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91 Cards in this Set
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Heart Failure |
abnormal clinical syndrome that involves inadequate pumping and or filling of the heart. |
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Primary Risk factors for HF |
Coronary artery disease Hypertension |
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Cardiac Output depends on: |
Preload Afterload Myocardial contractility Heart Rate |
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Primary causes of HF |
Coronary artery disease (including MI) Hypertension (including hypertensive crisis) Rheumatic Heart Disease congenital heart defects pulmonary hypertension cardiomyopathy hyperthyroidism vavular disorders myocarditis |
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Precipitating causes of HF |
Anemia infection thyrotoxicosis hypothyroidism dysrhythmias bacterial endocarditis pulmonary embolism pagets disease nutritional deficiencies hypervolemia
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2 classifications of HF |
Systolic Failure Diastolic Failure |
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Systolic Failure causes |
Inability of heart to pump blood effectively. Caused by impaired contractile function increased after load cardiomyopathy and mechanical abnormalities. |
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Systolic Failure end results |
Left ventricle loses ability to generate enough pressure to eject blood forward thru the aorta. eventual it becomes dilated and hypertrophied. |
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Hallmark of systolic failure |
decrease in the left ventricular ejection fraction. (defined as amount of blood ejected from the LV with each contraction. |
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Ventricular ejection fraction normals |
55-60% normal 40-55% less than normal >40% may confirm dx HF >35% is seriously low |
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Diastolic Failure |
inability of the ventricles to relax and fill during diastole. Decreased filling of the ventricles results in decreased stroke vol. and CO. It's characterized by high filling pressures because of stiff ventricles |
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Diastolic Failure results |
venous engorgement in both the pulmonary and systemic vascular systems |
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Diastolic failure causes |
left ventricular hypertrophy from hypertension myocardial iscemia valve disease cardiomyopathy |
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4 main compensatory mechanisms a heart in failure utilizes |
1) Sympathetic nervous system activation 2) Neurohormonal Response 3) Dilation 4) Hypertrophy |
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Compensatory mechanism: Sympathetic nervous system activation |
First triggered but least effective Causes release of catecholamines (nor/epinephrine). Triggering increased HR, myocardial contractility, & peripheral vasoconstriction. Initially the increase in HR improve but overtime become harmful increasing the workload of an already failing heart. |
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Compensatory Mechanism: Neurohormonal Response (Release of Amino Acid Peptides) |
Released by stretch receptors in atria/ventricles in response to excess blood volume Primary Purpose is to: -cause loss of NA and H2O Via Kidneys -vasodilate veins/arteries decreasing BP -reduce aldosterone levels -activation or renin-angiotension-aldosterone system in response to low cardiac output |
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Compensatory mechanism: Dilation |
enlargement of the chambers of the heart. occurs after pressure in the heart chambers is elevated over time. at first this leads to increased CO & maintains BP but eventually this causes the elastic elements of the muscle fibers to overstretch & no longer contract effectively thus decreasing CO |
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Compensatory Mechanism: Hypertrophy |
an increase in the muscle mass and cardiac wall thickness in response to overwork and strain. occurs slowly and initially leads to increase CO & maintenance of of tissue perfusion but overtime the hypertrophic heart muscle has poor contractility requires more oxygen to perform work has poor coronary artery circulation & is prone to dysrhythmias. |
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2 Staging systems of HF |
ACC/AHA Staging System NY Heart Assoc. Classification System |
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ACC/AHA Staging |
Stage A-ideentifies pts at risk for CHF but don't have any structural heart disease or symptoms Stage B-Individual w/documented structural changes but don't yet have any symptoms Stage C-pts that have structural changes & have/had symptoms Stage D-Describe pts with refractory HF requiring support |
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AHA/ACC Staging of Heart Failure |
Class 1-Ordinary physical activity doesn't cause undue fatigue Class 2-Ordinary physical activity causes fatigue dyspnea and pain. However at rest are asymptomatic. Class 3-Less than ordinary activity causes symptoms. PT has marked limitations of physical activity but is typically asymptomatic at rest. Class 4-can't perform any level of physical activity w/o discomfort. w/activity discomfort increases. may need mechanical support rx support, consider transplant or end of life care. |
