Busy. Please wait.

Forgot Password?

Don't have an account?  Sign up 

show password


Make sure to remember your password. If you forget it there is no way for StudyStack to send you a reset link. You would need to create a new account.

By signing up, I agree to StudyStack's Terms of Service and Privacy Policy.

Already a StudyStack user? Log In

Reset Password
Enter the email address associated with your account, and we'll email you a link to reset your password.

Remove ads
Don't know (0)
Know (0)
remaining cards (0)
To flip the current card, click it or press the Spacebar key.  To move the current card to one of the three colored boxes, click on the box.  You may also press the UP ARROW key to move the card to the "Know" box, the DOWN ARROW key to move the card to the "Don't know" box, or the RIGHT ARROW key to move the card to the Remaining box.  You may also click on the card displayed in any of the three boxes to bring that card back to the center.

Pass complete!

"Know" box contains:
Time elapsed:
restart all cards

Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.

  Normal Size     Small Size show me how



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
HF heart sounds Right: TR murmur, Loud P2; Right sided S3 or S4, RV Lift; Left: S3 or S4, MR murmur, AI/ AS Murmur, Displaced PMI
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)
HTN not responsive to basic meds = think secondary HTN, most likely renal artery stenosis (infrarenal artery)
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; Longstanding 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 Left HF Ischemic heart dz (most common) 2/2 MI or chronic ischemia; chronic HTN; valvular heart dz; idiopathic; myocarditis (L & R); toxins (ETOH, cocaine, thyroid, lead); sepsis
Most common cause of Systolic Left Heart Failure Ischemic heart dz
Causes of Systolic HF (decreased EF) MI, chronic HTN, Dilated CM
Can Systolic & Diastolic CHF coexist? Yes
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; ARBs; Beta Blockers; Nitrates + hydralazine; AAs; 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)
ACEI effect on heart remodeling Decrease (reverse) remodeling, improving cardiac performance
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 DM
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
Created by: Adam Barnard Adam Barnard