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Cardiology (Fall 2023) > 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

Characterized by s/s of reduced CO and volume overload

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2
Q

What is the rate of mortality, hospitalization and readmission for patients with HF

A
  • 5 year survival rate - 50%
  • Severe disease could mean 1 year mortality as high as 40%
  • 83% of pts are hospitalized at least once
  • 20-25% chance of readmission in 60 days, 50% chance at 6 months
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3
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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4
Q

What are the risk factors for HF?

A
  • CAD/Atherosclerosis
  • DM
  • HTN
  • Metabolic syndrome/Obesity
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5
Q

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

A

HTN!

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6
Q

What are the common symptoms of acute HF?

A
  • SOB
  • PND
  • Orthopnea
  • RUQ pain

acute = symptoms began w/i last few days/weeks

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7
Q

What are the common symptoms of chronic HF?

A
  • Fatigue
  • Anorexia
  • Abdominal distension
  • Edema

You can have an acute exacerbation still.

chronic = symptoms present for months

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8
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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9
Q

What is low output HF?

A

Insufficient forward output
* reduced EF, hypovolemia

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10
Q

What is the difference between HF w/ reduced left ventricular EF (HFrEF) and HF with preserved EF (HFpEF)?

A
  • HFrEF is systolic HF with reduced EF <= 40%
  • HFpEF is diastolic HF with normal EF >= 50%
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11
Q

What are the classifications of HF?

A
  • Type I - HFrEF (EF </=40%)
  • Type II - HFpEF (EF >/= 50%)
  • Type a - HFpEF, borderline (EF 41-49%)
  • Type b - HFpEF, improved (EF >40%)
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12
Q

What is the MC type of HF? what does this type of HF lead to?

A
  • Left sided systolic HF/HFrEF
  • Leads to DOE, PND, orthopnea, fatigue
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13
Q

What is the MCC of right sided HF? How does it present?

A
  • Left sided HF
  • presents with JVD, hepatic congestion, ascites, anorexia, LE edema

Isolated is rare unless lung disorder is present.

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14
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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15
Q

What do NYHA classes quantify?

A
  • The functional limitation caused HF to estimate severity of disease.
  • Assesses effort needed to elicit symptoms in a HF patient.

Class I-IV

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16
Q

Describe the 4 classes of NYHA severity for HF.

A
  1. Class I = no limitation of activity/ ordinary activity does not cause HF symptoms
  2. Class II = Slight limitation with symptoms upon ordinary activity but not at rest
  3. Class III = Marked limitation with symptoms upon less than ordinary activity but still NOT at rest
  4. Class IV = Complete inability to do activity with symptoms at rest

Limitation varies by patient based on their baseline.

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17
Q

What is the main difference between ACC/AHA staging and NYHA classes?

A
  • AHA Describes the evolution of heart failure
  • AHA are progressive stages and CANNOT change
  • AHA Helps define appropriate therapeutic approach and determine prognosis
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18
Q

Define Stages A-D for the ACC/AHA 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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19
Q

comparison pic of NYHA/ACC/AHA stages combined

A
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20
Q

What are the two neurohumoral compensatory mechanisms in HF?

A
  • Vasoconstriction to maintain systemic pressure
  • Increased myocardial contractility and HR to restore CO

These mechanisms/adaptations occur with systolic and diastolic dysfunction

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21
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.

this is enochs card, i actually have no clue whats going on here ahahahaha. good luck

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22
Q

What is one of the first responses to low cardiac output? what does this do?

A
  • activation of the SNS!
  • Increases release and decreases uptake of NE –> increased ventricular contractility and HR
  • Also leads to vasoconstriction and enhanced venous tone, increasing preload
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23
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 NE, which correlates to the severity of HF and inversely w/ survival.
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24
Q

What stimulates RAAS?

A
  • Decreased glomerular filtration
  • Increased Beta-1 adrenergic activity
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25
Q

what are the results of activation of RAAS system

A
  • increases sodium reabsorption
  • Induces systemic renal vasoconstriction
  • Can act directly on myocytes to promote pathologic remodeling via hypertrophy, apoptosis, necrosis
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26
Q

What cell type can RAAS affect?

A

Myocytes. it causes them to develop more AT receptors which results in cell apoptosis.

27
Q

What is the order of events 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
  4. Promotes water retention and stimualtes thirst
  5. increases SVR
  6. leads to reduced sodium (via dilution). degree of hyponatremia parallels the severity of HF
28
Q

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

A
  • ANP: response to atrial volume expansion, rises eary in HF.
  • BNP: response to high ventricular filling pressures, long half-life. Present in chronic or advanced HF.
  • BNP: Reduces SVR and central venous pressure and increases natriuresis to reduce afterload.
29
Q

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

A
  • Pulmonary vascular congestion
  • Peripheral edema
30
Q

What does increased afterload do in HF?

