M103 T3 L12 Flashcards

1
Q

When does high output HF occur?

A

when the heart can’t provide for the unusually high demand for blood to organs with normal functioning

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2
Q

What conditions result in high output HF? (SATT.PAPP)

A

sepsis, acromegaly, thyrotoxicosis (SAT)

Profound anaemia, Pregnancy, Pagets disease (PAPP)

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3
Q

What are causative conditions of HF?

A
Cardiomyopathies
Congenital Heart Disease
Coronary Heart Disease
Hypertensive Heart Disease
Myocardial Disease
Valvular Heart Disease
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4
Q

What are the causes of dilated cardiomyopathy?

A
alcohol, pregnancy
systemic disease 
muscular dystrophies 
Drug toxicity (chemotherapy)
Myocarditis – common viruses
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5
Q

What are the three types of cardiomyopathy? (DHR)

A

dilated
hypertrophic
restrictive

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6
Q

What is the main cause of restrictive cardiomyopathy?

A

amyloid

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7
Q

What does the activation of neurohormonal system involve?

A

the release of noradrenaline
the release of ANP / BNP
the activation of RAAS

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8
Q

Which compensatory mechanisms may successfully restore cardiac output but can also worsen HF?

A

vasoconstriction
Na and water retention
excessive tachycardia

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9
Q

What is excessive tachycardia caused by?

A

→ ↓diastolic filling time → ↓ventricular filling → ↓SV and CO

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10
Q

What are the clinical types of HF?

A
Left sided, right sided and biventricular 
Acute and chronic
Compensated and decompensated
Systolic and Diastolic
High and Low out put
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11
Q

What happens during left sided HF?

A

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

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12
Q

What conditions cause left sided HF? (VIM Him)

A

Valvular heart disease
Ischaemic heart disease
Myocardial disease
Hypertension

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13
Q

How does left ventricular HF cause heavy wet lungs?

A

pulmonary vein pressure is transmitted retrogradely to the capillaries and arteries
< pulmonary congestion and oedema < heavy wet lungs

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14
Q

What conditions cause heavy wet lungs?

A

dyspnoea exaggeration of the normal breathlessness that follows exertion
Orthopnoea
Paroxysmal nocturnal dyspnoea

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15
Q

How does left ventricular HF affect the kidneys?

A

Decreased cardiac output results in decreased renal perfusion
Activation of RAAS
Retention of salt and water with consequent expansion of interstitial fluid and blood volumes

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16
Q

What neurological conditions cause left ventricular failure?

A

Hypoxic encephalopathy
Irritability, Loss of attention, Restlessness
Stupor and coma

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17
Q

What conditions cause right sided HF?

A

usually left sided HF - congestive cardiac failure
cor-pulmonale
valvular heart disease
congenital heart disease

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18
Q

What is cor-pulmonale caused by?

A

increased resistance within the pulmonary circulation due to respiratory disease e.g. COPD or pulmonary emboli
leads to significant pulmonary hypertension
causes right HF

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19
Q

Which parts of the body does HF affect? (PASST)

A

Portal system, Abdomen, Spleen, Subcutaneous Tissue
the liver
the pleural and pericardial space

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20
Q

What conditions does right HF cause in the liver or in the portal system?

A

Congestive hepatomegaly
Centrilobular necrosis when severe
Cardiac cirrhosis

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21
Q

What abdominal condition is caused by right HF?

A

Congestive splenomegaly

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22
Q

How does right HF affect the subcutaneous tissue?

A

Peripheral oedema of dependent portions of the body esp. ankle and pretibial oedema

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23
Q

How does right HF affect the pleural and pericardial space?

A

effusions

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24
Q

What can cause biventricular failure?

A

the same pathological process on each side of the heart

left HF leading to volume overload of the pulmonary circulation and eventually the right ventricle

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25
Q

In patients with HF, what conditions does excess fluid accumulation cause? (HODA)

A

Hepatic congestion
Orthopnoea, Oedema
Dyspnoea, paroxysmal nocturnal dyspnoea
Ascites

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26
Q

In patients with HF, what does a reduction in HF cause?

A

Fatigue

Weakness

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27
Q

What are the different classes of HF?

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

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28
Q

What are the clinical signs of HF?

A

Cool, Ascites, pale (CAP)
Peripheral oedema, Displaced apex (PO.DA)
cyanotic extremities, Tachycardia (CET)
Hepatomegaly, Elevated jugular venous pressure (HEj)
the presence of an S3 sound
Crackles or decreased breath sounds at bases on chest auscultation

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29
Q

What clinical tests are used to pin point HF?

A

CXR, ECG
Blood investigations
Echocardiogram / Cardiac MRI or CT / CT-PET
CTCA / Coronary angiography

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30
Q

What are two examples of loop diuretics?

A

frusemide

bumetanide

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31
Q

What can potent loop diuretics lead to?

A

electrolyte abnormalities
hypovolaemia
diminished renal perfusion

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32
Q

How are loop diuretics administered?

A

iv / orally

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33
Q

How do loop diuretics work?