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Left Ventricle Failure |
Most common
fluid accumulates behind the failing chamber first
causes either pulmonary congestion or a disturbance in the respiratory control mechanisms -> respiratory distress |
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Signs of Left Sided Heart failure |
LV Heaves Pulsus Alternans (alternating strong/weak beat) Increased HR PMI displaced Inferiorly & posteriorly Decreased PaO2 & slightly increased PaCO2 Crackles S3 & S4 heart sounds pleural effusion
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Renal Changes of Left Sided HF |
Nocturia Oliguria Activation of renin-angiotension-aldosterone system |
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Left sided HF Symptoms |
Weakness, Fatigue anxiety depression dyspnea shallow respirations up to 32-40 per min paroxysmal nocturnal dyspnea orthopnea dry hacking cough nocturia frothy pink-tinged sputum |
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Right Sided Failure |
Right ventricle fails causing peripheral edema and venous congestion of the organs |
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Right Sided HF Signs |
Edema Anasarca (massive generalized body edema) Hepatomegly Ascities (Lungs/Abdomen feels full) Decreased exercise tolerance murmurs Jugular Venous Distention Weight Gain Increased HR |
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Right Sided Symptoms |
Fatigue anxiety & depression dependent, bilateral edema RUQ Pain Anorexia and GI Bloating Nausea |
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backward failure |
term used to denote venous congestion arising from the damming of blood behind the failing chamber |
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forward failure |
refers to problems of inadequate perfusion secondary to reduced contractility producing a decrease in stroke volume cardiac output and blood flow to the organs |
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High Output Failure |
occurs when the heart despite normal to high output levels is simply not able to meet the accelerated needs of the body
volume of blood required exceeds what the L ventricle can eject |
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Low Output Failure |
Occurs in most forms of failure
Occurs when the heart is unable to pump an adequate supply of blood to the body
low output results in decreased perfusion of cells |
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Cardinal signs of HF |
Dyspnea fatigue Fluid Retention |
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Acute Pulmonary Edema |
Medical Emergency (usually results of left sided failure) left untreated pts will drown in own fluids
treated with lasix IV, Airway & O2, Elevated HOB
Eventually Morphine but not given early due to risk of morbidity |
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Refractory Heart Failure |
Heart failure when despite diet changes, medications, interventions fail to alleviate symptoms and restore partial cardiac reserve.
Treatment: prolonged bed rest, seer NA restriction, restrict fluids, diuretic therapy. |
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Clinical Manifestations of Chronic Heart Failure |
Fatigue Dyspnea Paroxysmal Nocturnal Dyspnea Tachycardia Edema Nocturia Skin Changes Behavioral Changes Chest Pain Weight Changes |
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Complications of HF |
Pleural effusion Dysrhythmias L Ventricular Thrombus Hepatomegaly Renal Failure |
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Drug Therapy for Acute HF |
Diuretics-decrease Na reabsorption Vasodilators Morphine Positive Inotropes-increases myocardial contractility
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Rein-Angiotensin-Aldosterone System Inhibitors for Chronic HF |
Angiotensin-Converting Enzyme Inhibitors (primary drug of choice for blocking RAAS system in HF pts w/systolic failure) Angiotensin 2 receptor blocker(alternate to ACEs) Aldosterone Aantagonists Beta Adrenergic Blockers |
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Medical Management Goals for HF |
1. Improve Ventricular Pump Performance
2. Reduce Myocardial workload
3. Prevent further HF by affecting process of remodeling |
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Treatment Of Heart Failure 3 Broad Components |
European Guidelines-less on devices/surgery
General Measures-teaching, counseling very important, lifestyle changes
Pharmacological Therapy |
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HF Interventions |
Positioning-high fowlers or in a chair to decrease pulmonary venous congestion
Oxygen Administration |
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Pharm. for improving ventricular Pump Performance |
Digoxin (lanoxin)
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Preload Reduction |
decrease circulating blood vol. Preload reduction 1st line tx for heart failure achieved through -diuretics -vasodilators
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Afterload Reduction |
Venous Dilators-relax smooth muscles and increase the capacity of the systemic venous bed
Arteriole Dilators-reduce systemic arteriole tone which decreases pVR afterload, L ventricular workload and increases C.O.
