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CV <3 > Lecture 13: Heart Failure 1 > Flashcards

Lecture 13: Heart Failure 1 Flashcards

1
Q

Define Heart Failure.

A

It is a complex clinical syndrome that RESULTS from any structural or functional impairment of ventricular filling or ejection of blood.

AHA/ACC definition

AKA inability to have proper ventricular output or filling.
Ultimately means we have poor cardiac output.

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2
Q

What are the MCC of death in people with HF?

A

Progressive HF or SCD.

Arrhythmia is common as the left ventricle keeps stretching.

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3
Q

What are the risk factors for HF?

A
  • CAD/Atherosclerosis
  • DM
  • HTN
  • Metabolic syndrome/Obesity
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4
Q

What is the #1 risk factor for HF in both genders?

A

HTN!

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5
Q

What are the common symptoms of acute HF?

A
  • SOB
  • PND
  • Orthopnea
  • RUQ pain
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6
Q

What are the common symptoms of chronic HF?

A
  • Fatigue
  • Anorexia
  • Abdominal distension
  • Edema

You can have an acute exacerbation still.

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7
Q

What is high output HF?

A
  • Unable to meet demands of peripheral needs.
  • Thyrotoxicosis, severe anemia, sepsis
  • Symptoms of reduced CO.
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8
Q

What is low output HF?

A

Insufficient forward output, such as reduced EF or hypovolemia

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9
Q

What are HFrEF and HFpEF?

A
  • HFrEF is systolic HF with reduced EF <= 40%
  • HFpEF is diastolic HF with normal EF >= 50%
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10
Q

What is the MC type of HF?

A

Left sided systolic HF/HFrEF

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11
Q

What is the MCC of right sided HF?

A

Left sided HF

Isolated is rare unless lung disorder is present.

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12
Q

How does left-sided HF typically present? Right-sided?

A
  • Left-sided: DOE, PND, Orthopnea, fatigue
  • Right-sided: JVD, hepatic congestion, ascites, anorexia, LE edema
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13
Q

What do NYHA classes quantify?

A
  • The functional limitation caused by HF.
  • The effort needed to elicit symptoms in a patient.

Class I-IV

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14
Q

Describe the 4 classes of NYHA severity for HF.

A
  1. Class I = no limitation
  2. Class II = Slight limitation with symptoms upon ordinary activity.
  3. Class III = Marked limitation with symptoms upon less than ordinary activity.
  4. Class IV = Complete limitation with symptoms at rest

Limitation varies by patient based on their baseline.

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15
Q

What is the main difference between HF staging and NYHA classes?

A
  • Staging cannot CHANGE.
  • It stages the structural changes of the heart.

Progresses.

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16
Q

Define Stages A-D for the stages of HF.

A
  1. A = At risk but no disease or symptoms.
  2. B = Structural disease but no S/S.
  3. C = Structural dsease with prior or current S/S
  4. D = Refractory HF that requires specialized interventions (Usually class IV patients)
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17
Q

What are the two neurohumoral compensatory mechanisms in HF?

A
  • Vasoconstriction to maintain pressure
  • Increased myocardial contractility and HR to maintain CO
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18
Q

Why is hyponatremia common in HF?

A
  1. Poor renal perfusion due to poor CO causes the RAAS system to activate.
  2. RAAS will cause us to retain fluid and therefore dilute our sodium.
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19
Q

How does the sympathetic NS boost vasoconstriction and enhance venous return?

A

Increased release of NE, which also increases ventricular contractility and HR

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20
Q

What occurs in the kidney due to SNS stimulation in HF?

A
  1. Increased proximal tubular sodium reabsorption, which contributes to sodium retention in HF.
  2. Increases plasma concentration of Plasma NE.
21
Q

What stimulates RAAS?

A
  • Decreased glomerular filtration
  • Increased Beta-1 adrenergic activity
22
Q

What cell type can RAAS affect?

A

Myocytes, causing remodeling of the heart.

Also increases the # of AT2 receptors in the heart.

23
Q

What is the pathway that triggers ADH release and what is the effect of ADH release?

A
  1. Low CO
  2. Activates carotid sinus and aortic arch baroreceptors
  3. Release of ADH and stimulates thirst
  4. Increased SVR
  5. Promotes water retention
24
Q

What are the two natriuretic peptides released by the heart and what triggers each?

