NURS 8022 Exam 3; Cardiac Study with Complete Solutions | Rated A+, Exams of Nursing

Download NURS 8022 Exam 3; Cardiac Study with Complete Solutions | Rated A+ and more Exams Nursing in PDF only on Docsity! NURS 8022 Exam 3; Cardiac Study with Complete Solutions | Rated A+ guideNURS8022 Exam #3 Study Guide: Cardiac STRUCTURE AND FUNCTION OF THE CV AND LYMPHATIC SYSTEMS 1. Understand the basics of cardiac muscle contraction > Cross-bridge cycling -Attachment of actin to myosin at the cross bridge -Myosin head molecule undergoes a position change -Causes thin filaments to slide past thick filaments (contraction) ➤Calcium -Is stored in the tubule system and the sarcoplasmic reticulum -Enters the myocardial cell from the interstitial fluid after electrical excitation, which increases membrane permeability to calcium -Diffuses toward the myofibrils, where it binds with troponin > Excitation contraction coupling - Is the process by which an action potential triggers the cycle of events, leading to cross-bridge activity and contraction - Requires calcium - Calcium-troponin complex facilitates the contraction process > Myocardial relaxation - Is vital to optimal cardiac function as is contraction - Calcium, troponin, and tropomyosin also facilitate relaxation > Troponin release of calcium begins myocardial relaxation. 2. Understand cardiac cycle and what each part represents > Cardiac cycle -One contraction and one relaxation -Makes up one heartbeat > Diastole (D=R) -Relaxation: Ventricles fill > Systole (S=C) -Contraction: Blood leaves the ventricles `Phases of the cardiac cycle > Phase 1: Atrial systole or ventricular diastole > Phase 2: Isovolumetric ventricular systole > Phase 3: Ventricular ejection (semilunar valves open) > Phase 4: Isovolumetric ventricular relaxation (aortic valve closes) > Normally heart can pump 3-4 times as much blood as is needed > Therefore if atria fail, not normally symptomatic patient, unless under stress; ex: exercise 6. Understand volumes, EF, Cardiac output, preload, and afterload Cardiac output > Is the volume of blood flowing through either the systemic or the pulmonary circuit > Is expressed in liters per minute (L/min) > Is calculated: CO = HR x SV > Normal adult cardiac output at rest is 5 L/min Factors that affect CO: > Preload > Afterload > Frank Starling Law of the heart > Laplace’s Law Ejection fraction > Is the amount of blood ejected per beat > Normal is 55% or higher > stroke volume divided by end-diastolic volume > Is an indicator of ventricular function Cardiac Index Definition > CO indexed against body size > Formula- CI = CO/ BSA > Normal value = 2.5-4.0 L/min/m2 Decreased CO/CI Increased CO/CI MI HTN Shock Dec vascular resistance Dec HR Pulmonary edema Dec SV Inc metabolic state Negative inotropes Positive inotropes Cardiac tamponade Hypovolemia Valvular heart disease High PEEP Preload: the pressure generated at the end of diastole ➤also called left ventricular end-diastolic pressure (LVEDP) ➤determined by 2 primary factors -Amount of venous return to the ventricle -Blood left in the ventricle after systole or end-systolic volume > When preload exceeds physiologic range, further muscle stretching causes a decline in cardiac output > Preload is assessed by measuring the filling pressure of each ventricle > RV preload = CVP (central venous pressure) (3-8mmHg) > LV preload = PAOP (pulmonary artery occlusion pressure) aka PCWP (2- 15mmHg) Clinical significance > Represents fluid returning to the heart > aka the “filling pressure” > Increased preload represents increased myocardial oxygen consumption or (MVO2) Afterload: Is the resistance to ejection during systole > Aortic systolic pressure is a good index of afterload for the left ventricle > Decreased afterload: Heart contracts more rapidly > Increased afterload: Slows contractions and increases work load > Afterload is assessed by measuring the resistance in the ventricle during systolic ejection > Right ventricle afterload = PVR (100 -250 dynes/sec/cm-5) > Left ventricle afterload = SVR (800-1200dynes/sec/cm-5) Clinical significance: > Increased afterload = increased work of the heart and increased oxygen demand > Factors that increase afterload - Vasoconstriction - Valvular stenosis - Increased blood volume - Factors that decrease afterload: Vasodilation 7. Know different valves and which type they are Purpose of valves -Ensure one way blood flow Atrioventricular valves (AVs) > One-way flow of blood from the atria to the ventricles > Tricuspid valve: 3 leaflets or cusps > Bicuspid (mitral) valve: 2 leaflets or cusps Semilunar valves > One-way flow from the ventricles to either the pulmonary artery or to the aorta > Pulmonic semilunar valve > Aortic semilunar valve HEART SOUNDS > No sound with opening of valves > Heart sounds a result of valve closure and vibration of surrounding fluids under sudden pressure changes - 1st Heart Sound is low in pitch and long-lasting - Closure of the A-V valves - 2nd Heart Sound is a rapid snap - Closure of