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CVS > L9: Congestive Heart Failure: evidence-based treatment > Flashcards

L9: Congestive Heart Failure: evidence-based treatment Flashcards

1
Q
A

MYOCARDIAL INFARCTION is death of part of myocardium AKA HEART ATTACK.
Caused by total occlusion of a coronary artery. However, if narrowing of coronary artery not complete -> patients may develop ANGINA (chest pain on exhersion); can progress & may develop pain at rest called UNSTABLE ANGINA.

MI -> cardiac arrest -> death

ALL OF THE ABOVE IS RELATED TO A DISEASE PROCESS CALLED ATHEROSCLEROSIS

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2
Q

What is atherosclerosis??

A

The process of progressive thickening and hardening of the walls of medium and large-sized arteries as a result of cholesterol deposition mainly in the presence of high BP/hypertension.

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3
Q

Cardiovascular disease risk factors:

A

Non-Modifiable Risk Factors:
- Age
- Male sex
- Family History
- Low Birth weight
- Premature Birth

Modifiable Risk Factors:
- Hypertension
- Smoking
- Diabetes mellitus
- Hypercholesterolemia
- Obesity
- Physical inactivity

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4
Q

Which types of risk factors can we treat for cardiovascular diseases?

A

Modifiable risk factors

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5
Q

How can MI occur due to an atheroma?

A

Plaque rupture -> atheroma in contact with blood -> initiates thrombosis -> expands and may block entire lumen = acute myocardial infarction = necrosis = heart failure

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6
Q

Cardiovascular Continuum Concept

A

The diagram shows how heart failure progresses and can cause death

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7
Q

Definition of heart failure + what is forward + backward symptoms

A
  • A complex of symptoms: shortness of breath, fatigue, and congestion
  • Due to an impairment of the heart’s ability to (contract) empty* or (relax) fill* properly,
  • Leading to inadequate perfusion of tissues during exertion (causes forwards symptoms), and retention of fluid (causes backward symptoms)
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8
Q

Types of heart failure

A
  1. Systolic Heart Failure = Unable to contract
  2. Diastolic Heart failure = heart muscle unable to relax
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9
Q

Forward + Backward Symptoms

A

Heart = pump
Inedeuqate supply = tiredness + fatigue; blood stagnation + congestion = oedema

Forward:
- Tiredness,
- shortness of breath,
- coughing

Backward:
- Odema in legs + ankles
- Ascites
- Pleural effusion
- Pulmonary odema

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10
Q

Heart failure Prevalance

A
  • Affects 1-2% of population
  • 10% among persons ≥ 70 years
  • Prognosis 25-40% mortality ~ 5 years (similar to cancer)
  • Prognosis worse if:
    1. severe symptoms
    2. high dose of diuretics
    3. low BP
    4. low sodium
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11
Q

Why is low BP = worse prognosis?

A

Drugs needed to prevent heart failure further reduce BP

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12
Q

Causes of Heart Failure?

A
  1. Decreased Contractility, due to:
    - Coronary heart dis.
    - Cardiomyopathies (Primary disease of myocardium - independent of coronary arteries): Viral myocarditis (Covid can increase these); Infiltrations (e.g. lymphoma)
    - Drugs (that make myocardium weaker): ß-adrenergic blockers, Verapamil (CCB), Doxorubicin (cancer drug)
    - Arrhythmias (atrial fibrillation)
  2. Increased Afterload (myocardium normal but in front of LV, obstruction/increased resistance):
    - Hypertension
    - Valvular disease (e.g. aortic stenosis- narrowing of aorta)
    - HOCM (hypertrophic obstructive cardiomyopathy) - myocardium v. thick between ventricles = block outflow of LV.
  3. Increased Output (heart is normal but body needs more cardiac output due to):
    - Anaemia
    - Hyperthyroidism
    - AV shunts (blood goes from artery to vein)
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13
Q

What is acute decompensation of heart failure?

A

Means the patient had been treated, symptoms resolved but there’s a reappearance of symptoms

Can be due to one or more of these events:
- Discontinuation of treatment
- ACS (new event e.g. another MI or developed arrhythmia)
- Arrhythmias (AF)
- Infection in urine or chest
- Anaemia
- Pulmonary Embolism

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14
Q

The stages/classification of Heart Failure: New York Heart Association (NYHA) Classification

A

Class I:
- No limitation of physical activity
- Ordinary physical activity does not cause SOB (dyspnoea) or fatigue

Class II:
- Slight limitation of physical activity (running after bus)
- Ordinary physical activity result in dyspnoea or fatigue

