Aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle Results in two separate, parallel circuits Unoxygenated blood continuously circulates through the systemic circulation Oxygenated blood continuously circulates through the pulmonary circulation Extrauterine survival requires communication between the two circuits Clinical manifestations: Cyanosis may be mild shortly after birth and worsen during the first day Treatment: Surgery to switch the arteries Figure 33.12, Rogers, 2023, p. 1119 49  Total Anomalous Pulmonary Venous Connection Pulmonary veins connect to the right side of the heart, directly or indirectly, through one or more systemic veins that drain into the right atrium Nonobstructive vs. obstructive Clinical manifestation Cyanosis Treatment Obstructed lesions are repaired at the time of diagnosis Unobstructed lesions are generally repaired during infancy Surgery: Anastomosis of the common pulmonary vein to the left atrium; closure of the atrial septal defect Figure 33.13, Rogers, 2023, p. 1120 50  Truncus Arteriosus Is failure of embryonic artery to divide into pulmonary artery and aorta Trunk straddles an always present ventricular septal defect Types I through IV I: Most common; main pulmonary artery arises from truncus II: Pulmonary arteries arise from posterior aspect of truncus III: Pulmonary arteries arise from lateral aspect of truncus IV: Pseudotruncus; is a severe form of tetralogy of Fallot with bronchial arteries arising from descending aorta to supply lungs Clinical manifestations Mild-to-moderate cyanosis that worsens with activity Murmur Treatment Modified Rastelli procedure involving VSD patch closure to divert the blood flow from the left ventricle outflow tract into the truncus Correct pulmonary arteries 51 Hypoplastic Left Heart Syndrome Abnormal development of left-sided cardiac structures Obstructs blood flow from the left ventricular outflow tract Left ventricle, aorta, and aortic arch are underdeveloped; mitral atresia or stenosis is observed Clinical manifestations As ductus closes, systemic perfusion is decreased, resulting in hypoxemia, acidosis, and shock Loud and single second heart sound Treatment Prostaglandin administration Correction of acidosis Inotropic support for adequate cardiac output Ventilatory manipulation Surgery Cardiac transplantation 52 Figure 33.15, Rogers, 2023, p. 1122  Cardiovascular Pharmacotherapy (Review this pharmacotherapy PowerPoint before class. Recall that these drugs/classifications of drugs were taught in PAT201/PAT202) PAT401 Fall 2023 Week 1 1  Cardiovascular Pharmacotherapy Classification Drug Glucocorticoids -prednisone NSAIDS (non-selective inhibitors) -ibuprofen Non-opioid analgesics -acetaminophen Shorter acting thiazide diuretics -hydrochlorothiazide Loop diuretics -furosemide Mineralocorticoid receptor antagonists -spironolactone Angiotensin-converting enzyme (ACE) inhibitors -lisinopril Non-selective beta-adrenergic blockers -propranolol Anticoagulants -warfarin Antidote for warfarin therapy -vitamin K 2  Recall The Overall Cardiovascular Pharmacological Goals 1 2 3 4 5 Treat symptoms Decrease heart Improve Improve cardiac Reduce pain workload & oxygenation function oxygen demands 3 Pharmacotherapy: Glucocorticoids Classification Drug Glucocorticoids -prednisone 4  Classification: Synthetic glucocorticoid Indications for use: anti-inflammatory; pericarditis Prednisone Mechanisms of Action: decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation Desired effects: prevent inflammation, reduce risk of bronchospasm in patients with asthma or certain cancers; immunosuppressive at higher dose Adverse effects: Cushing’s syndrome (long-term), fluid retention 5  Pharmacotherapy: Analgesics Classification Drug NSAIDS (non-selective inhibitors) -ibuprofen Non-opioid analgesics -acetaminophen 6  Recall NSAIDs NSAIDs inhibit cyclooxygenase An enzyme responsible for formation of prostaglandins When cyclooxygenase is inhibited, inflammation and pain are reduced! Use Relieve mild to moderate pain, especially for pain associated with inflammation Desired effects Anti-pyretic, anti-inflammatory, analgesic Figure 23.4 Adams et al., 2021, p. 282 7 Recall What The COX Enzymes Do 8 Adapted from: https://science.sciencemag.org/content/336/6087/1386/tab-figures-data CREDIT: C. BICKEL/SCIENCE Recall The Arachidonic Acid Pathway Arachidonic acid is released