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103 theme 3 > heart failure > Flashcards

heart failure Flashcards

1
Q

what is heart failure

A

fails to maintain an adequate cardiac output to meet the demands of the body
-any structural or functional abnormality that impairs ability of ventricle to eject blood (systolic HF) or fill with blood (diastolic HF)

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2
Q

the impact of heart failure in the UK

A

In-hospital mortality - 9.4%
30 day mortality in those surviving to discharge - 6.1%
Overall 30 day mortality - 14.9% (almost 1 in 7 pts)
Mortality affected by place of care
cardiology ward – 7%
general medical ward – 11%
Other ward – 14%

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3
Q

what is the pathophysiology of heart failure

A

stroke volume (contractility, preload and afterload) x heart rate = cardiac output

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4
Q

what is heart rate and its affect on the heart

A

inc HR, inc Cardiac output
Excessively high HR results in a decrease in the amount of time allowed for the ventricles to fill in diastole which causes SV and, thus CO to fall

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5
Q

what is stroke volume, pre and afterload

A

Contractility: the intrinsic ability of the myocardium to contract
Preload: the volume of blood or stretching of cardiomyocytes at the end of diastole prior to the next contraction
Afterload: the resistance/end load against which the ventricle contracts to eject blood

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6
Q

what is the frank-starling law

A

An increase in volume of blood filling the heart stretches the heart muscle fibres causing greater contractile forces which increases the stroke volume
true to a certain point… at some stage the fibres become over-stretched and the force of contraction is reduced
inc PL>inc stretch>dec contraction>dec SV + CO

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7
Q

What effects afterload

A

The greater the aortic/pulmonary pressure, the greater the afterload on the ventricles
increases with hypertension and vasoconstriction
decreases with vasodilatation
afterload increases, cardiac output decreases

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8
Q

what are the types of low output heart failure

A

Systolic heart failure

Diastolic heart failure

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9
Q

what is high output heart failure

A

increase demands on cardiac output, causing a clinical HF
heart functioning normally but cannot keep up with 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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10
Q

what is systolic heart failure

A

Progressive deterioration myocardial contractile function
Ischaemic injury
Volume overload
Pressure overload

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11
Q

what is diastolic heart failure

A

Inability of the heart chamber to relax, expand and fill sufficiently to accommodate an adequate blood volume
Significant left ventricular hypertrophy (LVH) e.g HCM
Infiltrative disorders
Constrictive pericarditis
Restrictive cardiomyopathy

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12
Q

what are the causes of heart failure

A 
Coronary Heart Disease
Hypertensive Heart Disease
Valvular Heart Disease
Myocardial Disease/ Cardiomyopathies
Congenital Heart Disease
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13
Q

cardiomyopathies

A

Diffuse disease of the heart muscle leading to functional impairment

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14
Q

what causes dilated cardiomyopathy

A

various causes, 50% familial
ETOH, pregnancy, systemic disease (SLE), muscular dystrophies
Drug toxicity (chemotherapy – anthracyclines, herceptin)
Myocarditis – Aetiology includes viral (enteroviruses – coxsackie B), HIV

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15
Q

what are other types of cardiomyopathy

A 
Hypertrophic Cardiomyopathy (hereditary)
Restrictive Cardiomyopathy (rare) – Amyloid the main cause in the UK
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16
Q

what is the pathophysiology of heart failure

A

Compensatory to maintain arterial pressure and perfusion of vital organs- FSM
vasoconstriction - increased venous return to the heart, increased preload, heart muscle fibres stretch, enhanced contractility

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17
Q

what myocardial structural change results from heart failure

A

Augmented muscle mass (hypertrophy) with/without cardiac chamber dilatation
Activate neurohormonal system:
Release Noradrenaline – increases heart rate and myocardial contractility. Causes vasoconstriction
Release of ANP/BNP
Activation of RAAS

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18
Q

what is the renin angiotensin aldosterone system

A

sympathetic and aldosterone increase - na+ retention and vasoconstriction
decrease in CO and BP - increase renin and angiotensin

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19
Q

what does angiotensin result in

A

Angiotensinogen > angiotensin I >angiotensin II
Arteriolar vasoconstriction
sympathetic activity
ADH secretion, H20 absorption
Adrenal gland: Aldosterone secretion - tubular Na+, Cl- reabsorption, H20 retention, K+ excretion
Water and Sodium retention
increased circulating volume, increased renal perfusion

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20
Q

What is the NP system

A

Distended ventricular wall
proBNP > NT-proBNP (non active) > excreted renally
BNP (diuresis, vasodilation, RAAS inhibition, SNS inhibitors)

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21
Q

what is the CNS sympathetic outflow

A

inc cardiac sympathetic activity (B1, B2, a1) - myocyte hypertrophy, myocyte injury, increased arrhythmias
increased vascular sympathetic activity (a1)- vasoconstriction
increased renal sympathetic activity (B2, a1) - activate RAAS and sodium retention
all leads to disease progression

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22
Q

how can compensatory mechanisms worsen heart failure

A

Vasoconstriction: ↑resistance against which heart has to pump (i.e.↑afterload), and may therefore ↓ CO
Na and water retention: ↑fluid volume, which ↑ preload. If too much “stretch” → ↓ contractile strength and CO
Excessive tachycardia → ↓diastolic filling time → ↓ventricular filling → ↓SV and CO

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23
Q

what are the clinical types of heart failure

A

Left sided, right sided and biventricular failure
Acute and chronic heart failure
Compensated and decompensated heart failure

24
Q

what is left sided heart failure

A 
Blood backs up progressively from the left atrium to the pulmonary circulation 
Causes:
Ischaemic heart disease
Hypertension
Valvular heart disease
Myocardial disease
25
Q

how does left ventricular failure effect the lungs

A

Pressure in the pulmonary veins is transmitted to the capillaries and arteries
This leads to pulmonary congestion and oedema