A
  • ANP: response to volume expansion, rises earlier.
  • BNP: response to high ventricular filling pressures, long half-life.
  • BNP: Reduces SVR, and increases natriuresis to reduce afterload.
25
Q

As we get increased filling pressures/diastolic pressures, what occurs in our lung?

A
  • Pulmonary vascular congestion
  • Peripheral edema
26
Q

What does increased afterload do in HF?

A
  • Depress cardiac function
  • Enhance deterioration of the heart
27
Q

What two hormones can promote myocyte loss and cardiac remodeling?

A
  • Catecholamines
  • Angiotensin II
28
Q

Define preload, contractility, and afterload.

This is VERY IMPORTANT TO KNOW for all heart stuff

A
  1. Preload: venous return and EDV (end-diastolic volume)
  2. Contractility: force generated at any given EDV.
  3. Afterload: Aortic impedance, SVR, and wall stress.

Afterload is essentially the pressure the heart must overcome during systole.

29
Q

What happens to myocardial contractility in systolic dysfunction?

A

Decreased contractility, aka decreased SV and therefore CO.

CO = HR x SV

30
Q

How does the body compensate for reductions in CO and SV?

A
  1. SNS will activate first, increasing contractility and HR.
  2. Salt and water retention will also occur to raise EDV.
31
Q

What are the cardinal symptoms of HF?

A
  1. Dyspnea
  2. Fatigue
  3. Fluid retention
32
Q

What are common vitals seen in HF?

A
  • Resting sinus tach
  • narrow PP (< 25 mm Hg)
  • Diaphoresis
  • Peripheral vasoconstriction
33
Q

What lung sounds might be heard in a volume assessment for HF?

A
  • Inspiratory rales
  • Dull breath sounds at the bases
34
Q

How do you properly assess for LE edema?

A

Start at the feet then work up

35
Q

How is pitting edema graded?

A

0-4, with 0 being none and 4 being a lot.

Also note when the pitting edema stops

36
Q

What is a pathognomonic finding in HF?

A

Pulsus alternans

Evenly spaced strong and weak peripheral pulses

Also seen in DCM along with tach and LBBB

37
Q

What HFs are associated with S3 and S4?

A
  • S3: systolic (because it occurs in early diastole)
  • S4: diastole (because it occurs in late diastole/early systole)

S4 = diAstole (4 = A and d is the 4th letter)

38
Q

What is the main purpose of an EKG in HF?

A

Looking for arrhythmias or underlying causes of the HF.

39
Q

What CXR findings suggest HF?

A
  • Diffuse infiltrates
  • KERLEY B lines
  • Waterbottle heart
  • Pleural effusions
40
Q

Kerley B lines CXR image

A

Horizontal lines that begin in the periphery and extend to the pleural surface.

Suggests pulmonary edema.

41
Q

What is the primary treatment for reducing pulmonary vascular congestion?

A

Lasix

42
Q

What is the primary use of BNP tests?

A

Excluding HF due to its high negative predictive value

43
Q

Between BNP and NT-proBNP, which range is higher?

A

NT-proBNP can go up to 300 before considering it as positive.

BNP only needs to be higher than 100 to be positive.

44
Q

What is the primary difference between NT-proBNP and BNP?

A

NT-proBNP has a longer half-life.

45
Q

What can cause elevated BNP?

A
  • ACS
  • LVH
  • Pulmonary HTN
  • Afib
  • S/P Cardioversion
  • PNA
  • Sepsis
  • Severe burns
  • Increased age
  • Severe anemia
  • Renal failure
  • Chronic HF

It is a poor indicator in patients with chronic HF.

46
Q

Why can trops be elevated in HF that does not have CAD or ischemia?

A

Remodeled myocytes can be irritated more easily and is suggestive of ongoing injury.

Suggests increased mortality rate.

47
Q

What measurements does an echo give that we want to know about in a patient with HF?

A
  • Ventricular size and function
  • Regional wall motion abnormalities
  • Thickening
  • RV function and pulmonary pressure estimates
48
Q

How do we rule out CAD in HFrEF?

A
  • Stress testing
  • Potentially coronary angiography

Denial of symptoms is NOT exclusion of CAD.

49
Q

What is most clinical evidence regarding HF based on? (Which HF type?)

A

HFrEF patients

CV <3 (25 decks)

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