from cell membrane phospholipids using phospholipase Then…arachidonic acid is converted by enzymes within two different pathways Leukotriene Pathway Cyclooxygenase Pathway Cyclooxygenase enzymes (COX-1; COX-2) Can be expressed under normal conditions i.e. homeostasis Lipoxygenase enzyme (LOX) (COX-1 & COX-2) or in response to triggering event i.e. injury (COX-2) Leukotrienes Prostaglandins & Thromboxane Smooth muscle contraction, constricts pulmonary airways Maintain organ function, protect gastric mucosa, mediate (bronchoconstriction), vasoconstriction, vascular pain & inflammation, vasodilation/vasoconstriction, permeability 9 bronchoconstriction, platelet function Ibuprofen Indications for use: relieve mild to moderate pain, fever, and inflammation Mechanisms of action: inhibition of prostaglandin synthesis Desired effects: reduction of pain, temperature, and inflammation Adverse effects: Nausea, heartburn, epigastric pain, dizziness, GI ulceration with occult or gross bleeding 10 Acetaminophen Indications for use: Treatment of fever, relief of mild to moderate pain Action (unclear): Inhibits synthesis of prostaglandins in central nervous system; direct action at level of hypothalamus and causes dilation of peripheral blood vessels, enabling sweating and dissipation of heat Desired effect: Reduces fever and pain Adverse effects (very rare at therapeutic dose): Acetaminophen inhibits warfarin (Coumadin) metabolism, causing warfarin to accumulate to toxic levels. High-dose or long-term acetaminophen usage may result in elevated warfarin levels and bleeding. Acute toxicity includes nausea, vomiting, chills, and abdominal discomfort 11  Pharmacotherapy: Diuretics Classification Drug Shorter acting thiazide diuretics -hydrochlorothiazide Loop diuretics -furosemide Mineralocorticoid receptor antagonists -spironolactone 12 Recall How The Thiazide, Loop, and Potassium- Sparing Diuretics Work 13 Figure 52-2, Adams et al., 2021, p. 701 Thiazide Diuretics: Hydrochlorothiazide Indications Mechanisms of action HF, HTN, edema Reduces Na+ and Cl- reabsorption by inhibiting Na+/Cl- symporter, reducing water reabsorption in nephron distal convoluted tubule Desired effects Adverse effects Promotes diuresis→ decreases Hypotension, orthostatic hypotension, preload dizziness, H/A Decreases BP Electrolyte imbalances Hypokalemia (dysrhythmias), hyponatremia, hypercalcemia 14 Loop Diuretics: Furosemide Indications - Treatment of acute edema associated with liver cirrhosis, CKD, HF, pericardial effusion - HTN Mechanisms of action - Blocks sodium/potassium/chloride symporter in ascending limb of loop of Henle - Increased urinary excretion of sodium, chloride, potassium, hydrogen ions - Region of nephron that normally filters bulk of sodium → causes +++ diuresis Desired effect - Removes large amounts of fluid in a short time - Decreases preload, decreases BP Adverse effects - Hypovolemia (orthostatic hypotension, syncope) - Electrolyte imbalances - Tachycardia, dysrhythmias, N/V - Hypokalemia and metabolic alkalosis 15  Recall that aldosterone Indications increases Na+ Severe stages of HF and H2O Liver disease (aldosterone not metabolized) resorption! Mechanisms of action Blocks aldosterone receptors (distal convoluted tubules & collecting ducts) Mineralocorticoid Blocks sodium reabsorption Receptor Desired effects Sodium and water excretion is increased Antagonists: Decreases cardiac preload Decreases morbidity and mortality rates in severe HF when Spironolactone added to standard therapy K+ sparing diuretic! Adverse effects Na+ is lost and K+ is retained Hyperkalemia Muscle weakness, ventricular tachycardia, fibrillation 16 Pharmacotherapy: ACE Inhibitors & Beta-Blockers Classification Drug Angiotensin-converting enzyme (ACE) inhibitors -lisinopril Non-Selective Beta-Adrenergic Blockers -propranolol 17 Recall what the ACE normally does Soooo…what happens if we inhibit the ACE? 18 Figure 51.6, Adams et al., 2021, p. 685  Prevents intense vasoconstriction Recall that caused by angiotensin II decreased SVR (decreased afterload) ACE inhibitors Both decrease myocardial O2 demand! block the Decrease blood volume by RAAS blocking aldosterone → Decrease preload 19 ACE Inhibitors (“prils”): Lisinopril Indications HF, HTN Mechanisms of Action Inhibits angiotensin-converting enzyme (ACE) Angiotensin I cannot be converted to angiotensin II Desired