Heart Failure Flashcards

1
Q

What are the traditional and universal definitions for heart failure?

A

Traditional definition

Failure of the heart to pump blood at a rate commensurate with the requirements of the metabolizing tissues or is able to do so only with an elevated diastolic filling pressure.

Universal definition and classification of heart failure

HF is a clinical syndrome with symptoms and/or signs caused by a structural and/or functional cardiac abnormality and corroborated by elevated natriuretic peptide levels and/or objective evidence of pulmonary or systemic congestion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ACCF/AHA (2013) and ESC (2016) definition of HF

A

ACCF/AHA (2013)

complex clinical syndrome that results from any structural or functional impairment of ventricular filling or ejection of blood. The cardinal manifestations of HF are dyspnoea and fatigue, which may limit exercise tolerance, and fluid retention, which may lead to pulmonary and/or splanchnic congestion and/or peripheral oedema.

ESC (2016)

A clinical syndrome characterized by typical symptoms (e.g. breathlessness,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the AHA/ACC Classification of HF?

A

• Stage A - At risk for HF

Patients at risk for HF but without current or prior symptoms or signs of HF and without structural, biomarker, or genetic markers of heart disease

Patients with HTN, CVD, DM, obesity, known exposure to cardiotoxins, family history of cardiomyopathy

• Stage B - Pre-HF

Patients without current or prior symptoms or signs of HF but evidence of one of the following:

Structural heart disease:
e.g. LVH, chamber enlargement, wall motion abnormality, myocardial tissue abnormality, valvular heart disease

Abnormal cardiac function: e.g. reduced LV or RV ventricular systolic function, evidence of increased filling pressures or abnormal diastolic dysfunction

Elevated natriuretic peptide levels or elevated cardiac troponin levels in the setting of exposure to cardiotoxins

• Stage C - Symptomatic HF

Patients with current or prior symptoms and/or signs of HF caused by

Structural and/or functional cardiac abnormality

Heart Failure in Remission
Persistent Heart Failure

• Advanced HF (Stage D)

Severe symptoms and/or signs of HF at rest, recurrent hospitalizations despite GDT, refractory or intolerant to GDMT

Requiring advanced therapies such as consideration for transplant, mechanical circulatory support, or palliative care

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the classification of HF According to left ventricular ejection fraction (LVEF)?

A

• HFrEF - symptomatic HF with LVEF ≤40%
• HFmrEF - symptomatic HF with LVEF 41–
49%
• HFpEF - symptomatic HF with LVEF ≥50%;
• HFimpEF - symptomatic HF with a
baseline LVEF ≤40%, a ≥10 point increase
from baseline LVEF, and a second
measurement of LVEF > 40%.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the NYHA Classification - The Stages of Heart Failure?

A

• Class I - No symptoms and no limitations in ordinary physical activity
• Class II - Mild symptoms (mild shortness of breath and/or angina) and slight limitation during ordinary activity.
• Class III - Marked limitation in activity due to symptoms, even during less-than-
ordinary activity. Comfortable only at
rest.
• Class IV - Severe limitations. Experiences symptoms even whilst at rest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the three major determinants of LV performance (reflected as stroke volume)?

A

• the preload (reflected by venous return and end-diastolic volume)
• myocardial contractility (the force generated at any given end-diastolic
volume)
• the afterload (aortic impedance and wall stress)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is pre-load and its association with Frank Sterlings Law?

A

Preload— Preload is defined as the particular stretch or length of LV myocardial fibres at end-diastole, which is determined by the resting force, myocardial compliance, and the degree of filling from the left atrium.

• Landmark studies by Frank and Starling established the relationship between ventricular end-diastolic volume (which is a measure of preload) and ventricular performance (stroke volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Discuss contractility

A

Contractility— Myocardial contractility is defined by the force generated at any given preload.
• Thus, the stroke volume at any given fibre length is a function of contractility, as variations in contractility create nonparallel shifts in the developed force-length relation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the two major types of ventricular dysfunction that lead to HF?

A

• Systolic dysfunction (impaired cardiac contractile function)
• Diastolic dysfunction (impaired cardiac filling)
• Although these mechanisms are interrelated and often concurrent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is LVSD?

A

LV systolic dysfunction (LVSD) refers to decreases in the length-tension relationship and myocardial contractility.

