HF II - Dx and Tx Flashcards
Major symptoms associated with heart failure due to decreased cardiac output
FATIGUE
Symptoms of decreased organ perfusion
Muscle→fatigue, tiredness/sleepiness
Gut→anorexia, wasting (cachexia)
Kidney→↓urine output, renal dysfunction
Exercise intolerance→inability to augment cardiac output to meet increasing demands of stress/exercise.
Major symptoms associated with heart failure due to increased pulmonary venous pressure
DYSPNEA (breathlessness)
Dyspnea on exertion
Orthopnea→SOB when lying flat (blood pooling in legs now pulling in abdomen/thorax)
Paroxysmal nocturnal dyspnea (PND)→delayed SOB, waking patients from sleep→mobilization of edema from tissue through lymphatics back into blood stream.
Acute pulmonary edema: acute, intense shortness of breath; occurs once fluid retention/left atrial pressure overwhelms compensatory mechanisms→fluid spills from the pulmonary vasculature into the interstitial space and then into the alveoli→hypoxia
“fluffy” infiltrates on an CXR
Major symptoms associated with heart failure due to increased central venous pressure
Peripheral swelling/dependent EDEMA
Ascites
Hepatic congestion
Intestinal congestion (protein-losing enteropathy)
New York Heart Association Functional Class
o I: asymptomatic
o II: symptomatic with moderate exertion
o III: symptomatic with minimal exertion
o IV: symptomatic at rest
ACC/AHA HF Stage
o A: At high risk for heart failure but without structural heart disease or symptoms of heart failure
o B: Structural heart disease but without symptoms of heart failure.
o C: Structural heart disease with prior or current symptoms of heart failure.
o D: refractory heart failure requiring specialized interventions
Common precipitants of worsening heart failure
o Increased circulating volume (Preload)→sodium load in diet, renal failure
o Increased pressure (afterload)→uncontrolled hypertension (LV), worsening aortic stenosis (LV), pulmonary embolism (RV)
o Worsened contractility (inotropy)→myocardial ischemia, initiation of negative inotrope (beta-blocker or calcium channel blocker)
o Arrhythmia (rate)→bradycardia, atrial fibrillation
o Increased metabolic demands→fever, infection, anemia, hyperthyroidism, pregnancy
o NON-ADHERENCE WITH HF MEDICATIONS
Variable clinical course of heart failure
o HF is marked by a non-linear course. It is typically marked by episodic exacerbations with significant symptoms (sometimes requiring hospitalization), with intervening periods of relative stability. Patients rarely stay at a singly NYHA class over time; they may move between functional classes depending on a number of factors that dictate cardiac function and symptomatology. However, the usual course is an average of progressive decline over time.
Physical signs of heart failure and their relation to underlying pathology: Signs of low flow:
Cool extremities—peripheral vasoconstriction to redirect what existing blood flwo there is to vital organs.
Tachycardia—compensate for low stroke volume
Low pulse pressure—reflection of low output.
Physical signs of heart failure and their relation to underlying pathology: Signs of elevated left-sided filling pressures
rales (pulmonary crackles)—fluid in the lungs, wet alveoli opening. Hypoxia Tachypnea Sitting bolt upright Popping open of alveoli
Physical signs of heart failure and their relation to underlying pathology: Signs of elevated right-sided pressures
Edema—dependent=follows gravity
Hepatic congestion/hepatomegaly
Jugular venous distention (JVD) = ↑ central venous pressure
JVP = CVP = right atrial pressure
Normal < 5 cm H2O.
With a person lying flat or a person with JVD in HF, the jugular vein (internal and external) will fill with blood. Thus the neck veins will appear full on visual examination. More importantly, they will transmit pressure changes in the right atrium as waves, visible fluctuations in the vein size and in the meniscus.
Physical signs of heart failure and their relation to underlying pathology: Gallops
S3 gallop—rapid expansion of the ventricular walls in early diastole
HFrEF/dilated heart
Ken-tuc-ky (S1-S2-S3)
S4 gallop—atria contracting forcefully in an effort to overcome abnormally stiff or hypertrophic LV
Ten-ne-ssee (S4-S1-S2)
Natriuretic peptides
B-type natriuretic (BNP) is secreted by the myocardium in response to
Primary: ventricular stretch
Secondary: hyperadrenergic state, RAAS activation, ischemia
BNP: cutoff for diagnosis is relative (100 pg/mL)
NT-proBNP: n-terminus breakdown product of BNP (sticks around longer and easier to measure)
Use of BNP/NT-proBNP: clinically used to rule out HF, very unlikely that you have HF if you have a low BNP. Hard to rule-in, lots of causes (even ones associated secondarily with HF) that can raise BNP
CXR:
Enlarged cardiac silhouette in HFrEF
↑upper lobe vascular markings with acute decompensation
fluffy infiltrates of pulmonary edema
pleural effusions
Electrocardiogram (EKG)
No direct diagnosis of HF
Infer possibility of HF from other findings
Q waves—prior MI
Increased voltage—LVH
Arrhythmia (AF, PVCs), non-sustained ventricular tachycardia (NSVT)
Echocardiography
Provides: LVEF, chamber size (dilation), LV wall thickness (hypertrophy), measures of relaxation (diastology), valvular anatomy and function, filling pressures, pulmonary pressures.
Advantages: real time, non-invasive, no radiation, inexpensive