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Clinical Medicine 3 > Lecture 3 (Cardio)-Exam 1 > Flashcards

Lecture 3 (Cardio)-Exam 1 Flashcards

1
Q

American College of Cardiology defines Heart Failure as what?

A

“as a complex clinical syndrome that results from structural or functional impairment of ventricular filling or ejection of blood, which in turn leads to the cardinal clinical symptoms of dyspnea and fatigue and signs of HF, namely edema and rales”

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2
Q

What is HF? Increased prevalence due to what?

A
  • Pathophysiologic state in which abnormal cardiac function renders the heart unable to pump blood at a rate to meet the metabolic requirements of the tissues
  • Increased prevalence due to aging population and prolongation of life
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3
Q

Lower Yield

Epidemiology
* How many world wide?
* How many people over 65?
* Male vs Female?
* Improved therapeutic intervention for certain conditions has caused what?

A
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4
Q

Lower Yield

Impact on Public Health
* Common or not?
* Can be what?
* How is it disabling?
* Increased mortality?

A
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5
Q

What happens happen to the survival rate over the years?

A

“There have been modest improvements in survival rates for people with chronic HF over the past 70 years. Despite this, the 5-year survival rate is close to 50% and many people will die directly from HF or from related cardiovascular disease. Older populations are at the greatest risk of death, presenting a looming challenge to healthcare systems given changing global demographics”

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6
Q

Cardiac Physiology
* Heart Rate is dependent on what?

A

is dependent on the conduction system as well as sympathetic and parasympathetic tone

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7
Q
  • Stroke volume is dependent on what?
  • How do you get the Stroke volume?
A

Stroke volume is dependent on preload, afterload and ventricular contractility
* Not all of the blood that fills the heart by the end of diastole (end-diastolic volume or EDV) can be ejected from the heart during systole. Thus the volume left in the heart at the end of systole is the end-systolic volume (ES V). Thus, the stroke volume is not equal to the end-diastolic volume but the EDV- ESV

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8
Q

What are factors what affect the HR and SV?

A
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9
Q

Preload:
* What is it?
* Approximated by what?

A

Preload: The passive load or filling pressure of the LV.
* Approximated by the left ventricular end diastolic pressure (LVEDP) and pulmonary capillary wedge pressure (PCWP)
* “Preload isproportional to the end-diastolic ventricular volume, or the amount of blood in the ventricles immediately before systole. Greater end-diastolic volumes of blood returned to the heart, increase the passive stretching of the heart muscles. This in turn results in the ventricles contracting with more force- a phenomenon called the Frank-Starling law of the heart”

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10
Q

Afterload
* What is it?
* What is it estimated by?

A

Afterload: The resistance against which the LV contracts.
* Estimated by the systemic vascular resistance
* “Afterload represents all the factors that contribute to total tension during isotonic contraction.As such afterload can be related to the amount of systemic resistance the ventricles must overcome to eject blood into the vasculature. Afterload is proportionate to systemic blood pressures and is inversely related to stroke volume, unlike preload and contractility.”

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11
Q

Contractility
* What is it?
* Approximated by what?

A
  • Approximated by ejection fraction (EF)
  • “Contractility describes the force of myocyte contraction, also referred to as inotropy. As the force of contraction increases,the heart is able to push more blood out of the heart, and thus increases the stroke volume”
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12
Q

PATHOPHYSIOLOGY OF HEART FAILURE
* Compensatory mechanisms are trigged by what?
* Preload increases as a result of what?
* LV dilation occurs with what?
* Neuro-humoral mechanisms are activated when what happens?
* Vicisous cycle of what?

A
  1. Compensatory mechanisms are trigged by an initial drop in cardiac output
  2. Preload increases as a result of sodium retention
  3. LV dilation occurs with a resultant increase in contractility (Frank-Starling relation)
  4. Neuro-humoral mechanisms are activated when contractility begins to fail
  5. Vicious cycle of failure, attempted compensation, failure, compensation…etc
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13
Q

NEURO-HUMORAL COMPENSATORY MECH ANISMS
* What is released? What does that increase?
* What occurs to assure adequte organ perfusion?
* As heart failure worsens, what rises?

A
  • Norepinephrine is released and increases heart rate and contractility
  • Peripheral vascular vasoconstriction occurs to assure adequate organ perfusion
  • As heart failure worsens, norepinephrine rises with a paradoxical decrease in organ perfusion
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14
Q

Renin-Angiotensin-Aldosterone System
* Activated by what?
* Explain the pathway and the effects?

