Heart Failure 2

Question 1

Common symptoms of left-side heart failure

Answer 1

Dyspnea (Shortness of breaths)

• increase left side filling pressures→incre. pulmonary venous pressure→Acute pulmonary edema: leads to transudation of fluid into the pulmonary interstitium and congestion of the lung parenchyma→ reduced pulmonary compliance and increases the work of breathing to move the same volume of air, also excess fluid in the interstitium compresses the walls of the bron- chioles and alveoli, increasing the resistance to airflow and requiring greater effort of respiration
• Reduce CO-> reduced blood flow to overworked respiratory muscles and ac- cumulation of lactic acid may also contribute to that sensation.

Orthopnea: sensation of labored breath- ing while lying flat and is relieved by sitting upright

• results from the redistribution of in- travascular blood from the gravity-dependent portions of the body (abdomen and lower ex- tremities) toward the lungs after lying down.

Paroxysmal noctural dyspnea: severe breathlessness that awakens the patient from sleep 2 to 3 hours after retiring to bed. **(Different from orthopnea is this is delayed, and orthopnea is immediate) **

• results from the gradual reabsorption into the circulation of lower extremity interstitial edema after lying down, with subsequent expansion of intra- vascular volume and increased venous return to the heart and lungs

Impair urine output during the day because of decreased renal perfusion and increased urinary frequency at night (nocturia) when, while supine, blood flow is redistributed to the kidney, promoting renal perfusion and diuresis

Fatigue and weakness : because reduce CO -> Reduced skeletal muscle perfusion may result in fatigue and weakness.

Question 2

Common symptoms of ride-side heart failure

Answer 2

Abdominal discomfort

• the elevated systemic venous pressures can result the liver becomes engorged and its capsule stretched
• anorexia (decreased appetite) and nausea may result from edema within the gastrointesti- nal tract

Peripheral edema, especially in the ankles and feet, also reflects increased hydrostatic venous pressures. ​

Question 3

Precipitating factors that make symptoms worse

Answer 3

Increased circulating volume (preload)

• Sodium load in diet
• Renal failure

Increased pressure (afterload)

• Uncontrolled hypertension (LV)
• Worsening aortic stenosis (LV)
• Pulmonary embolism (RV)

Worsened contractility (inotropy)

• Myocardial ischemia
• Initiation of negative inotrope (beta-blocker or calcium channel blocker)

Arrhythmia (rate)

• Bradycardia (slower than normal heart rate)
• Atrial fibrillation

Increased metabolic demands

• Fever, infection
• Anemia
• Hyperthyroidism
• Pregnancy

**Non-adherence with HF medications **

Question 4

Eccentric hypertrophy

Answer 4

Chronic volume overload (e.g., chronic mitral or aortic regurgitation) results in the synthesis of new sarcomeres in series with the old, causing the myocytes to elongate. The radius of the ventricular chamber therefore en- larges, doing so in proportion to the increase in wall thickness

Question 5

Concentric hypertrophy

Answer 5

Chronic pressure overload (e.g., caused by hypertension or aortic stenosis) results in the synthesis of new sarcomeres in parallel with the old (i.e., the myocytes thicken). In this situation, the wall thickness increases without proportional chamber dilatation, and wall stress may therefore be reduced substantially (reduce compliance).

Question 6

SYMTOMATIC CLASSIFICATIONS

Answer 6

Symptoms are important in heart failure for a number of reasons

• 1. Symptoms decrease quality of life and are highly relevant to patients.
• 2. Symptoms define the severity of the disease. Disease severity is one of the strongest predictors of death in heart failure.
• 3. Symptoms are often used to determine therapy (e.g. more aggressive therapies are indicated for more advanced disease)

There are 2 classification systems for heart failure which are largely based on symptoms (these classifications are frequently used to describe patients with HF).

Question 7

Clinical Course of HF

Answer 7

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 single NYHA (New York Heart Association) 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.

Question 8

Physical signs of HF

Answer 8

SIGNS OF LOW FLOW

• Cool extremities: Peripheral vasoconstriction to redirect what existing blood flow there is to vital organs
• Tachycardia: Compensate for low stroke volume
• Low pulse pressure (difference between systolic and diastolic pressure): Reflection of low output

SIGNS OF ELEVATED LEFT-SIDED FILLING PRESSURES

• Pulmonary rales (pulmonary crackles):Sounds like Velcro pulling apart on inspiration due to wet alveoli opening
• Hypoxia
• Tachypnea
• Sitting bolt upright
• Popping open of alveoli

SIGNS OF ELEVATED RIGHT-SIDED PRESSURES

• Edema: Dependent = follows gravity (legs, sacrum, scrotum)
• Hepatic congestion / hepatomegaly
• Jugular venous distention (JVD) = ↑ central venous pressure (CVP)
  