A

Inhibit Na+ re-absorption from the proximal tubule

K+ loss from distal tubule

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34
Q

What are two examples of Mineralocorticoid Receptor Antagonists?

A

EPLERENONE

SPIRONOLACTONE

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35
Q

How do Mineralocorticoid Receptor Antagonists work?

A

they promote Na+ excretion and K+ re-absorption

in distal tubule

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36
Q

What is the effect of Mineralocorticoid Receptor Antagonists?

A

they reduce hypertrophy and fibrosis

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37
Q

What are the main side effects of Mineralocorticoid Receptor Antagonists?

A

Gynaecomastia (esp. Spironolactone)

Electrolyte (K+ high) and renal function abnormalities

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38
Q

What are examples of ACE Inhibitors? (RECord Perilous Liars)

A
Ramipril
Enalapril
Captopril
Perindopril
Lisinopril
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39
Q

What do ACE Inhibitors act on?

A

the activated RAAS

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40
Q

How are ACE Inhibitors administered?

A

given orally in small doses with slow titration

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41
Q

How do ACE Inhibitors block the production of angiotensin?

A

Vasodilatation
BP lowering
Reduce cardiac work

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42
Q

What are the main side effects of ACE inhibitors?

A

cough
hypotension
renal impairment

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43
Q

What are three examples of beta blockers? (BCM - Back CAR MEeT)

A

BISOPROLOL
CARVEDILOL
METOPROLOL

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44
Q

How do beta blockers block the action of adr and noradr?

A

they slow the HR, which reduces BP

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45
Q

What is the function of beta blockers?

A

to block the action of adrenaline and noradrenaline on adrenergic b-receptors

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46
Q

How are beta blockers administered?

A

they are given orally in small doses with slow titration

treat arrhythmias

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47
Q

What are the two main side effects of beta blockers?

A

Bronchospasm

Claudication

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48
Q

What is an example of a SA node blockade?

A

ivabradine

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49
Q

How do SA node blockades work?

A

Slow HR, no effect on BP

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50
Q

How are SA node blockades administered?

A

Given orally with dose titration

51
Q

What is the function of SA node blockades?

A

blocks the If channel within the SA node

52
Q

What are the two main side effects of SA node blockades?

A

Visual aura

Bradycardia

53
Q

What is the effect of digoxin?

A

it increases myocardial contractility

it slows conduction at the AV node

54
Q

What conditions is digoxin used to treat?

A

acute HF, chronic HF

arrhythmias, AF

55
Q

What happens to digoxin once it has made its way through the body?

A

it is excreted by kidney

56
Q

What is an example of an ARNI?

A

SACUBITRIL VALSARTAN

57
Q

What is the function of an ARNI?

A

it acts on the activated RAAS
it blocks the breakdown of ANP/BNP
it blocks the production of angiotensin
it promotes natriuresis

58
Q

How do ARNIs block the production of angiotensin?

A

vasodilatation
lowers the bp
reduces cardiac work

59
Q

What are the main side effects of ARNIs?

A

hypotension

renal impairment

60
Q

How do ARNIs promote natriuresis?

A

sodium excretion
vasodilatation
reduce hypertrophy
fibrosis

61
Q

What are other therapies for HF?

A

Cardiac Resynchronisation Therapy
Cardiac transplantation
Stem cell therapy

62
Q

What is the difference between standard pacemakers and biventricular pacemakers?

A

standard - equipped with two leads that conduct pacing signals to specific regions of heart
biv - have an additional third lead designed to conduct signals directly into the left ventricle

63
Q

What is an adv of biventricular pacemakers?

A

the combination of all three leads promotes synchronised pumping of ventricles
there is increasing efficiency of each beat
pumps more blood on the whole

64
Q

What is the usual cardiac output at rest?

A

70mls/kg/min

65
Q

What two things does the Frank Starling law relate to eachother?

A

Preload

Cardiac Output

66
Q

What does the Frank Starling law state?

A

that 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

67
Q

Why is the Frank Starling law only true up to a certain point?

A

at some stage the fibres become over-stretched and the force of contraction is reduced

68
Q

What is the effect of noradrenaline?

A

increases heart rate
increases myocardial contractility
causes vasoconstriction

69
Q

What does the activated RAAS do and how?

A

it elevates blood volume by increasing Na and water reabsorption

70
Q

What is the natriuretic peptide system activated by?

A

increased ventricular wall stretch

71
Q

What is the effect of active BNP?

A

diuresis

vasodilationinhibits the RAAS and the sympathetic NS

72
Q

What is the half life of active BNP in circulation?

A

20 mins - very short lived

73
Q

What does high NT-proBNP indicate?

A

increased risk of HF

74
Q

What are the effects of the natriuretic peptide system?

A

Increase GFR
decrease bp
increased water & sodium excretion in urine

75
Q

What happens when the natriuretic peptide system is activated?

A

pro-BNP is released

is cleaved

76
Q

What is pro-BNP cleaved into?

A

active BNP

NT-proBNP

77
Q

From where is NT-proBNP excreted?

A

renally

78
Q

What is the half life of NT-proBNP in circulation?

A

2 hrs

79
Q

Why is sympathetic NS activity counter productive in a HF situation?