A
  • Depress cardiac function
  • Enhance deterioration of the heart
31
Q

What two hormones can promote myocyte loss and result in cardiac remodeling?

A
  • Catecholamines
  • Angiotensin II

Catecholamine-stimulated contractility and increased HR can worsen coronary ischemia

32
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.

These three are the major determinants of the LV stroke Volume

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

33
Q

What happens to myocardial contractility in systolic dysfunction?

A

Decreased contractility, assocaited with a decreased SV and therefore CO.

CO = HR x SV

34
Q

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

A
  1. SNS will activate first, increasing contracility and HR.
  2. Salt and water retention will also occur to raise blood volume and therefore EDV.
35
Q

What are the cardinal symptoms of HF?

A
  1. Dyspnea
  2. Fatigue
  3. Fluid retention

fluid retention presents as LE edema

these symptoms are d/t low CO and fluid accumulation

36
Q

What are common general PE findings in HF?

A
  • Resting sinus tach
  • narrow PP (< 25 mm Hg)
  • Diaphoresis
  • Peripheral vasoconstriction
37
Q

What are some positive findings when doing a volume assessment on PE

A
  • pulmonary congestion - inspiratory rales or dull breath sounds at bases
  • peripheral edema - LE, scrotum, ascites
  • Elevated jugular venous pressure - present if edema is d/t HF
38
Q

How do you properly assess for LE edema?

A

Start at the feet then work your way proximally to see how far the edema extends.

DONT FORGET ABOUT SCROTAL AREAS

39
Q

How is pitting edema graded?

A

0-4
1. mild pitting (2mm depression)
2. moderate pitting (4mm depression that disapears in 10-15s)
3. moderate/severe - (6mm depression that last >1 min)
4. severe - (8mm depression lasting >2 min)

40
Q

What is a pathognomonic finding in severe LV failure?

A

Pulsus alternans

Evenly spaced strong and weak peripheral pulses

41
Q

what PE finding would suggest LV enlargement

A

laterally displaced apical impulse

42
Q

what PE finding would suggest Pulmonary HTN

A

parasternal lift of RV on precordial palpation

43
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)

S3S

44
Q

what is the goal of diagnostic studies in HF patients

A

not only to confirm that symptoms are d/t heart failure but also to determine the cause of HF

45
Q

What is the main purpose of an EKG in HF?

A
  • can detect findings that specify a cause of HF
  • can show arrhythmias that is the cause or result of HF
46
Q

What CXR findings suggest HF?

A
  • Pulmonary vascular congestion
  • KERLEY B lines
  • cardiomegaly
  • Pleural effusions
47
Q

Kerley B lines CXR image

A

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

Suggests pulmonary edema.

48
Q

What is the primary treatment for reducing pulmonary vascular congestion?

A

Lasix

49
Q

what are the initial tests in evaluation of HF

A
  • CBC - anemia, pericarditis, leukocytosis
  • CMP - electrolytes, BUN, Cr, Mg, LFTs
  • Coag studies
  • fasting BG
  • Lipid panel

CXR and EKG are also initial

50
Q

what are additional lab tests that could be done in evaluation of HF when supporting or determining the etiology of HF

A
  • TFTs
  • Iron studies
  • ANA
  • Viral Serology
  • Genetic testing
51
Q

what is the BEST test for HF evaluation

A
  • BNP and NT-proBNP
  • used when excluding HF as a dx due to its high negative predictive value
  • also good for establishing severity of disease
52
Q

what is BNP and NT-proBNP

A

a biomarker released from the ventricles while in HF

53
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.

54
Q

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

A

NT-proBNP has a longer half-life.

55
Q

What are the limitations of BNP and NT-proBNP

A
  • pt may present with more than one cause of their symptoms
  • pts with chronic severe HF may have persistently elevated levels of BNP
  • there can be other causes of elevated BNP aside from HF (will be covered on next card)
56
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.

57
Q

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

A

suggestive of ongoing myocardal injury or necrosis

Suggests increased mortality rate.

58
Q

what imaging is always indicated in new onset HF patients

A

Echoooo

59
Q

What infromation can be given with an echo

A
  • Ventricular size and function
  • LV diastolic function
  • Regional wall motion abnormalities
  • Pericardial Thickening or effusion
  • Valvular disease
  • RV function and pulmonary pressure measurements
60
Q

How do we rule out CAD in HFrEF?

A
  • Stress testing
  • Even if stress test is normal, coronary angiography should be considered
  • May also perform left ventriculogram during cardiac cath to evaluate LV function

Denial of symptoms is NOT exclusion of CAD.

61
Q

what additional diagnostic evaluations for HF can be considered if necessary

A
  • cardiac MRI
  • Cardiac CTA
  • endomyocardial biopsy
62
Q

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

A

HFrEF patients

63
Q

youre all donneee, flash back to when rhys had a bad hair day

A

Cardiology (Fall 2023) (45 decks)

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