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)

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

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

what is the pathophysiology of heart failure

A

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

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

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

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

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

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

what are the types of low output heart failure

A

Systolic heart failure

Diastolic heart failure

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

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

what is systolic heart failure

A

Progressive deterioration myocardial contractile function
Ischaemic injury
Volume overload
Pressure overload

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

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

cardiomyopathies

A

Diffuse disease of the heart muscle leading to functional impairment

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

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

what are other types of cardiomyopathy

A
Hypertrophic Cardiomyopathy (hereditary)
Restrictive Cardiomyopathy (rare) – Amyloid the main cause in the UK
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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

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

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

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
how does left ventricular failure effect the lungs
Pressure in the pulmonary veins is transmitted to the capillaries and arteries This leads to pulmonary congestion and oedema
26
what results from heavy wet lungs
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
how does left ventricular failure affect the kidneys
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
how does left ventricular failure affect the brain
``` Hypoxic encephalopathy Irritability Loss of attention Restlessness Stupor and coma ```
29
what is right sided heart failure
Usually consequence of left sided HF (congestive cardiac failure (CCF))
30
what is 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
31
what are other causes of right sided heart failure
Valvular heart disease | Congenital heart disease
32
what are the systemic effects of right heart failures
``` 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
what is biventricular failure
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
what is the clinical presentation of heart failure
``` Due to excess fluid accumulation Dyspnoea Orthopnoea, paroxysmal nocturnal dyspnoea Oedema Hepatic congestion Ascites Due to reduction in cardiac output Fatigue Weakness ```
35
how is heart failure classified
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
what are the 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 ```
37
what clinical tests are done for heart failure to determine underlying cause
``` CXR ECG Blood investigations Echocardiogram / Cardiac MRI or CT / CT-PET CTCA / Coronary angiography ```
38
how is heart failure diagnosed
``` 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
how can heart failure be treated
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
what are loop diuretics
FRUSEMIDE, BUMETANIDE Inhibit Na+ re-absorption from the proximal tubule K+ loss from distal tubule
41
how are loop diuretics given
Can be given iv or orally can- electrolyte abnormalities hypovolaemia and diminished renal perfusion
42
what are Mineralocorticoid Receptor Antagonists
EPLERENONE, SPIRONOLACTONE Acts on distal tubule Promotes Na+ excretion and K+ re-absorption Reduces hypertrophy and fibrosis
43
what are side effects of Mineralocorticoid Receptor Antagonists
Gynaecomastia (esp. Spironolactone) | Electrolyte (K+ high) and renal function abnormalities
44
what are 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
45
what are side effects of ACE inhibitors
cough, hypotension, renal impairment
46
what are 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)
47
what are side effects of beta blockers
Bronchospasm | Claudication
48
what are SA node blockades
IVABRADINE Blocks the If channel within the SA node Slow HR, no effect on BP Given orally with dose titration
49
what are side effects of SA node blockades
Visual aura | Bradycardia
50
what does digoxin do
Increases myocardial contractility Slows conduction at the AV node (use in AF) Excreted by kidney - Toxicity important
51
when is digoxin used
Acute HF especially in AF | Chronic HF in selected cases
52
what are ARNIs
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
what are side effects of ARNIs
hypotension, renal impairment
54
what are other therapies for heart failure
``` 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
what is CRT (Biventricular Pacing)
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
what do CRT s (Biventricular Pacing) do
Combination of all three leads promote synchronised pumping of ventricles, increasing efficiency of each beat and pumping more blood on the whole.