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CHF
Cardiology
| Question | Answer |
|---|---|
| ACC/AHA CHF Guidelines: Stage A | At risk without known disease |
| ACC/AHA CHF Guidelines: Stage B | Structural heart disease - asymptomatic |
| ACC/AHA CHF Guidelines: Stage C | Prior or current symptoms |
| ACC/AHA CHF Guidelines: Stage D | Advanced or refractory |
| NYHA Class I: | No limitations or symptoms with normal activity |
| NYHA Class II: | Slight limitations; normal activity (moderate exertion) results in symptoms. |
| NYHA Class III: | Marked limitation; minimal activity/ exertion/ ADLs results in symptoms (none at rest) |
| NYHA Class IV: | Symptoms present with minimal activity and at rest/nocturnally |
| CHF risk factors | Age; HTN; Tobacco; DM; Obesity; ETOH/Substance abuse |
| Most common causes of HF: | Ischemic cardiomyopathy; Valvular cardiomyopathy; Hypertensive cardiomyopathy |
| Most common form of HF is caused by: | chronic ischemic heart disease |
| Relationship: CHF & age | HF incidence due to diastolic dysfunction increases with age (due to increasing noncompliance of LV from long-standing HTN) |
| CHF Sx/Sx | SOB/dyspnea on exertion; edema (LE, abdomen (ascites), sacral/low back if bedbound); PND; orthopnea; fatigue, weakness, anorexia, nausea, wt change; tachycardia/palpitations |
| CHF physical exam findings | Skin (pallor, cyanosis, cool/moist); Tachypnea; JVD; HJR, hepatomegaly |
| CHF: Systemic Findings | Hepatomegaly; Pulsatile liver, tender RUQ; Ascites, Abd Swelling; edema (Low Back or sacrum if in bed); diminished or bounding pulses; Pulse, Pressure, 02 sat, weight |
| Right-sided HF heart sounds | TR murmur, Loud P2; Right sided S3 or S4, RV Lift |
| JVP elevation: | Assess R internal jugular vein: reflects right atrial pressure elevations |
| HJR = | Hepatojugular reflux |
| CHF pts w/low EF (<35%) are at risk of developing: | V-tach or V-fib |
| Heart failure after URI: | Myocarditis |
| Sudden triggers for Acute HF | Massive MI; Tachyarrhythmia with a very rapid rate; rupture of valve secondary to infective endocarditis |
| Decompensated CHF: | Pt is clinically deteriorating or unstable; begin early & aggressive tx as sort out Etiology |
| Acute CHF S/S | Severe SOB, Rales, Hypoxic, Cyanotic, Pale; CP; Tachy, BP may be hyper or hypo; cool or not perfused, poor pulses; distress (tachypneic, accessory mx); poor mental status |
| Tests to determine cause of Decompensated CHF | EKG (ischemia), HTN, atrial or other arrhythmia; Echo to assist dx; CXR to assess pulmonary edema |
| Acute Decompensated CHF: Tx | Diuretics (Natriuretics); O2 (CPAP or BiPAP); morphine? ; Nitrates (Vasodilators); Inotropes (Dobutamine, Milrinone); Hold/Do not start Beta; ACE/ ARB or other afterload reduction; Balloon pump; ID & tx underlying cause |
| Pulmonary diseases associated with HF: | COPD, Interstitial Lung Dz; Pulmonary emboli; Pulmonary HTN (idiopathic, connective tissue dz) |
| A change in structure and function of the right ventricle of the heart as a result of a respiratory disorder = | cor pulmonale |
| Acute (flash) pulmonary edema occurs when: | fluid balance is disturbed between vascular bed & lung interstitium; tachypnea, tachycardia, HTN, hypoxemia, crackles; grave prognosis if hypotensive |
| Causes of acute pulmonary edema: | MI; Acute Valvular lesion (MR, AI); HTN/Renovascular dz; End stage valvular dz (AS, MS); Systemic illness (sepsis, anemia, thyrotoxicosis, severe resp illness); poss other causes (PE, MI) |
| Acute pulmonary edema: mgmt | Pt upright, O2/CPAP, IV diuretics, nitrates, inotropes (or BNP nesiritide), pressors (dopamine, dobutamine), ACE/ARB or hydralazine + nitrate; HOLD beta in acute phase; morphine, antiarrhythmics PRN |