the semilunar valves - 3rd Heart Sound - Very low pitch - Caused by inrushing of blood into ventricles - 4th Heart Sound - Atrial contraction late in diastole - Hard to hear with stethoscope except in hypertensive patients with a thick left ventricle 8. Potassium and calcium do what to the heart > Excess K+ decreases contractility - Cause heart to become dilated and flaccid, slows heart rate - Rise to just 2-3 times normal (8-12mEq/L) can lead to death > Excess Ca++ causes spastic contraction, and low Ca++ causes cardiac dilation - Calcium abnormalities not as big of a concern as potassium because blood levels more regulated 9. Understand electrical pathway of the heart – basics. Know different nodes and what they do PATHWAY OF HEARTBEAT > Begins in the sinoatrial (S-A) node > Internodal pathway to atrioventricular (A-V) node > Impulse delayed in A-V node and bundle (allows atria to contract before ventricles) > A-V bundle takes impulse into ventricles > Left and right bundles of Purkinje fibers take impulses to all parts of ventricles ➤Norepinephrine and Epinephrine Beta-2- vascular and nonvascular smooth muscle (“2 lungs = Beta-2) ➤Regulatory; inverse response of cell (stimulation =decreased activity or muscle tone of the cell is decreased) ➤Located on smooth muscle; GI tract, urinary bladder, skeletal muscle arteries, bronchial tree, and some coronary arteries ➤Epinephrine mostly, only interacts with norepinephrine released from the adrenal gland not from nerve endings ➤Activation leads to vascular and nonvascular smooth muscle relaxation β3 receptors > Decrease myocardial contractility (negative inotropic effect) > May provide a “safety mechanism” to prevent an overstimulation of the heart by the sympathetic nervous system. Stimulation of both the β1 and β2: Increases the heart rate (chronotropy) and force of the myocardial contraction (inotropy) > If the heart rate is affected, then the effect is called chronotropy - Negative chronotropy: Decreases heart rate - Positive chronotropy: Increases heart rate > If the heart contraction is affected, then the effect is called inotropy - Negative inotropy: Decreases force of contraction ➤Acetylcholine released from the vagus nerve - Positive inotropy: Increases force of contraction ➤Norepinephrine from the sympathetic nerves supplying the heart ➤Epinephrine from the adrenal medulla. ➤Thyroid hormone and dopamine **hypoxia dec contractility 11. Understand basics about capillary hydrostatic pressure, plasma oncotic/colloid pressure, interstitial pressure, and interstitial fluid oncotic/colloid pressure = Starling forces - Starling Forces 4: 1. Hydrostatic pressure in the capillary 2. Hydrostatic pressure in the interstitium 3. Oncotic pressure in the capillary 4. Oncotic pressure in the interstitium https://www.anaesthesiamcq.com/FluidBook/fl4_2.php http://www.pathwaymedicine.org/starling-forces Frank-Starling Law > Related to the volume of blood at the end of diastole/ preload and stretch placed on the ventricle *** More stretch = Increased force of contraction - Greater stretch during diastole = greater force of contraction = greater amt of blood pumped out Laplace’s law > Contractile force within a chamber depends on the radius of the chamber and the thickness of its wall - Smaller chambers and thicker chamber walls equal increased contraction force - In ventricular dilation, the force needed to maintain ventricular pressure lessens available contractile force Poiseuille’s law o Greater the resistance, the lower the blood flow. ➢ Pressure o Force is exerted on a liquid per unit area. ➢ Resistance o Is the opposition to blood flow. o Diameter and length of the blood vessels contribute to resistance. o Vessel radius or diameter greatly affects resistance. ➢ Velocity o Is the distance blood travels in a unit of time. ➢ Viscosity o Thick fluids move more slowly and cause greater resistance to flow than thin fluids. o High hematocrit reduces the flow through the blood vessels. ➢ Laminar and Turbulent Flow o ➢ Laminar flow – occurs when fluid or layers of molecules go straight ahead ➢ Turbulent flow – some sort of turn or something in the vessel, produces a really wind of flow ➢ Vascular compliance o The increase in volume a vessel is able to accommodate for a given increase in pressure. o Stiffness is the opposite of compliance. o Veins are more compliant than arteries 12. Understand basic functions of lymphatic system > Special vascular system picks up excess fluid and returns it to the venous circulation > Moving lymphocytes and leukocytes between different components of the immune system is another important function > Has lymph nodes and vessels > Valves allow one way flow > Lymphatic fluid is made up of primarily water and small amounts of dissolved proteins, mostly albumin -maintains fluid balance AGING AND THE CARDIOVASCULAR SYSTEM > Cardiovascular disease -the most common cause of morbidity and mortality in older adults > Physiologic changes - Myocardial and blood vessel stiffening - Changes in neurogenic control over vascular tone - Increased occurrence of atrial fibrillation - Loss of exercise capacity - Left ventricular hypertrophy and fibrosis > Arterial stiffening Vasculitis o Benign cases are thrombosis, histoplasmosis, tuberculosis, mediastinal fibrosis, cystic fibrosis, and benign tumors (retrosternal goiter) o Clinical manifestations ▪ Edema and venous distention in the upper extremities and face ▪ Fullness feeling in head ▪ Headache, visual disturbances, impaired consciousness ▪ Skin of face and arms purple and taut ****Oncologic emergency · Inflammation of blood vessels · Caused by Hepatitis B/C, EBV, CMV, drugs (PCN, Sulfa, quinolones), autoimmune disease (SLE, RA) or independent vasculitic syndromes · Clinical manifestations: o Constitutional symptoms of wt loss, fatigue, fever o Consequences of ischemia – skin rashes/ulcers, renal dysfunction, neuropathy, or bowel infarction o Must rule out underlying cause o Arterial biopsy and/or angiogram is necessary for definitive diagnosis 15. Hypertension – different types, pathogenesis, and s/s, including malignant hypertension Hypertension · Isolated systolic hypertension: Elevated systolic blood pressure accompanied by normal diastolic blood pressure · Hypertension o Consistent elevation of systemic arterial blood pressure o JNC 8 Guidelines o < 150/90 is goal, unless underlying co-morbidities, DM, Renal disease then 140/90. · Primary (essential) hypertension o No known cause; is 95% of those with hypertension. · Secondary hypertension o Is caused by altered hemodynamics from an underlying primary disease or drugs. · Affects the entire cardiovascular system o Systolic hypertension: Most significant factor in causing target organ damage o Increases the risk for myocardial infarction (MI), kidney disease, and stroke · Risk factors o Positive family history* o Advancing age* o Gender: Female >70 years of age; male <55 years of age o Race: Black o ↑Sodium (Na+) intake o Glucose intolerance (diabetes mellitus) o Heavy alcohol use o Obesity o Cigarettes o ↓Potassium (K+), magnesium (Mg++), calcium (Ca++) · Caused by increases in cardiac output or total peripheral resistance, or both o Cardiac output increased: Any condition that increases heart rate or stroke volume · Peripheral resistance increased: Any factor that increases blood viscosity or reduces vessel diameter (vasoconstriction) · Primary hypertension o Extremely complicated interactions of genetics and the environment mediated by neurohumoral effects ▪ Genetics interact with diet, smoking, age, and other risk factors to cause chronic changes in vasomotor tone and blood volume. o Overactivity of sympathetic nervous system and renin-angiotensin- aldosterone system (RAAS), and alterations in natriuretic peptides o Inflammation, endothelial dysfunction, obesity-related hormones, and insulin resistance · Secondary hypertension o Caused by systemic disease that raises peripheral vascular resistance and/or cardiac output o Renal artery stenosis, renal parenchymal disease, pheochromocytosis, and drugs are examples. · Complicated hypertension o Hypertrophy and hyperplasia with associated fibrosis of the tunica intima and media in a process called vascular remodeling ▪ Kidneys, brain, heart, extremities, and eyes all most at risk · Malignant hypertension o Rapidly progressive hypertension o Diastolic pressure is usually >140 mm Hg o Can lead to encephalopathy – d/t high arterial pressure in cerebral arteries which renders those arteries incapable of regulating blood flow. o Result of gene dysfunction · Clinical manifestations o Early stages of hypertension have no clinical manifestations other than elevated blood pressure ▪ Called silent (lanthanic) disease o Sustained uncontrolled hypertension leads to target organ damage ▪ Heart disease ▪ Renal insufficiency ▪ CNS dysfunction ▪ Impaired vision ▪ Impaired mobility ▪ Vascular occulsion ▪ Edema Orthostatic (Postural) Hypotension · Decrease in the systolic and diastolic blood pressures on standing by 20 mm Hg or more and by 10 mm Hg or more, respectively · Lack of normal blood pressure compensation in response to gravitational changes on the circulation, leading to pooling and vasodilation · Acute versus chronic orthostatic hypotension · Clinical manifestation: o Fainting upon standing, may involve CV symptoms, impotence, and bowel and bladder dysfunction 16. Aneurysm patho Aneurysm · Local dilation or outpouching of a vessel wall or cardiac chamber · True aneurysms o Involvement of all three layers of the arterial wall o Fusiform aneurysms o Circumferential aneurysms · False aneurysms – extravascular hematoma o Leak between a vascular graft and a natural artery · Saccular aneurysms – spherical in shape · Clinical manifestations o Heart ▪ Include dysrhythmias, heart failure, and embolism of clots to the brain or other vital organs. o Aorta ▪ Is asymptomatic until it ruptures, then it becomes painful. o Thoracic ▪ Dysphagia (difficulty in swallowing) and dyspnea (breathlessness) are caused by the pressure. o Abdomen ▪ Flow to an extremity is impaired, causing ischemia. · Complication Aortic dissection (not same thing as rupture) ▪ Tear in intima of aorta, into which blood flows furthering the tear. o Review again: damaged endothelium, causes reponse with activation of macrophages , leading to foam cells which then create fatty streak with the lipid core formation and oxygenation of the LDL. Then formation and covering causing the fibrous plaque. That’s unstable. If ruptures – complicated plaque. · Clinical manifestations o Depends on the organ affected o Symptoms and signs are the result of inadequate perfusion of tissues 20. CAD, angina, MI. Understand pathogenesis of these and s/s Coronary Artery Disease · Any vascular disorder that narrows or occludes the coronary arteries · Results in an imbalance between coronary supply of blood and myocardial demand for oxygen and nutrients o Reversible myocardial ischemia or irreversible infarction may result. · Most common cause: Atherosclerosis · Nonmodifiable risk factors o Advanced age; family history · Modifiable risk factors o Dyslipidemia o Hypertension ▪ Endothelial injury, increase in myocardial demand o Cigarette smoking ▪ Vasoconstriction and increase in LDL, decrease in high-density lipoproteins (HDL) o Diabetes mellitus and insulin resistance ▪ Endothelial damage, thickening of the vessel wall o Obesity and/or sedentary lifestyle ▪ Obesity, dyslipidemia, and hypertension: Metabolic syndrome o Atherogenic diet- HIGH FAT · Nontraditional risk factors o Markers of inflammation and thrombosis ▪ C-reactive protein – mostly synthesized in liver, something can be drawn and indirect measure of atherosclerotic plaque • Will be elevated with any time of inflammation o Troponin I ▪ Serum protein, measurement used as sensitive and specific diagnostic test to help identify MI injury during ACS. o Hyperhomocysteinemia ▪ Result of genetic lack of enzyme that breaks down homocysteine (amino acid) or folate, B12, or B6 deficiency ▪ Increased LDL oxidation – lead to foam cells and plaque ▪ Decreases naturally occurring vasodilator, smooth muscle o Adipokines - Group of hormone released from adipose cells ▪ Adiponectin and leptin ▪ Adiponectin is normally antiatherogenic ▪ Decreased Adiponectin and leptin (hypertension) ▪ Decreased in obesity o Infection ▪ Microorganisms and periodontal disease ▪ Infection results in local inflammation of vessels and therefore contributes to vascular disease · Air pollution · Coronary artery calcification, carotid wall thickness Dyslipidemia · Strong link between lipoproteins and coronary artery disease · Abnormal concentrations of serum lipoproteins · Dietary fat packaged into chylomicrons for absorption in the small intestine o Chylomicrons: Function by transporting exogenous lipid from the intestine to the liver and peripheral cells (by LDL) o Primarily contains triglyceride; triglycerides may be removed and either stored by adipose tissue or used by muscle as an energy source. o Remnant contains cholesterol, which is taken up by the liver. · Lipids o Very low–density lipoproteins (VLDL): Mainly triglycerides plus a carrier protein o LDL: Mainly cholesterol plus a carrier protein ▪ Are responsible for the delivery of cholesterol to the tissues and periphery from liver where if its transported, it can be incorporated into the atherosclerotic lesion o HDL: Mainly phospholipids plus a carrier protein ▪ Are responsible for “reverse cholesterol transport,” which returns excess cholesterol from tissues to the liver, where it is eliminated as bile or converted to cholesterol-containing steroids. ▪ Can remove excess cholesterol from arterial walls. ▪ Mostly returns cholesterol back to the liver from the peripheries · Is an indicator of coronary risk. o Increased LDL: Play a role in endothelial injury, inflammation, and immune responses that are important in atherogenesis. o Low levels of HDL: Are responsible for “reverse cholesterol transport,” which returns excess cholesterol from the tissues to the liver. o Elevated serum VLDL (triglycerides) o Increased lipoprotein (a) – genetically determined molecular complex between LDL and serum glycoprotein a ▪ Elevated lipoprotein A known risk factor for CAD esp women Myocardial Ischemia · Supply vs demand o coronary blood cannot meet the demand of the myocardium for oxygen and nutrients. · During exertion, heart beats faster and stronger to sypply O2 to muscles. Vasodilation of myocardial vasculature increases BF to cardiac muscle to meet need of increased O2 demand. If heart with bad atherosclerotic disease, vessels are narrowed and blood supply to the heart is diminished. In milder cases, heart might be fine at rest but if increased demand, heart can’t get enough O2, because it can’t adequately vasodilate. · Types o Stable angina: predictable chest pain. ▪ Relieved with rest ▪ Exertional type of CP. ▪ Relieved when person stops exerting themselves o Prinzmetal angina (variant): unpredictable