effects Enhanced excretion of Na+ and H2O (decreases blood volume) Decreases BP (afterload) and increases CO Combination decreases Dilation of veins returning blood to heart workload of heart! Decreases preload and reduces peripheral edema Adverse effects Hyperkalemia, hypotension, H/A, dizziness, cough 20 Don’t suddenly stop this drug! Why? Indications Adverse effects HTN, angina, prevent MI Bradycardia, hypotension, fatigue Non-Selective Mechanisms of Action Affects beta1 receptors in heart Contraindicated in clients with Beta- and beta2 receptors in pulmonary and vascular smooth asthma! WHY??? Adrenergic muscle Blockers Desired effects Reduces HR, slows conduction (“olols”): velocity, lowers BP Propranolol Very effective for tachycardia caused by excessive sympathetic stimulation 21 Pharmacotherapy: Anticoagulants Classification Drug Anticoagulants -warfarin Antidote for warfarin therapy -vitamin K 22  Recall that anticoagulant activity of warfarin can take several days to reach its maximum effect. This is why heparin and warfarin therapy are overlapped! Indications Prophylaxis of Thromboembolic events DVT, PE, AF Anticoagulants: Arterial thromboembolism Prevention of CVA/MI Valvular dysfunction Warfarin Long-term anticoagulation Mechanisms of action Inhibits action of vitamin K Without adequate vitamin K, synthesis of clotting factors II, VII, IX, and X is diminished Decreases production of clotting factors including thrombin Desired effects Prevents intravascular clots/thrombosis Adverse effects 23 Abnormal bleeding  Reverses anticoagulant activity of warfarin Vitamin K is essential for synthesis of blood coagulation factors Indications Antidote for When PT/INR indicates blood taking too long to clot Warfarin Mechanisms of action Vitamin K overrides mechanism by which warfarin inhibits Therapy: production of vitamin K-dependent clotting factors Vitamin K Desired effects Effective blood clotting Adverse effects Vitamin K is relatively nontoxic and causes minimal adverse effects May have hypersensitivity reactions 24  Warfarin maintenance dose can fluctuate significantly Warfarin : depends on amount of vitamin K in diet do not need to avoid but need to be consistent with Dietary diet of leafy green veggies once warfarin maintenance dose established Requirements i.e. kale, Swiss chard, spinach, collard greens so…food high in vitamin K may ↓ warfarin’s ability to prevent clots remember…vitamin K is an antidote for warfarin! Monitor PT/INR regularly! Food-drug measures how long it takes blood to clot interaction! 25 Electrocardiography (ECG) Interpretations PAT401 Week 2 Fall 2023 1 FIRST…SOME BACKGROUND KNOWLEDGE 2 The Five Phases of the Cardiac Cycle 3 Figure 31.5, Rogers, 2023, p. 1026 Conduction System of the Heart Figure 31.7, Rogers, 2023, p. 1029 4  Electrocardiogram (ECG) and Cardiac Electrical Activity Electrocardiography Serial 12-lead ECGs establish the presence of myocardial ischemia and infarction or conduction defects and dysrhythmias Holter monitoring 5 Figure 31.9, Rogers, 2023, p. 1031  Anatomy of an ECG Christianson, J. (2019). An EKG Interpretation Primer. Nurses International Team. 6 https://open.umn.edu/opentextbooks/textbooks/814 Basic ECG interpretation 1. ECG rate 2. Is there a P wave for every QRS complex? Is there a QRS complex for every P wave? 3. Do the P waves come at consistent intervals or “march out”? The QRS complexes? 4. Is the QRS complex wide or narrow? Christianson, J. (2019). An EKG Interpretation Primer. Nurses International Team. 7 https://open.umn.edu/opentextbooks/textbooks/814  Putting it all together Christianson, J. (2019). An EKG Interpretation Primer. Nurses International Team. 8 https://open.umn.edu/opentextbooks/textbooks/814  Normal Sinus Rhythm The normal rhythm of heart is sinus rhythm Recognized on ECG by regular P-waves, at a rate between 60 and 100 beats per minute (bpm), with every P-wave followed by a QRS complex and every QRS complex preceded by a P-wave Depolarization and repolarization of the atria and ventricles show as 3 distinct waves/deflections (P, QRS, T) on ECG Richley, R. (2019). Recognising and treating arrhythmias in primary care. Practice Nursing, 30(6), 270-275 9 Composite Chart of Heart Function 10 Figure 31.4, Rogers, 2023, p. 1025 ACUTE CORONARY SYNDROMES (ACS) Unstable angina NSTEMI STEMI 11  Types of Myocardial Ischemia and Infarction Degree of