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248 Cards in this Set
- Front
- Back
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What is the Bruce Heller mnemonic for acute congestive heart FAILURE?
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F - failure to take medications (digoxin, etc)
A - atrial fibrillation I - ischemia, infarct, infections L - lifestyle (salt load) U - upregulation (thyroid hormone) R - rheumatic valve disease E - embolism like PE |
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What are the basic types of CHF?
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Acute - symptoms of HoTN without edema
Chronic - symptoms of vascular congestion develop progressively Right - lung obstruction - "back fill" edema, congestive hepatomegaly, systemic venous distension Left - dyspnea and orthopnea from pulmonary congestion - Diastolic (preserved EF >40) and Systolic dysfunction (depressed EF) |
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Describe the epidemiology of left sided HF - what are the lifetime risks, incidence of diagnosis, etc.
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20 million people worldwide
Affects 4.9 million Americans 1 million hospitalizations/year Most common hospital discharge diagnosis among patients over 65 Lifetime risk is 1 in 5 for a 40 year old Increases in prevalence with aging population |
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What may cause low cardiac output?
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Increased work to eject blood
CAD HTN DM Obesity MI Valvular disease |
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What may cause high cardiac output?
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Body has higher metabolic demand for O2
Metabolic disorders - thyrotoxicosis, nutritional disorders like beriberi Excessive blood flow requirements - systemic arteriovenous shunting, chronic |
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What is associated with left ventricular systolic dysfunction? (regarding pressure, volume...)
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Disorders of rate and rhythm
Chronic volume overload - HTN, valvular disease, obesity Chronic volume overload - Intracardiac (left-right) shunting, regurgitant valvular disease, extracardiac shunting Damage to myocardium - CAD (MI, ischemia) in 60-70% of all cases Also Nonischemic Dilated Cardiomyopathy |
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What is associated with left ventricular diastolic dysfunction? (regarding heart cells)
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Usually from a thickening of the ventricular walls
Pathological hypertrophy - primary HCMs, secondary (HTN) Restrictive cardiomyopathy - infiltrative disorders (amyloidosis, sarcoidosis), storage diseases (hemochromatosis) Fibrosis Endomyocardial disorders Aging |
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What are some S/S of CHF (4 major ones, describe each) - per Gayer?
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Dyspnea: activation of juxtacapillary J receptors is induced by pulmonary congestion breathing characteristic of cardiac.
Orthopnea, which is defined as dyspnea occurring in the recumbent position, produced with increased severity of heart failure. Relieved by sitting up. Paroxysmal Nocturnal Dyspnea (PND) severe shortness of breath and coughing that generally occur 1–3 h after the patient is a asleep. Produced by increased airway compression and resistance Cheyne-Stokes Respiration: depressed CO2 and O2 response, leads to quick shallow breadth that repeat in a cyclic fashion. |
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What is the diuretic of choice with edema?
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Furosemide
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What is included in the ddx for a respiratory pump problem?
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COPD, Asthma, Kyphoscoliosis
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What is included in the ddx for respiratory gas exchange dyspnea?
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PE
Pneumonia Interstitial Lung Disease |
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What is included in the ddx for respiratory controller dyspnea?
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Pregnancy
Metabolic acidosis |
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What is included in the ddx for cardiovascular low output dyspnea?
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CHF
MI Constrictive pericarditis |
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What is included in the ddx for cardiovascular normal output dyspnea?
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Deconditioning
Obesity Diastolic dysfunction |
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What is included in the ddx for cardiovascular high output dyspnea?
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Anemia
Hyperthyroidism Arteriovenous shunt |
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What are the most common history findings for CHF (per KBIT)?
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Dyspnea with exertion (fatigue, SOB)
Heart disease Orthopnea |
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What are some common history findings for CHF (per KBIT)?
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BIlateral peripheral edema
Tobacco use Dyspnea at rest Dull chest pain Acute dyspnea (lasting minutes-hours) |
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What are some less common history findings for CHF (per KBIT)?
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Intermittent episodes of dyspnea
Nocturnal episodes of dyspnea Fatigue/weakness Subacute dyspnea (lasting days) |
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What are some physical exam findings for CHF?
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Early CHF: Normal/high BP, increased S-ANS compensation, low pulse pressure, low stroke volume
Late CHF: low BP, from compensation with low stroke volume, palpable pulse pressure at dicrotic notch (from decreased aortic compliance), pulsus alternans Increased HR (increased S-ANS compensation) Cool periphery - from increased vasoconstriction (increased S-ANS) PMI below 5th intercostal, lateral to midclavicular line - from cardiomegaly (LVH) Heart sounds (late CHF) - S3 (dilated ventricle), S4 (rigid ventricle wall), Murmurs - from enlarged or remodeled ventricle Jugular venous pressure > 8cm Peripheral and pulmonary edema - leg swelling, lung crackles, rales and wheezes - from volume overload |
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What are some lab/radiology tests for CHF?
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TFT - for thyrotoxicosis
LFT - for hepatic congestion CBC - rule out anemia ECG - determine LVH, MI, rhythm issues CXR - Cardiomegaly, pulmonary vasculature 2D ECG - LV enlargement and function, valvular abnormalities MRI - cardiac anatomy and function Biomarkers - BNP (brain type natriuretic peptide) - also released from atrium, Tn Treadmill - Prognostic, CAD |
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What are some S/S of Cor Pulmonale (Right Ventricular Dysfunction)
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Dyspnea
Pitting edema Caused by back-pressure into the RV from problems in the lungs |
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What are some causes of right side pulmonary heart disease?
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Left sided HF
Diseases leading to hypoxic vasoconstriction - chronic bronchitis, COPD, Cystic fibrosis Chronic hypoventilation - obesity, neuromuscular disease, chest wall dysfunction, living at high altitude Diseases that cause occlusion of pulmonary vascular bed - recurrent pulmonary thromboembolism, primary pulmonary HTN, venocclusive disease, collagen vascular disease, drug induced lung disease Diseases that lead to parenchymal - chronic bronchitis, COPD, bronchiectiasis, cystic fibrosis, pneumoconiosus, sarcoid idiopathic pulmonary fibrosis |
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What are the four classes for CHF (per NYHA)?
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Class I - symptoms of HF only at activity that would limit normal individuals
Class II - symptoms of HF with ordinary exertion, comfortable at rest Class III - symptoms of HF with less than ordinary exertion - comfortable at rest Class IV - symptoms of HF at rest increased with any physical activity |
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What are the four stages for CHF (per ACC/AHA task force)?
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Stage A - high risk for HF, without structural heart disease or symptoms
Stage B - heart disease with asymptomatic LV dysfunction Stage C - Prior or current symptoms of HF Stage D - Refractory end stage HF |
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Describe the pathogenesis of heart failure with depressed EF?