| Pleural effusions in CHF: caused by: | increase in interstitial edema |
| Acute CHF: hypotension is: | Ominous (if bradycardia this may be cause, as is inappropriate) |
| Why do initial CHF Sx/Sx occur w/ exertion? | Exertion: Decrease ventricular filling time; Increase HR; Inability to increase CO (end result = supply & demand mismatch); ischemia may worsen situation |
| CHF & output | Most right/ left heart failure is low output |
| High-output HF (rare) is associated with: | Elevated cardiac index but low SVR; chronic activation of symp N.S. & RAA systems; chronic volume overload and remodeling; heart cannot meet the metabolic demands; ultimately result in same neurohormonal imbalances as low output HF |
| High output heart failure (normal cardiac fn but excess tissue demands for CO): causes | Pregnancy, thyrotoxicosis, anemia, beriberi, Paget’s disease, AV fistula with shunting |
| Low output heart failure: causes | Common: ischemic heart disease & HTN. Less common: dilated CM, valve disease (eg stenosis), dysrhythmias |
| 3 major adaptive mechanisms to compensate for CHF | Frank-Starling mechanism (rapid); Neurohumoral system activation (rapid); Myocardial remodeling (slow) |
| Frank-Starling mechanism | Increased ventricular filling during diastole results in increased volume of ejected blood during systolic contraction (CO = HR x SV; norm is about 5L/min) |
| Neurohumoral release | Norepinephrine stimulates cardiac contraction & activation of renin-angiotensin-aldosterone system; fn = to maintain arterial pressure & perfusion of vital organs |
| Cardiac Remodeling (decline in function) | Compensatory response following injury to cardiac tissue; LV dilates, damaged area forms scar (over time progresses to noncompliance of ventricle, inhibiting relaxation & filling) |
| ACEI effect on heart remodeling | Decrease (reverse) remodeling, improving cardiac performance |
| Heart Contraction & Relaxation with respect to energy: | Both are energy requiring |
| Systolic Dysfunction | Defect is in the expulsion of blood from the left ventricle, leading to inadequate cardiac output |
| Causes of Systolic Left Heart Failure | Ischemic heart dz (most common) due to MI hit or chronic ischemia. Chronic HTN. Valvular heart dz. Idiopathic. Myocarditis (L & R). Toxins (ETOH, Cocaine, Thyroid, Pb). Sepsis |
| Systolic component of CHF is caused by: | chronic loss of contracting myocardium due to prior MI & acute loss of myocardial contractility induced by transient ischemia |
| Systolic left heart failure MOA: | Contraction: heart does not squeeze well, low EF (<55%) |
| Most common cause of Systolic Left Heart Failure | Ischemic heart dz |
| Prior histories most often associated with systolic CHF | CAD; valvular heart dz |
| Diagnostic features of systolic CHF | Echo reduced EF; CXR Cardiomegaly; CXR Pulm edema |
| Echo features present in systolic HF & absent in diastolic HF | Reduced EF; LV dilation |
| Causes of Systolic HF (decreased EF) | MI, chronic HTN, Dilated CM |
| Can Systolic & Diastolic CHF coexist? | Yes |
| Sx/Sx of CHF with preserved systolic function | Clinical Sx/Sx similar to systolic dysfunction |
| Diastolic left heart failure MOA: | Relaxation or Filling: heart does not relax normally, filling pressures are high but EF is preserved (over 55%) |
| Diastolic component of CHF is due to: | ventricles reduced compliance due to chronic scarring & acute loss of distensibility during ischemia |
| Prior histories most often associated with diastolic CHF | HTN |
| Diagnostic features of diastolic CHF | Echo LVH; EKG LVH; CXR Pulm edema |
| Causes of diastolic HF (preserved EF) | Restrictive, infiltrative CM (amyloidosis, sarcoid), pericardial effusion, HOCM, MI, HTN |