occlusion caused Rupture of plaque and Arterial occlusion tends not by plaque and oxygen Vascular occlusion may also formation of a thrombus can to be a significant factor demand of myocardium be masked by formation of drastically and quickly until the lumen is occluded determine degree of anastomoses reduce lumen and blood by about 70 percent ischemia that can develop flow But when ischemia is Degree and duration of prolonged then MI becomes ischemia determine type of more likely Mild or brief ischemia can acute coronary syndrome lead to angina Significant changes in ECG and (ACS) that occurs and the release of cardiac enzymes are clinical impact seen Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. 12 https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0.  Sudden coronary obstruction caused by thrombus formation over ruptured atherosclerotic unstable plaque → ACS results Plaque progression, disruption, & subsequent clot formation ACS Unstable Angina (UA) MI (Non-STEMI & STEMI) Common complications Arrhythmias/dysrhythmias, heart failure, pericarditis, aneurysm/rupture of wall or septae of infarcted ventricle, systemic arterial thromboembolism, pulmonary thromboembolism, sudden cardiac death 13 Unstable Angina, Non- STEMI and STEMI Figure 32.11, Rogers, 2023, p. 1081 14 Unstable Angina (UA) EMERGENCY! Transient episodes of thrombotic vessel Form of acute coronary Sign of impending occlusion and syndrome infarction! vasoconstriction at site of plaque damage 15 Diagnostics: ECG Affected area can be identified on 12-lead ECG Ischemic / injured / UA infarcted tissue Non-STEMI does not function like normal STEMI myocardial tissue! ECG changes depend on Duration of ischemic event (acute vs evolving) Extent (partial/subendocardial vs full wall thickness/transmural) Location 16 UA ECG Presentation UA is first step in progressive spectrum of ischemia-related myocardial injury Now is grouped under classification of Non-STEMI The ECG most commonly shows ST segment depression and T wave inversion 17  SUBENDOCARDIAL INFARCTION If thrombus disintegrates before complete distal tissue necrosis has occurred Infarction will involve only the myocardium directly beneath endocardium Partial wall thickness damage Present with ST segment depression and T wave inversion without ST elevation on ECG Types of MI and Non ST-Segment Elevation MI (Non-STEMI) ECG TRANSMURAL INFARCTION Presentations If thrombus lodges permanently in vessel, infarction will extend through myocardium all the way from endocardium to epicardium Full wall thickness damage Presents with ST segment elevation on ECG ST-Segment Elevation MI (STEMI) Clients with STEMI at highest risk for serious complications Should receive definitive intervention without delay! 18 Types of MI and ECG Presentations (cont.) Non-STEMI: ST segment depression and T-wave inversion indicative of partial wall thickness (subendocardial) damage STEMI: ST segment elevation indicative of full myocardial wall thickness (transmural) damage 19 Figure 32.8, Rogers, 2023, p. 1078 ARRHYTHMIAS/ DYSRHYTHMIAS 20 Arrhythmias/Dysrhythmias Are disturbances of the heart rhythm Ranges from an occasional “missed” beat or rapid beats to severe disturbances that affect the pumping ability of the heart Can be caused by an abnormal rate of impulse generation or an abnormal impulse conduction 21 Atrial Fibrillation Most common cardiac arrhythmia Caused by rapidly firing potentials in atrial myocardium Aberrant depolarizations often result of myocardial remodeling Causes include HTN, valvular and ischemic heart disease, genetics Rapid depolarizations result in very fast atrial rate 400 to 600 bpm Because atrial rate is so fast, ECG shows very rapid, irregular atrial deflections of varying shapes and sizes called “fibrillatory waves” Action potentials produced are low amplitude, so P-waves will not be seen Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0. 22 Richley, R. (2019). Recognising and treating arrhythmias in primary care. Practice Nursing, 30(6), 270-275  Atrial Fibrillation: ECG Fibrillatory waves indicated by arrows 23 Richley, R. (2019). Recognising and treating arrhythmias in primary care. Practice Nursing, 30(6), 270-275 Atrial Fibrillation: Summary No visible P-Waves Irregularly irregular QRS complexes High ventricular rate Atrial fibrillatory waves Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. 