Combination Venous/Arteriole Dilators-decrease preload & afterload (Ex. Nipride) |
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Dietary Management of Heart Failure |
Sodium Restrictions (2-4gms)
Potassium Supplements (foods like potatoes & bananas)
Fluid Restriction-maybe necessary for 1000 cc's daily |
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Other measures for HF Tx |
Rest
Sedatives/Anxiety Meds-to promote rest
Exercise-limited but can do passive/active ROM
Anticoagulation therapy-risk vs. benefit for each pt |
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Surgical Management of HF |
Intra aortic Balloon Pump
Venoarterial bypass
heart transplant or artificial heart
Heart Assisted Pump |
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Pt teaching for pts w/HF |
Set up med schedule discourage OTC drugs dietary teaching when to call dr energy exercise in chair skin assessment |
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Hypertension |
Persistant elevation of the systolic BP at 140 or greater and diastolic BP at 90 or greater |
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Subtypes of Hypertension |
Isolated Systolic Hypertension-SBP of 140 or greater w/Dpb of less than 90
Pseudohypertension-occurs with advanced atherosclerosis (loss of elasticity of arteries)
*only way to determine is inter arterial cath
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Degree of severity of Hypertension |
Borderline Hypertension
White Coat Hypertension
Benign Hypertension
Accelerated Hypertension |
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Accelerated Hypertension |
if pt is on beta blocker peril, HCTZ, diuretic & still elevated. |
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Blood Pressure |
the force exerted by the blood against the walls of the blood vessel
*BP=CO x SVR |
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Primary HTN |
elevated BP w/o an identified cause
accounts for 90-95% of HTN
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Secondary HTN |
elevated BP with a specific cause that often can be identified and corrected.
should be suspected in pts who suddenly develop HTN and it's severe |
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Etiology of Primary Hypertension |
Response to increased: 1) CO 2) Systemic Vascular Resistance (SVR) |
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Factors affecting 2 causes of Primary Hypertension |
Heightened Response to stress Defect in renal excretion or cellular transport of sodium obesity associated w/increased insulin levels loss of elastic tissue environmental stressors |
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Secondary HTN non-modifiable risk factors |
Family history
age
gender
ethnicity |
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Secondary HTN Modifiable risk factors |
Stress
Obesity
Nutrients
Substance Abuse |
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4 control systems that play a role in maintain BP |
Arterial Baroreceptors/chemoreceptors
Regulation of body fluid vol
The renin-angiotension system
vascular autoregulation |
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Arterial baroreceptors |
monitor arterial pressure & counteract increases with vasodilation and slowing of heart rate
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arterial chemoreceptors |
sensitive to changes in concentrations of O2, CO2, and H+ ions
Drop in O2 or pH -> BP elevates Rise in CO2-> BP drops |
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Regulation of body fluid vol in BP Control |
When total blood vol. increase BP Elevates
In healthy kidneys a rise in pressure leads to diuresis
pathological changes alter the pressure threshold at which kidneys excrete salt & H2O |
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Renin-angiotension system |
renin transforms angiotension to angiotension 1
ACE converts angiotension 1 to angiotension 2
angiotension 2 increases BP by 2 different mechanisms.
