Cardiology
Quiz yourself by thinking what should be in
each of the black spaces below before clicking
on it to display the answer.
Help!
|
|
||||
|---|---|---|---|---|---|
| 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
🗑
|
Review the information in the table. When you are ready to quiz yourself you can hide individual columns or the entire table. Then you can click on the empty cells to reveal the answer. Try to recall what will be displayed before clicking the empty cell.
To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
To hide a column, click on the column name.
To hide the entire table, click on the "Hide All" button.
You may also shuffle the rows of the table by clicking on the "Shuffle" button.
Or sort by any of the columns using the down arrow next to any column heading.
If you know all the data on any row, you can temporarily remove it by tapping the trash can to the right of the row.
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
Normal Size Small Size show me how
Created by:
Abarnard
Popular Medical sets