A
  • Activated by Norepi levels, decreased renal perfusion, and increased PVR (peripheral vascular resistance)
  • Renin secretion leads to formation of Angiotensin II
  • Angiotension II causes vasoconstriction, increased afterload, and the release of aldosterone and vasopressin
  • Aldosterone contributes to sodium and water retention
  • Preload increases
  • The pituitary releases vasopressin which causes fluid retention and vasoconstriction

Picture is extra if needed

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15
Q
A
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16
Q

Congestive Heart Failure Pathophysiology

A
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17
Q

Frank-Starling law
* Relationship between what?
* Systolic contractile performance (stroke volume or CO) is proportional to what?
* What is normal heart?
* Failing heart: with exertion produces less what?
* When preload is low (at rest), there is little what?

A
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18
Q

Congestive Heart Failure: Frank-Starling Relationship
* Explain this chart

A

Normally (top curve), as preload increases, cardiac performance also increases. However at a certain point, performance plateaus, then declines. In heart failure (HF) due to systolic dysfunction (bottom curve), the overall curve shifts downward, reflecting reduced cardiac performance at a given preload, and as preload increases, cardiac performance increases less. With treatment (middle curve), performance is improved, although not normalized.

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19
Q

KNOW

HF with reduced EF (HFrEF)
* Formerly know as what?
* Happens happens?

A
  • formerly systolic HF
  • Ventricle fails to contract properly. This is a pumping problem so the EF will be less than 40%

Can have combined CHF which has factors of both systolic and diastolic CHF

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20
Q

KNOW

HF with preserved EF (HFpEF)
* Formerly known as what?
* What happens during this?
* Diagnosis of exclusion, how?

A
  • formerly diastolic HF
  • Ventricular muscles become stiff, causing impaired ventricular filling during diastole. Either impaired relaxation or increased stiffness of ventricles or both. LV EF will be normal (sometimes elevated)
  • Diagnosis of exclusion: IF systolic function is normal and there is evidence of CHF

Can have combined CHF which has factors of both systolic and diastolic CHF

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21
Q

What does systolic dysfunction and diastolic dysfunction look like?

A
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22
Q
A
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23
Q

HF with reduced ejection fraction (HFrEF)
* Also called?
* leads to what?
* What happens to EF?
* May have defects in what?

A
  • Global LV systolic dysfunction
  • Leads to increased diastolic volume and pressure
  • Ejection fraction decreased (< or = 40%)
  • May have defects in metabolism, electrophysiologic function, contractile elements, intracellular calcium modulation and cAMP production
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24
Q

HF with reduced ejection fraction (HFrEF)
* May be due to what?

A
  • May be due to CAD/MI (most common), valvular heart disease (valve not working so increase work or volume backed up), myocarditis/sarcoidosis (w/n wall), dilated cardiomyopathy, sustained arrhythmia such as AF, and sustained HTN (starts as LVH and diastolic heart failure, ending in systolic heart failure)
  • May be due to LV or RV failure – if LV primary – can cause RV failure
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25
Q

HF with Preserved Ejection Fraction (HFpEF)
* What is the prior name?
* What is impaired? What does that result in?
* Usually has a norma what?
* What is normal?

A
  • Prior name: diastolic heart failure
  • LV filling is impaired, resulting in – Increased LV end-diastolic pressure at rest or during exertion
  • Usually has a normal LV end-diastolic volume
  • Global contractility and ejection fraction remain normal (= or > 40%)
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26
Q

HF with Preserved Ejection Fraction (HFpEF)
* What are the causes?

A

HTN leading to myocardial hypertrophy (most common cause), Aging (normal), Obesity, DM (significant risk factor- associated with myocardial fibrosis), Valvular heart disease (AS and AI), Pulmonary HTN/MS, SLE, OSA

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27
Q

What are the different classfications of HF?

A
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28
Q

Signs/Symptoms of HF
* What are cardinal sxs?
* What happens with breathing?
* What type of congestions? What does that cause?
* What are other breathing issues? (3)

A
  • Cardinal symptoms – fatigue, SOB
  • Dyspnea with exertion in early disease, at rest in later disease
  • Pulmonary congestion with accumulation of interstitial or intra-alveolar fluid/Pulmonary edema (CXR changes)
  • Orthopnea
  • Nocturnal cough (non-productive), worse in recumbent position
  • Paroxysmal nocturnal dyspnea
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29
Q

Signs/Symptoms of HF
* What happens in 40% of late stages?
* What happens with GI?
* Neuro?
* What happens to extremities?

A
  • Cheyne-Stokes respiration - ~40% of patients with advanced HF
  • GI – anorexia, nausea, early satiety – abdominal bloating
  • Confusion and memory impairment in advanced HF (inadequate brain perfusion)
  • Diaphoresis and cool extremities at rest (NYHA class IV)
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30
Q

What is the sx in acute left and right HF?