chest pain. ▪ Result of intermittent vasospasm as opposed to actual vascular occlusion ▪ Can occur at any time and not necessarily related to activity so its unpredictable o Silent ischemia: no detectable symptoms. ▪ Common in diabetic patients o Angina pectoris: transient substernal chest discomfort · Necrotic center, hypoxic xone around that, and zone of ischemia around that. o Its tissue that can save, but is at a high risk for becoming infarcted tissue if right treatment isn’t initiated · Clinical manifestations o Sudden severe chest pain, ▪ N/V, Diaphoresis, Dyspnea ▪ Zones ▪ ECG changes ▪ Troponin I: Most specific • Elevates in 2 to 4 hours • Only 1 elevated is needed ▪ Creatine phosphokinase-MB (CPK-MB), LDH • LDH – elevated 24 usually after ▪ Hyperglycemia · Severity of functional impairment depends on the size and site of infarction o Ischemia of conduction symptoms · Functional changes o Decreased cardiac contractility, with abnormal wall motion o Altered left ventricular compliance o Decreased stroke volume o Decreased EF o Increased left ventricular end-diastolic pressure o SA or AV node malfunction o Papillary muscle rupture = MR o Septal rupture = VSD = systolic murmur o Ventricular free wall rupture = tamponade · RCA block – high risk for dysrhythmias · Significant heart failure issues with left sided coronary conclusion · Complications o Dysrhythmias o Cardiogenic shock o Pericarditis o Dressler (postinfarction) syndrome**** ▪ Pericarditis after MI ▪ Delayed form of acute pericarditis ▪ May occur 1 week to several months later. ▪ Thought to be related to antigen-antibody response to the necrotic myocardium o Organic brain syndrome ▪ Can result in TIA or CVA if blood flow to brain is impaired Peripheral Vascular Disease · Atherosclerosis of peripheral arteries · Same patho as atherosclerosis of coronary arteries · Same consequences · Clinical manifestattions o Atherosclerotic lesion of peripheral vasculature causes claudication (exercise induced pain in the periphery) o 6 Ps ▪ Pallor, pulselessness, pain, paresthesias, paralysis, and poikilothermia (cold temperature to touch) o Changes in hair, nail, and skin o Confirmed by Doppler US, angiography, and/or ABI – ankle/brachial index – meausres the difference in BP from ankle or arm. Normally should be equivalent (ratio of 1. Ratio <1= decreased BP in ankle compared to upper extremity) Thromboangiitis obliterans (Buerger disease) o Occurs mainly in young men who smoke. o Is an inflammatory disease of the peripheral arteries. ▪ Digital, tibial, plantar, ulnar, and palmar arteries o Obliterates the small- and medium-sized arteries. ▪ Lesions accompanied by thrombi and vasospasm of arterial segments o Inflammation, thrombus formation, and vasospasms will lead eventually to occlude and obliterate small and medium sized arteries o Thought to occur from significant T cell activation and autoimmunity o Pain and tenderness develop in the affected part. ▪ Hair loss in affected area o Sluggish blood flow, rubor, and cyanosis result. o Can often lead to gangrenous lesions if blood supply is not restored 21. Pericarditis and tamponade patho Infective Endocarditis · Inflammation of the endocardium from infectious agents o Most common: Bacteria, especially streptococci, staphylococci, and enterococci o Common in IV drug users o Vegetations – when bacteria begins to collect on the valve leaflets o If IE left unchecked, can be more severe cardiac abnormalities o Can break off and go through blood stream · Pathogenesis o Endocardial damage o Bloodborne microorganism adherence o Course can be acute or subacute o Formation of infective endocardial vegetations · Clinical manifestations o Fever o New or changed cardiac murmur o Petechial lesions of the skin, conjunctiva, and oral mucosa o Osler nodes: Painful erythematous nodules on the pads o of the fingers and toes o Degeneration with aging o Inflammatory damage caused by rheumatic heart disease o Risk factors same as with CAD · Carotid upstroke – clinical finding o How the carotid feels o Instead of the blood usually slamming upwards through the carotid its sent slowly with less force bc its being help up by the narrowed aortic valve o Instead of brisk pulse, its called parvis atartis? Weakened or delayed o If brain doesn’t get enough blood, can result in syncope, lightheadedness · Orifice of the aortic semilunar valve narrows, causing diminished blood flow from the left ventricle into the aorta · Clinical manifestations: Angina (from thicker ventricular wall that can’t get adequately perfused), syncope, faint pulses, and heart failure · Weak, fatigued · See decreased stroke volume, reduced systolic BP, and narrowed pulse pressure, systolic ejection murmur, crescendo-decrescendo murmur, softer S2 · Murmur – when does blood go across this? o Blood flows across aortic valve when the left ventricle contracts or during systole. Systole time between S1 and S2 (closure of semilunar valve). Blood flowing across the valve between S1 and S3. So in