| Classifications of Left Heart Failure: | Systolic & diastolic |
| Cardiac Exam: Left HF / dilated cardiomyopathy: | S3 or S4 or Summation gallop; MR murmur |
| Lung Exam: Left HF | Crackles/Rales; poss wheezing; dullness at bases; sputum (frothy/pink) |
| Percentage of people with LV dysfunction who are symptomatic | 50% |
| What % of CHF patients have LVH? | 20% |
| Causes of Right HF | Left HF; congenital heart dz (ASD); right valve dz (MS, tricuspid, pulmonic); RV infarct; pHTN; pulmonary dz (COPD w/cor pulmonale) |
| Cardiac Exam: Right HF / dilated cardiomyopathy: | Right sided S3 or S4; TR murmur, loud P2 (delayed closing of pulmonic valve |
| Most common cause of Right HF | Left HF |
| Lung Exam: Right HF | Possibly clear; dullness at bases (consider pleural effusion) |
| CHF: Cardiac Cath consists of: | Left ventriculogram; Arch shot; Coronary angiography to assess for blockages |
| Left ventriculogram (MUGA scan): | Evaluate LV fn w/ calculated EF, assess wall motion, look for evidence of Mitral Regurgitation |
| Arch shot: | Assess for Aortic Insufficiency, defects in aorta (dissection/aneurysm) |
| CHF: Echocardiogram is performed to assess: | Assess for EF (LV function); for LVH; RV & Pulmonary pressures; Cardiac valves/murmurs; diastolic fn/ relaxation; WMAs; Pericardium (for effusion or mass) |
| CHF: EKG | Global low voltage possible in end stage CHF; Evidence of Ischemia or prior infarction (Q waves) |
| CHF: Cardiac Biomarkers | (CK/MB, Troponin levels): indicated if suspect ischemic etiology |
| Cardiac Cath: Indicated in: | MI, USA |
| CHF: on CXR (PA/Lateral), what is important? | Size & Shape of cardiac silhouette |
| CHF: CXR findings | Kerley B lines; pleural effusions; batwing pattern of pulmonary edema; increased vascular markings & cephalization |
| Kerley B lines = | sharp, linear densities of interlobular interstitial edema |
| Pleural effusions in CHF: caused by: | increase in interstitial edema |
| Pleural effusions most often assoc with: | LV dysfunction |
| CHF is the most common cause of what pulmonary outcome? | Pleural effusion |
| Describe pleural effusions: | Typically transudative, small to moderate in size, & free flowing (LLD view may be helpful) |
| CHF: Echo provides: | structural, anatomic & physiologic info about the heart |
| BNP: CHF | BNP secreted from ventricles under stress in CHF |
| BNP Levels | Levels vary dependent on alterations in intracardiac filling pressure |
| BNP = proposed marker for : | severity of CHF & potentially useful for Rx management |
| BNP may be falsely elevated in: | renal failure |
| HF Management Algorithm | H&P / Sx&Sx; EKG /Labs (assess etiology); Echo (MRI): preserved EF (diastolic) or poor EF (Systolic); cardiac cath |
| Pharm mgmt of CHF | ACEI, ARB, BB, CCB. Inotropes (digoxin). Nitrates + hydralazine. AA. Diuretics. Digoxin. Statins |
| CHF: Pharm mgmt w/ proven mortality benefit | ACEI; ARBs; Beta Blockers; Nitrates + hydralazine; AAs |
| CHF: Non-Pharm chronic tx | Multi-disciplinary team approach; Wt mgmt (Na+ / Fluid balance; ETOH/Toxin avoidance; Behavioral/ Risk modification; Palliative Care/ Hospice when appropriate |
| Exercise in CHF pts | Pts limited in even daily activity by poor functional status; even if cannot fix heart, make body more efficient at given work load to allow independence; allows for weight loss, mx strength, rehab enough to be able to get transplant |
| Resynchronization therapy (Biventricular pacing): indications | If low EF, Wide QRS > 130 ms and Class III or IV |
| Anticoagulation for CHF | Consider Coumadin (chronically) for Low EF; Hosp pt: prophylactic anticoag; aspirin if CAD (but no evidence for non-ischemic) |