A
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31
Q
  • New York Heart Association (NYHA) functional classification system is a widely used tool for assessing what?
  • What are the categorization? (general)
A
  • New York Heart Association (NYHA) functional classification system is a widely used tool for assessing the severity of heart failure symptoms and functional limitations
  • Categorizes HF patients into 1 of 4 classes based on the degree of physical activity limitations experienced
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32
Q

KNOW

What is NYHA Class 1?

A

no limitations of physical activity – able to carry out usual activities without experiencing fatigue or other symptoms

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33
Q

KNOW

What is NYHA Class 2?

A

slight limitations of physical activity – comfortable at rest or with mild exertion but experience symptoms such as fatigue, dyspnea or angina with moderate exertion

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34
Q

KNOW

What is NYHA Class 3?

A

NYHA Class III – marked limitations of physical activity – significant symptoms of heart failure that result in marked limitations of physical activity. Comfortable at rest but experience symptoms of fatigue, dyspnea, and angina with less than ordinary exertion (mild exertion like walking short distances)

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35
Q

KNOW

What is NYHA Class 4?

A

NYHA Class IV – unable to carry out any physical activity without discomfort – have severe symptoms of heart failure that severely limit physical activity – happen at rest and are unable to carry out any physical activity without experiencing significant discomfort

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36
Q

New York Heart Association Functional Classification

A
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37
Q

KNOW

What are the major sx of Right sided heart failure?

A

Right sided HF: Ascites, congestive hepatomegaly, pedal edema, decreased bowel perfusion, jugular venous distension, and weight gain. Appears like hepatic dysfunction.

SYSTEMIC ISSUES

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38
Q

Cor Pulmonale
* What is it?
* Progresses into what?

A

Cor pulmonale is right ventricular enlargement secondary to a lung disorder that produces pulmonary artery hypertension.
* Progresses to right ventricular failure follows.

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39
Q

Cor Pulmonale
* What are the Physical exam findings? (systemic vs cardiac)
* What is the txt?

A
  • Systemic- Findings include peripheral edema, neck vein distention, hepatomegaly,
  • Cardiac - Palpable left the parasternal lift, loud S2 (accentuation of the pulmonary component of the second heart sound) narrow splitting of S2, a holosystolic murmur of tricuspid regurgitation at the left lower sternal border, right-sided S4 heart sound
  • Treatment is directed at the cause.
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40
Q

Cor Pulmonale
* Alteration of what?
* usually what?
* May be caused by what?

A
  • Alteration of right heart structure or function
  • Usually chronic, may be acute and reversible
  • May be caused by any disease which leads to elevated pressure in the lungs
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41
Q

Again, what is cor pulmonale?

A
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42
Q

What are the cor pulmonale sx?(6)

A
  • Asymptomatic at first
  • Dyspnea
  • Exertional fatigue
  • Edema
  • Chest pain
  • Syncope
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43
Q

What are Cor Pulmonale PE Findings?

A
  • Left parasternal systolic lift
  • Loud pulmonic component of the 2nd heart sound (S2)
  • Murmurs of functional tricuspid
  • Right sided S3 gallop
  • JVD
  • Hepatomegaly/Ascites
  • Lower extremity edema
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44
Q

Cor Pulmonale PE Findings
* pHTN is caused by what?
* Elevated what? What does that cause?

A

Pulmonary hypertension
* Increased afterload in RV, similar to what occurs in LV failure

Elevated end-diastolic, central venous pressure
* ventricular hypertrophy and dilation

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45
Q

Cor Pulmonale Diagnostic testing
* What do you see on EKG?
* What do you see on CXR?

A

EKG
* RVH and strain
* tall peaked P waves (P-pulmonale),
* Right axis deviation
* RBBB

CXR:
* Enlargement of pulmonary arteries
* Dilation of the right atrium
* Dilation of right ventricle

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46
Q

Cor Pulmonale Diagnostic testing
* What od you see on Echo? (4)

A
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47
Q

Cor Pulmonale Diagnosis
* What is the gold standard to dx? What does it provide?
* What are the values?

A

Right heart catheterization
* Invasive hemodynamic assessment with right heart catheterization is considered the gold standard for diagnosing pulmonary hypertension and cor pulmonale. RHC provides direct measurements of right atrial pressure, pulmonary artery pressure, pulmonary capillary wedge pressure, and cardiac output, which are essential for confirming the diagnosis and guiding treatment.
* Elevation of pulmonary artery (mean greater than 25mmHg), RV and RA pressures

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48
Q

How does COPD and unresolved PE cause cor pulmonale?

A
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49
Q

Cor Pulmonale Treatment
* What is the txt for the cause?
* What is the txt for the symptoms?