  • JVP = CVP = right atrial pressure
  • Assumes no blockage or valve in between RA and neck
  • Normal is < 5 cm H2O, so jugular vein is typically collapsed – with a person standing up, only the carotid pulsation should be visible (brisk upstroke during systole only)
  • With a person lying flat or with JVD in HF, the jugular vein (internal and external) 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 as fluctuations in the vein size and in the meniscus (location of the highest point in filling).
• Unlike the single systolic pulsation of the carotid, the jugular veins will have multiple fluctuations during a cardiac cycle (triphasic). These waves are:
  
  • A wave: atrial contraction
  • C wave: closing of the tricuspid valve early early in systole
  • V wave: movement of the RV annulus and tricuspid valve backward at the very end of systole (before the valve opens)
• One of the only ways to noninvasively assess vascular filling pressures.

GALLOPS

• [S1 is mitral (tricuspid) valve closure; S2 is aortic (pulmonary valve closure)]
• S3 gallop is thought to be caused by rapid expansion of the ventricular walls in early diastole
  
  • Can be present in normal young people; abnormal after age 40
  • Typical of HFrEF / dilated heart
  • Cadence of “Ken-tuc-ky” (S1-S2-S3)
• S4 gallop is 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)
  • By definition, absent in atrial fibrillation

Question 9

Heart failure

STUDIES / LABORATORY TESTING

Designed to:

Answer 9

•  Confirm the diagnosis of HF
  
  •  Rule in HF
  •  Rule out other potential causes
•  Characterize HF
  
  •  Type
  •  Severity
•  Assess response to therapy

Question 10

CHEST RADIOGRAPHY (CXR) for HF

Answer 10

• Enlarged cardiac silhouette in HFrEF (HF with reduce Ejection Fraction, eg. systolic HF)
• Increased upper lobe vascular markings with acute decompensation
• Fluffy infiltrates of pulmonary edema (not on this image)
• Pleural effusions (not on this image)

Question 11

NATRIURETIC PEPTIDES in blood of HF patient

Answer 11

• B-type natriuretic (BNP) is secreted by the myocardium in response to
  
  • Primary: ventricular stretch (measure of preload)
  • Secondary: hyperadrenergic state, RAAS activation, ischemia
• Two assays:
  
  • BNP level: Cutoff for diagnosis is relative (100 pg/mL often used)
  • NT-proBNP: N-terminus breakdown product of BNP, inactive, half life ~120 minutes (BNP 20 minutes), ~6 times the BNP
• Both increase with age
• NT-proBNP especially increased with renal failure
• Practical use of BNP / NT-proBNP
  
  • Elevations are most often due to HF
    
    • Other reasons ↑BNP include sepsis, pulmonary embolism (PE), … 
  • Clinically BNP = “rule out symptomatic HF”
    
    • In patients with chronic HF, 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)

Question 12

ELECTROCARDIOGRAM (EKG) for HF

Answer 12

• No direct diagnosis of HF
• Infer possibility of HF from other findings
  
  • Prior myocardial infarction (e.g. Q waves)
  • LVH (increased voltage)
  • Diffuse conduction disease from fibrosis or myocardial damage (e.g. LBBB)
  • Arrhythmia (atrial fibrillation [AF], paroxysmal ventricular contractions
  • [PVCs], non-sustained ventricular tachycardia [NSVT] are more common in HF)

Question 13

CARDIAC IMAGING (Echo, CT, MR, nuclear MUGA/SPECT) for HF

Answer 13

Gross measure of systolic function: left ventricular ejection fraction (LVEF):

see equation below

• Examples:
  
  • Normal = (100 ml – 40 ml) / 100 ml = 60%
  • HFrEF = (200 ml – 150 ml) / 200 ml = 25%
    
    • Dilated AND reduced stroke volume

Question 14

ECHOCARDIOGRAPHY (ultrasound of the heart)

Answer 14

• Provides
  
  •  LVEF (systolic function)
  •  Chamber size (dilation)
  •  LV wall thickness (hypertrophy)
  •  Measures of relaxation (diastology)
  •  Valvular anatomy and function
  •  Estimated filling pressures (LA, CVP)
  •  Estimated pulmonary pressures (pulmonary hypertension)
•  Advantages
  
  •  Real time
  •  Non-invasive
  •  No radiation
  •  Relatively “inexpensive”

Question 15

RIGHT HEART CATHETERIZATION

Answer 15

Also called a Pulmonary Artery (PA) Catheter, or a Swan-Ganz catheter (or “Swan”) after the physicians who invented it.

•  A plastic catheter introduced into one of the major veins and 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
•  The balloon also 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.
• Gives 2 major types of measurements
  
  •  Pressures (CVP/RA, RV, PA, PCWP)
  •  Flow = cardiac output
    
    • • Fick CO (oxygen consumption measure)
    • • Thermodilution CO (timed flow measure) 
• Resistances can be calculated from pressures and flow
  
  •  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)