Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
29 Cards in this Set
- Front
- Back
|
What is forward failure?
What is backward failure? |
*Forward Failure
-Inability to pump blood forward to meet the body’s demands. *Backward Failure (1/3 of patients) -Ability to meet the body’s demands, at the cost of abnormally high filling pressures. -LV is operating at a higher point on the Starling curve. |
|
|
Compare systolic and diastolic dysfunction:
|
*Systolic dysfunction
-Decreased stroke volume (followed by +HR, activated by SNS) -Decreased forward cardiac output -Almost always associated with DIASTOLIC dysfunction as well -Forward failure. *Diastolic Dysfunction -One third of patients with clinical heart failure have normal systolic function – i.e. “pure” diastolic dysfunction. Abnormal filling curves. -Backward failure. |
|
|
Clinical Findings in Heart Failure:
|
*Elevated PCW pressure leads to fluid in lungs (transudation thru capillaries to lungs).
-Dyspnea on exertion. -Orthopnea. -Paroxysmal nocturnal dyspnea (PND--wake up SOB). *Reduced cardiac output leads to fatigue and decreased organ perfusion -Cool extremities. -Reduced urinary output. -Decreased mentation. |
|
|
New York Heart Association Classification of Chronic Heart failure:
describe the 4 classes of it-- |
Class I: No limitation of physical activity.
Class II: Slight limitation of activity. Dyspnea and fatigue with moderate exertion (e.g. walking upstairs quickly). Class III: Marked limitation of activity. Dyspnea with minimal exertion (e.g. walking slowly upstairs). Class IV: Severe limitation of activity. Symptoms present even at rest. This is end-stage heart failure. |
|
|
What are the general characteristics of left heart failure?
|
4 broad categories of left heart failure.
Pressure overload --> Diastolic dysfunction. Restrictive cardiomyopathy --> amyloidosis. |
|
|
What is diastolic dysfunction?
|
*Impaired early diastolic relaxation (this is an active, energy dependent process)
*Increased stiffness of the left ventricle (this is a passive phenomenon) -LVH -LV fibrosis -Restrictive or infiltrative cardiomyopathy |
|
|
Discuss Diastolic dysfunction due to LVH:
|
*Patients with diastolic dysfunction have chronically elevated PCWP (25-30), and that's why they're SOB.
|
|
|
Diastolic dysfunction: Discuss changes in the Pressure – Volume Loop:
|
-Slight decrease in SV.
|
|
|
Compensatory Mechanisms for Heart Failure: 3 categories
|
*Frank – Starling Mechanism
*Neuro-humoral alterations *Left ventricular enlargement -LV Hypertrophy --> ↑ contractility (stronger heart) -LV “remodeling” --> ↑ stroke volume (bigger heart) |
|
|
Discuss the Frank –Starling mechanism as a compensatory mechanism for heart failure:
|
Go from A to B after MI. Only way to maintain CO is by upping the PCWP, and going to C. Good short term, not good long term.
|
|
|
Changes in levels of Neuro-humoral mediators during heart failure: 3 mediators
|
*SNS is turned on as soon as you start to have heart failure.
*We block these mediators with drugs (ACEi, ß-blockers). |
|
|
Discuss Neuro-humoral mediators as a compensatory mechanism for heart failure:
|
*Vasoconstriction to maintain BP. Can eventually lead to fluid in lungs. These are all short term fixes that lead to HF eventually.
|
|
|
Discuss two kinds of Left Ventricular enlargement:
|
*Concentric LVH.
-Increased LVEDP -Increased incidence of backward failure -Decreased wall stress at expense of increased oxygen demand and increased LVEDP -This one is maybe less bad? *Eccentric hypertrophy (cavity dilation and hypertrophy). -Seen in volume-overload states -Seen after acute MI (post-infarction “remodeling”) -Increased stroke volume at the expense of increased wall stress, oxygen demand and LVEDP -Worse due to scar zones and death post-MI? |
|
|
What are the end results of “compensatory mechanisms” for heart failure?
|
*Proarrhythmic effect! As EF goes < 40 it gets bad. Under 30 is really bad --> implant a defibrillator.
|
|
|
Discuss "pseudo left heart failure":
|
*Obstruction of LV filling causes pseudo HF. LV is functioning totally fine.
|
|
|
Physiology of Mitral Stenosis:
|
*MV isn't opening probably. Almost always due to rheumatic fever.