A

increased cardiac, vascular and renal sympathetic activity

80
Q

Why is increased cardiac sympathetic activity counter productive in a HF situation?

A

myocytes hypertrophy
increased arrhythmia
increased ischaemic demand

81
Q

Why is increased vascular sympathetic activity counter productive in a HF situation?

A

vasoconstriction mediated by the peripheral vascular circulation

82
Q

Why is increased renal sympathetic activity counter productive in a HF situation?

A

causes sodium retention

further activates the RAAS - RAAS activates this sympathetic NS and vice versa

83
Q

What happens during decompensated HF?

A

occurs when patients have ended up with worsening symptoms

often admitted to hospital

84
Q

What causes decompensated HF?

A

an additional medical condition - puts extra pressure on the balance of their HF
disease progression / further cardiac insult

85
Q

When is Cardiac Resynchronisation Therapy (CRT) offered to a HF patient?

A

when the patient is deemed to be at risk of sudden cardiac death

86
Q

When is Dialysis & Ultrafiltration used on a HF patient?

A

when the patient become resistant to diuretics

87
Q

What treatments are used on HF patients who are very unstable and extremely unwell with cardiogenic shock?

A

Ventricular Assist Device (LVAD/RVAD)

Intra-aortic balloon pump

88
Q

What are the two types of defibrillator?

A

System ICD

Transveous ICD

89
Q

How is the Transveous ICD positioned?

A

a lead inside the heart is connected to a pulse generator under the skin

90
Q

How does a Transveous ICD work?

A

an electrical shock wave is passed through the heart from the generator to the lead and back
this reverts unstable ventricular arrhythmias back to sinus rhythm

91
Q

What is an advs of using a Transveous ICD?

A

can be achieved completely subcutaneously

avoids the need for placing electrodes within the circulation or within the heart itself

92
Q

How is the System ICD positioned?

A

the lead is placed to the left of the sternum

93
Q

What is Cor pulmonale otherwise known as?

A

right-sided HF

94
Q

What is cardiac cirrhosis caused by?

A

right sided HF

95
Q

What is S3 otherwise known as?

A

the third heart sound

ventricular gallop

96
Q

What is a displaced apex caused by?

A

LV enlargement

97
Q

What medication may work for swelling when other medications have not?

A

bumetanide

98
Q

What is frusemide used to treat?

A

hypertension

fluid build-up due to HF, cirrhosis, or kidney disease

99
Q

What is bumetanide used to treat?

A

swelling (cardiac AAR of HF) and hypertension

100
Q

What is Eplerenone used to treat?

A

HF, hyperaldosteronism

reduces the risk other heart problems / a stroke

101
Q

Is Gynaecomastia benign?

A

usually but breast cancer can develop in about 1% of cases

102
Q

What causes Gynaecomastia?

A

an imbalanced ratio of oestrogen and androgen activity

103
Q

What causes high output HF?

A

when CO is higher than normal due to increased peripheral demand

104
Q

What conditions an result from high output HF?

A

a circulatory overload
pulmonary oedema secondary
elevated diastolic pressure (left ventricle)

105
Q

What is claudication usually a symptom of?

A

peripheral artery disease caused by atherosclerosis

106
Q

When does claudication occur?

A

when there is too little blood flow to the limbs due to atherosclerosis

107
Q

What is peripheral artery disease usually caused by?

A

atherosclerosis

108
Q

What is a symptom of claudication?

A

pain in the limbs associated with walking or using the arms

109
Q

What is the difference between angina and chest pain?

A

Not all angina is chest pain

angina is pain caused by narrowed coronary arteries

110
Q

What conditions is ivabradine used to treat?

A

the symptoms of stable heart-related chest pain

HF not fully managed by beta blockers

111
Q

What do the cardiac glycosides affect?

A

they ics the force of the heart and its rate of contractions

112
Q

How do the cardiac glycosides work?

A

by acting on the cellular Na/K ATPase pump

113
Q

What is digoxin used for?

A

to control some heart problems

114
Q

How does neprilysin work to inactivate peptide-based hormones?

A

they cleave peptides at the amino side of hydrophobic residues

115
Q

What are examples of peptide hormones that are inactivated by neprilysin? (GES NOB)

A

glucagon, enkephalins, substance P, neurotensin, oxytocin, and bradykinin.

116
Q

When are ARNIs used?

A

when other treatments for HF aren’t working in certain cases / patients

117
Q

Where is B-type natriuretic peptide made?

A

inside the pumping chambers of the heart

118
Q

When is B-type natriuretic peptide made?

A

when pressure builds up from HF

119
Q

What substance serves as an indicator of HF?

A

B-type natriuretic peptide

120
Q

What does CRT involve?

A

implanting a small pacemaker just below the collarbone
three leads are connected to a device that monitors the heart rate to detect heart rate irregularities and emit tiny pulses of electricity to correct them

121
Q

What gender(s) is androgen present in?

A

both genders

122
Q

What is the role of androgen?

A

contributes to male traits and reproductive activity

123
Q

What are the two main androgens?

A

testosterone and androstenedione