• LVSD causes a shift in the Frank-Starling curve downward and to the right, a downward shift in the end-systolic pressure-volume relationship (ESPVR), and a decrease in the slope of the ESPVR
relationship over a range of pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Hemodynamic changes associated with systolic dysfunction

A

Hemodynamic changes associated with systolic dysfunction trigger neurohumoral activation as well as cardiac remodeling.
• The fall in cardiac output leads to increased sympathetic activity,
which helps to restore cardiac output by increasing both contractility and heart rate.
• The fall in cardiac output also promotes renal salt and water retention, leading to expansion of the blood volume, thereby raising end-diastolic pressure and volume.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Left ventricular hypertrophy

A

• Left ventricular hypertrophy is also part of the adaptive response to systolic dysfunction since it unloads individual muscle fibres and thereby decreases wall stress and afterload.
• Decreased compliance due to hypertrophy and fibrosis may eventually produce disturbed diastolic function in many patients with advanced HF.
• The failing heart is progressively more afterload-dependent, and small changes in afterload can produce large changes in stroke volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is cardiac remodeling?

A

Remodelling is defined as an alteration in the structure of the heart in response to hemodynamic load and/or neurohormonal activation.

Cardiac remodelling may transition from an apparently compensatory process to a maladaptive one.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the factors of cardiac remodeling?

A

Factors influencing remodelling include alterations in hemodynamic load in response to myocardial injury, blood pressure, and neurohormonal activation.

• It generally includes increases in myocardial mass. The myocyte is the
major cell involved.

Other components include the interstitium, fibroblasts, collagen, and coronary vasculature.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Structural remodelling is often associated with

A

• Structural remodelling is often associated with molecular events leading to changes in the expression and/or activity of proteins
involved in virtually every aspect of myocardial function, including the
hemodynamic, energetic, and electrical properties of the heart.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the three general patterns of remodelling?

A

• Concentric LV remodelling (in response to pressure overload)
• Eccentric LV hypertrophy (in response to volume overload)
• Mixed concentric/eccentric hypertrophy as may occur following MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cellular and molecular alterations

A

• Myocyte hypertrophy
• Loss of myocytes due to apoptosis or necrosis
• Fibroblast proliferation and fibrosis
• Increased expression of genes that are typical of the fetal heart (eg, B-type natriuretic peptide, myosin heavy chain).
• Increased collagen synthesis and degradation
• Increases in circulating proinflammatory cytokines
• Oxidative stress
• Alteration in calcium handling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is the Aetiology of Heart failure?

A

• Hypertensive heart disease
• Dilated cardiomyopathy
• Rheumatic valvular heart disease
• Ischemic heart disease
• Peripartum cardiomyopathy
• Restrictive cardiomyopathy– Cardiac amyloidosis
• Myocarditis
• Pericardial diseases
• Adult congenital heart disease
• Infections – HIV, Chagas disease
• DRUGS – Anthracyclines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the Risk factors for heart failure?

A

• Older age
• Hypertension
• Coronary disease particularly MI
• Diabetes mellitus
• Valve disease
• Cigarette smoking
• Obesity
• LVH on ECG or ECHO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the Precipitants Of Heart Failure?

A

• Infection
• Acute myocardial dysfunction (e.g. ischaemia due to myocardial infarction)
• Uncontrolled hypertension
• Arrhythmias
• Worsening chronic valve disease
• Non-adherence with drugs/diet
• Others-Anaemia, thyrotoxicosis
• Change in drug regimen
• Withdrawal/reduction of heart failure medications inappropriately
• Initiation/increase of rate-control medications inappropriately
• Other medications: steroids, non-steroidal anti-inflammatories, pioglitazones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the Clinical Features (signs and symptoms) of HF?

A

SYMPTOMS
• Exertional dyspnea and/or dyspnea at
rest
• Orthopnea
• Chest pain/pressure and palpitations
• Fatigue and weakness
• Nocturia and oliguria
• Anorexia, weight loss, nausea

SIGNS
• Tachycardia
• Distention of neck veins
• Weak, rapid, and thready pulse
• Rales, wheezing
• S 3 gallop and/or pulsus alternans
• Increased intensity of P 2 heart sound
• Hepatojugular reflux
• Ascites, hepatomegaly, and/or
anasarca
• Central or peripheral cyanosis, pallor

22
Q

Discuss the Framingham criteria for the diagnosis of heart failure

A

The Framingham criteria for the diagnosis of heart failure consists of the concurrent presence of either two major criteria or one major and two minor criteria.

Minor criteria

Accepted only if they cannot be attributed to another medical condition are as follows
• Nocturnal cough
• Dyspnoea on ordinary exertion
• A decrease in vital capacity by one-third of
the maximal value recorded
• Pleural effusion
• Tachycardia (rate of 120 bpm)
• Hepatomegaly
• Bilateral ankle oedema

Major criteria

• Paroxysmal nocturnal dyspnoea
• Weight loss of 4.5 kg in 5 days in response to treatment
• Neck vein distention
• Rales
• Acute pulmonary oedema
• Hepatojugular reflux
• S 3 gallop
• Central venous pressure greater than 16 cm of water
• Circulation time of 25 seconds or longer
• Radiographic cardiomegaly

23
Q

What are the Investigations for HF?