*Mitral valve leaflets become thickened and can't open all the way -- "doming." *Note elevated LA pressure and everything else upstream in MS. |
|
|
Findings with Mitral Stenosis:
|
*Prominent first heart sound-- S1 is louder.
*Opening snap after S2. *Pre-systolic rumble (murmur). *Signs of right heart failure: -Prominent P2. -Prominent jugular venous A wave. -Prominent Jugular V-wave (if TR present). |
|
|
Discuss Right Heart Failure:
|
*Left failure strains the right heart.
*"Pure" causes: -pulmonic valve stenosis -COPD -Embolism -etc. |
|
|
Compare Right heart vs. Left heart failure based on symptoms:
|
*Left Heart failure:
-Pulmonary congestion. -Reduced forward cardiac output: Fatigue. Renal insufficiency. Cool extremities. Decreased mentation. *Right Heart failure: -Neck vein distension. -Hepatic congestion (hepatomegaly and hepatojugular reflux--HJR). -Peripheral edema. Swolled up cankles. -Also may result in reduced forward cardiac output, but with clear lung fields. |
|
|
Auscultatory findings in CHF: 2 main sounds
|
*S4 gallop – decreased compliance (“diastolic dysfunction”). Occurs just before S1. Coincides with atrial kick, just before mitral/tricuspid close. Low pitched.
*S3 gallop – systolic dysfunction or volume overload. Much more ominous. EF would be 30 or less. |
|
|
Chest X-ray findings in heart failure:
What PCWPs do different findings correlate to on X-ray? 3 |
*Upper lung field vascular re-distribution:
Correlates with PCW pressure > 15 mm Hg *Interstitial edema --> Kerley B lines: Correlates with PCW > 20 mm Hg *Pulmonary edema --> opacification of alveoli: Correlates with PCW pressure > 25 – 30 mm Hg |
|
|
*Normal Chest X ray. Heart is less than half the chest width across.
*Sharp costophrenic angles. |
|
|
*Chest X-ray in CHF; PCWP >15
*Vascular redistribution (engorged vessels) and prominent cardiac silhouette; heart is enlarged. |
|
|
*Chest X-ray in CHF.
*Kerley “B” lines: *Suggest interstitial edema. *Look like horizontal lines perpendicular to the lateral aspects of the lower lungs. |
|
|
*Kerley A lines (arrows) are linear opacities extending from the periphery to the hila; they are caused by distention of anastomotic channels between peripheral and central lymphatics.
*Kerley B lines (white arrowheads) are short horizontal lines situated perpendicularly to the pleural surface at the lung base; they represent edema of the interlobular septa. *Kerley C lines (black arrowheads) are reticular opacities at the lung base, representing Kerley B lines en face. |
|
|
*Pulmonary edema:
-Findings include diffuse “fluffy” infiltrates representing alveolar edema. PCWP here is 30-35. Fluid is pouring into alveoli. Looks like a cotton ball. If there's no increase in WBC or other pneumonia findings, you know it's CHF. |
|
|
Pulmonary edema. Very fluffy pattern.
|
|
|
*CXR with pleural effusion
-Pleural fluid in CHF: -Usually occurs on the right side first. -Blunting of the “costo-phrenic” angles. -Layering out of fluid with patient lying on their side. |
|
|
Biomarkers for Congestive heart failure:
|
*BNP = Brain Natriuretic Peptide
*Elevated in Congestive heart failure -The heart secretes natriuretic peptides as a homeostatic signal to maintain stable blood pressure and plasma volume and to prevent excess salt and water retention. Increases diuresis and natriuresis (Na excretion). -BNP primarily is secreted by the ventricles as a response to left ventricular stretching or wall tension. -Higher BNP level correlates with worse prognosis. -But, BNP isn't totally specific for HF. Other things can cause it to be elevated. |