1) A2 is potent vasoconstriction & increases SVR resulting in immediate increase in BP
2) increases BP indirectly by stimulating the adrenal cortex to secret aldosterone |
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Vascular Autoregeneration |
normally constriction/vasodilation is auto regulated
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Vessel changes that occur with hypertension |
Silent killer: often no S&S of the damage being caused to organs
initially no changes in blood vessels/organs |
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damage to lg vessels in HTN |
sclerosed and tortuous lumens narrow-blood flow decreases eventual occlusion or hemorrhage |
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damage to sm vessels in HTN |
sm vessels of the brain, heart, kidneys are affected |
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HTN damages what layer causing what |
intimal layer
1) Fibrin accuulation 2) local edema 3) intravascular clotting
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In development of hypertensive cardiovascular disease a vicious cycle of pathologic changes occur |
arterioles contract -> contractility increases to maintain normal CO and over come increased After load
leads to hypertrophy of heart and coronary insufficience
L Ventricle fails -> increase diastolic press causing congestion pulmonary tree -> r sided heart failure |
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HTN Clinical Manifestations |
Early stages-no S&s
Advanced Stages-occipital headache, unexplained dizziness, palpitations, flushing, blurred vision, epistaxis (nosebleed) |
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Prognosis of HTN |
If left untreated -1/2 die from heart disease -1/3 die from stroke -remaining die from kidney disease |
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Goal of HTN Treatment |
prevent morbidity/mortality |
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Objective of HTN Treatment |
to achieve/maintain arterial BP <140/90 |
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Nonpharmacologic interventions of HTN |
Weight Reduction Sodium Restriction Modification of Dietary Fat DASH Eating plan Exercise Alcohol Restriction Caffeine Restriction Relaxation Techniques Smoking Cessation
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Herbal Remedies in HTN |
many herbal drugs interact with cardiac medications |
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Potassium Supplements in HTN |
Increased ratio of NA+ : K+ has been found to be responsible for development of HTN
Reduce High Sodium Diet Add High Potassium Diet
Potassium supplements may be helpful to lower BP but costly and dangerous (cardiac Contractility) |
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Pharmacologic interventions |
Debate on when to start them. Do benefits outweigh risk/inconvience Drug selection is critical part of management of HTN
Diuretics Vasodilators Adrenergic Inhibiting Agents Central Acting Adrenergic Inhibitors Calcium Channel Blockers Angiotension Converting Enzyme Inhibitors Angiotensin Receptor Blockers Peripheral Acting Adrenergic Inhibitors |
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Diuretics in HTN |
Mainstay of Therapy Thiazides-promote renal excretion of NA H20 K+
Loop Diuretics-act on loop of hence minimize NA and H20 reabsorption
Potassium Sparing-block action of aldosterone -side-effects:elevated K+, low Na, Elevated BUN, Impotency, ataxia |
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Vasodilators in HTN |
Used to tx resistant or accelerated HTN
Acts directly on smooth muscles of arterioles cause vasodilation
Used in combo w/other drugs |
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Adrenergic Inhibiting Agents in HTN |
Beta Blockers Block beta receptors thus dilating blood vessels decreasing contractility lowering heart rate.
Alpha-Adrenergic: Cause vasodilation of peripheral attires thus decreasing PVR. (not 1st line tx) best effective in combo w/diuretics(*take at bedtime to decrease episodes of orthostatic hypotension & other side effects) |
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Central Acting Adrenergic Inhibitors in HTN |
suppresses CNS sympathetic outflow and block release of catacholemines (2nd or 3rd line of defense)
Very effective for severe HTN
Don't Stop Abruptly |
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Calcium Channel Blockers in HTN |
Block entry of calcium into smooth muscle cells cause arterial vasodilation and lower PVR |
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Angiotension Converting Enzyme Inhibitors in HTN |
"Pril" inhibit conversion angiotension 1 to angiotension 2 therefore decreasing PVR |
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Stepped-care approach goal |
To control blood pressure with minimal side-effects. |
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Stepped-Care Step1 |
Implement lifestyle changes |
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Stepped-Care Step 2 |
Continue lifestyle changes
start with one drug (lowest does or long acting daily)
Diuretics or beta blockers recommended |
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Stepped-Care Step 3 |
Change 1st drug, increase dose or add another drug from a different class |
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Stepped-Care Step 4 |
Add a 2nd, 3rd, or 4th drug from other classes and evaluate effectiveness
may also change doses of current drugs
must consider cost and compliance |
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Complications of HTN |
Hypertensive crisis |