A

• Complete blood cell (CBC) count
• Electrolyte levels
• Renal and liver function studies
• Fasting blood glucose levels
• Lipid profile
• B-type natriuretic peptide levels/ N-
terminal pro-B-type natriuretic
peptide levels
• 12 lead Resting Electrocardiography
• Chest radiography
• Two-dimensional (2-D)
echocardiography
• Cardiac enzymes
• Urinalysis
• Iron studies
• Thyroid stimulating hormone (TSH) levels
• Lung ultrasound scan
• Nuclear imaging [10]
• Maximal exercise testing
• Pulse oximetry or arterial blood gas
• Noninvasive stress testing.

24
Q

How can Natriuretic peptide be used for investigations?

A

• B-type natriuretic peptide (BNP): BNP is a sensitive but non- specific marker of heart failure.
• AHF is unlikely and can be ruled out if:
• BNP is less than 100 ng/litre
• NT-proBNP is less than 300 ng/litre

25
Q

Chest radiography –PA view

A

• ABCDE:
• A: alveolar oedema (perihilar/bat-wing opacification)
• B: Kerley B lines (interstitial oedema)
• C: cardiomegaly (cardiothoracic ratio >50%)
• D: dilated upper lobe vessels
• E: effusions

26
Q

12 lead Resting Electrocardiography

A

a diagnostic test used to assess the electrical activity of the heart while the patient is at rest.

• Abnormalities (e.g. signs of ischaemia or arrhythmias) are very common in AHF
• An alternative diagnosis should be considered if the ECG is completely
normal.
• Findings
• Sinus tachycardia
• Arrhythmias
• Q waves
• LV hypertrophy (LVH)
• widened QRS complex – suggestive of bundle branch block

27
Q

Two-dimensional (2-D) echocardiography

A

• Biventricular systolic function (Ejection fraction)
• Diastolic function
• Ventricular dilation, ventricular hypertrophy and poor contractility
• Valve Disease
• Ventricular wall rupture
• Pericardial effusion
• Intracardiac shunts: the presence of a dilated inferior vena cava with
reduced respiratory variation is indicative of high venous pressure

28
Q

Management of AHF- Principles

A

• Brief History and Examination
• Resuscitation –ABCDE
• Investigate
• Identify precipitants and treat
• Manage heart failure
• Identify co-morbidities and treat
• Rehabilitate

29
Q

Management of AHF- Resuscitation

A

• ABCDE
• Nurse in cardiac position
• Strict bed rest
• Input output monitoring
• Intranasal oxygen therapy -titrate oxygen to maintain saturations
between 94-98% (or 88-92% in those with COPD).
• Dietary sodium and fluid restriction, physical activity as appropriate,
and attention to weight gain

30
Q

What are the CHAMP conditions (triggers for heart failure)?

A

• Acute Coronary syndrome (ACS)
• Hypertensive crisis
• Arrhythmias, e.g. atrial fibrillation, ventricular tachycardia,
bradyarrhythmia
• Mechanical problems, e.g. myocardial rupture as a complication of
ACS, valve dysfunction
• Pulmonary embolism

31
Q

Management of AHF

A

• All ‘WET’ patients will require diuretics as the cornerstone of their management to improve symptoms of congestion fluid overload.
• E.g. Furosemide, Torsemide, bumetanide
• Beware of electrolyte derangement
• Natriuresis-guided diuretic therapy advocated (PUSH-AHF trial).
• Further data is needed to support the addition of acetazolamide or hydrochlorothiazide to a standard diuretic regimen in patients hospitalized due to AHF

• Nitrates
Do not use nitrates in those with SBP <90mmHg or aortic stenosis, who rely on
sufficient preload to overcome their pressure gradient.
Nitrates cause venous and/or arterial dilation to reduce preload and/or
afterload.
They are given to patients with concomitant myocardial ischaemia or hypertension.

Non-invasive ventilation (NIV)
CPAP or BiPAP are used for those with cardiogenic pulmonary oedema and
dyspnoea
NIV improves ventilation to reduce respiratory distress and drives fluid out of
alveoli and into vasculature in those whose respiratory failure is not controlled
with oxygen therapy given via a face mask.