24 https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0.  Atria contract very rapidly – usually 300 times a minute! Recognized by characteristic ‘sawtooth’ pattern Not all atrial impulses conduct to ventricles (i.e. 1 in 4 impulses) Results in ventricular rate less than atrial rate i.e. approx. 75 bpm Important not to assume on basis of normal heart rate that this must be sinus rhythm Atrial Flutter Atrial flutter of new onset often assoc. with HR of 150 bpm because 1 in 2 atrial impulses conducted to ventricles A useful tip is to suspect atrial flutter in anyone with resting HR of 150 bpm Once atrial flutter is suspected, flutter waves can often be identified Richley, R. (2019). Recognising and treating arrhythmias in primary care. Practice Nursing, 30(6), 270-275 25 Atrial Flutter: ECG Note ‘sawtooth’ pattern 26 Richley, R. (2019). Recognising and treating arrhythmias in primary care. Practice Nursing, 30(6), 270-275 Atrial Flutter: Summary Regularly High Sawtooth irregular QRS ventricular atrial pattern complexes rate Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. 27 https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0.  Premature Atrial Contractions Generated by a depolarization instigated The early P-wave is usually followed by Premature atrial contractions are outside of SA node normal or near-normal QRS complex, considered benign and rarely need Produces premature P-wave after which there is a short pause before treatment the next sinus beat appears Premature P-wave is a different shape from normal P- wave of sinus node origin In this case, the premature P-wave is superimposed on the T-wave of previous beat Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0. 28 Richley, R. (2019). Recognising and treating arrhythmias in primary care. Practice Nursing, 30(6), 270-275 Premature Atrial Contractions: ECG Premature P-wave indicated by arrow 29 Richley, R. (2019). Recognising and treating arrhythmias in primary care. Practice Nursing, 30(6), 270-275  Extra P-wave with abnormal Premature Atrial morphology Contractions: Compensatory pause leading to atrial bigeminy (complexes appear Summary to be in pairs) 30 Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0. Premature Ventricular Contractions Originates in ventricles Occurs when a focus in the ventricle generates an action potential before the pacemaker cells in SA node depolarize As a result, are not preceded by a premature P-wave and QRS is broad and bizarre A compensatory pause follows the premature ventricular contraction as the unscheduled depolarization puts the ventricular myocardium into refractory state Forces it to “skip a beat” Common and often occur in healthy individuals BUT…more common in people with heart disease Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0. 31 Richley, R. (2019). Recognising and treating arrhythmias in primary care. Practice Nursing, 30(6), 270-275 Premature Ventricular Contractions: ECG Indicated by arrow 32 Richley, R. (2019). Recognising and treating arrhythmias in primary care. Practice Nursing, 30(6), 270-275 Premature Ventricular Contraction: Summary Out of step with normal R-R interval Wider complex Followed by compensatory pause Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. 33 https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0. Ventricular Tachycardia Arises in ventricles and is recognized on ECG by a regular rhythm and broad and bizarre QRS complexes not preceded by P-waves Fast rhythm, between 120 and 250 bpm With disorganized contractility and reduced filling time, ventricular tachycardia can lead to hemodynamic instability and severe hypotension Is a potentially life-threatening arrhythmia Needs to be identified and dealt with quickly Is considered an emergency! Can progress to ventricular fibrillation Occurs most commonly in clients with significant structural heart disease Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0. 34 Richley, R. (2019). Recognising and treating arrhythmias in primary care. Practice Nursing, 30(6), 270-275 Ventricular Tachycardia (cont.) Can be monomorphic or polymorphic QRS complexes in monomorphic ventricular tachycardia Have same shape and are symmetrical because they start in same place in myocardium Polymorphic ventricular tachycardia Has variable QRS shape because depolarizations are instigated at multiple points Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. 