Class III:
- Marked limitation of physical activity (walk to toilet)
- Less than ordinary physical activity result in dyspnoea or fatigue

Class IV:
- Inability to carry out any physical activity without discomfort
- Symptoms are present at rest

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15
Q

Diagnosis of Heart Failure

A
  • NT-proBNP (ANP derivative) – measured in urine; if <400 ng/L = HF unlikely
  • If NT-proBNP high -> ECHO cardiogram (ultrasound of heart - tells us what type of HF (diasytolic or systolic): can diagnose with:
    1. HFrEF (heart failure with reduced ejection fraction)
    2. or HFpEF (heart failure with preserved ejection fraction)
  • Cardiac MRI (CMR)
  • Other tests: ECG, CXR, U&Es, ABGs, D-dimer
  • Look for cause(s) of decompensation: Troponin for ACS, ECG for Arrhythmias, etc..
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16
Q

What is ejection fraction?

A

= % of how much blood left ventricle pumps out with each contraction. (by seeing on echocardiogram the reduction in size of LV)

EF of 60% = 60% of total amount of blood in left ventricle is pushed out with each heartbeat – 50% is normal

EF also called Fractional shortening

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17
Q

Types of HF + when do we diagnose people with them?

A
  1. HFpEF (Heart failure with preserved ejection fraction >50%)
    - Aka Diastolic HF
    - HFpEF patients are older, female, hypertension, obesity, anemia, and AF
    - Failure of filling of blood
  2. HFrEF (Heart failure with reduced ejection fraction ≤40%)
    - Failure of ejection of blood
    - Systolic HF
  3. HFmrEF (mid-range ejection fraction)
    - in between normal of 50 and abnormal of 40 (41-49%), now name changed to mildly reduced ejection fraction (no treatment options yet)
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18
Q

What are the aims of HF treatment?

A
  1. Removal of the underlying or precipitating causes
  2. Improving survival & reducing mortality
  3. Relief of symptoms (& Improvement in quality of life)
  4. Prevention of re-admissions to hospital, recurrent ischaemic events, and further deterioration in left ventricular function
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19
Q

How do we remove precipitating causes?

A
  • Treatment of hypertension
  • Correction of valvular lesions
  • Treat anaemia, thyrotoxicosis, fluid overload, increased dietary salt intake
  • Improve compliance with treatment
  • Drugs that worsen HF: beta-blockers, salt-retaining drugs (NSAIDs, steroids)
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20
Q

How do we treat HF with drugs?

A

Standard Drug Therapy:

  1. First-Line Drugs:
    - ACE inhibitors
    - ARNI (angiotensin receptor blockers/neprilysin inhibitor) e.g. Sacubitril-Valsartan
    - Beta Blockers
  2. Second-line
    - Angiotensin receptor antagonists (ARBs)
    - Aldosterone antagonists
    - Hydralazine/nitrate
  3. Third-line
    - Diuretics
    - Digoxin
    - SGLT2 inhibitors
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21
Q

RAAS System

A

Angiotensinogen (made in liver)

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22
Q

Examples of ACE inhibitors + when indicted?

A

Indicated in all patients with heart failure (EF<40 - HFrEF) (unless contraindicated)

Examples:
- Captopril ( do not use as short-acting
- Enalapril
- Lisinopril
- Perindopril
- Ramipril - most commonly used
- Trandolapril

23
Q

ACE inhibitors side effects

A
  • Reduce angiotensin II levels -> induce arteriolar vasodilatation
  • Reduce systemic vascular resistance -> Lower BP
  • Reduce norepinephrine release
  • Decrease sympathetic activity
  • Decrease aldosterone secretion
  • Suppress vasopressin release
  • Increase bradykinin levels -> cough
24
Q

Evidence Based medicine for ACE inhibitors + HF

A
  1. Documented survival benefit
  2. Several large, controlled double-blind trials:
    - CONSENSUS
    - SOLVD
    - SAVE
    - AIRE
    - TRACE
25
Q

What is the Acute Infarction Ramipril Efficacy (AIRE) trial?

A
  • Effect of Ramipril on mortality and morbidity of survivors of acute MI with HF
  • 2006 patients, EF ≤ 35% post-MI
  • Follow-up average 15 months
  • Overall mortality significantly reduced 27%
  • Development of severe HF reduced by 23%
26
Q

Where else are ACE inhibitors used?