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An initial event/condition results in damage, which provokes compensatory mechanisms, which stimulates secondary damage from remodeling of the heart.
Gradually, ejection fraction decreases, becomes more symptomatic |
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What kind of dysfunction (systolic of diastolic) is caused by inability to contract normally, and is responsive to positive inotropes?
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Systolic dysfunction
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What kind of dysfunction (systolic or diastolic) is caused by an inability to relax due to hypertrophy and stiffening?
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Diastolic dysfunction
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How does neurohormonal reflex compensation affect cardiac output?
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There is decreased carotid sinus firing from decreased CO, which stimulates increased sympathetic discharge that causes increased force, rate, and preload = increased CO
Decreased CO also decreases renal blood flow, stimulating renin release and thus angiotensin II which increases preload/afterload and remodeling |
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What kind of hypertrophy is caused by pressure overload?
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Concentric hypertrophy - increased number of myofibrils
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What kind of hypertrophy is caused by volume overload?
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Eccentric hypertrophy - increased stretch of myocytes, sarcomeres
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What are some acute compensatory mechanisms in CHF (also adaptive, hemorrhage, etc)?
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Augments preload, Frank Starling increased contractile force
Vasoconstriction maintains tissue perfusion pressure Increased S-ANS stinulation increases HR and contraction, renin release Hypertrophy unloads strain on individual muscle fibers Collagen deposition reduces dilation Cytokine production and vasodilator release effects vasodilation |
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What are some chronic compensatory mechanisms in CHF?
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Salt and water retention leads to pulmonary congestion, ventricular enlargement
Vasoconstriction - exacerbates pump dys, increasing afterload and energy use S-ANS stimulation increases energy use, desensitizes beta-receptors, and maybe increases remodeling Hypertrophy - increases death of cardiac cells, myofibril disorganization Collagen deposition - decreased organization, decreased myocyte support, less relaxation Cytokine production and vasodilators - skeletal muscle catabolism, deterioration of endothelial function, impaired contraction, LV remodeling |
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What is the 5 year survival rate after CHF diagnosis?
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30-40% - better for women than men
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What are some reliable drugs that can increase duration of life?
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ACE inhibitors, vasodilators, beta blockers, spironolactone
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What are some non-drug therapies?
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CABG, biventricular pacing
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What drugs inhibit cardiac remodeling?
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Beta Blockers
Ace Inhibitors AVP antagonists |
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What drugs inhibit vasoconstriction, salt and water retention?
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Vasodilators, Diuretics
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What drugs inhibit left ventricular dysfunction?
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Positive Inotropes
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What drugs are used to increase exercise tolerance and help patients maintain a functional lifestyle?
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Positive Inotropes
Cardiac glycosides or cardenolides - Digoxin Phosphodiesterase inhibitors - Amrinone (Inamrinone) Mmilrinone, Methylxanthine Beta-adrenergic Receptor Agonist - Dobutamine, Dopamine |
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What is the action of Digitalis/Digoxin?
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It inhibits Na+/K+ ATPase - it has a very narrow therapeutic window - idea is to slightly decrease the activity of Na+/K+ ATPase.
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How does Digoxin distribute, get metabolized, excreted...?
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Inactivated by enteric bacteria in 10% of patients - watch dose with antibiotic use
Widely distributed to tissues (well absorbed) Vd depends on plasma protein binding vs tissue binding - highest in kidney, heart, and liver Metabolism/excretion - 2/3 excreted unchanged by the kidneys - dosage related to creatine clearance and body weight |
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What is the dosing for Digoxin?
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Long half life: 40 hours - steady state in about 1 week
Slow increases are safest Loading dose - larger dose given 4x every 8-12 hours, for three doses, followed by a maintenance dose. Monitor patient plasma levels |
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What is the effect of reversible inhibition by Digoxin?
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As Na+K+ATPase activity decreases, there is more less Na+ being pumped out of the cell, and less Ca++ being pumped out as Na+ is pumped back in...
Net result: increased amount of Ca++ stored and a cardiac myocyte is more depolarized |
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What is included within Mitral Valve diseases?
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Mitral stenosis
Mitral regurgitation Mitral valve prolapse |
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What is included within Aortic Valve diseases?
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Aortic stenosis
Aortic regurgitation |
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What is included in Tricuspid Valve disease?
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Tricuspid stenosis
Tricuspid regurgitation |
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What is included in Pulmonic Valve disease?
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Pulmonic stenosis
Pulmonic regurgitation |
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What is the normal cross-sectional area of the mitral valve? At what reduced area do hemodynamic changes become clinically evident?
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Normal: 4-6 cm2
Reduced < 2 cm2 |
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How does mitral valve stenosis affect pressure in the heart?
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LA pressures increase, and impaired filling of the LV contributes to decreased stroke volume and cardiac output
Increased LA pressure also increases pulmonary venous and capillary pressures, which can induce transudation of plasma into the lung interstitium and alveoli |
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What conduction abnormality is a consequence of LA enlargement?
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LA dilation stretches the atrial conduction fibers, and may disrupt the conduction integrity. This would result in atrial fibrillation.
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What is mitral valve regurgitation?
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This occurs when the mitral valve incompletely closes and backward flow of blood occurs.
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What is mitral valve stenosis?
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The mitral valve becomes stiff and thickened, introducing a degree of obstruction.
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What are major presenting symptoms of mitral valve regurgitation?
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Chronic MR - decreased CO, fatigue/weakness with exertion, LV failure: dyspnea; RV failure: peripheral edema;
Acute MR - pulmonary edema, dyspnea Clinically significant MR in about 2% of the population |
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What are some causes for chronic MR?
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Myxomatous degeneration of the MV
Rheumatic Fever Infective Endocarditis Calcification of the mitral annulus associated with HTN/DM/Renal disease, and HCM |
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What are some causes for acute MR?
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Idiopathic rupture of the chordae tendinae
Papillary muscle dysfunction secondary to MI |
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What is the link between Fen-phen and MR?
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The weight-loss drug combo of fenfluramine and phentermine promoted MR as well as aortic regurgitation and/or tricuspid valve disease - withdrawn in 1997
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What are the consequences of MR pathophysiologically?
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During systole, a portion of the LV stroke volume is ejected backward into the LA, reducing the cardiac output through the aorta
Direct consequences: elevation of the LA volume and pressure, reduction of forward CO, volume-related stress on the LV (the regurgitated volume adds to the fill volume, thus requiring more ejection force) |
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What are some factors that affect the severity of MR and its effect on CO?
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Size of the mitral orifice during regurgitation
Systolic pressure gradient between the LV and LA Systemic vascular resistance opposing forward LV blood flow LA compliance Duration of regurgitation with each systolic contraction |
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What is the pathophysiology behind acute MR?
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LA is relatively stiff, so LA pressure increases substantially, transmitting increased pressure into the pulmonary circulation.
