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Cardiovascular System > Session 10 > Flashcards

Session 10 Flashcards

1
Q

What is heart failure?

A

The inability of the heart to meet the demands of the body; a clinical syndrome (collection of signs) of reduced cardiac output, tissue hypoperfusion, increased pulmonary pressures and tissue congestion.

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2
Q

What enables the heart to function effectively?

A
  • One-way valves
  • Functioning cardiac muscle
  • Chamber size

Any impairment = impairment in cardiac function

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3
Q

What is the most common cause of heart failure?

A

Ischaemic heart disease that causes myocardial dysfunction through fibrosis and remodelling which impairs contractility of heart

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4
Q

What are the other causes of heart failure?

A
  • Hypertension (afterload)
  • Aortic stenosis (afterload)
  • Cardiomyopathies (dilation)
  • Arrhythmias
  • Pericardial disease
  • Acquired/congenital valvular or myocardial structures
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5
Q

What can cause high output heart failure and why?

A

Occurs when there is a very elevated demand on cardiac output (eg. during thyrotoxicosis) even for a healthy heart

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6
Q

How do you measure the cardiac output?

A

CO = SV x HR

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7
Q

What is stroke volume?

A

A fraction of the total volume within the ventricle at the end of diastole (EDV)

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8
Q

What is ejection fraction?

A

Stroke volume / EDV x 100

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9
Q

What can DECREASE stroke volume?

A

Total peripheral resistance (afterload) = More constriction in smooth muscle vessels means that less blood can get through

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10
Q

What can INCREASE stroke volume?

A
  • Pre load (increasing volume in ventricles at end of diastole as there is more stretch and a higher pressure)
  • Myocardial contractility
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11
Q

What is the Frank-Starling’s law?*

A

More ventricular distention during diastole will result in a greater volume of blood being ejected during systole (up to a certain point)

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12
Q

What can increase the contractility of the heart?*

A

Increased sympathetic activity (inotropy)

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13
Q

Why can cardiac output be reduced in heart failure?

A

Due to a reduction in stroke volume, which can be caused by:

  • Reduced preload (impaired ventricular filling)
  • Reduced myocardial contractility (unable to produce the force of contraction for given volume)
  • Increased afterload (higher pressure against which ventricles must contract)
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14
Q

What is DIASTOLIC heart failure?*

A
  • Problems with FILLING of the heart

- Reduced ventricular capacity (reduced space available in ventricle)

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15
Q

What can cause diastolic heart failure?

A
  • Ventricle muscle wall being hypertrophied
  • Ventricular chambers being too stiff and not relaxing enough
  • Ventricular muscle remodelling which has encroached the ventricular chamber size
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16
Q

Why is there a limit to which cardiac muscle can stretch?

A

Degree of overlap between actin and myosin = stretching too far means that they are pulled too far away from each other to effectively contract

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17
Q

What is SYSTOLIC heart failure?*

A
  • Space in heart available but there is a poor degree of ventricular contraction
  • Heart unable to empty as well because it can’t pump with enough force
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18
Q

What can cause systolic heart failure?

A
  • Thin or fibrosed muscle wall
  • Enlarged chambers due to overstretched sarcomeres
  • Abnormal/uncoordinated contraction
  • EJECTION PROBLEM
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19
Q

What is heart failure with reduced ejection fraction?*

HFrEF

A

Heart failure that causes systolic dysfunction (i.e. contractility problem)

Most common

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20
Q

What is heart failure with preserved ejection fraction?*

HFpEF

A

Heart failure that causes diastolic dysfunction and indicates a filling problem

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21
Q

What should the NORMAL ejection fracture?

A

Above 50% (normal usually above 60%)

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22
Q

What is REDUCED ejection fracture?

A

Below 40%

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23
Q

How can the heart be failing with a preserved ejection fraction?

A
  • The ventricle will eject less volume in a heart beat as it can only accommodate a smaller volume
    Fraction of what’s available is still above 50%, even though not all is ejected
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24
Q

How can you calculate the ejection fracture?

A

Echocardiogram (cheap, non-invasive)

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25
Q

Which ventricle is most commonly involved in heart failure?

A

Left ventricle, but the right ventricle will be involved subsequently

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26
Q

What is congestive/biventricular heart failure?

A

Both ventricles being involved in heart failure

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27
Q

When can right ventricular heart failure occur in isolation and why?

A

Can occur secondary to chronic lung diseases due to changes in the pulmonary oxygenation of blood etc.

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28
Q

What is the most common cause for RV heart failure?

A

LV heart failure

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29
Q

What does an increase in LV filling in the healthy heart lead to?

