CVPR 03-27-14 09-10am Heart Failure-Diagnosis - Allen Flashcards Preview

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Flashcards in CVPR 03-27-14 09-10am Heart Failure-Diagnosis - Allen Deck (51):

HF symptoms associated with decreased Cardiac Output

Decreased organ perfusion, FATIGUE


HF symptoms associated with increased Pulmonary Venous Pressure (Left-sided)

---> increases pressure in the lungs ---> Breathlessness (DYSPNEA)


HF symptoms associated with increased Central Venous Pressure (Right-sided)

Edema (ascites, pleural edema/effusion, swelling in ankles/legs)


HF symptoms associated with Low Flow

1. Decreased cerebral perfusion (sleepiness, confusion); 2. Decreased muscle perfusion (fatigue, weakness); 3. Decreased gut perfusion (anorexia, wasting/cachexia); 4. Decreased kidney perfusion (RAAS activation, reduced urine output, progressive renal dysfunction)


HF symptoms associated with increased Left-Sided Pressure

Increased Pulmonary venous pressure --> breathlessness (dyspnea), dyspnea on exertion, orthopnea (dyspnea when lying flat), paroxysmal nocturnal dyspnea, acute pulmonary edema


Positional Shortness of Breath - Orthopnea

Immediate SOB when lying flat; in HF, relates to lost venous pooling of blood in legs ---> when lie down, no longer gravity working against heart ---> rt. atrial filling pressure immediately goes up ---> rt. ventricular contractions thus go up, pushing more blood to lt side ---> if lt. ventrical is already stiff w/ already high pressure, back up of pressure in lungs


Positional Shortness of Breath -Paroxysmal nocturnal dyspnea (PND)

Delayed SOB, waking pts from sleep; classically relieved by pt getting out of bed & ambulating; relates to mobilization of edema from tissue through lymphatics back into blood stream (over the day, gravity pools fluid in lower extremities, increasing pressure & causing edema; when lie flat, no longer this pressure --> fluid leaches back into veins over time, increasing venous pressure --> increases preload & thus rt. ventricular contraction, filling of dysfunctional lt side, pressure build up in lungs (but delayed b/c fluid must leach back in)


HF symptoms associated with increased Right-Sided Pressure

Increased central venous pressure (RV failure) ---> Peripheral swelling/dependent edema, Ascites, Hepatic congestion, Intestinal congestion (protein-losing enteropathy)


Edema in HF

Increased central venous pressure (CVP) upsets the balance of Starling forces: Ventricular dysfunction ---> Increased filling/venous pressure ---> Hydrostatic pressure pushing water out of veins is greater than normal so that oncotic pressure can’t make up for it & pull water back into veins ---> Edema


Precipitating factors producing acute or worsening symptoms in HF

1. Increased circulating volume (preload)…..2. Increased pressure (afterload)…..3. Worsened contractility (inotropy)…..4. Arrhythmia (rate).....5. Increased metabolic demands…..6. Non-adherence with HF meds!!!


Factors that increase circulating volume (preload) & thus exacerbate HF

SODIUM LOAD IN DIET; Renal failure


Factors that increase pressure (afterload)) & thus exacerbate HF

Uncontrolled HTN (LV); Worsening aortic stenosis (LV); Pulmonary embolism


Factors that worsened contractility (inotropy) & thus exacerbate HF

Myocardial ischemia; Initiation of negative inotrope (beta-blocker, calcium channel blocker)


Factors related to Arrhythmias (rate) that thus exacerbate HF

Bradycardia, Atrial fibrillation


Factors that increase metabolic demands & thus exacerbate HF

Fever/infection, Anemia, Hyperthyroidism, Pregnancy


NYHA HF rating

Based on assessment of symptoms: I Asymptomatic….II Symptomatic w/moderate exertion….III Symptomatic w/minimal exertion (going up flight of stairs)…..IV Symptomatic at rest


American College of Cardiology and American Heart Association (ACC/AHA HF) Stages

A – High risk for HF (HTN, CAD) but w/out structural heart disease or symptoms of HF….. B – Structural heart disease but w/out symptoms of HF….. C – Structural heart disease w/prior or current symptoms of HF….. D – Refractory HF requiring specialized interventions…. Can move between stages (can move from C after a salty meal, back to B with treatment, etc)


Importance of Symptoms

Symptoms decrease quality of life, define the severity of the disease (which is one of the strongest predictors of death in HF), often determine therapy (e.g., more aggressive therapies for more advanced disease); Can treat heart disease before HF develops & prevent it!