32
Q

Drug therapy in HFrEF - “4 pillars” of medical care

A

Combinations of: ARNI/ACEi/ARB + SGLT2i + BB + MRA in HFrEF

• Offer patients with reduced ejection fraction (LVEF <40%) heart failure the following medications that reduce mortality

• SGLT -2 inhibitors– dapagliflozin, Empagliflozin

• Angiotensin Receptor Neprilysin Inhibitor (ARNI)– Sacubitril/valsartan

• B-blocker– Carvedilol, Bisoprolol, Metoprolol succinate

• Mineralocorticoid receptor antagonist– Aldactone, Eplerenone

33
Q

Drug therapy in chronic heart failure

A

• Patients experiencing an episode of worsening HF might require a
fifth drug, vericiguat –VICTORIA study
• Hydralazine/isosorbide dinitrate (HYD/ISDN)
• Ivabradine
• Mavacamten in hypertrophic cardiomyopathy
• Tafamidis in transthyretin cardiac amyloidosis

34
Q

Surgical treatment

A

• Electrophysiologic intervention
• Revascularization procedures
• Valve replacement/repair
• Ventricular restoration
• Extracorporeal membrane oxygenation
• Ventricular assist devices
• Heart transplantation
• Total artificial heart

35
Q

Mortality/prognosis

A

• National statistics in the United States showed a rise in the death rate
attributable to HF from 5.8 per 1000 in 1970 to 16.4 per 1000 in 1993.
• This upward trend contrasts with reported declines in overall and
coronary mortality and at least in part reflects avoidance of premature mortality from these predisposing conditions, which are only palliated, not cured, by advances in therapy.
• Average survival remained poor after hospitalization for a first episode of HF
• HFpEF appears to be associated with a better prognosis than HF due to systolic dysfunction

36
Q

Raised JVP in a sign of what kind of HF?

A

Right sided HF

The right ventricle is weak and can’t pump blood forward effectively.
This causes blood to back up into the right atrium and then into the jugular veins, leading to a raised JVP.

37
Q

Pulmonary edema is a sign of what kind of HF? And what can it result in?

A

Left-Sided Heart Failure (LV Dysfunction)

If the left ventricle fails, it cannot effectively pump blood forward to the body.
This causes blood to back up into the left atrium and then into the pulmonary veins.
The increased pressure in the pulmonary veins leads to fluid leaking into the alveoli in the lungs → pulmonary edema (fluid buildup in the lungs).

However over time, this increases pressure in the right heart, leading to secondary right-sided heart failure and jugular venous distension.

38
Q

What are the Symptoms of right-sided heart failure?

A
  • Right hypochondriac pain
  • ankle swelling
  • abdominal swelling
  • early satiety (due to enlarged liver limiting stomach expansion/ size)
39
Q

What are the Symptoms of right-sided heart failure?

A
  • Right hypochondriac pain
  • ankle swelling
  • abdominal swelling
  • early satiety (due to enlarged liver limiting stomach expansion/ size)
40
Q

What are the Symptoms and signs of left-sided heart failure?
How would you ask a patient if they have orthopnea?
Most common cause of right HF?

A

Symptoms:
* dyspnea is sudden in onset
* orthopnea
* paroxysmal nocturnal dyspnea
* cough productive if pink frothy sputum (due to rupture of capillaries)
*fatigue

Signs and on examination:
Pulmonary edema (congestion)
Crackles (rales) on auscultation
S3 (ventricular gallop) or S4 (atrial gallop) heart sound

To ask about orthopnea - ask how many pillows they use? 2 or more signifies possible orthopnea

Most common cause of right HF is left HF

41
Q

What are the Symptoms of congestive heart failure?

42
Q

If the cough is productive of whitish/yellowish/brownish sputum the possible precipitation of heart failure could be what?

43
Q

What are the common causes for pericarditis?

A

Infections such as TB
SLE and RA (causing serocites)

44
Q

What question would you ask a patient you suspect of pericarditis caused by TB?
What is the treatment protocol for TB?

A
  • Were you on any drugs everyday for 6 months
  • Have you ever treated a chronic cough

DOTS
Direct observed therapy shortcut

45
Q

A patient came in with abdominal swelling and leg swelling, why does it matter which symptom came first in order to make a diagnosis?

A

Because abdominal swelling coming first points to a hepatic cause eg. Liver disease
Leg swelling first points to heart failure

46
Q

Why are some Causes of dilated cardiomyopathy?

A

Drugs (Anthracyclins)
Infections (HIV, chagas disease )
Pregnancy
Vitamin B1 deficiency
DM
Obesity
Irradiation

47
Q

What is the commonest Heart defect amongst generally and specifically among adults?

A

Generally: VSD
Amongst adults: ASD

48
Q

2 most important features of infective endocarditis and myocarditis

A

IE:
Fever
Changes in heart murmur

Myocarditis:
Fever
Catarrh

49
Q

Causes of restrictive cardiomyopathy

A

Restrictive cardiomyopathy (RCM) is a condition where the heart’s ventricles become stiff and have impaired filling, while systolic function is usually preserved.

Massive ascites
Amyloidosis
Sarcoidosis

50
Q

What is Cor Pulmonale

A

Chronic lung disease leading to right heart failure/dysfunction
It is a cause of congestive heart failure

51
Q

What is the most common precipitation in Heart failure?

A

Poor drug compliance