A

A bigger increase in cardiac output

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30
Q

What does an increased LV filling cause in a failing heart?*

A
  • Very small increase in CO
  • Worsening CO
  • Marked increase in LVEDP to increase SV, which can result in a failing CO and pulmonary congestion due to the pressure being so high that it impedes return of the blood from the lungs
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31
Q

What physiological mechanisms are triggered by drops in cardiac output that will correct it?*

A
  • Damaged ventricular tissue
  • Reduction in efficiency of contraction
  • Reduced SV and therefore CO
  • NEURO-HORMONAL ACTIVATION
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32
Q

What can neuro-hormonal activation eventually cause?

A

Increased cardiac demand, which will reduce the stroke volume even more (helpful if the heart is healthy)

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33
Q

What is activated if cardiac output is reduced and BP drops?*

A
  • Baroreceptors in carotid sinus and aortic arch detect BP drop
  • Increased sympathetic drive increases HR and TPR (so needing more oxygen)
  • Increased afterload and cardiac workload
34
Q

How can the RAAS be activated?

A
  • Drop in BP causes a drop in renal perfusion

- Activation of RAAS

35
Q

What does RAAS do?*

A
  • Increases circulating volume (Na+ and H20 retention)
  • ADH stimulated
  • Vasoconstriction
  • Enhanced sympathetic activity
  • Increased preload (which increases stretch more and WILL NOT HELP)
36
Q

What can long-term activation of SNS and angiotensin II cause?

A

Cardiotoxic effects

37
Q

What are the most common symptoms and signs of heart failure?

A
  • Fatigue and lethargy (not perfused)
  • Breathlessness (depends on if RV or LV affected)
  • Leg swelling (oedema, pulmonary or peripheral)
38
Q

How does tissue fluid form?* SLIDE 23!

A

High pressure in arterial circulation: H&raquo_space; O (H out, O in = fluid into interstitium)
Low pressure: O&raquo_space; H (fluid back into capillary)

39
Q

What causes tissue oedema?

A

Increased capillary hydrostatic pressure leading to less fluid being drawn back into venules
(higher pressure = higher hydrostatic pressure)

40
Q

What is pulmonary oedema?*

A

Accumulation of fluid in the lungs

41
Q

What is peripheral oedema?*

A

Accumulation of fluid in the peripheries

42
Q

What are the features of left ventricular heart failure?

*- caused by pulmonary oedema

A

Fluid in lungs

  • Fatigue and lethargy
  • Exertional breathlessness
  • Orthopnoea (breathlessness made worse lying flat)*
  • Paroxysmal nocturnal dyspnoea (waking up gasping for breath)*
  • Basal pulmonary crackles*
  • Cardiomegaly
43
Q

What are the features of right ventricular heart failure?

A

Fluid in body

  • Fatigue and lethargy
  • Breathlessness
  • Peripheral/pitting oedema (tissue fluid accumulation)
  • Raised JVP
  • Liver congestion (smooth, tender, enlarged liver)
44
Q

What is a raised jugular venous pressure used to diagnose and how is it relevant?*

A
  • If distended = elevated
  • Is a marker of pressure in the right side of the heart
  • Will only go up if right side of heart is struggling
45
Q

What is the risk of readmission/death within 60 days in heart failure?*

A

30-50%

46
Q

What is the ‘organ system failure’ trajectory?*

A
  • Patient constantly gradually declines
  • Has dips where they become acutely unwell
  • You never know if the patient will get better or if they will die
  • Death often ‘sudden’ but time is about 2-5 years from when they have to be hospitalised
47
Q

What is Class I heart failure?

A

No symptomatic limitation of physical activity

48
Q

What is Class II heart failure?

A
  • Slight limitation of physical activity
  • Ordinary physical activity resulting in symptoms
  • No symptoms at rest
49
Q

What is Class III heart failure?

A
  • Marked limitation of physical activity
  • Less than ordinary physical activity = symptoms
  • No symptoms at rest
50
Q

What is Class IV heart failure?

A
  • Inability to carry out any physical activities without symptoms
  • Symptoms at rest
  • Discomfort increasing with any physical activity
51
Q

What are the key questions to ask in investigations?

A

Does the patient have heart failure?

  • Diagnose with clinical investigations (symptoms, tests, etc)
  • Differential diagnoses? (eg. anaemia)
52
Q

What is the next question?

A

What sort of heart failure does a patient have?

  • HFrEF
  • LV systolic dysfunction
  • Valvular/structural
  • RV failure
  • High output cardiac failure
  • HFpEF (stiffness)
53
Q

What is the final question to ask?

A

What is causing the patient’s heart failure?