A
  • Heart failure
  • Hypertension
  • Post-Myocardial Infarction (LVD)
  • Diabetic nephropathy (kidney disease in diabetes)
  • Diabetic retinopathy (renal disease in diabetes)
27
Q

ACE inhibitor side effects:

A
  • First dose may cause hypotension (patients on very high dose thus recommended to start with small dose in HF (not hypertension patients))
  • Cough
  • Angioedema – most dangerous, swelling of lips and tongue, difficulty breathing
  • Rash
  • Neuropathy (pins + needles)
  • Deterioration of renal function (in RAS (renal artery stenosis- narrowing of kidney arteries))
28
Q

Contraindications of ACEi:

A
  • Pregnancy or at risk of pregnancy
  • Renal artery stenosis (bilateral, single k)
  • Caution with patients that have:
    >Peripheral vascular disease
    >Low BP
    >High dose diuretic, hypovolemia
    >Age >70 ys
    >Creatinine >150µmol/L
    >+NSAIDs
29
Q

What if ACEi are contraindicated or untolerated?

A
  • Other vasodilators:
    1. Angiotensin Receptor Blockers e.g. Candesartan, Losartan
    2. Hydrallazine & Nitrates
    3. Angiotensin receptor-neprilysin inhibitor (ARNI )
30
Q

What are Angiotensin Receptor Blockers (ARBs) + examples

A

= Block angiotensin II type 1 receptors

Examples:
- Losartan
- Candesartan
- Irbesartan
- Valsartan
- Eprosartan

31
Q

ELITE study: (Evaluation of Losartan In The Elderly) with Losartan (ARB)

A

Evaluation of Losartan In The Elderly
- 722 patients with CHF
- Designed to study effects of losartan on renal function (vs captopril)
- All cause mortality was 46% lower

32
Q

What is Sacubitril-Valsartan (Entresto)?

A

=Angiotensin receptor-neprilysin inhibitor (ARNI) (one end acts as ARB + other acts as diuretic so 1 molecule acting as 2 drugs)

  • Moderate to severe heart failure [NYHA class II–IV]
  • LV ejection fraction of ≤35%
  • Already on a stable dose of ACEi or ARBs
  • PARADIGM-HF Trial produced these results
    43% reduction in mortality (better than ACEi alone)
33
Q

What does PARADIGM-HF stand for?

A

Prospective comparison of Angiotensin II Receptor blocker neprilysin inhibitor with Angiotensin-converting enzyme inhibitor to Determine Impact on Global Mortality and morbidity in heart failure

34
Q

positive + negative effects of Beta Blockers

A
  • Reduce sympatho-adrenergic activity
  • Reduce afterload
  • Decrease myocardial oxygen demand – important for patients that have angina
  • Reduce ventricular remodelling
  • Reduce renin release
  • Coronary and peripheral vasodilatation
  • Negative inotropic effect/direct weaking affect on the myocardium – can make HF worse
35
Q

evidence for beta-blockers

A
  • reduce mortality in mild-to-moderate HF, reduce hospitalization, improve symptoms
  • Benefit not clear in class I or class IV
  • Reduction in mortality may not be a class effect (not every BB has the same effect + not all used in HF)
  • e.g. Bisoprolol metoprolol, carvedilol)
36
Q

MERIT-HF Study for BB

A
  • 39991 patients in USA & Europe
  • NYHA II- III
  • Metoprolol-XL (extneded release) 12.5mg up to 200mg once a day
  • Total mortality: Decreased by 34%
  • CV mortality: Decreased by 38%
  • Sudden death: Decreased by 41%
37
Q

Negative side effects of beta-blockers

A
  • Fatigue
  • Sleep disturbances
  • Bradycardia (slowing down of heart)
  • Hypotension
  • can worsen Heart failure (start low doses, slowly increase)
  • Conduction disorders
  • Bronchospasm
  • GI disturbances
  • can make asthma or COPD worse
38
Q

BB cautions + contradictions

A
  • Asthma, COPD – can be made worse
  • Uncontrolled heart failure
  • Severe bradycardia
  • Hypotension or shock
  • AV block (2nd & 3rd degrees), SSS
  • Pheochromocytoma (tumour that secretes adrenaline + NO + can cause severe hypertension) (unless with a-blocker)
  • Peripheral vascular disease
39
Q

What is Spironolactone?