A
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50
Q

She has the big section of CCB, i think it is low yield

What is the role of CCB for pHTN?

A

Calcium channel blockers (CCB) were the first vasodilator agents to gain popular acceptance in the treatment of pulmonary arterial hypertension (PAH). They have been shown to be particularly effective in patients who show a significant immediate hemodynamic response to pulmonary vasodilators (“responders”). The application of CCB is currently restricted to “responders” only. It is believed that no more than 5% of PAH patients will benefit from CCB long term. The response rate of most non-idiopathic forms of PAH is considered to be even lower. The “non-responders” as well as “responders” who fail to benefit from CCB should be treated with newer agents, collectively called “advanced PAH therapy.” The basis of this consensus rests on empiric experience gained in the PAH community over the years. However, the cut-points where advanced agents are more effective than CCB and where there is no additional role for CCB remain unknown.

51
Q

Cor Pulmonale Prognosis
* What is the prognosis?
* What is it a marker of?

A
  • In patients with lung disease, the development of cor pulmonale is associated with poor prognosis
  • Usually a marker of severe end-stage lung disease
52
Q

KNOWWWW

What are the left sided heart failures?

A

L sided HF: Paroxysmal nocturnal dyspnea, orthopnea, crackles at lung bases, dullness to percussion, decreased urine output, palpitations, and chronic cough.
High risk for pleural effusion

53
Q

What is the most common cause of right sided heart failure?

A

Left sided heart failure

54
Q

Physical Exam findings for HF
* What is going on with the heart? (think HR, Sounds, veins and displacement)

A
55
Q

Physical Exam findings for HF
* What is going on with the lungs?

A
  • Pulmonary crackles
  • Diminished breath sounds (pleural effusion)
56
Q

PHYSICAL EXAM of HF (BODY)
* What is going on with the liver?
* Peripheral?
* What is in severe chronic HF?

A
  • Hepatomegaly – important sign – late in disease, ascites present due to increased pressure in the hepatic veins
  • Jaundice is a late sign
  • Peripheral edema is a cardinal sign – but non-specific and does not happen with adequate diuretic use
  • In severe chronic HF – marked weight loss or cardiac cachexia may be present
57
Q
  • Right side failure, think what?
  • Left side failure, think what?
A
  • Right side failure, think systemic
  • Left side failure, think pulmonary
58
Q

What is going on with the Physical exam in terms of neuro?

A

Cerebral symptoms, especially common in elderly
* Confusion
* Anxiety
* Headaches
* Delirium
* Insomnia
* Secondary to poor perfusion

59
Q

Heart Failure – diagnostic testing
* What does the EKG show?

A

LVH, check for myocardial infarction (MI), screen for Arrhythmias, Q waves (old infarct)

60
Q

Heart Failure – diagnostic testing
* What do the labs show?

A

CBC, CMP (check LFTs), TSH, Lipid panel, troponin, A1C and BNP
* Hyponatremia
* Hypokalemia-diuretics
* Hyperkalemia- low cardiac output leads to renal insufficiency, ACEI use, K-sparing diuretics
* Elevated LFTs – liver congestion

61
Q

Heart Failure – diagnostic testing: BNP
* What is it secreted by?
* When are there higher levels?
* What are the classes (3)
* Used for what?

A
62
Q

Heart Failure – diagnostic testing on CXR?

A

Cardiomegaly

Pulmonary edema
* Increased pulmonary vasculature
* Diffuse bilateral opacities

Pleural effusions

Kerley B lines

Indicate interstitial edem

63
Q

What are these?

A

Heart Failure –
* Right: Intersitital markings
* Left: Kerley B lines

64
Q

What does this show?

A

Pleural effusion

65
Q

KNOW

Heart Failure – Diagnostic testing
* What is the dx test of choice?
* What does it show?

A
66
Q

Heart Failure – DiAGOSTIC testing
* What is MUGA?
* What does it provide?

A

MUGA (multi-gated acquisition scan) scan
* Provides measurement of left and right ventricular EF
* Useful when Echo is technically suboptimal
* Nuclear scan calculating EF

67
Q

Heart Failure – diagnostic testing: Stress test
* What is it used for?
* Identifies what?
* Quantitates what?
* Can help differentiate what?
* Assess what?

A

Stress test: This is mainly for risk stratification and class placement.
* Identifies if ischemia present
* Quantitates level of conditioning
* Can help differentiate cardiac versus pulmonary etiology of dyspnea
* Assess dynamic responses of HR, rhythm, BP

68
Q

Heart Failure – diagnostic testing
* If ischemia is a possible contributing factor then get what? What does it tell

A

If ischemia is a possible contributing factor then get cardiac angiography
* Quantitative information regarding systolic and diastolic dysfunction
* Excludes CAD as underlying cause of CHF

69
Q

HF: Treatment
* What med guidelines?
* What about risk factors?
* Diet?
* Moving?
* Fluid?