This can result in overt pulmonary edema, a medical emergency LV accomodates the increased volume load with a compensatory increase in the stroke volume |
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What is the pathophysiology behind chronic MR?
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The LA undergoes gradual compensatory dilation and increased compliance, so there is less impact on the pulmonary circulation - allow a larger LA volume without a substantial increase in pressure
There is inadequate forward CO, the compliant LA becomes a preferred low-pressure sink, and the more blood that flows into the LA, the more dilated and compliant it becomes. With increased dilation, comes increased risk of atrial fibrillation |
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What is the most common finding on a physical exam for MR?
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In chronic MR, there will be an apical holosystolic (pansystolic) murmur that radiates to the axilla
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What results may be shown to indicate MR in...
...CXR? ...ECG? ...Doppler ECG? |
CXR: In chronic MR may show LA and LV enlargement
ECG: LA enlargement and LV hypertrophy Doppler ECG: identify structural causes and grade MR severity |
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What are some treatment options for acute MR?
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IV diuretics - relieve pulmonary edema
Vasodilators (IV sodium nitroprusside) - reduce resistance to forward flow and augment forward CO |
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What is the goal of surgical intervention in MR and what kind of surgery is performed?
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The goal is to prevent development of LV failure
Surgery is done to reconstruct the native valve (2-4% operation mortality) is preferred, followed by mitral valve replacement (5-7% operation mortality) |
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What is mitral valve prolapse?
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A common and usually asymptomatic condition consisting of billowing of the mitral leaflets into the LA during ventricular systole - in 2% of population, more often in women
Sometimes accompanied by MR |
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How does mitral valve prolapse usually present?
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Usually asymptomatic, but may be associated with chest pain or palpitations - usually due to premature atrial or ventricular contractions
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What are some causes of mitral valve prolapse?
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Inherited forms: A primary autosomal dominant disorder, or in association with a connective tissue disorder such as Marfan's or Ehlers-Danlos syndrome
Consequence of myxomatous degeneration of the MV |
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How does MV prolapse typically present?
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Usually identified in an asymptomatic patient during a routine exam
Typically presents with a mid-systolic click and late systolic murmur loudest at the cardiac apex |
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What evidence is there for MV prolapse on...
CXR? ECG? |
CXR and ECG typically normal
ECG - demonstrates posterior displacement of one or both mitral leaflets into the LA during systole |
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What is the clinical course of MV prolapse? Treatment?
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Typically, it is not progressive - rarely it is.
Treatment is not indicated unless MR is present |
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What are the direct effects of Digoxin?
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Increased contractility from inhibition of Na+K+ATPase pump
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How does Digoxin cause indirect electrical effects?
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Via sensitization of the baroreceptors, central vagal stimulation and facilitation of muscarinic transmission at the cardiac muscle cells
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What are the effects on the SA node, AV node, atrial muscle, purkinje system/ventricular muscle, and ECG when Digoxin is at the therapeutic dose?
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SA node - decreased rate (P-ANS)
AV node - decreased conduction velocity, increased refractory period (P-ANS) Atrial muscle - decreased refractory period Purkinje system/ventricular muscle cells - slight decrease in refractory period Electrocardiogram - increased PR interval (P-ANS), decreased QT interval |
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What are the effects on the SA node, atrial muscle, etc. of Digoxin at toxic levels?
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Decreased rate, refractory period;
Arrhythmia Extrasystole, tachycardia, fibrillation in purkinje/ventricular muscles ECG: Tachycardia, fibrillation, arrest at high doses |
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What are the effects of Digitalis-induced P-ANS stimulation?
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Rate control similar to BB, CCB
Treats atrial arrhythmias (slows AV conduction, controls high ventricular rate) Paroxysmal atrial and AV nodal tachycardia Contraindicated in WPW |
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What are some positive inotropic effects of Digitoxin?
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Alleviates acute symptoms of CHF
May break downward spiral of CHF Neutral effect on mortality: decreases progression, despite the sudden death at high dosages |
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What are the toxicities of Digoxin?
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Common toxicity - very narrow therapeutic window
5-25% had a toxic response requiring temporary cessation Arrhythmia is #1 side effect, from Calcium overload - such as AV junctional rhythm, premature ventricular depolarizations, bigeminal rhythms, second degree AV block Gynecomastia in men ATPase-dependent transport inhibition - aqueous humor and CSF fluid and Na+ reabsorption in kidney Increase in SM tone in gut - anorexia, diarrhea CNS effects - hallucinations, visual disturbances, agitation, convulsions, etc. |
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What is used when there is calcium overload?
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Oral Magnesium or Potassium, stop use
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How does Potassium affect Digoxin?
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They inhibit one another (act at same pump)
Abnormal cardiac automaticity is inhibited by hyperkalemia |
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How do magnesium levels relate to arrhythmias and Digoxin?
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Hypomagnesemia and Digoxin combine to increase risk of arrhythmias.
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How does Quinidine affect Digoxin?
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Quinidine displaces Digoxin from tissue binding site, and decreases renal clearance, increasing plasma levels up to 2x. Similar effects may be seen with CCB and NSAIDs.
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How do Antibiotics interact with Digoxin?
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Antibiotics reduce gastric microbial metabolism, thus increasing Digoxin availability
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If a patient is on Digoxin, what risk is there if the patient takes agents that release catecholamines?
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It may sensitize the myocardium to digitalis-induced arrhythmias.
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What should be done to treat Digitalis induced arrhythmias?
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Low doses - Oral K+ and withdrawal of digitalis
More serious arrhythmias use parenteral potassium and lidocaine Overdoses - expect elevated K+ levels, released from muscle. Depressed automaticity. Treat with cardiac pacemaker catheter and digoxin immune fab (Digibind). Cardioversion makes things worse. |
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What are the two main groups of phosphodiesterase inhibitors?
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Methylxanthines
Bipyridines |
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What are the two main beta adrenoceptor stimulants with positive inotropic effects?
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Dobutamine, Dopamine (medium dose)
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How do beta adrenoceptor agonists and phosphodiesterase inhibitors affect cAMP? What are the subsequent effects?
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They increase cAMP mediated phosphorylation of the voltage gated Ca++ channel - resulting in increased Ca++ conductance
There is also inhibition of Phospholamban, activates Ca++ uptake in the SR |
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What phosphodiesterase inhibitor is used most often? Where does it act?
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Inamrinone - used for refractory CHF and acute HF. Enhances effects of cAMP and cGMP by preventing breakdown to ADP.
In cardiac muscle cells - increased calcium influx through plasma membrane channels, increased release from sarcoplasmic reticulum In blood vessels - vasodilation - most beneficial |
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What are the toxic effects of phosphodiesterase inhibitors?
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N/V, thrombocytopenia, liver enzyme changes, Inamrinone (and possibly milrinone) may cause BM changes and liver toxicity
Inamrinone is only used via IV in acute HF |
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What beta adrenoceptor agonist is used most often for CHF? How does it behave? What are its toxicities?