A

= mineralocorticoid inhibitor
= Blocks aldosterone receptors on the distal convoluted tubule

  • RALES study showed its efficacy

Side effects:
- Gynaecomastia (painful)(doesn’t regress even after stopping drug)
- Testicular atrophy
- Menstrual irregularities
- Hyperkalaemia (esp. renal impairment)(drug is high K sparing diuretic)

40
Q

RALES (Randomised Aldactone Evaluation Study)

A

1663 patients, severe heart failure (NYHA IV) (LVEF<35%)
- Rx ACEi + Loop diuretic ± Digoxin
- Spironolactone 25mg - 50mg od
- Total mortality : 30% reduction p<0.001
- Cardiac mortality : 31% reduction
- Hospitalization: 35% reduction

41
Q

What is epleronone + state the EPHESUS study

A

= mineralocorticoid inhibitor
- produces less painful gynaecomastia than spironolactone

EPHESUS study:
- 13% reduction in mortality from cardiovascular causes or hospitalization
- 21% reduction in sudden death
- Causes hyperkalaemia + renal dysfunction

42
Q

What is Digoxin?

A
  • Inhibits Na+-K+ ATPase pump, inactivating Na+-Ca2+ exchanger, increasing Ca2+ intraceullularly
    = Increases force of contraction

Other effects:
>Decrease in AV conduction
>Increase in vagal activity
>Decrease in heart rate

43
Q

Uses of Digoxin

A
  • Slowing ventricular rate in rapid AF (atrial fibrillation)
  • Treatment of heart failure in patients who remain symptomatic despite optimal doses of diuretics and ACE inhibitors

Side effects:
- Nausea, vomiting, arrhythmias, confusion
- Toxicity enhanced by hypokalaemia

44
Q

Which trial studied Digoxin?

A
  • Digoxin has no effect on mortality (DIG trial)
  • Clinical effects are not dramatic
  • Withdrawal of digoxin may cause clinical deterioration in 1/4 of patients stable on digoxin and diuretic ±ACEi (RADIANCE and PROVED trials)
  • Reduces hospitalization rates
45
Q

What are the positive and negative consequences of diuretic use?

A
  • Relieve symptoms
  • Relieve circulatory congestion and pulmonary and peripheral oedema
  • Reduce atrial and ventricular diastolic pressure
  • Do not improve LV dysfunction
    -Little impact on mortality (so third-line of treatment)
46
Q

What are the positive and negative consequences of diuretic use?

A
  • Relieve symptoms
  • Relieve circulatory congestion and pulmonary and peripheral oedema
  • Reduce atrial and ventricular diastolic pressure
  • Do not improve LV dysfunction
    -Little impact on mortality (so third-line of treatment)
47
Q

Examples of diuretics

A

-Frusemide
-Other loop diuretics e.g. bumetanide
-Metolazone

48
Q

Side effects of diuretics

A

Metabolic effects:
- Hypokalaemia (low K) 🡺 (arrhythmias) – most dangerous
- Hyperglycaemia (high glucose) 🡺 (diabetes)
- Hyperuricaemia (high uric acid) 🡺(gout)

Social disruption:
- Frequency, urgency, incontinence of urine

49
Q

Importance of Hydralazine in combination with Nitrate

A
  • patient is of African or Caribbean origin and moderate to severe heart failure [NYHA class III–IV]

Trials (evidence-based)
- V-HeFT (Vasodilator-Heart Failure Trial) - 43% reduction in mortality
- A-HeFT (African American-Heart Failure Trial)

used in patients who cannot tolerate ACEi or ARBs.

50
Q

What are sodium-Lucose co-Transporter-2 inhibitors (aka gliflozins) + examples

A

= Inhibit reabsorption of glucose in the kidney and lower blood sugar in distal renal tube= increase loss of sugar in urine

  • Indicated in Type 2 Diabetes mellitus

Examples: Dapagliflozin (EMPEROR-preserved trial used in patients with HF + preserved ejection fraction), Empagliflozin, Canagliflozin, Ertugliflozin, Sotugliflozi

51
Q

What if all drugs are not effective?

A

Non-Drug therapy

52
Q

Example of non-drug therapy?

A
  • Cardiac-Resynchronization Therapy (RCT)
  • Surgery
53
Q

What is Cardiac-Resynchronization Therapy (RCT)

A
  • Using atrial-synchronized bi-ventricular pacing: device whereby electrodes are placed in both ventricles at the same time + adjust during to activity in atrium so both ventricles contract same time = improved cardiac output
  • Indicated for patients with severe symptoms with intra-ventricular conduction delays i.e. QRS ≥120 msec (ventricles do not contract at the same time as conduction system in heart damaged)
  • Leads to dys-synchronous LV contraction, impaired emptying, MR
  • Can reduce symptoms, improve functional capacity, reduce hospitalizations and increase survival
54
Q

What is RCT fails?

A

= Surgery
1.Ventricular Assist Devices – a pump put into the left ventricle, connects to aorta - not permanent solution but to improve survival until cardiac transplant procedure is available

  1. Cardiac Transplantation
  2. Xeno Cardiac transplantation (genetically modified pig heart)

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