aortic stenosis, where blood doesn’t flow normally across the valve, the murmur occurs between S1 and S2 systolic murmur. Murmur has to stop at S2 bc that means the aortic valve is closed. And if its closed then theres no blood flowing across it so no sound or murmur. o Shape would be of the murmur – crescendo-decresendo murmur because it gets louder as it perceeds but then decrescendos (diminishes before S2) Mitral Stenosis · Impairment of blood flow from the left atrium to the left ventricle o Occurs during diastole · If blood can’t get out of the left atrium, the left atrium dilates d/t increased volume. · Most common cause: Acute rheumatic fever · Higher risk of developing atrial fib and ultimately thrombi · Clinical manifestation: Opening snap heard, diastolic murmur · Murmur – when does blood pass across mitral valve? o Passing across valve during diastole so this is between S2 and S1. Diastolic murmur. The sound of the quick snapping can sometimes be heard as an opening snap. o Expect to hear when the valve opens – snap shortly after S2 which signifies the beginning of diastole o Timing of opening snap can reflect severity of stenosis o If severe can lead to very high increase of left atrial pressure o High pressures, valve snaps open quickly. If less severe, then it doesn’t snap open as much o Timing of opening snap is inversely proportional to severity of stenosis ▪ More severe – the earlier the opening snap · Untreated chronic mitral stenosis leads to pulmonary HTN, edema, and RVF Aortic and Mitral Regurgitation · Aortic regurgitation o Leaking of fluid back into the left ventricle o Leads to left ventricle dilation o Occurs to weakening of valve or dilatation of aortic root. o Marfans syndrome, syphilis o Murmur – after S2 during diastole o Inability of the aortic valve leaflets to close properly during diastole o Clinical manifestations: Widened pulse pressure as a result of increased stroke volume and diastolic backflow, diastolic murmur o BP – after a forceful squeeze and the valve closes, some of the blood that went forward will back up in the ventricle ▪ So diastolic will be affected, will be low (the squeeze is ok), systolic stays the same ▪ Distance between systolic and diastolic will be widened • Widened pulse pressure o Bounding pulses, gushing out and falling back. o Heart failure sx’s d/t decreased forward flow and increased back up · Mitral regurgitation o Most common causes: Mitral valve prolapse and rheumatic heart disease o Mitral valve is supposed to close tightly so blood does not flow back into the atrium, and to maximize forward flow of blood o Permits backflow of blood from the left ventricle into the left atrium during ventricular contraction ▪ Results in LV hypertrophy because of increased volume in LA entering the ventricle. ▪ Blood sent back to LA, but forward flow also decreased d/t more blood going back up into LA o Mitral valve prolapse and rheumatic heart disease – most common causes o If it exists for a long time, the heart will be start to compensate and dilate to compensate for the increased blood volume ▪ Can cause systolic dysfunction and S3 o Systolic murmur between S1-S2, pansystolic murmur o Presence of S3 – splashing sound Tricuspid Dysfunction and MVP · Tricuspid regurgitation o Very similar to mitral regurg o Leads to volume overload in the right atrium and ventricle, increased systemic venous blood pressure, and right heart failure o Elevated right atrial pressure, things will back up from right atrium and back up into the blood and elevated JVP. ▪ JVP – how we clinically see right sided pressures o Jugular vein connected to superior vena cava which is connected to right atrium. So if increase in right side of heart will lead to elevated JVP o Systolic murmur that increases with inspiration · Tricuspid Stenosis o Patho essentially the same as MS, except that it occurs on the right side of the heart o Diastolic murmur o Leads to left atrial dilation, increased pressure, so increased JVP · Mitral valve prolapse syndrome o Anterior and posterior cusps of the mitral valve billow upward (prolapse) into the atrium during systole o Most common valve disorder in US o Most common cause – degeneration of the leaflets which leads to cusps thickened. o More prevalent in young women o X Linked inheritance pattern o Clinical manifestations: Asymptomatic o Affected valves at greater risk of developing infective endocarditis Pulmonary Valve · Pulmonic Stenosis o Result of congenital anomaly o Systolic murmur o Normally heard best on left upper sternal border 2nd ICS · Pulmonic Regurgitation o Seen with pulmonary hypertension o Pulmonary system usually low pressure system so when patho present, becomes more high pressure system and PA dilate o Leads to separate of leaflets of pulmonic valve – resulting in regurg o Diastolic murmur – pulmonic area on left side o Lacks changes in BP and pulse changes ▪ Bc right side of heart doesn’t eject blood to systemic area 23. Rheumatic fever and disease patho