| Anticoagulation for CHF: Chronic Definite Use (Unless CI) | A-fib; LV Thrombus; Previous thrombo-embolic CVA; Coagulopathy; LV Aneurysm |
| Devices for CHF Mgmt | AICD; IABP; Ultrafiltration/hemofiltration to remove fluid; LVAD |
| AICD criteria | EF < 35% for most CHF etiologies |
| AICD Purpose: | Prevention of sudden death; also for some HCM |
| IABP = | Intra-aortic balloon pump, temporary measure for acute CHF in hospital |
| AICD = | Automatic Implantable Cardioverter Defibrillators |
| CHF: Nonpharm tx | Behavioral; Devices (AICDs, Pacing, LVADS or pumps); Transplant |
| LVAD = | Left Ventricular Assist Device |
| LVAD is considered a ____ tx | bridge therapy prior to heart transplantation |
| Placement of LVAD | May be internal or external |
| Frequency of heart transplants for CHF | 2500/yr for CHF |
| CHF Device Tx | AICD; IABP; Ultrafiltration/hemofiltration to remove fluid; LVAD |
| AICD for CHF = what type prevention? | Primary or Secondary Prevention |
| AICD indicated if: | Previous V-Tach, SCD |
| Effect of antiarrhythmics for VT/VF | (Amiodarone, Dofetilide) do not improve survival |
| Limitation in OHT (transplant) for CHF = | donor organs |
| OHT for CHF: Late Survival post one year: | Determined by devt CAD or vasculopathy |
| OHT for CHF: median survival = | 10 years |
| OHT for CHF: one-year mortality predicted by: | need for post-op dialysis or ventilation |
| OHT for CHF: Hx of sepsis, CAD, DM, CVA predict: | decreased 5 year survival |
| AICD for CHF = what type prevention? | Primary or Secondary Prevention |
| OHT for CHF: Hx of sepsis, CAD, DM, CVA predict: | decreased 5 year survival |
| Loop diuretics (furosemide, bumetanide, torsemide) mechanism of action: | Inhibits reabsorption of Na & Cl in ascending loop of Henle & distal renal tubule, interfering with Cl-binding cotransport system -> increased excretion of H2O, Na, Cl, Mg, and Ca |
| Metolazone mechanism of action: | Inhibits Na reabsorption in distal tubules -> increased excretion of Na and H2O, as well as K and H+ ions |
| Thiazide diuretics (HCTZ, chlorthalidone) mechanism of action: | Inhibits Na reabsorption in distal tubules -> increased excretion of Na and H2O, as well as K and H+ ions |
| Positive inotropes are: | increase cardiac efficiency (eg, digoxin increases force of heartbeat by increasing myocardium Ca) |
| Negative inotropes are: | weaken force of contractions & slow heart rate |
| Negative inotrope examples: | BB: block beta-adrenergic receptors; CCB: relaxes vessels (lowers BP); antiarrhythmics |
| AHA/ACC Mgmt of HF: Stage A | Tx HTN (thiazides, ACEI, ARB), HLD, DM, OSA. Lifestyle (low Na, smoking cessation, exercise, wt loss, no EtOH) |
| AHA/ACC Mgmt of HF: Stage B | Prevent disease progression: Stage A measures PLUS ACE or ARB; consider BB in CAD patients with angina / past MI |
| AHA/ACC HF: Stage C: Initial Mgmt | Tx Symptomatic HF: Daily wts, VTE stockings, ACEI, diuretics (loops +/- metolazone) for sx control; ARB (decrease mortality); BB (Coreg, Lopressor) |
| Mainstay of therapy in AHA/ACC stage 3 tx = | ACEI |
| AHA/ACC HF Stage C subsequent mgmt | Consider hydralazine + Imdur (esp in AA); spironolactone; digoxin (esp in Afib); AICD / BiV PM |
| In HF with normal EF, this Rx may be helpful: | CCB |
| Consider AICD in these HF patients: | NYHA Class II or III and LVEF <35% |
| Consider biventricular pacemaker in these HF patients: | cardiac dyssynchrony and QRS >0.12ms; LVEF <35%; and NYHA class III or IV |
| Young patients / any age with few comorbidities, in AHA/ACC stage D (refractory) should be: | referred for LVAD and transplant |
| Young athlete with syncope during exercise; no physical exam abnormalities | Hypertrophic CM or fatal arrhythmia. Get EKG or Echo |