A
70
Q

According to the 2022 American College of Cardiology/American Heart Association/HeartFailure Society of America heart failure (HF) guidelines, initiation of what is the first step of txt of HFrEF?

A

initiation of quadruple therapy with renin-angiotensin-system inhibitors including angiotensin-converting enzyme inhibitor (ACEI)/angiotensin receptor blockers (ARBs)/angiotensin and neprilysin inhibitor (ARNI), beta-blocker, mineralocorticoid receptor antagonist (MRAs), and sodium-glucose cotransporter 2 inhibitors (SGLT2is)

71
Q

Medications

  • Patients with tachycardia, active ischemia, recent myocardial infarction, or ventricular ectopy may be initiated on what?
  • Patients with significant congestion and volume overload may be initiated on what?
A
  • Patients with tachycardia, active ischemia, recent myocardial infarction, or ventricular ectopy may be initiated on beta-blocker.
  • Patients with significant congestion and volume overload may be initiated on SGLT2i or MRA after diuretics.
72
Q

When should quadruple therpy happen?

A

There is evidence of early benefit with GDMT in patients with HFrEF, as early as within the first 30days of treatment with SGLT2i or ARNI, and within 2weeks of initiation of SGLT2i in patients with HFrEF or HFpEF. It is therefore important for quadruple therapy to be initiated within the first 4 to 6weeks.

73
Q

After initiation and optimization of doses of quadruple therapy, the following steps are important to consider in patients with HFrEF.
* What is indicated in African-American patients with NYHA functional class III-IV HFrEF?
* For patients with symptomatic stable chronic HFrEF in sinus rhythm with a heart rate of≥70 beats/min despite beta-blocker, what can be useful?

A
  • Hydralazine and nitrates are indicated in African-American patients with NYHA functional class III-IV HFrEF.
  • For patients with symptomatic stable chronic HFrEF in sinus rhythm with a heart rate of≥70 beats/min despite beta-blocker, ivabradine can be beneficia
74
Q
  • In patients with symptomatic HFrEF, what can be considered to decrease hospitalizations for HF?
  • In selected high-risk patients with HFrEF and recent worsening of HF, what can be used?
  • In patients with LVEF<35% and NYHA functional class II-III symptoms on chronic GDMT, who have reasonable expectation of meaningful survival for >1 year, what is recommended?
A
  • In patients with symptomatic HFrEF, digoxin might be considered to decrease hospitalizations for HF.
  • In selected high-risk patients with HFrEF and recent worsening of HF, vericiguat may be considered to reduce HF hospitalization and cardiovascular death.
  • In patients with LVEF<35% and NYHA functional class II-III symptoms on chronic GDMT, who have reasonable expectation of meaningful survival for >1 year, implantable cardioverter-defibrillator therapy is recommended.
75
Q
  • Patients with left bundle branch block and wide QRS interval also have indications for what?
  • Important additional considerations include appropriate treatment strategies for comorbidities, such as what?
A
  • Patients with left bundle branch block and wide QRS interval also have indications for cardiac resynchronization therapy.
  • Important additional considerations include appropriate treatment strategies for comorbidities, such as iron deficiency, atrial fibrillation, ischemic heart disease, valvular heart disease, sleep apnea, and diabetes, and treatment of specific etiologies, such as cardiac amyloidosis or sarcoidosis
76
Q

What is the evoluion of HF txt?

A
77
Q

Guideline Directed Therapy
* What has it reduced?

A

GDMT : proven to reduce mortality and morbidity

78
Q

Guideline Directed Therapy: Beta-blocker
* What is the MOA?
* What does it decrease?
* Improves sx of what?
* Off loads what?

A

Beta-blockers: decrease catecholamine levels and dysrhythmias
* Decreases mortality for all classes
* Improves symptoms of CHF
* Off loads the work of the heart, decrease heart rate which decreases forcefulness of contraction

79
Q

Beta-blockers
* What are the receptors? What does it cause?
* May slow progression of what?
* Contraindicated while what?
* Which BB are more effective?

A
80
Q

HFrEF:
* What are the standard therapies?
* What are additional interventions?
* What is the follow up?
* What should you also treat?

A
81
Q

GDMT: Carvedilol (Coreg)
* Preferred when?
* Reduced all what?
* Contraindicated for who?

A
  • Preferred beta-blocker in patients with HFrEF and NYHA II-IV
    symptoms
  • Carvedilol reduced all-cause
    mortality compared to metoprolol tartrate (COMET Trial)
  • Contraindicated for acute/decompensated heart failure due to acute negative inotropic effects
82
Q

GDMT: ACEI
* What is the MOA?
* In addition, ACE inhibitors increase what? What does that cause?
* What does it reduce?

