Heart Failure Flashcards

(53 cards)

1
Q

Heart failure definition

A

Failure to maintain an adequate cardiac output to meet the demands of the body

Structural or functional abnormality - impairs ability of ventricles to eject blood or fill

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2
Q

CO

A

HR x SV

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3
Q

Preload

A

Is affected by venous blood pressure and the rate of venous return to the heart

This, in turn, is affected by venous tone and volume of circulating blood

Preload increases with increasing blood volume and vasoconstriction

Preload decreases with blood volume loss and vasodilatation

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4
Q

Frank-Starling Law

A

An increase in volume of blood filling the heart stretches the heart muscle fibres causing greater contractile forces which, in turn, increases the stroke volume

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5
Q

Afterload

A

It is the pressure in the aorta/pulmonary artery that the left/right ventricular muscle must overcome to eject blood

The greater the aortic/pulmonary pressure, the greater the afterload on the left/right ventricle respectively

Afterload increase with hypertension and vasoconstriction

Afterload decreases with vasodilatation

As the afterload increases, cardiac output decreases

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6
Q

LOHF

A

Systolic heart failure

Diastolic heart failure

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7
Q

HOHF

A

The heart itself is functioning normally but cannot keep up with the unusually high demand for blood to one or more organs in the body

Causes: thyrotoxicosis, profound anaemia, pregnancy, pagets disease, acromegaly, sepsis

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8
Q

Systolic heart failure

A

Progressive deterioration myocardial contractile function

Ischaemic injury
Volume overload
Pressure overload

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9
Q

Diastolic heart failure

A

Inability of the heart chamber to relax, expand and fill sufficiently during diastole to accommodate an adequate blood volume

Significant left ventricular hypertrophy (LVH) e.g HCM
Infiltrative disorders
Constrictive pericarditis
Restrictive cardiomyopathy

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10
Q

HF causes

A
Coronary Heart Disease
Hypertensive Heart Disease
Valvular Heart Disease
Myocardial Disease/ Cardiomyopathies
Congenital Heart Disease
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11
Q

Activation of neurohormonal system

A

Release of Noradrenaline – increases heart rate and myocardial contractility. Causes vasoconstriction
Release of ANP/BNP
Activation of renin-angiotensin – aldosterone system

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12
Q

Compensatory mechanisms

A

Vasoconstriction
Na and water retention
Excessive Tachycardia

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13
Q

Pressure Overload

A

Concentric left ventricular hypertrophy
E.g. Hypertension or aortic stenosis
Augmented muscle may reduce the cavity diameter
Cross sectional areas of the myocytes are increased

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14
Q

Volume overload

A

Chamber dilatation with increased ventricular pressure
E.g. mitral or aortic regurgitation
Deposition of new sarcomeres
Increased cell length and width
Muscle mass and wall thickness are increased in proportion to chamber diameter

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15
Q

Left side HF

A

Blood backs up progressively from the left atrium to the pulmonary circulation

Causes:
Ischaemic heart disease
Hypertension
Valvular heart disease
Myocardial disease
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16
Q

Left side HF - lungs

A

Breathlessness
Orthopnoea
Paroxysmal nocturnal dyspnoea

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17
Q

Left side HF - kidneys

A

Decreased cardiac output

Reduction in renal perfusion

Activation of renin - angiotensin – aldosterone system

Retention of salt and water with consequent expansion of interstitial fluid and blood volumes

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18
Q

Left side HF - brain

A
Hypoxic encephalopathy
Irritability
Loss of attention
Restlessness
Stupor and coma
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19
Q

Right side HF

A

Usually as a consequence of left sided heart failure (congestive cardiac failure

Cor-pulmonale:
Right sided HF due to significant pulmonary hypertension due to increased resistance within the pulmonary circulation
Usually as a result of respiratory disease e.g. COPD or pulmonary emboli

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20
Q

Right side HF- Cor Pulmonale

A

Right sided HF due to significant pulmonary hypertension due to increased resistance within the pulmonary circulation
Usually as a result of respiratory disease e.g. COPD or pulmonary emboli