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Dobutamine - drug of choice
For refractory CHF Affects beta 1 receptors on the heart - increases HR, increases pacemaker activity Toxicity - reflex tachycardia, arrhythmias, angina from increased oxygen consumption, decrease in long term survival rates |
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What is the mechanism by which diuretics decrease preload and afterload?
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They reduce preload by decreasing salt and water retention, decrease venous return, and decrease ventricular size
It allows Frank Starling effects, decreases edema |
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What congestive symptoms are treated by diuretics? What symptoms are corrected by the effects of diuretics on control filling pressures?
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Reduce congestive symptoms: dyspnea, orthopnea, edema
Reduce rales, jugular venous distension, peripheral edema |
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What are some loop diuretics used for patients with CHF/edema?
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Bumetanide
Furosemide Torsemide |
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What diuretic is used in combination with a loop diuretic to treat mild heart failure?
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Thiazides (Hydrochlorothiazide)
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What K+ sparing drugs are used? (to prevent hypokalemia)
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Spironolactone - anti-aldosterone effects
Eplerenone Triamterene |
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What are the toxicities of Spironolactone?
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It's a steroid, since it inhibits aldosterone, so...
Gonadal hormone issues like gynecomastia, hirsutism, decreased libido, etc. Hyperkalemia Gastric dyspepsia and ulcers |
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How does inhibition of angiotensin II conversion affect beta blockers?
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ACE inhibitors, and other drugs that inhibit angiotensin II production, decrease S-ANS stimulation of beta receptors on juxtaglomerular cells
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What are the beneficial mechanisms of ACE-inhibitors?
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decrease afterload (prevents vasoconstriction)
decrease preload (decreases aldosterone release, so less retention) decreased S-ANS activity reduced remodeling - fibrosis of the heart and vasculature |
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When would one use ARBs in place of ACE inhibitors?
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If a patient has troubles with cough while using ACE inhbitors, switch them to an ARB - which has no bradykinin effects and thus less cough, but also less vasodilation.
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What drugs end with -sartan?
Which drugs end with -pril? |
-sartan = ARB
-pril = ACE |
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By what path does myocardial failure increase Na+ reabsorption and vasoconstriction?
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Myocardial failure --> impaired renal perfusion --> RAAS stimulation --> renin secretion --> constriction of arterioles --> increased Na+ reabsorption and vasoconstriction
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By what path does myocardial failure decrease Na+ reabosrption and vasoconstriction?
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Myocardial failure --> increased atrial or ventricular distension (pressure) --> ANP release --> inhibition of Na+ reabsorption and vasoconstriction
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What endogenous compound is Nesiritide analagous to?
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B-type natriuretic peptide
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A 73 yo m with CHF has been taking Digoxin for several years - now having frequent bouts of atria arrhythmia. Because the patient's levels of digoxin are not excessive, an antiarrhythmic agent is given concurrently with the digoxin. Soon after, the patient begins taking both drugs, he begins suffering from anorexia, nausea, vomiting, and diarrhea. Lab studies show an increase in the plasma level of digoxin - which of the following antiarrhythmic agents was most likely prescribed?
Hydrochlorothiazide Lisinopril Phenytoin Procainamide Quinidine |
Quinidine
Other drugs that increase Digoxin: Verapamil |
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A 62 yo m has PE precipitated by acute LV failure. Which of the following is the drug of choice to induce diuresis and reduce fluid volume?
Acetazolamide Furosemide Hydrochlorothiazide Mannitol Triamterene |
Furosemide
Hydrochlorothiazide - not strong enough Mannitol - used for hemorrhages and such, not HTN |
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What would be expected to occur in normal (healthy) subjects treated with a digitalis glycoside? (regarding CO, SV, HR, peripheral vascular resistance)
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CO - no change *HEALTHY!*
SV - increases HR - decreases Peripheral vascular resistance - increases |
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72 yo m suffers from HTN and CHF for many years - two weeks after he begins a new therapeutic regimen that includes Digoxin, he complains of N/V. Cardiac glycosides cause these adverse effects by acting on...
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Chemoreceptor area in the medulla - that is where the BBB is thinnest for the brain - idea is that if you ingest something really bad for you, it'll hit that area first, and induce N/V and get it out of your system before you DIE
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An elderly woman accidentally takes 5mg of Digoxin and 12 h later begins to suffer from N/V and diarrhea. Labs and other findings include a high plasma sodium level, a low potassium level, and an abnormal ECG pattern - which of the following is the most effective treatment for this patient?
Atropine Calcium chloride Digoxin Immune Fab Potassium Chloride Quinidine |
Digoxin immune Fab - necessary for really high doses of Digoxin
Lower doses - supplementing with KCl or MgCl is adequate |
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57 yo m has been treated for HTN the past 7 years - lately has gained 15 lbs and begun to complain his feet are swollen and he is SOB. When he is admitted, clinical findings have high BP, tachycardia, significant ankle edema, cyanosis, dyspnea. He is currently taking hydrochlorothiazide, propranolol, and ibuprofen. Which of the following drugs would be most appropriate for this patient?
Diazoxide Digoxine plus Quinidine Furosemide plus Lisinopril Hydralazine plus Spironolactone Prazosin plus Verapamil |
Furosemide plus Lisinopril
Furosemide for the edema Lisinopril to stop remodeling of the heart |
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What changes are expected to occur when patients with CHF are treated with a digitalis glycoside? (with regard to CO, SV, HR, Peripheral Vascular Resistance)
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CO - increased *CHF PATIENT*
SV - increased HR - decreased Peripheral vascular resistance - decreased via baroreceptor reflex - already have a lot of compensatory reflexes and in this state the baroreceptors are overstimulated so giving Digoxin will reset the baroreceptors so they can function more normally. |
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When is BNP released? Why? From where?
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It is released upon increased ventricular pressure (wall distension)
Opposes many vasoconstrictor and salt/water retaining effects of S-ANS, RAAS, and AVP systems. Reduces Renin secretion Produces vasodilation by increasing cGMP release in SM cells of venules and arterioles |
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How is BNP administered?
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Bolus dose, followed by continuous IV infusion
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In what cases is BNP elevated?
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Dyspnea - CHF, Renal Failure - elevated
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What is the effect of preload reduction on the heart (physically)?
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Reduces wall stress
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What is the physical effect of afterload reduction on the heart (physically)?
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Easier aortic outflow - easier for weak heart to eject blood
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What are the effects on preload and afterload from NO donors?
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Marked decrease in preload
Slight decrease in afterload |
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What are the effects on preload and afterload from ACE inhibitors?
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Moderate decrease in preload and afterload
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What are the effects on preload and afterload from ARBs?