| Alcoholic with DOE, heart failure | Primary dilated CM |
| History of CHF on diuretic & digoxin: | Suspect dig toxicity (hypokalemia from diuretic -> dig toxicity) |
| Cardiomyopathy Pathophysiology: | HCM (50% familial, auto dom), dilated CM, restrictive (2/2 amyloidosis, sarcoid, scleroderma, hemochromatosis) |
| 3 functional categories of primary cardiomyopathy | dilated; hypertrophic; restrictive |
| Causes of Acute Pulmo Edema: | MI; acute valvular lesion (MR, AI); HTN / renovascular dz; end stage valvular dz (AS, MS); systemic illness (sepsis, anemia, thyrotoxicosis, severe resp illness); poss other causes (PE, MI) |
| Pleural effusions are most often associated with: | LV dysfunction |
| Describe pleural effusions: | Typically transudative, small to moderate in size, & free flowing (LLD view may be helpful) |
| Cardiomyopathy types | HCM (auto dom), DCM, restrictive (2/2 amyloid) |
| Cardiomyopathy EKG/CXR | CXR cardiomegaly, effusions; EKG: ST/TW changes |
| HCM pathophysiology: | LV myocardium becomes hypertrophic (esp at septum) -> diastolic dysfn -> outflow obstruction -> increased risk of arrhythmia & syncope with exertion |
| HCM dx tests: | Echo (often diagnostic); cardiac MRI; cardiac cath; 24h Holter monitor to assess for VT (if syncope / palpitations) |
| HCM tx: | Beta blockers; +/- CCB (verapamil) +/- disopyramide. AVOID Diuretics & nitrates (decrease preload & thus increase outflow obstruction) |
| TTE: dilated thin LV and low EF in pt with EtOH hx = | dilated CM |
| Categories of secondary cardiomyopathy: | myocardial dysfunction due to ischemia/CAD; HTN; VHD |
| Purpose of TTE in HF | r/o ischemia, assess valve gradients, filling pressures, consider bx; start acute or chronic tx; reduce concomitant risk factors |
| Dilated Cardiomyopathy etiology | up to 50% idiopathic; infective myocarditis; drugs (cocaine, adriamycin); ALCOHOL; Auto (SLE/scleroderma); hemachromatosis; thyroid |
| Infective myocarditis bugs | Enterovirus (Coxsackie group B), Lyme, HIV |
| Dilated Cardiomyopathy clinical findings | tachy/tachy, pulsus alternans (strong/weak), cyanosis, cool extremities, JVD/HJR, S3, S4, MR murmur |
| Dilated Cardiomyopathy mgmt | Na restriction, diuretics, ACE/ARB, dopamine in hospital, nitrates, hydralazine, digoxin, warfarin? |
| What medication is contraindicated in HCM? | Digoxin (except for A-fib with uncontrolled RVR) |
| Decreased elasticity & compliance of ventricles (often from infiltrativ process) -> high filling pressures & diastolic dysfn & HF = | Restrictive CM |
| Restrictive CM etiology: | Amyloidosis, sarcoidosis, hemachromatosis, scleroderma, Freidreich ataxia |
| Restrictive CM mgmt: | Loop diuretics, vasodilators (ACEI, nitrates), consider digoxin; transplant if refractory |
| 3 BBs shown to be effective vs mortality from CHF: | bisoprolol, carvedilol, metoprolol succinate |
| Ranolazine MOA | Inhibit the inactivating component of Na channel & Inhibit rapid inward current => prolonged ventricular action potential. Tx of chronic angina |
| Left-sided HF heart sounds | S3 or S4, MR murmur, AI/ AS Murmur, Displaced PMI |
| Right HF clinical exam S/S | LE edema, HJR, dilated neck veins, ascites |
| In a patient with CAD and CHF currently on atenolol and furosemide, what med should be added? | Lisinopril (ACEI) |
| Which BP (SBP vs DBP) is predictor of CHF in patients <50 y.o.? | DBP |
| Which BP (SBP vs DBP) is predictor of CHF in patients >50 y.o.? | SBP |
| Bilateral carpal tunnel syndrome is the most common noncardiac manifestation of which type of CHF? | Cardiac amyloidosis (ATTR type). Can precede HF sxs by 5-10 years |
Created by:
Abarnard
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