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21
Q

Right side HF - other causes

A

Valvular heart disease

Congenital heart disease

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22
Q

RHF - liver and portal system

A

Congestive hepatomegaly
Centrilobular necrosis when severe
Cardiac cirrhosis

23
Q

RHF - spleen

A

Congestive splenomegaly

24
Q

RHF - abdomen

A

Ascites - accumulation of transudate in peritoneal cavity

25
RHF - subcutaneous tissue
Peripheral oedema of dependent portions of the body esp. ankle and pretibial oedema Sacral oedema if bedridden
26
RHF - Pleural and pericardial space
Effusions
27
RHF systemic effects
``` Liver and portal system Spleen Abdomen Subcutaneous tissue Pleural and pericardial space ```
28
Biventricular failure
Either due to the same pathological process on each side of the heart OR Consequence of left heart failure leading to volume overload of the pulmonary circulation and eventually the right ventricle causing right ventricular failure
29
HF clinical presentation
``` Due to excess fluid accumulation Dyspnoea Orthopnoea, paroxysmal nocturnal dyspnoea Oedema Hepatic congestion Ascites ``` Due to reduction in cardiac output Fatigue Weakness
30
HF clinical presentation - due to excess fluid accumulation
``` Dyspnoea Orthopnoea, paroxysmal nocturnal dyspnoea Oedema Hepatic congestion Ascites ```
31
HF clinical presentation - Ddue to reduction in cardiac output
Fatigue | Weakness
32
Classification of HF
I: No limitation II: Slight limitation III: Marked limitation IV: Severe limitation
33
Clinical signs of cardiac failure
``` Cool, pale, cyanotic extremities Tachycardia Elevated JVP Third heart sound (S3) – gallop rhythm Displaced apex (LV enlargement) Crackles or decreased breath sounds at bases on chest auscultation Peripheral oedema Ascites Hepatomegaly ```
34
Acute Pulmonary Oedema
``` Acute Breathlessness Pallor Cyanosis Sweating Rapid Pulse Hypoxia Crackles in Lungs ```
35
Clinical tests in HF
``` CXR ECG Blood investigations Echocardiogram / Cardiac MRI or CT / CT-PET CTCA / Coronary angiography ```
36
Current drug treatment
``` Aldosterone antagonists ARNI ACEi/ARBs Beta-blockers SA Node Blockade ```
37
Current drug treatment - ACEi / ARBs
Enalapril, Ramipril, Perindopril | Losartan, Candesartan, Irbesartan
38
Current drug treatment - ARNI
Sacubitril Valsartan
39
Current drug treatment - Aldosterone antagonists
Spironolactone, Eplerenone
40
Current drug treatment - Beta-blockers
Carvedilol, Bisoprolol, Metoprolol
41
Current drug treatment -SA Node Blockade
Ivabradine
42
Current drug treatment - Diuretics
Loops – Furosemide, Bumetanide Thiazides – Bendrofluamethiazide, Indapamide Quinazolines - Metolazone
43
Loop diuretics
FRUSEMIDE, BUMETANIDE Inhibit Na+ re-absorption from the proximal tubule K+ loss from distal tubule Can be given iv or orally Potent – can lead to: electrolyte abnormalities hypovolaemia and diminished renal perfusion
44
Mineralocorticoid Receptor Antagonists
EPLERENONE, SPIRONOLACTONE Acts on distal tubule Promotes Na+ excretion and K+ re-absorption Reduces hypertrophy and fibrosis Principle Side-Effects Gynaecomastia (esp. Spironolactone) Electrolyte (K+ high) and renal function abnormalities
45
ACE Inhibitors
RAMIPRIL, PERINDOPRIL, ENALAPRIL, CAPTOPRIL, LISINOPRIL Act on activated renin - angiotensin system Given orally in small doses with slow titration Block production of angiotensin: Vasodilatation BP lowering Reduce cardiac work Principle Side-Effects: cough, hypotension, renal impairment
46
ARNI
SACUBITRIL VALSARTAN Acts on activated renin - angiotensin system Also blocks breakdown of ANP/BNP Block production of angiotensin: Vasodilatation, BP lowering, reduce cardiac work Promote natriuresis Sodium excretion, vasodilatation, reduce hypertrophy and fibrosis Principle Side-Effects: hypotension, renal impairment
47
Beta blockers
BISOPROLOL, CARVEDILOL, METOPROLOL Block the action of adrenaline and noradrenaline on adrenergic beta receptors Slow HR, reduce BP Given orally in small doses with slow titration (treat arrhythmias) Principle Side-Effects Bronchospasm Claudication
48
SAN blockade
IVABRADINE Blocks the If channel within the SA node Slow HR, no effect on BP Given orally with dose titration Principle Side-Effects Visual aura Bradycardia
49
Digoxin
Action: Increases myocardial contractility Slows conduction at the AV node (use in AF) Excreted by kidney - Toxicity important Given: Acute HF especially in AF Chronic HF in selected cases
50
Treatment of Acute Pulmonary Oedema - Immediate
High flow oxygen IV Morphine IV Nitrates IV Frusemide +/- Assisted Ventilation
51
Treatment of Acute Pulmonary Oedema - Definitive
Identify Cause Oral diuretics Medical Therapy Revascularisation if appropriate
52
Other therapies
``` Cardiac Resynchronisation Therapy (CRT) Implantable Cardioverter Defibrillator (ICD) Dialysis & Ultrafiltration Ventricular Assist Device (LVAD/RVAD) Intra-aortic balloon pump Cardiac transplantation (Stem cell therapy) ```
53
CRT (Biventricular pacing)
Standard pacemakers equipped with two wires (or "leads") conduct pacing signals to specific regions of heart. Biventricular pacemakers have an additional third lead designed to conduct signals directly into the left ventricle. Combination of all three leads promote synchronised pumping of ventricles, increasing efficiency of each beat and pumping more blood on the whole.