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Moderate decrease in preload and afterload
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What are the effects on preload and afterload from direct acting vasodilators (Hydralazine, Minoxidil)?
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Slight decrease in preload
Marked decrease in afterload |
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Which BBs are known to reduce mortality and improve symptoms of CHF?
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Metoprolol
Bisoprolol Carvedilol |
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What is the MOA by which BBs reduce M/M and improve symptoms from CHF?
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Block high concentrations of catecholamines
CHF patients can have 2-3x the catecholamine levels as a normal person Up-regulation of beta receptors Reduce calcium depletion of sarcoplasmic reticulum Decreased HR Reduced remodeling via mitogenic activity of catecholamines Reduction in renin release from kidneys |
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How are BBs used in CHF?
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Start at low doses and work up slowly over weeks
After 2-4 months, systolic function gradually recovers |
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What are some specific uses of carvedilol in CHF?
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Dose dependent increase in LV ejection fraction
65% reduction in mortality Now FDA approved for Class II and III symptoms of CHF and an ejection fraction < 35% |
|
|
What is an adverse effect from BBs, within the context of CHF?
|
Direct decrease in LV function
|
|
|
How should one managed acute heart failure?
|
Evaluate hemodynamic status - left ventricular filling pressure, cardiac output, heart rate, blood pressure
|
|
|
What therapy should be used in cases of MI subset hypovolemia?
|
Volume replacement
|
|
|
What therapy should be used in cases of MI subset pulmonary congestion?
|
Diuretics
|
|
|
What therapy should be used in cases of MI subset power failure?
|
Vasodilators, inotropic drugs
|
|
|
What therapy should be used in cases of MI subset peripheral vasodilation?
|
None, or vasoactive drugs
|
|
|
What therapy should be used in cases of MI subset severe shock?
|
Vasoactive drugs, inotropic drugs, vasodilators, circulatory assist
|
|
|
What therapy should be used in the case of MI subset right ventricular infarct?
|
Provide volume replacement for LVFP, inotropic drugs, avoid diuretics
|
|
|
What therapy should be used in the case of MI subset mitral regurgitation, ventricular septal defect?
|
Vasodilators, inotropic drugs, circulatory assist surgery
|
|
|
What can cause a hypovolemia subtype MI?
|
Excess diuretics, inadequate fluid intake
|
|
|
What are the symptoms of a power failure subtype MI?
|
Decrease in arterial pressure
Elevation in left ventricular filling pressure Reduction in CO |
|
|
What are the symptoms of a severe shock subtype MI?
|
Very low arterial pressures, very high filling pressures, very low cardiac indices
|
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|
What is aortic stenosis?
|
A thickened, stiff aortic valve, usually the result of age-related degenerative calcific changes. Especially in patients who present with AS after age 65 - causes impaired blood through the valve during systole
|
|
|
What are the major presenting symptoms of aortic stenosis?
|
Angina
Syncope CHF |
|
|
What are the main causes of aortic stenosis?
|
Aging
1-2% of population is born with an abnormal aortic valve, which carries increased risk of degenerative changes RF |
|
|
How does aortic stenosis progress pathophysiologically?
|
The aortic valve orifice gradually reduces - when it is at <50% of its original size, significant LV pressure is needed to eject blood.
Because it develops over years, hypertrophy develops in the LV, reducing compliance and the LA begins to undergo hypertrophy as well, accounting for up to 25% of the ejection force. |
|
|
How does aortic stenosis cause angina?
|
Hypertrophied muscle requires more oxygen, and there is increased wall stress
Elevated LV diastolic pressure also reduces coronary perfusion, reducing blood supply to the heart |
|
|
How does aortic stenosis cause exertional syncope?
|
LV hypertrophy creates pressure sufficient for normal CO at rest, but because the stenotic orifice is fixed, CO cannot increase with excertion, thus decreasing cerebral perfusion, causing dizziness and possibly syncope.
|
|
|
How does aortic stenosis cause CHF?
|
As the stenosis progresses, LV becomes less able to cope with the gradually increasing afterload - LV diastolic volume and pressure increase, LA pressure increases, pulmonary venous pressure increases, pulmonary alveolar congestion occurs
|
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|
What are the grades of aortic stenosis?
|
Normal aortic valve cross sectional area: 3-4 cm2
Mild AS: < 2 cm2 Moderate AS: 1.0-1.5 cm2 Severe AS: <1.0 cm2 |
|
|
What are the mean survival times of a patient with aortic stenosis and...
...syncope? ...angina? ...CHF? ...atrial fibrillation? |
with syncope: 3 years
with angina: 5 years with CHF: 2 years with atrial fibrillation: 6 months |
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|
What kind of murmur is auscultated for aortic stenosis? What else may be noted during this part of the physical exam?
|
There are early and late peaking murmurs, early has a crescendo that enters decrescendo closer to S1, while late peaking murmurs have the decrescendo starting closer to S2.
Weakened and delayed upstroke of the carotid artery pulsations due to the obstructed LV outflow May have an S4 (atrial kick into stiff LV) |
|
|
What may show up on an ECG, CXR, doppler ECG in a patient with aortic stenosis?
|
ECG: LVH in advanced AS
CXR: may reveal LVH Doppler ECG: best and most sensitive for assessing aortic valve and LV wall |
|
|
What is the average survival for aortic stenosis? What treatments are available?
|
Untreated, symptomatic patients have a 57% 1-year survival rate
Only effective treatment in advanced AS is surgical replacement of the valve - indicated when those with severe AS develop symptoms or when there is progressive LV dysfunction |
|
|
What is aortic regurgitation? How does it develop?
|
AR occurs when there has been damage to the aortic leaflets or there has been significant aortic dilation, allowing abnormal regurgitation of blood from the aorta into the LV during diastole
|
|
|
What are the major presenting symptoms of aortic regurgitation?
|
Dyspnea on exertion
Fatigue Decreased exercise tolerance Sometimes patient is aware of the feeling of uncomfortably strong, forceful heart beats |
|
|
What are some causes for aortic regurgitation?
|
Valve leaflet abnormalities - congenital (bicuspid valve), endocarditis, RF
Dilation of the aortic root - aortic aneurysm, aortic dissection, annuloaortic ectasia, syphilis |
|
|
How does aortic regurgitation affect the rest of the heart, pathophysiologically?
|
Blood regurgitating from the aorta during diastole is added to the normal amount of blood from the LA, forcing the LV to increase stroke volume.
Amount of blood determined by size of regurgitant orifice, pressure gradient across the aortic valve during diastole, duration of the diastole |
|
|
What is acute aortic regurgitation?
|
A surgical emergency, requiring valve replacement.
LV pressure will substantially increase with the increased volume, transmitting pressure to the LA and pulmonary circulation, causing pulmonary edema and dyspnea |
|
|
What is a hallmark of early aortic regurgitation?
|
A widened pulse pressure
|
|
|
How does the LV adapt over time in aortic regurgitation (early chronic AR)?
|
LV dilation predominates, and hypertrophy is a lesser process.