A
  • ACE Inhibitors: work by preventing ACE from converting angiotensin I to angiotensin II in the lungs. This prevents an elevation in blood pressure, reduces sodium reabsorption, and reduces ventricular remodeling.
  • In addition, ACE inhibitors increase bradykinin and prostaglandin levels, which leads to vasodilation of the arterioles, decreasing afterload and SVR (Decrease BP)
  • ACEI reduce mortality (CONSENSUS and SOLVD) trials
83
Q

GDMT: ACEI
* What are the positvies of this drug?
* Class effect so you can use any medication within what?
* Dosage? Monitor what?

A
  • Prolong survival, increase quality of life by alleviating symptoms in mild, moderate and severe CHF
  • Class effect so you can use any medication within the class to reduce overall mortality. Both ACEI or ARB
  • Always start low dose to prevent hypotension
  • Monitor BUN and Creatinine
84
Q

GDMT: ARB
* What is it?
* Used in patients who cannot take what?
* Should not replace what?
* Help limit the growth of what?
* What is not advisable?

A

Angiotensin II receptor blockers (ARBs)
* Used in patients who cannot take ACEI due to dry cough side effect
* Should not replace ACEI if patient can tolerate it
* ARB’s can help limit the growth of aneurysms (ex. Losartan)
* Combination ACE inhibitor + ARB is not advisable and places patients at risk for side effects such as hyperkalemia

85
Q

GDMT: Aldosterone antagonists
* What is aldosterone? What does it help control? (2)

A
  • Aldosterone - A steroid hormone made by the adrenal cortex(the outer layer of the adrenal gland)
  • Helps control the balance of water and salts in the kidney by keeping sodium in and releasing potassium from the body
  • Aldosterone also helps control the amount of water yourkidney reabsorbs; this increases blood volume and also impacts blood pressure
86
Q

GDMT: Aldosterone antagonists
* Blocking aldosterone helps what?
* Decreases what?
* Spironolactone and eplerenone will do what?
* They have been shown to do what?

A
  • Blocking aldosterone helps to increase sodium and water excretion
  • Decreases mortality
  • Spironolactone and eplerenone (less endocrine side effects than spironolactone – use this in males) will reduce preload and increase sodium/water excretion.
  • These have been shown to reduce mortality in Class III and class IV patients.
87
Q

GDMT: SGLT-2 Inhibitor
* What do they do?

A

SGLT2 inhibitorsreduce sodium and glucose flow into the blood, reduce fluid load, and exert an indirect osmotic diuretic effect. Also with myocardial energy supply affect to decrease oxygen consumption and cardiac sympathetic nerve activity

88
Q

SGLT-2 INHIBITOR
* What does the meta-analysis confirm?

A

“The results of this meta-analysis confirm the growing evidence in the literature of the favorable profile of SGLT2 inhibitors in cardiovascular outcomes and mortality in patients with heart failure regardless of the baseline diabetes status.”

89
Q

SGLT2 inhibitors:
* What are the MOA?
* What are the examples?

A
90
Q

SGLT2 inhibitors:
* What are the major advantages?
* What is contraindications?

A
91
Q

SGLT2 inhibitors:
* What are the common side effects and important toxicities?

A
92
Q

GDMT: NEPRILYSIN INHIBITOR (ARNI)
* What is an example?
* Decreases what?
* What is the MOA? When combined with ARB, it can improve what?

A
  • Sacubitril/Valsartan (Entresto)
  • Decreases mortality
  • Sacubitril is a neprilysin inhibitor (First FDA approved NI).
  • When combined with an ARB, this can improve blood pressure, HR, and EF. ->relax blood vessels and decrease sodium and fluid in the body.
93
Q

GDMT: Neprilysin inhibitor (ARNi)
* For what disease?
* Can be used in place of what?
* Reduces what?
* What do you need to before initating therapy?

A
  • For use in chronic heart failure with reduced EF (<40%) – not enough data to use in HFpEF
  • Can be used in place of ACE inhibitor monotherapy and/or if an ACE inhibitor isn’t tolerated (cough). This medication is better than ARB monotherapy.
  • Reduces the risk of cardiovascular death and hospitalization (NYHA class II-IV) with reduced ejection fraction
  • Must allow at least 36 hours after the last ACEI dose before initiating therapy
94
Q

GDMT others: Loop Diuretics
* Used for what?
* What does loop diuretics do?
* What is the MOA?