Clinical Course of HF

Nonlinear; Can look really bad after a big salty meal (Class C), but then go back to Class B w/no symptoms after treatment


Signs of Low Flow in HF

1. Cool extremities (peripheral vasoconstriction to redirect scant existing blood flow to vital organs)….. 2. Tachycardia (Compensation for low SV)….. 3. Low pulse pressure = difference btwn systolic & diastolic pressure (reflection of low output; in late HF, go from HTN to Hypotension = bad sign of advanced disease)


Signs of Increase Left-Sided Pressure in HF

1. Rales (pulmonary crackles, like Velcro, due to wet alveoli opening)….. 2. Hypoxia….. 3. Tachypnea….. 4. Sitting bolt upright (b/c of orthopnea, etc., & to optimize their lung capacity = tripod position)


Signs of Increased Right-Sided Pressure in HF

1. Edema (follow gravity – lefts, sacrum, scrotum)…..2. Hepatic congestion / hepatomegaly….. 3. Jugular venous distention (JVD)


Jugular venous pressure – defn.

JVP = CVP (central venous pressure ) = right atrial filling pressure………..Assuming no blockage or valve between; Normal is


Jugular venous distension

= Increased central venous pressure (CVP) ---> fills up normally collapsed jugular vein; measurement of rt atrial filling pressure


Jugular venous pressure – Waves

Triphasic wave (distinguish from carotid): ..... A wave: atrial contraction; ….. C wave: closing of the tricuspid valve early early in systole; ….. V wave: movement of the RV annulus & tricuspid valve backward at the very end of systole (before the valve opens)


Normal heart sounds

The sound made as the valves shut closed; S1 = lub = Mitral & Tricuspid..... S2 = dub = Aortic & Pulmonary


Heart sounds in HF

In normal heart, lub-dub (S1, S2); In HF, Gallops (extra heart sounds due to abnormal heart)


Gallops – S3

Thought to be caused by rapid filling/expansion of the ventricular walls in early diastole; Can be present in normal young people, but abnormal after age 40; Typical of HFrEF / dilated heart; Cadence of “Ken-tuc-ky” (S1-S2-S3, lub-dub-dub, S3 right after S2)


Gallop - S4

Caused by atria contracting forcefully in an effort to overcome an abnormally stiff or hypertrophic LV; Usually abnormal; Cadence of “Ten-ne-ssee” (S4-S1-S2, dub-lub-dub, S4 right before S1); Absent in AFIB


Gallop - “Summation gallop”

All 4 (S1-S2-S3-S4), S3 & S4 come together as loud sound?


Keys to HF diagnosis

Hx (symptoms); PE (signs); Labs (testing)…Consider other possibilities (DDx) to help guide the evaluation


Typical symptoms of HF

Breathlessness, Orthopnea, Paroxysmal nocturnal dyspnea [pretty specific to HF], Reduced exercise tolerance, fatigue, tireness, increased time to recover after exercise, ankle swelling


Typical Signs of HF

Elevated jugular venous pressure, Hepatojugular reflux, Third heart sound (gallop rhythm), Laterally displaced apical impulse; Cardiac murmur


Less typical symptoms of HF

Nocturnal cough, Wheezing, Weight gain (>2kg/wk), Weight loss (in advanced HF), Bloated feeling, Loss of appetite, Confusion (esp. in elderly), Depression, Palpatations, Syncope


Less typical signs of HF

Peripheral edema (ankle, sacral, scrotal), Pulmonary crepitations, Reduced air entry & dullness to percussion at lung bases (pleural effusion), Tachycardia, Irregular pulse, Tachypnea (>16 breathes/min), Hepatomegaly, Ascites, Cachexia