It keeps dilating to accommodate the increasing volume, aortic diastolic pressure drops, and coronary artery perfusion drops. Stroke volume increases, producing a high systolic arterial pressure, producing increased or widened pulse pressure. |
|
|
What is characteristic of late phase chronic AR?
|
As AR progresses, LV enlargement surpasses preload reserve on the Frank-Starling curve, with the EF falling to normal and then subnormal levels.
Eventually the LV reaches its maximum diameter and diastolic pressure begins to rise, resulting in exertional dyspnea. May also lower coronary perfusion gradients, causing angina and ischemia. |
|
|
What sound is associated with aortic regurgitation?
|
a "blowing" diastolic decrescendo starting at S2
May also be accompanied by a low-frequency, Austin-Flint murmur thought to represent turbulent blood flow across the mitral valve during diastole. |
|
|
What will show up on an ECG, CXR, and doppler ECG of a patient with aortic regurgitation?
|
CXR: can demonstrate LV enlargement
ECG: may show LVH, depending on the degree of hypertrophy Doppler ECG: best for quantifying the degree of AR and identifying the cause |
|
|
What treatments are available for aortic regurgitation?
|
Severe AR - asymptomatic with preserved LV function - medical therapy such as afterload reducing vasodilators (CCB, ACE-I) with goal of delaying need for surgery
Severe AR - symptomatic or asymptomatic with impaired LV function - surgery should be offered. Without surgery, death occurs within about 4 years of the onset of angina, and 2 years of HF symptoms. |
|
|
What is tricuspid stenosis? What does it sound like?
|
A rare disease usually associated with rheumatic fever (particularly IV drug abusers), often present along with mitral stenosis.
Has a similar sound to mitral stenosis - an opening snap and diastolic rumble after S2 It creates obstruction that can cause neck vein distension, abdominal distension, or hepatomegaly. Surgery usually required, whether valvuloplasty or valve replacement |
|
|
What heart valve problem is associated with an a wave in the internal jugular veins just before S1?
|
Tricuspid stenosis
|
|
|
What is tricuspid regurgitation? What are its causes?
|
Often a secondary development to right ventricle enlargement, rheumatic fever.
Very rare cause is carcinoid syndrome - produced by a type of GI tumor that secretes serotonin metabolites that are thought to promote endocardial plaques on the right side of the heart |
|
|
How would tricuspid regurgitation sound?
|
The systolic murmur is typically a high-pitched, blowing, holosystolic, nonradiating murmur best heard at the lower left sternal border. It becomes louder on inspiration.
|
|
|
What heart problem is associated with a v wave in the internal jugular veins, approximately coinciding with the second heart sound?
|
Tricuspid regurgitation
|
|
|
What is the best method to evaluate tricuspid regurgitation (CXR, ECG...)
|
Doppler ECG
|
|
|
What treatments are indicated for tricuspid regurgitation?
|
Primary treatment is for focus on the conditions responsible for the RV hypertrophy as well as diuretic therapy. Surgery is indicated for severe cases.
|
|
|
What is pulmonic stenosis? What causes it?
|
This is a rare disease, almost always due to congenital valve deformity (eg Tetralogy of Fallot). Another rare cause is carcinoid syndrome.
|
|
|
What kind of murmurs would be heard in pulmonic stenosis?
|
It has a crescendo-decrescendo pattern following S1, but with the crescendo growing longer as stenosis progresses from mild to moderate to severe
|
|
|
What is the most common acquired abnormality affecting the pulmonary valve? Is it primary or secondary?
|
Pulmonic regurgitation
Usually secondary to dilation of the pulmonic valve ring by severe pulmonary hypertension |
|
|
What kind of murmur is associated with pulmonic regurgitation?
|
A high-pitched blowing decrescendo diastolic murmur (from S2), virtually indistinguishable from aortic regurgitation.
|
|
|
How do the different classes of functional capacity help determine when surgical intervention is needed?
|
Functional capacity can help determine when surgery is needed to improve quality of life
|
|
|
What is the primary goal of the NYHA classification of function assessment?
|
It acts as a guide for physical activity recommendations - can also determine when surgical intervention is needed
|
|
|
What viruses are the most common cause for viral myocarditis?
|
Adenovirus - has become the most common
Group A and B Coxsackieviruses |
|
|
What viruses may cause viral myocarditis?
|
Adenovirus
Group A, B Coxsackievirus Echovirus Parvovirus B19 HIV CMV Influenza Mumps |
|
|
What are some groups who are at risk of contracting viral myocarditis?
|
Infants and young adults, especially those who are physically active
|
|
|
What is the mortality rate for acute viral MC?
|
0-4%
|
|
|
What are some histological characteristics of viral myocarditis?
|
Inflammatory infiltrates
Lymphocytic infiltration of the myocardium with myocytolysis |
|
|
What percentage of cases of myocarditis are caused by viruses?
|
70%
|
|
|
How does the virus cause myocarditis?
|
The virus enters the body, enters the lymph nodes, replicates and causes acute viremia
It then disseminates to the heart and replicates further, leading to acute or chronic myocarditis |
|
|
What type of cardiomyopathy may develop from chronic viral myocarditis?
|
Dilated cardiomyopathy
|
|
|
How would a patient present who has viral myocarditis?
|
Patient may have a history of a recent URT or GI infection, or a flu-like syndrome within the past 1-2 weeks
Shortness of Breath Chest Pain Fever |
|
|
About how many cases of viral myocarditis develop into...
...acute viral myocarditis? ...chronic myocarditis? |
If viral myocarditis does not resolve itself, it may develop into acute or chronic viral myocarditis.
Acute: 9% Chronic: 10-40% |
|
|
What percentage of cases of chronic viral myocarditis end in sudden death? End with a heart transplant (from DCM)?
|
Sudden death: 20%
Heart transplant: 80% |
|
|
What are some lab tests that aid in diagnosing viral myocarditis?
|
Blood cultures
PCR will help determine which virus is the cause Anti-viral antibody titers ECG to rule out other heart problems Heart MRI |
|
|
How would one treat viral myocarditis? What should be avoided?
|
Start with supportive therapy for LV dysfunction
Limit physical activity AVOID corticosteroids AVOID immunosuppression/immunotherapy (mixed results) |
|
|
What is a virulence factor associated with viral myocarditis (CVB)?
|
(Coxsackie virus B) Viral protease 2A - may cleave certain host proteins and effect ongoing myocyte injury. Also cleaves dystrophin, thus disrupting the dystrophin glycoprotein complex which is necessary for cardiac function
|
|
|
What are the main pathogens that cause infective endocarditis?
|
Staphylococci
Streptococci Enterococci Fungi |
|
|
How do these organisms invade, adhere, and proliferate?