A

Used for symptom control only, does not decrease mortality

Loop Diuretics: Decrease blood pressure andremoves excess fluid.
* inhibiting the sodium-potassium-chloride (Na+/K+/2Cl) co-transporter in the thick ascending loop of Henle (hence the name loop diuretic), which is located in the kidneys.
* This reduces or abolishes sodium, chloride, and potassium reabsorption, leading to increased loss of sodium, chloride, and potassium into the nephron (the functional unit of a kidney). As a result, water is also drawn into the nephron and urine volume increases

95
Q

GDMT others: Loop Diuretics
* Can cause what levels to decrease?
* beware of what?
* Does not improve what?
* What should you remember?

A
  • Can cause hypokalemia and reduced magnesium levels
  • Beware over-diuresis, orthostatic hypotension; worsening renal insufficiency
  • Does not improve LV contractility (only reduces preload – prevent pulm edema)
  • Remember: patients with diastolic dysfunction need elevated filling pressures(HOCM, severe AS)- care when using diuretics
96
Q

Gdmt Add-Ons: Hydralazine + Nitrates (isosorbide dinitrate)
* Reduces what?
* Hydralazine does what?
* This medication combo is especially effective in who?

A

Reduces mortality
* Hydralazine dilates arteries and Nitrates will dilate veins and decrease preload.
* This medication combo is especially effective in African Americans.

97
Q

Gdmt Add-Ons: Hydralazine + Nitrates (isosorbide dinitrate)
* Used if cannot tolerate what?
* Not as effective as what?
* Dosage?

A
  • Used IF cannot tolerate ACEI/ARB
  • Not as effective as ACEI
  • Inconvenient dosage schedule (TID)
98
Q

GDMT: more add-ons (digoxin)
* What is the MOA?
* What are the mechanical affects?
* What are the electrical affects?
* What are the toxicity issues?

A
  • Selectively and reversibly inhibits the Na-K ATPase ion transport system (increased sodium inside the cell slows it down and calcium builds which triggers myocyte- increases force of contraction)
  • Mechanical affects: increases contractility, EF, CO
  • Electrical affects: decrease heart rate, increase PR interval, decrease QT interval, increases refractory period at AV node (Afib therapy)
  • Toxicity issues – check dig levels, digibind. Also interacts with lots of other medications
99
Q

GDMT: more add-ons (Ivabradine)
* Belongs to what drug class?
* Is works by what?

A
  • Belongs to drug class: hyperpolarization-activated cyclic nucleotide-gated (HCN) channel blockers
  • It works by slowing the heart rate so the heart can pump more blood through the body each time it beats
100
Q

-

Acute Decompensated heart failure (ADHF)
* What are the Acute Onset or Worsening of Symptoms?
* What happens with volume?

A
  • Acute Onset or Worsening of Symptoms: Patients with ADHF typically present with a sudden onset or exacerbation of symptoms related to heart failure, such as dyspnea (often orthopnea or paroxysmal nocturnal dyspnea), fatigue, exercise intolerance, peripheral edema, and/or weight gain.
  • Volume Overload: ADHF is characterized by volume overload, which may manifest as pulmonary congestion (pulmonary edema) leading to dyspnea, orthopnea, and cough, or systemic congestion leading to peripheral edema, ascites, and hepatic congestion. Patients may exhibit signs of fluid overload, such as jugular venous distention (JVD), hepatomegaly, and ascites.
101
Q

Acute Decompensated heart failure (ADHF)
* When are they hemodynamic instable?
* What are preipating factors?

A
  • Hemodynamic Instability: Patients with ADHF may exhibit hemodynamic instability, including hypotension, tachycardia, and/or evidence of end-organ hypoperfusion (e.g., altered mental status, cool extremities). In severe cases, patients may present with cardiogenic shock, characterized by severe hypotension and evidence of tissue hypoperfusion.
  • Precipitating Factors: ADHF often occurs in the setting of precipitating factors or triggers, such as myocardial ischemia/infarction, uncontrolled hypertension, arrhythmias (e.g., atrial fibrillation/flutter), infection, medication non-adherence, dietary indiscretion (e.g., excessive sodium intake), or exacerbation of comorbid conditions (e.g., chronic kidney disease, chronic obstructive pulmonary disease).
102
Q

Heart failure requiring inpatient admission:Acute decompensated heart failure (ADHF)
* What are the five goals?

A
  • Manage oxygenation, ventilation
  • Treat unstable dysrhythmias if present
  • Preload reduction, fluid removal
  • Afterload reduction, lower BP and work of the heart
  • Improve contractility
103
Q

Treatment of ADHF
* The first goal is oxgenation ventilation, what are the different types and how they help?