  • Viral
  • Ischaemic heart disease
  • Hypertension
54
Q

What is used to symptomatically treat heart failure?

A

Furosemide (diuretic to reduce fluid buildup)

55
Q

What is the prognostic treatment for left ventricular systolic dysfunction?

A
  • Cardiac rehabilitation
  • ACE/ARB (angiotensin receptor blockers)
  • Betablockers
  • MRA (Spironolactone) - aldosterone receptor antagonist
  • Biventricular pacemaker
  • Sacubitril valsartan
  • Ivabradine, nitrate, IV iron
56
Q

What is the immediate treatment for an emergency heart failure?

A
  • Furosemide (80mg stat)
  • Oxygen if hypoxic
  • Respiratory support?
57
Q

What can cause tachycardia in heart failure ?

A

Pulmonary oedema (must be treated immediately!)

58
Q

What can cause fast atrial fibrillation?*

A

Heart trying to decompensate

59
Q

How does respiratory/heart failure present on a CXR?*

A
  • Cardiomegaly
  • Fluid in fissure
  • Pleural effusion
60
Q

Why is IV furosemide used?

A
  • Reduces preload and therefore afterload
  • Immediate venodilation
  • Diuretic action 30 minutes, peak at 60-90 min
  • Getting rid of excess fluid

AROUND 40mg NEEDED TO MAXIMISE DIURESIS IF KIDNEYS GOOD

61
Q

What needs to be monitored when giving furosemide?

A
  • Heart rate
  • Blood pressure
  • Resp rate
  • Partial pressure of O2
  • Chest x-rays
  • Fluid balance
  • Weight loss (1kg/day)
  • Hourly urine output
62
Q

How does a LBBB appear on an ECG?*

A

Slide 22

- Biventricular pacemaker if weak heart to allow coordination

63
Q

Why would you do a full blood count on a patient with heart failure?

A
  • Patients with HF often anaemic

- Anaemia might explain symptoms

64
Q

Why would you do a NTpro-BNP?

A
  • Natriuretic peptide: released in response to ventricular stretch due to fluid overload
  • Afib can triple
65
Q

Why would you do U&E tests?

A
  • Check for renal function deterioration

- Na/K levels for medication

66
Q

Why would you do LFTs?

A

Patients’ livers can get congested

67
Q

Why would you do clotting tests?

A

May consider anticoagulants for Afib

68
Q

Why would you check the CRP?

A

To look for inflammation and infection as a cause

69
Q

What is the NTpro-BNP test?***

A
  • Test for a hormone released in response to atrial and ventricular stretching due to fluid overload
  • Can triple in Afib
  • Negative predictive value 97%
70
Q

What does it mean when a patient has a very HIGH BNP?

A
  • Severe heart failure
  • Heart is working to counteract (natriuresis, diuresis, vasodilation)
  • Values around 2000 = strong indication of heart failure
  • Values under 400 = probably not heart failure
71
Q

What is the role of the sympathetic nervous system in the heart?

A

A baroreceptor-mediated response that aims to improve CO by promoting cardiac contractility, vasoconstriction, tachycardia

72
Q

What is a transthoracic echocardiogram used for?

A

To check for severe LV impairment

73
Q

What are the long term effects of sympathetic activation?

A
  • Downregulation of beta adrenergic receptors

- Noradrenaline inducing hypertrophy and upregulates RAAS

74
Q

What are the physiological effects of beta-blockers?

A
  1. Reducing heart rate
  2. Reducing BP
  3. Reduced CO so less oxygen demand
75
Q

How do you prescribe beta-blockers?

A
  • Initiate at a low dose and titrate slowly

- Alter other medication if needed

76
Q

How do you prevent the activation of RAAS in heart failure?

A
  • ARB/angiotensin receptor blockers

- ACE inhibitors

77
Q

What is the function of spironolactone?*

A

Prevents the aldosterone concentration from rising to prevent arrhythmias

78
Q

How do you manage and treat a patient with HFrEF?***

A

NYHA I: treat underlying risk factors
NYHA II: refer for cardiac rehab, ACEI, ARB, beta blockers, diuretics
NYHA III: consider implantable monitoring device, evaluate risk
NYHA IV: end of life discussion, ventricular assist device

CONSIDER TRANSPLANT AND PALLIATIVE CARE THROUGHOUT THE TREATMENT

79
Q

When is a biventricular pacemaker good?

A

In heart failure with a NATURAL LOSS OF SYNCHRONY

80
Q

How to approach HFrEF patient with involvement?

A
  • Educate patient
  • Involve MDT
  • Cardiac rehabilitation

Cardiovascular System (11 decks)

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