Rheumatic fever cough of frothy sputum, fatigue, decreased urine output, and edema, drowsy d/t decreased BF to brain o Physical examination often reveals pulmonary edema (cyanosis, inspiratory crackles, pleural effusions), hypotension or hypertension, an S3 gallop (from slapping of excess fluid), and evidence of underlying CAD or hypertension Diastolic heart failure o Heart failure with preserved ejection fraction o In isolated diastolic HF, heart usually able to metabolically meet the body’s needs but has a higher diastolic pressure o LV stiff o Decreased compliance of the left ventricle and abnormal diastolic relaxation which leads to increased end diastolic pressure o Higher end diastolic left ventricular pressure transmitted to pulmonary circulation ▪ Leads to pulmonary congestion, dyspnea and other sx’s of HF o Causes: chronic HTN (most common cause), Ischemia, HR, Afib, ventricular hypertrophy, aging (d/t increased collagen, smooth muscle content, and loss of elastic fibers) o Clinical manifestations non-specific; dyspnea, exercise intolerance, fatigue, weakness High output failure o Occurs when CO is higher than normal o Underlying patho = reduced systemic vascular resistance o Is the inability of the heart to supply the body with bloodborne nutrients, despite adequate blood volume and normal or elevated myocardial contractility. o Common causes ▪ Anemia, septicemia, hyperthyroidism, and beriberi, shunting of blood, peripheral vasodilation o Leads to fall in systemic arterial BP o Neurohormonal activation – RAAS and ADH o Causes salt water retention, can cause high ouput failure d/t reduced systemic vascular resistance Diseases of the Electrical System Dysrhythmia o Are disturbances of the heart rhythm. o Ranges from an occasional “missed” beat or rapid beats to severe disturbances that affect the pumping ability of the heart. o Can be caused by an abnormal rate of impulse generation or an abnormal impulse conduction. Disorders of impulse generation o Sinus bradycardia ▪ Pulse 60 beats per minute (bpm) or less o Simple sinus tachycardia ▪ Pulse rate 100 to 150 bpm o Premature atrial contractions ▪ Early P waves o Atrial flutter ▪ P rate 251 to 300 bpm o Atrial fibrillation ▪ P rate over 300 bpm Bradycardia o Pulse 60 beats per minute (bpm) or less o Pathological causes ▪ Results from block in conduction system or problem with SA node o Physiological causes ▪ Trained athletes o Abnormal Conduction (heart block) – 4 types ▪ First –degree ▪ Second- degree Mobitz I (Wenckebacke) ▪ Mobitz II • Generally blockage in bundle of HIS ▪ Third –degree (complete heart block) • AV node OR bundle of HIS OR purkinje system • Escape rhythm originating from ventricles o Originates outside the normal conduction system. · Ventricular tachycardia o QRS complex is >0.11 ms, with a rate of 100 bpm or more. · Ventricular fibrillation o Results from multiple reentrant circuits o Electrical and muscle activity even more uncoordinated than that of Vtach bc multiple circuits o Can result from ischemia or infarct or from Vtach o QRS complex is characterized by a heart rate of >300 bpm and is usually not observable; is not compatible with life. 25. Pediatric congenital heart defects, identify different types, s/s and how they are classified Heart Failure · Is a common condition associated with congenital birth defects. · Is also called congestive heart failure · (CHF). · Occurs when the heart is unable to maintain sufficient cardiac output to meet the metabolic demands of the body. · Neurohumoral and hemodynamic changes create abnormal ventricular wall stress and cause the myocardium to hypertrophy. · Clinical manifestations o Poor feeding and sucking; leads to failure to thrive o Dyspnea, tachypnea, diaphoresis, retractions, grunting, nasal flaring, wheezing, coughing o Skin changes, such as pallor or mottling o Hepatomegaly o Pulmonary overcirculation: Predominant cause associated with congenital defects Congenital Heart Defects · Is the leading cause of death (except for prematurity) in the first year of life. · Cause is known in only 10% of defects. · Prenatal, environmental, and genetic risk factors o Maternal rubella, insulin-dependent diabetes, alcoholism, phenylketonuria (PKU), and hypercalcemia o Drugs o Chromosomal aberrations Hypoxemia · Is a condition associated with congenital birth defects. o Heart defects that allow desaturated blood to enter the systemic system without passing through the lungs result in hypoxemia and cyanosis. ▪ Hypoxemia: Arterial oxygen tension is below normal and results in low oxygen arterial saturations and cellular function alteration. ▪ Cyanosis: Blue discoloration of mucous membranes and nail beds; is the result of deoxygenated hemoglobin. Classifications · Based on blood flow o Lesions increasing pulmonary blood flow ▪ Defects that shunt from high-pressure left side to low-pressure right side with pulmonary congestion; acyanosis o Lesions decreasing pulmonary blood flow ▪ Generally complex with right-to-left shunt and