35 https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0.  Ventricular Tachycardia: ECG At 190 bpm 36 Richley, R. (2019). Recognising and treating arrhythmias in primary care. Practice Nursing, 30(6), 270-275 Ventricular Ventricular rate >100 bpm Tachycardia: QRS complex not associated with P-wave Wide QRS complex morphology Summary Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0. 37 Ventricular Fibrillation Occurs when ventricular rate exceeds 400 bpm! Disorganized and uncoordinated contraction of myocardium Rates of survival for out-of-hospital ventricular fibrillation are causes cardiac output to fall to low catastrophic levels Coronary artery disease and Tissue damage allows formation of reentry patterns that cause resultant myocardial ischemia or chaotic ventricular depolarization tissue scarring are most common These reentry patterns break up into multiple smaller wavelets causes that cause high frequency activation of the myocytes Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. 38 https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0. Ventricular Fibrillation: ECG No recognizable P-waves or QRS complexes Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. 39 https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0.  Chaotic, irregular, and varying intervals Ventricular No P-waves, QRS Fibrillation: complexes, or T-waves Summary High rate 40 Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0.  Heart Block: Atrioventricular (AV) Block Three categories First-degree heart block Results from slow action potential conduction through AV node Second-degree heart block Not all atrial impulses are conducted to the ventricles Second-degree heart block is sub-divided Wenckebach (Mobitz I) Mobitz II Third-degree heart block Commonly known as complete heart block No atrial impulses conduct to the ventricles Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0. 41 Richley, R. (2019). Recognising and treating arrhythmias in primary care. Practice Nursing, 30(6), 270-275  Generally, is asymptomatic and But long-term monitoring for worsening conduction is advisable does not require any treatment Results from slow Slowing can be due to changes in action potential Vagal tone or structural changes associated with damage or disease conduction through First-Degree AV node affecting conductive tissue of atria, AV node (most common), bundle of His or bundle branches, and Purkinje system Heart Block Defined by prolonged P-R Takes longer for action potential to reach ventricles, so P and R appear further apart interval Exceeds 0.20 seconds Each P-wave is accompanied by a All impulses get through QRS complex Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. 42 https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0. First-Degree Heart Block: ECG P-R interval >0.20 seconds P-R interval = 6 small boxes = 0.24 seconds = first-degree block Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. 43 https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0. Second-Degree Heart Block Also has changes in P-R interval But starts to show failure as some P-waves not followed by a QRS complex Depolarization intermittently fails to reach ventricles Pattern of missed ventricular depolarizations, or blocked P-waves, is often very regular and described as a ratio of P-waves to QRS complex Way in which P-R interval changes in relation to blocked P-waves produces subclassifications of second-degree blocks, Mobitz I and II Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0. 44 Wenckebach (Mobitz I) After the pause, the P-R P-R is longest before Often a benign finding and P-R interval increases from interval returns to normal, dropped QRS complex and may be due to high vagal beat to beat until then starts increasing again shortest immediately after tone in successive beats But…may be P-wave is not Sequence typically associated with followed by a QRS repeats symptoms of possible cardiac origin Results in a pause Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0. 