|
Survive host defenses - resist complement-mediated bactericidal activity of serum, escape phagocytosis
Adherence Resistance to platelet microbicidal proteins |
|
|
What are some predisposing factors for infective endocarditis?
|
Congenital cardiac defects
Degenerative heart disease Mitral valve prolapse Prosthetic heart valves Rheumatic heart disease Valvular damage from previous endocarditis Intravenous drug use |
|
|
What are some of the pathological effects of infective endocarditis?
|
Persistent bacteremia
Release of cytokines Tissue damage Fragmentation of vegetations into the circulation Secondary autoimmune effects |
|
|
How does acute infective endocarditis progress in a native valve?
|
Febrile toxic course (days-weeks)
Structurally abnormal or normal valves 60% from virulent agent like S. aureus (others: pneumococci, streptococci, gram negative rods) |
|
|
How does subacute infective endocarditis progress in a native valve?
|
Low fever, anorexia, weakness, lasting weeks+
Structurally abnormal valves Less virulent bacteria cause: alpha-hemolytic streptococci (60%), enterococci, staphylococci, gram negative |
|
|
How does early prosthetic valve infective endocarditis progress?
|
Within first 3 months of surgery
Often nosocomial or from contamination Caused by...staphylococcus (55%), gram negative rods, fungi (candida, aspergillus) |
|
|
How does late prosthetic valve infective endocarditis progress?
|
3 months or more after surgery
Consequence of transient bacteremia Causative organisms: alpha-hemolytic streptococci, enterococci, staphylococci |
|
|
What are the causative organisms with infective endocarditis related to IV drug abuse? What valve is most often involved?
|
Tricuspid valve - 50%
Causative microorganisms - S. aureus, coagulase negative staphylocci, others. |
|
|
What are some characteristics of S. aureus: Gram stain? Positive/negative tests?
|
Gram + cocci
Arranged in clusters Catalase positive Coagulase positive beta hemolysis Mannitol positive Yellow colonies |
|
|
What are some virulence characteristics of S. aureus (particularly those that play a role in infective endocarditis)?
|
Protein A - inhibits phagocytosis
Fibrinogen-binding protein - clumping factor Coagulases - convert fibrinogen to a fibrin clot Cytotoxic toxins - pore-forming toxins |
|
|
What medium can be used to grow S. aureus that is selective and differential?
|
Mannitol salt agar
|
|
|
What are some positive/negative tests for S. epidermidis? How does it infect people, and what is a major virulence factor?
|
Gram + cocci
Arranged in clusters Catalase positive Hemolysis negative Mannitol negative Coagulase negative Infections via catheters, prosthetic devices, IV drug abuse, prosthetic valves Virulence factor: biofilm |
|
|
Where is Viridans Streptococci found?
Positive/negative tests? |
Normal flora in oral/nasopharyngeal cavities
Dental caries Gram + cocci in chains Catalase negative alpha hemolysis Optochin resistant BIle resistant *low virulence* |
|
|
What is the most common cause of subacute IE in patients with abnormal or damaged heart valves?
|
Viridans Streptococci
|
|
|
How does Viridans usually gain access to a person?
|
During oral/dental surgery or procedures
|
|
|
What is a major virulence factor of Viridans Streptococci?
|
Dextran-mediated adherence (biofilm) - form on damaged heart valve surfaces
|
|
|
What are characteristics of Enterococcus faecalis?
|
Gram + cocci
Single cells, diplococci, short chains Catalase negative Group D Lancefield antigen Grown in 6.5% NaCl *Normal intestinal flora* |
|
|
How is E. faecalis acquired? What does it cause?
|
Nosocomial infections most often
Urinary tract infections Endocarditis - 3rd most common cause |
|
|
What are some characteristics of Pseudomonas aeruginosa?
|
Aerobic Gram - motile rod
Produces pigments May adapt to low nutrients Uncommon with IE, mostly drug abusers and those with prosthetic valves Has pili, capsule, extracellular enzymes/toxins |
|
|
What are the HACEK organisms?
|
Haemophilius aphrophilus
Actinobacillus actinomycetemcomitans Cardiobacterium hominis Eikenella corrodens Kingella kingae |
|
|
What are some characteristics of HACEK organisms? how often do they cause IE?
|
Cause about 5% of cases of IE
Fastidious organisms - require 5-10% CO2 and 3 weeks for growth |
|
|
How do Bartonella sp. bacteria cause IE? In whom?
|
Typically in homeless males with poor hygiene
Must be considered in cases of culture-negative endocarditis in homeless |
|
|
What is polymicrobial IE?
|
A combination, usually Pseudomonas and Enterococci
Observed in IV drug users Mortality is 2x that of single-agent IE |
|
|
Who tends to get fungal endocarditis? What kind of fungi?
|
Generally IV drug abusers and ICU patients with broad-spectrum antibiotics
Blood cultures often negative Candida spp. Aspergillus spp. |
|
|
How do patients present with subacute IE?
|
85% have patients within 2 weeks of a dental or other procedure
Low grade fever/chills (90%) Fatigue, anorexia, weight loss (25%) New or changing heart murmurs Various skin lesions in about 20% of patients |
|
|
How does a patient present with acute IE?
|
Acute onset of high-grade fever and chills
Rapid onset of CHF Murmurs absent in about 1/3 of patients |
|
|
How would one diagnose IE?
|
Duke clinical criteria
Blood cultures - 3 sets, different sites, 24-48 hours. Multiple positives = persistent bacteremia If multiple are all same bacteria, isolate and identify, test sensitivity Culture-negative IE in about 5% - causes include recent antibiotic treatment, fastidious organisms, fungi |
|
|
What can be observed in an ECG in a patient with IE?
|
Vegetations - especially with BC-negative cases
Negative does not rule it out |
|
|
What are some ways to prevent IE?
|
Maintain good oral hygiene
Prophylaxis with patients at high risk before the procedures |
|
|
What causes Rheumatic Fever?
|
Systemic inflammatory disease, a sequela of group A streptococcus infection - due to cross reactivity between M proteins and antigens of heart or joint tissue
signs include carditis - pericarditis, myocarditis, endocarditis |
|
|
What is shock?
|
The clinical syndrome that results from inadequate tissue perfusion
Definition: Inadequate delivery of substrates and oxygen to meet the metabolic needs of the tissues |
|
|
What are the consequences of shock?
|
Inadequate tissue perfusion
Imbalance between O2 supplied and O2 needed Cellular dysfunction Cellular injury produces and releases inflammatory mediators Perfusion further compromised via functional and structural changes in microvasculature. ... Death |
|
|
How does shock produce an ever-worsening cycle?
|
Hypoperfusion --> decreased O2 delivery and increased O2 needs --> cellular injury --> release of inflammatory mediators --> functional and structural changes in microvasculature --> more hypoperfusion
|
|
|
What are some of the morbidities associated with shock?
|
Renal failure
Brain damage Gut ischemia Hepatic failure Metabolic derangements Diffuse intravascular coagulation Acute respiratory distress syndrome Cardiac failure Death |
|
|
How is microcirculation affected by shock?
|
CO falls, SVR rises to maintain a level of pressure adequate to perfuse the brain and heart. SVR is determined by the luminal diameter of the arterioles, and constriction of arterioles leads to reductions in the number of capillary beds that are perfused.