cyanosis o Obstructive lesions ▪ Right- or left-sided outflow tract obstructions that curtail or prohibit blood flow out of the heart o Mixing lesions ▪ Desaturated blood and saturated blood mix in the chambers or great arteries of the heart · Key to remember o Acyanotic defects have left to right shunting with pulmonary congestion o Cyanotic has right to left shunting Defects Increasing Pulmonary Blood Flow – Acyanotic Defects · Allow shunting of blood from high-pressure left heart to lower-pressure right heart · Manifest as acyanotic · Shows symptoms of CHF · Untreated leads to pulmonary hypertension Acyanotic Defects (increased pulmonary blood flow) · Patent ductus arteriosus (PDA) o Vessel located between junction of main and left pulmonary arteries o Failure of the ductus arteriosus to close results in persistent patency of the ductus arterisus o PDA allows blood to shunt from the aorta to pulmonary artery causing left-to-right shunt o Hemodynamic effect is increased pulmonary blood flow, resulting in increased pulmonary venous return to the LA and LV with increased workload on the left side of the heart o Dyspnea, fatigue, low feeding o Clinical manifestation ▪ Continuous, machinery-type murmur ▪ Risk for bacterial endocarditis · Atrial septal defect o Abnormal opening between the atria; blood flows from left atria to right atria o Three major types: ▪ Ostium primum defect – opening found low in septum, may be associated with AV abnormalities, esp. mitral valve insufficiency ▪ Ostium secundum defect – opening in center of septum, most common ▪ Sinus venosus defect – opening is high in septum near superior vena cava and RA junction o Shunting from the left to right atrium because of higher pressure in left atrium and lower pulmonary vascular resistance ▪ Right atrial and ventricular enlargement o Clinical manifestations: Often asymptomatic; diagnosed by murmur; pulmonary symptoms on exertion at later age · Ventricular septal defect (VSD) o Abnormal communication between ventricles o Direction of shunting depends on the pressure difference between PA and aorta and location of the ductus (always high to low pressure) ▪ If blood pressure is greater in the aorta than PA = left to right shunting, resulting in increased pulmonary venous return to left side of heart, over time leading to hypertrophy of LV, and then HF o Clinical manifestations: Newborns usually exhibit CHF. ▪ Once the ductus closes, rapid deterioration occurs from hypotension, acidosis, and shock. o Clinical manifestations: Older children ▪ Hypertension in the upper extremities ▪ Decreased or absent pulses in the lower extremities ▪ Cool mottled skin ▪ Leg cramps during exercise Hypoplastic left heart syndrome o Left-sided cardiac structures develop abnormally. ▪ Left ventricle, aorta, and aortic arch are underdeveloped; mitral atresia or stenosis is observed. ▪ Obstruction to blood flow from the left ventricular outflow tract results in high pressure, leading to saturated blood entering the LA and then mixing with desaturated blood in the RA through atrial septal communication o As the ductus closes, systemic perfusion is decreased, resulting in hypoxemia, acidosis, and shock. o Fatal if left untreated Mixed Defects · Dependent of mixing of pulmonary and systemic circulations for survival during the postnatal period · This mixing results in desaturated systemic blood flow and cyanosis · Pulmonary congestion occurs because of preferential pulmonary blood flow = Heart Failure Transposition of the great arteries o Aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle. o Results in two separate, parallel circuits. ▪ Unoxygenated blood continuously circulates through the systemic circulation. ▪ Oxygenated blood continuously circulates through the pulmonary circulation. o Extrauterine survival requires communication between the two circuits. o Clinical manifestations: Cyanosis may be mild shortly after birth and worsen during the first day. Acquired Cardiovascular Disorders Systemic hypertension o Hypertension in children differs from adults. ▪ Children often have underlying renal disease or coarctation of the aorta. *** need to find cause if noted!! ▪ Cause of hypertension in children is almost always found. ▪ Children with hypertension are commonly asymptomatic. o Clinical manifestations: Systolic and diastolic blood pressure levels are greater than the 95th percentile for age and gender on at least three occasions. 26. Kawasaki disease Kawasaki disease o Is also known as mucocutaneous lymph node syndrome. o Is an acute, self-limiting systemic vasculitis that may result in cardiac sequelae. o Approximately 80% of cases occur in children under the age of 5. o Not contagious, usually self-limiting o But need medical treatment and if not, serious consequences o Cause ▪ Unknown ▪ Theories: An immunologic response to an infectious, toxic, or antigenic substance (including superantigen) **Coronary Aneurysms are most important complication, very important to recognize!! ***FEVER