45 Richley, R. (2019). Recognising and treating arrhythmias in primary care. Practice Nursing, 30(6), 270-275 Wenckebach (Mobitz I): ECG P-R interval (shown with blue bars) progressively lengthens until a P-wave is missed (indicated by arrows) Then goes back to its original length and starts increasing again 46 Richley, R. (2019). Recognising and treating arrhythmias in primary care. Practice Nursing, 30(6), 270-275 Mobitz II Mobitz II has blocked P-waves as well, but P-R interval remains unchanged There is a widening of the QRS complexes that are generated Rarer and more serious condition Usually involves problems with conduction system below AV node, most commonly in the bundle branches Usually associated with progressive disease of heart’s conduction system Normally leads to implantation of a permanent pacemaker Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0. 47 Richley, R. (2019). Recognising and treating arrhythmias in primary care. Practice Nursing, 30(6), 270-275 Mobitz II: ECG Blocked P-waves indicated by arrows 48 Richley, R. (2019). Recognising and treating arrhythmias in primary care. Practice Nursing, 30(6), 270-275  Complete heart block No atrial impulses conducted to ventricles To be compatible with life, AV node or ventricles must generate their own impulses No P-waves have associated QRS complexes P-waves and QRS complexes are completely unrelated to each other Termed “AV dissociation” Third-Degree Because of damage affecting AV node Heart Block Ischemia or disease (i.e. Lyme disease) Most worrying consequence is intermittent ventricular standstill May cause dizziness or, if prolonged, loss of consciousness Depending on client’s presentation Pacemaker may be implanted Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0. 49 Richley, R. (2019). Recognising and treating arrhythmias in primary care. Practice Nursing, 30(6), 270-275  Complete Heart Block: ECG Three hallmarks: Atrial rate is faster than ventricular rate i.e. 80 bpm and 35 bpm respectively Ventricular rate is slow and regular No relationship between atrial and ventricular impulses Atria contract completely independently of ventricles P-waves and QRS complexes indicated with arrows 50 Richley, R. (2019). Recognising and treating arrhythmias in primary care. Practice Nursing, 30(6), 270-275  First-degree Prolonged P-R interval (>0.20 seconds) Results from slow action potential conduction through AV node But all impulses get through! Second-degree Heart Block: Prolonged P-R interval (>0.20 seconds) Intermittently blocked P-waves Summary Variable P-R interval (Mobitz I) or stable P-R interval (Mobitz II) Third-degree Complete heart block No atrial impulses conducted to ventricles AV node or ventricles must generate their own impulses for survival Binks, Andrew., (2022). Cardiovascular Pathophysiology for Pre-Clinical Students, Roanoke: Virginia Tech Carilion School of Medicine. 51 https://doi.org/10.21061/cardiovascularpathophysiology. Licensed with CC BY NC-SA 4.0. Traumatic Brain Injury PAT401 Week 3 Fall 2023 1 CEREBRAL HEMODYNAMICS & INCREASED INTRACRANIAL PRESSURE (ICP) 2 Cerebral Hemodynamics Cerebral perfusion Cerebral blood flow pressure (CPP) Cerebral blood volume Cerebral blood (CBF) to brain (CBV) oxygenation (70–90 mm Hg) Normally maintained Pressure required to Amount of blood in Measured by oxygen at a rate that matches perfuse cells of brain intracranial vault at a saturation in internal local metabolic needs given time jugular vein of the brain CBF to gray matter is about 3 to 4 times greater than that to white matter because of increased metabolic activity 3 Alterations in Cerebral Hemodynamics Features of cerebral hemodynamic injury Alterations in cerebral blood flow, intracranial pressure, and oxygen delivery Goal of hemodynamics To balance intracranial pressure with internal jugular vein oxygen saturation Alterations in cerebral hemodynamics Increased ICP Cerebral edema 4 Increased ICP Normal is 1-15 mmHg or 5−15 mmHg Caused by Edema Excessive cerebrospinal fluid Hemorrhage Occurs when one or more of the contents of the cranial vault— brain tissue, CSF, and blood—increases in volume Because cranial vault itself is a rigid, fixed compartment! 5 Stages of Increased ICP 1 2 3 4 Stage 1 Stage 2 Stage 3 Stage 4 Vasoconstriction Compromised neuronal Brain hypoxia and Brain herniates; and external oxygenation; systemic hypercapnia; several herniation compression arterial vasoconstriction autoregulation syndromes occurs lost 6 Manifestations of Increased ICP 7 Figure 17.16, Rogers, 2023, p. 535 Therapeutic Management Goals for Individuals With Altered Cerebral Hemodynamics Central perfusion pressure >70mm Hg Intracranial pressure