26
Q

what results from heavy wet lungs

A

Breathlessness (dyspnoea) exaggeration of breathlessness that follows exertion
Orthopnoea – breathlessness lying flat that is relieved by sitting or standing
Paroxysmal nocturnal dyspnoea – an extension of orthopnoea with attacks of extreme dyspnoea bordering on suffocation usually occuring at night

27
Q

how does left ventricular failure affect the kidneys

A

Decreased cardiac output
Reduction in renal perfusion
Activation of renin - angiotensin – aldosterone system
Retention of salt and water with expansion of interstitial fluid and blood volumes

28
Q

how does left ventricular failure affect the brain

A 
Hypoxic encephalopathy
Irritability
Loss of attention
Restlessness
Stupor and coma
29
Q

what is right sided heart failure

A

Usually consequence of left sided HF (congestive cardiac failure (CCF))

30
Q

what is 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

31
Q

what are other causes of right sided heart failure

A

Valvular heart disease

Congenital heart disease

32
Q

what are the systemic effects of right heart failures

A 
Liver and portal system
Congestive hepatomegaly, Centrilobular necrosis when severe, Cardiac cirrhosis
Spleen
Congestive splenomegaly
Abdomen
Ascites
Subcutaneous tissue
Peripheral oedema pretibial oedema
Sacral oedema if bedridden
Pleural and pericardial space effusions
33
Q

what is biventricular failure

A

same pathological process on each side of the heart
or
consequence of left heart failure leading to vol overload of the pulmonary circulation and eventually the right ventricle causing right ventricular failure

34
Q

what is the clinical presentation of heart failure

A 
Due to excess fluid accumulation
Dyspnoea
Orthopnoea, paroxysmal nocturnal dyspnoea
Oedema
Hepatic congestion
Ascites
Due to reduction in cardiac output
Fatigue
Weakness
35
Q

how is heart failure classified

A

Class I: No limitation of physical activity
Class II: Slight limitation of ordinary activity
Class III: Marked limitation, even during less-than-ordinary activity
Class IV: Severe limitation with symptoms at rest

36
Q

what are the clinical signs of cardiac failure

A 
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
37
Q

what clinical tests are done for heart failure to determine underlying cause

A 
CXR
ECG
Blood investigations 
Echocardiogram / Cardiac MRI or CT / CT-PET
CTCA / Coronary angiography
38
Q

how is heart failure diagnosed

A 
detailed history and clinical exam
measure NT-proBNP
ECG (CXR, BT, PF, urinalysis)
may have specialist assessment 
assess severity, establish cause and correctable causes
39
Q

how can heart failure be treated

A

diuretics for congestive symptoms and fluid retention
preserved ejection fraction - manage cormorbidities
reduced ejection fraction - ACE I or BB
all personalised exercise based cardiac rehab programme
specialist re assessment

40
Q

what are loop diuretics

A

FRUSEMIDE, BUMETANIDE
Inhibit Na+ re-absorption from the proximal tubule
K+ loss from distal tubule

41
Q

how are loop diuretics given

A

Can be given iv or orally
can-
electrolyte abnormalities
hypovolaemia and diminished renal perfusion

42
Q

what are Mineralocorticoid Receptor Antagonists

A

EPLERENONE, SPIRONOLACTONE
Acts on distal tubule
Promotes Na+ excretion and K+ re-absorption
Reduces hypertrophy and fibrosis

43
Q

what are side effects of Mineralocorticoid Receptor Antagonists

A

Gynaecomastia (esp. Spironolactone)

Electrolyte (K+ high) and renal function abnormalities

44
Q

what are ACE inhibitors

A

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

45
Q

what are side effects of ACE inhibitors

A

cough, hypotension, renal impairment

46
Q

what are beta blockers

A

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)

47
Q

what are side effects of beta blockers

A

Bronchospasm

Claudication

48
Q

what are SA node blockades

A

IVABRADINE
Blocks the If channel within the SA node
Slow HR, no effect on BP
Given orally with dose titration

49
Q

what are side effects of SA node blockades

A

Visual aura

Bradycardia

50
Q

what does digoxin do

A

Increases myocardial contractility
Slows conduction at the AV node (use in AF)
Excreted by kidney - Toxicity important

51
Q

when is digoxin used

A

Acute HF especially in AF

Chronic HF in selected cases

52
Q

what are ARNIs

A

SACUBITRIL VALSARTAN
Acts on activated renin - angiotensin system
blocks breakdown of ANP/BNP
Block production of angiotensin:
Vasodilatation, BP lowering, reduce cardiac work
Promote natriuresis
Sodium excretion, vasodilatation, reduce hypertrophy and fibrosis

53
Q

what are side effects of ARNIs

A

hypotension, renal impairment

54
Q

what are other therapies for heart failure

A 
Cardiac Resynchronisation Therapy (CRT)
Implantable Cardioverter Defibrillator (ICD)
Dialysis & Ultrafiltration
Ventricular Assist Device (LVAD/RVAD)
Intra-aortic balloon pump
Cardiac transplantation
(Stem cell therapy)
55
Q

what is CRT (Biventricular Pacing)

A

Standard pacemakers equipped with two wires (or “leads”) conduct pacing signals to specific regions of heart. Biventricular pacemakers have an third lead to conduct signals directly into the left ventricle.

56
Q

what do CRT s (Biventricular Pacing) do

A

Combination of all three leads promote synchronised pumping of ventricles, increasing efficiency of each beat and pumping more blood on the whole.

103 theme 3 (20 decks)

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