A
104
Q

Treatment of ADHF
* Goal 2: How do you Treat any unstable dysrhythmias

A
  • Unstable brady dysrhythmias: pace
  • Unstable tachy dysrhythmias: shock
  • Afib RVR, slow down/convert
105
Q

Treatment of ADHF
* Goal 3: How do you reduce Preload?

A
  • Nitroglycerine
  • Loop diuretics
106
Q

Treatment of ADHF
* How do you reduce afterload?

A
  • IV milrinone
  • High dose NTG works, tricky with BP and headaches
  • ACE-inhibitors
  • Nitroprusside/Nipride (can lead to brain edema from vasodilation; prolonged use can also lead to cyanide toxicity)
107
Q

Treatment of ADHF
* How do you improve contractility?

A
108
Q

HF Treatment: IV medications used in hospital during ADHF-> dobutamine
* What class of CHF?
* Positive what?
* Improves what?
* Used in txt of what?
* Used to assess what?

A
  • Class IV CHF
  • Positive inotropic agent
  • Improves LV contractility and cardiac output
  • Used in treatment of acute decompensated CHF hospital admission
  • Used to assess cardiac contractile reserve

Proarrhythmic

109
Q

HF Treatment: IV medications used in hospital during ADHF-> milrinone
* What class of CHF?
* Positive what?
* What does it cause/decrease
* Improves what?

A
  • Class IV CHF
  • Positive inotropic agent
  • Vasodilator, decreases afterload (decrease BP)
  • Improves LV contractility and cardiac output
110
Q

Medications are great but also need to treat comorbidities
* Why do we need to tx a-fib?
* What are the two types of control?
* Restoration to what?
* What are the txt?

A
  • Afib leads to atrial cardiomyopathy, fibrosis, and heart failure
  • Rate control vs rhythm control
  • Restoration to NSR is key
  • Treatment: antiarrhythmic drugs, dccv, surgery
111
Q

What is the process of afib? What are the risk factors?

A
112
Q

HF treatment: Device Therapy Late Stage Management
* When is ICD a good rec?
* Used to prevent what?
* Improves what?

A
  • Implantable cardioverter-defibrillator (ICD) – rec’d for patients with good life expectancy (at least 1 year) if they have sustained v tach or v fib or unexplained syncope or are symptomatic with an EF less than 35% and on meds
  • Used to prevent arrhythmias/sudden cardiac death
    Improves survival

Appropriate for some patients

113
Q

Device Therapy
* Biventricular pacemaker (cardiac resynchronization therapy - CRT) may help with what?

A

may help with symptoms and decrease hospitalizations for HF patients with LVEF less than 35% and a widened QRS complex with left bundle branch block (NYHA Class III).

114
Q

Many CRT devices also have ICD function and indicated if what (3)?

A
  • Ejection fraction <30%, in normal sinus rhythm, and QRS >150ms.
  • Optimizes diastolic function by reducing mismatch between atria and ventricles.
  • Allows both ventricles to contract together
115
Q

Cardiac Resynchronization Therapy (CRT)
* CRT improves symptoms of heart failure in about 50% of patients who have been treated how?
* Improves what? (2)

A
  • CRT improves symptoms of heart failure in about 50% of patients who have been treated maximally with medications but still have severe or moderately severe heart failure symptoms.
  • Improves survival, quality of life, heart function, the ability to exercise, and helps decrease hospitalizations in select patients with severe or moderately severe heart failure.
  • Improves NYHA class
116
Q

Device Therapy: MCS (Mechanical circulatory support)
* What are the different types and what do they do? (3)

A
117
Q

What is the intra-aortic balloon pump?

A
117
Q
A
118
Q

LVAD – Left ventricular assist device
* What is ti?
* What type of pump?
* Helps with what?

A
  • Pump used for patients who have reached end-stage heart failure
  • Battery operated, mechanical pump
  • Helps the left ventricle pump blood to the rest of the body
119
Q

LVAD – Left ventricular assist device
* Can be used as what? (2)

A
  • Bride to transplant therapy – used while patients awaiting heart transplant
  • Destination therapy – for patients that are not candidates for heart transplants
120
Q

Surgical Intervention: Heart transplantation
* Choice of txt for who? (3)

A
  • patients under age 60 with severe refractory HF, have no other life threatening conditions and are highly adherent to treatment regimens
  • End stage heart failure
  • Severe CAD, not amenable to CABG or PCI
121
Q

Heart transplantation
* What is the survival?
* When was the first heart transplant?
* How many are performed each year?

A
  • Survival is 85-90% at 1 year, 75% at 5 yrs
  • The world’s first human heart transplant was on December 3, 1967
  • Worldwide there are 5,000 heart transplants performed every year
122
Q

What are Factors that affect eligibility for Heart Transplantation?

A

Clinical Medicine 3 (27 decks)

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