Limited surface area for filtration and gas exchange Derangement of cellular metabolism and organ failure |
|
|
What are the different classifications of shock (5-6)?
|
Hypovolemic
Distributive Cardiogenic Septic Obstructive Miscellaneous/Combination |
|
|
What is hypovolemic shock?
|
Results from absolute deficiency of intravascular blood volume
|
|
|
Which form of shock is the leading cause of pediatric death in the US and worldwide?
|
Hypovolemic shock
|
|
|
What complicates treatment of hypovolemic shock?
|
Rapid progression - rehydration is impeded by concurrent vomiting
Rapid loss of fluid --> reduced ventricular preload --> decreased stroke volume and CO --> decreased oxygen delivery |
|
|
What are common causes for hypovolemic shock (3 major)
|
Intravascular volume loss - gastroenteritis, burns, diabetes insipidus, heat stroke
Hemorrhage - trauma, surgery, GI bleeding Interstitial loss - burns, sepsis, nephrotic syndrome, intestinal obstruction, ascites |
|
|
What is distributive shock?
|
When normal peripheral vascular tone becomes inappropriately relaxed
Vasodilation --> increased venous capacitance --> relative hypovolemia --> decrease in preload --> decrease in oxygen delivery |
|
|
What are some common causes for distributive shock (4 major)?
|
Anaphylaxis - medication, blood products, foods, envenomation, latex
Neurological - head injury, spinal shocl Drugs - vasodilation Sepsis - release of vasoactive mediators may cause profound vasodilation |
|
|
What is cardiogenic shock?
|
Impairment of cardiac contractility, which decreases SV and CO and thus decreases oxygen delivery
|
|
|
What are some causes for cardiogenic shock (6)?
|
CHF
IHD Cardiomyopathy Cardiac Tamponade Sepsis Drugs |
|
|
What is obstructive shock?
|
Associated with physical obstruction of the great vessels or the heart itself
|
|
|
What are some common causes of obstructive shock? How does one approach it differently from other shocks?
|
Obstructive congenital heart disease - coarctation of the aorta, interrupted aortic arch, severe AV stenosis)
Acquired heart disease - rheumatic fever, subacute bacterial endocarditis, HCM, pulmonary embolism, cardiac tamponade Since it is often congenital, it is treatd with surgical intervention, and in neonates, maintenance of the patent DA. |
|
|
What is septic shock?
|
Sepsis = systemic inflammatory response triggered by the presence of infectious agents or toxins
|
|
|
How does oxygen delivery get impaired in septic shock?
|
Presence of infectious agents - endotoxin
The resultant release of inflammatory mediators and cytokines |
|
|
How does septic shock progress (several ways)?
|
Sepsis can induce the activity of the enzyme nitric oxide synthase, which induces potent dilation via NO - decreases CO and oxygen delivery
May also disrupt capillary integrity - result in intravascular fluid leaking into tissue third spaces --> hypovolemia Many different toxins and inflammatory mediators can depress cardiac function and reduce contractility Over-activation of the clotting cascade can result in DIC --> directly plug and block critical tissue beds (microvascular obstructive shock) Multiple system organ failure, including respiratory failure --> hypoxia |
|
|
What is systemic inflammatory response syndrome?
|
Defined as two or more of the following:
Fever > 38 degrees centigrade or < 36 degrees centigrade HR > 90 bpm RR > 20 breaths/min or PaCO2 < 32 mmHg Abnormal WBC >12,000/microL or <4,000/microL or >10% bands |
|
|
How is systemic inflammatory response syndrome (SIRS) caused?
|
It is a nonspecific syndrome which may be caused by ischemia, inflammation, trauma, infection, or a combination of things
NOT always related to infection |
|
|
How would one recognize shock?
|
It is a clinical physiological diagnosis
Symptoms and clinical findings relate to decreased perfusion - so lack of kidney perfusion = decreased UOP; lack of brain perfusion = mental status changes |
|
|
What kind of shock may be the result of vomiting/diarrhea, or a traumatic car accident?
|
Hypovolemic shock - due to fluid loss
|
|
|
What kind of shock may be the result of head trauma?
|
Distributive shock
|
|
|
What kind of shock may be associated with fever?
|
Septic shock
|
|
|
What kind of shock may be seen in a patient with a history of heart problems?
|
Cardiogenic shock
|
|
|
How do you evaluate a person for shock? What do you look for?
|
Blood pressure - Low
HR - usually high, unless impeded by Rx, nerve impairment, etc. Skin perfusion - Low - measure temperature of hands/feet, capillary refill, distal pulses (weak/thready) - may not show signs in early shock Urine output - Low (indicates decreased kidney perfusion) Assess mental status Look for areas of trauma, evidence of bleeding Temperature - hyperthermia, hypothermia |
|
|
How does compensated shock compare to decompensated?
|
Both have tachycardia, cold skin
Decompensated - HoTN, weak carotid pulses, absent distal pulses, global cyanosis, profound hypoventilation, little to no urine output Compensated - strong distal pulses, normal BP, tachypnea, moist skin, normal urine output |
|
|
What is the initial treatment for shock? ABC?
|
Start with the ABCs:
Airway - assurance of an airway Breathing - adequate ventilation - initially administer 100% O2 at high flow rate Circulation - establishment of adequate blood volume, chest compressions if inadequate heart rate Obtain access - multiple large-bore IVs Noninvasive monitors - pulse oximeter, cardiorespiratory monitor, obtain beside glucose measurement |
|
|
Once the patient is set up (ABCs, IVs, noninvasive monitors), what is the next step for stabilizing the patient?
|
Focus on improving circulation and systemic oxygen delivery
Volume expansion - IV fluids, blood products Vasopressors and cardiac inotropic agents If sepsis is a concern, start antibiotics Continue volume expansion with close monitoring of vital signs |
|
|
What are some blood tests that aid in diagnosing and treating shock?
|
CBC - check Hb, determine carrying capacity and need for transfusion
Complete metabolic panel - check volume status, electrolyte imbalances, liver and kidney perfusion CXR - evaluate cardiac silhouette, look for PNA, ARDS Blood gas - determine patient's blood pH |
|
|
If you are not in a clinical setting, how do you deal with a patient suffering shock?
|
Place victim in shock position (feet elevated)
Keep patient warm and comfortable Turn patient's head to one side, if neck injury is not suspected |