Relevant comorbidities of HF – Co-existing conditions which predispose to HF

Heart Disease (Coronary, Valve Disease, HTN, Other); Cardiac Risk Disorders (Diabetes, Renal Failure, etc.); Absence of Non-HF causes of dyspnea


Differential Dx for HF signs & symptoms

Short of breath, tired, swelling


Purpose of Studies/Tests to Dx HF

1. Confirm Dx (Rule in / out HF vs. other potential causes); Characterize HF (Type, such as systolic or diastolic, and Severity); Assess response to therapy


Chest radiography (CXR) in HF

Enlarged cardiac silhouette in HFrEF; Increased upper lobe vascular markings w/acute decompensation; Acute pulmonary effusion OR High EF


Acute pulmonary edema – what is it

Acute intense shortness of break; occurs once fluid retention / left atrial pressure overwhelms compensatory mechanisms (e.g. lymphathic fluid return)


Natriuretic peptide (BNP) – when released

B-type natriuretic is secreted by the myocardium in response to 1. Primary: ventricular stretch (measure of preload) and 2. Secondary: hyperadrenergic state, RAAS activation, ischemia


Assays for Natriuretic Peptides (BNP)

Two assays (Both Increase W/Age) : 1. BNP - Normal? (


Diagnostic use of BNP (Natriuretic Peptide Assay)

Best at ruling out HF through low (normal) BNP [negative predictive value] or assessing whether chronic HF is the reason for acute symptoms (less helpful to determine acute HF) ….1. Elevations most often due to HF (Other reasons ↑BNP include sepsis, PE, etc.)….. 2. Clinically = “rule out symptomatic HF” in pts w/chronic HF (decide if an elevated BNP is less useful to determine if new dyspnea is from acute HF decompensation or from some other process (e.g. COPD exacerbation)…..Thus the negative predictive value of BNP is more useful-- a low BNP makes HF unlikely as the cause of symptoms)



No direct Dx of HF; Infer possibility of HF from other findings -- Prior MI (e.g. Q waves), LVH (increased voltage), Diffuse conduction disease from fibrosis or myocardial damage (e.g. LBBB), Arrhythmia (AFib, ventricular ectopy)


Ejection Fraction equation

(END-DIASTOLIC - END SYSTOLIC VOLUME) / END-DIASTOLIC VOLUME….. EX: Normal = (100 ml – 40 ml) / 100 ml = 60% .......... HFrEF = (200 ml – 150 ml) / 200 ml = 25% [Dilated & reduced SV)


Cardiac imaging for LVEF

EF= Gross measure of systolic function [Normal = ~60%]…….Methods of measurement: Ultrasound (echocardiography), Nuclear (MUGA or SPECT), MRI, CT


Echocardiography (Ultrasound) – Information it provides

1. LVEF (systolic function)….. 2. Chamber size (dilation)….. 3. LV wall thickness (hypertrophy)….. 4. Measures of relaxation (diastology)….. 5. Valvular anatomy & function….. 6. Estimated filling pressures (LA, CVP)….. 7. Estimated pulmonary pressures (pulmonary HTN)


Echocardiography (Ultrasound) – Advantages

Real time, Non-invasive, No radiation, Relatively “inexpensive”


Right heart catheterization (Swan-Ganz catheter)

Plastic catheter introduced into one of the major veins, then “floated” through the right heart into the pulmonary artery; Has a balloon on the end of it to help blood flow carry it into the lungs and which allows a branch of the pulmonary artery to be occluded so that the downstream pressure (post-capillary wedge pressure [PCWP]) can be measured, which is equivalent to the left atrial pressure / left-sided filling pressure.


Hemodynamic measures – PA cather measurements

1. Pressures (CVP/RA, RV, PA, PCWP)….. 2. Flow = cardiac output (Fick CO = oxygen consumption measure; Thermodilution CO = timed flow measure)


Hemodynamic measures – Calculating Resistances

Resistances can be calculated from pressures and flow (gained from catheter measurements) via Ohm’s law: V=IR / Hemodynamic equivalent: ΔP = CO x R…… Across a body capillary bed: ΔP = mean arterial BP – central venous pressure………..Systemic vascular resistance = ΔP / cardiac output (in woods units)

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