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Cardiovascular > Heart Failure > Flashcards

Heart Failure Flashcards

1
Q

how many hospital admissions does HF account for yearly?

A

10%

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2
Q

how many people die yearly from HF?

A

100K

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3
Q

what conditions can lead to HF?

A
  • Ischaemia (CAD, AMI)
  • Hypertension
  • Diabetes (diabetic cardiomyopathy and CAD)
  • Valvular heart disease eg AS and MR
  • Cardiomyopathy
  • Pericardial disease
  • infection eg viral myocarditis
  • toxins and drugs (alcohol etc)
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4
Q

what happens when the ventricle is stretched more?

A

greater force of contraction to pump blood out
BNP secreted

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5
Q

what is ventricular remodelling?

A

any structural chnage in response to chnage in loading conditions
- change in mass, size, shape
can be reversed

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6
Q

what does ejection fraction approximate?

A

systolic function of LV

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7
Q

what is ejection fraction measuring?

A

proportion of blood present at he end of diastole that is ejected from ventricle on contraction

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8
Q

how do you calculate EF?

A

(EDV- ESV)/ EDV

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9
Q

what is a normal EF?

A

> 0.5 or 50-60%

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10
Q

what is n expected EF that is ‘reduced’?

A

<45%

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11
Q

what does HF start with?

A

damage to myocardium that leads to neurohumoral activation - adaptive mechanisms

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12
Q

what are signs of HF?

A
  • Breathlessness (exertion and rest)
  • Orthopnoea
  • Paraoxysmal nocturnal dyspnoea
  • Fatigue, lack of energy
  • Pitting oedema, coughing, elevated JVP, pulmonary oedema/ pleural effusion, ascites, tachycardia, S3 gallop (third heart sound – deceleration of blood entering LV from LA)
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13
Q

what are the NYHA stages defining HF?

A
  • Stage 1: no symptoms/ limitations or ordinary PA
  • Stage 2: mild symptoms – slight limitation of ordinary activity
  • Stage 3 – marked limitation during less than ordinary activities
  • Stage 4 – severe limitations – experience symptoms at rest
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14
Q

what investigations are carried out to diagnosis HF?

A
  • FBC, haematinics, U&E, TFT
  • Chest X ray
  • Brain derived natriuretic peptide (BNP), polypeptide produced by ventricles in response to stretching – of low very unlikely to have HF.
  • ECG – other arrhythmias
  • Echo – ejection fraction, assessment of valves
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15
Q

define heart failure

A

cardiac output is insufficient to adequately perfuse the tissues despite the normal filling of the heart
-pump mechanism doesnt work as well

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16
Q

what is the pathophysiology of HF?

A
  • Increased sympathetic nervous activity
  • Stimulating heart to beat and maintain the blood pressure by increasing the vascular resistance
  • Increase in the resistance against in which the heart has to pump (afterload)
  • Reduced renal blood flow results in renin secretion and has increased plasma angiotensin and aldosterone levels
  • Na and H2O retention to increase the blood volume increasing the central venous pressure (pre-load) and oedema and constricting vessels
  • Compensatory changes to help maintain cardiac output
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17
Q

what do the compensatory mechanisms cause within HF?

A
  • Decrease in BP and increase in sympathetic activity releasing catecholamines into circulation (dopamine, adrenaline, NA)
  • Increase in sympathetic activity and increase in ADH from posterior pituitary gland causing fluid retention by the kidneys
  • Reduced blood flow to the kidneys stimulates the production of renin which further increases oedema
  • Renin catalyses the production of potent vasopressor angiotensin – stimulates aldosterone by adrenal glands promoting salt and fluid retention by the kidneys
  • In the long term these can be deleterious and worsen HF
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18
Q

what occurs within HF-PEF?

A

left ventricular wall is stiff and does not relax adequately
doe not eject blood effectively
reduced compliance means it does not fill effectively

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19
Q

what is one of the main causes of HF-PEF?

A

years of hypertension

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20
Q

what is HF-REF?

A

common left ventricular failure
reduced ejection fraction

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21
Q

what are the main causes of HF?

A

CHD and hypertension

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22
Q

apart from CHD and hypertension, what else causes HF?

A

myocardial diseases, volume overload, congenital, arrhythmias, infiltrative disease, iatrogenic, systemic stressors

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23
Q

what are risk factors for HF?

A
  • MI, CAD/ angina
  • AF
  • Diabetes
  • Hypertension
  • Excessive alcohol consumption
  • Previous cardiotoxic chemotherapy eg doxorubicin/ daunorubicin (need echos to assess structure)
  • Family history of HF/ SCD from cardiomyopathy at a young age
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24
Q

what is primary prevention for HF?

A

control RF that predispose to impairment
BP control, weight management, CAD prevention, strict diabetes management, management of sleep apnoea

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25
Q

what are the main symptoms of chronic HF?

A

breathlessness ( orthopnoea/ paroxysmal nocturnal dsypnoea)
fatigue
oedema
decreased exercise tolerance

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26
Q

what are less common symptoms for chronic HF?

A

nocturnal cough, weight gain/ weight loss, bloated, loss of appetite, confusion, depression, palpitations, syncope

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27
Q

what are clinical signs of chronic HF?

A

laterally displaced apex beat (hypertrophy)
raised JVP, hepatomegaly, gallop rhythm, tachycardia, lung crepitiations

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28
Q

what is usually the cause of left sided HF?

A

CAD

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29
Q

what are common presentations of left sided HF?

A
  • Paroxysmal nocturnal dyspnoea
  • Elevated pulmonary capillary wedge
  • Pulmonary congestion – cough, crackles, wheezes, blood tinged sputum (alveoli ), tachypnea
  • Restlessness
  • Confusion
  • Orthopnoea
  • Tachycardia
  • Exertional dsyponea
  • Fatigue
  • Cyanosis
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30
Q

what is the usual causation for right sided HF?

A

pulmonary causation

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31
Q

what are the common presentations of right sided HF?

A
  • Fatigue
  • Increased peripheral venous pressure
  • Ascites
  • Enlarged liver and spleen
  • Distended JVP
  • Anorexia/ complaints of GI distress
  • Weight gain
  • Dependent oedema
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32
Q

what are the initial investigations for HF?

A

ECG, CXR, Bloods, echo, MI in past

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33
Q

on an ECG, what would indicate HF?

A

LV hypertrophy (increased amplitude and duration of QRS), evidence of prior MI, conduction defects m infiltrative cardiomyopathy

34
Q

on a chest X ray would would indicate HF?

A

ABCDE
Alveolar oedema (bat wings)
kerly B lines - interstitial oedema
cardiomegaly
Dilated prominent upper lobe vessels
pleural Effusion

35
Q

what would you look for within blood tests for HF?

A

FBC
U&E
BNP - secreted from heart wall when stretched

36
Q

what does BNP do?

A

secreted when ventricular wall is stretched
increases renal excretion of sodium/ water
relaxes smooth vascular muscle. >400pg/ml needs urgent referral

37
Q

what would an echo show for HF?

A

excluded valvular disease
assess systolic/ diastolic function
detects intracardiac shunts
measures ventricular function

38
Q

name some loop diuretics

A

furosemid, bumentanide, torasemide

39
Q

what is the action of loop diuretics?

A

inhibit reabsorption from ascending limb on loop of henle.
inhibits Na-K-Cl transporter in thick ascending limb
leads to both diuresis and natriuresis

40
Q

what is the function of loop diuretics?

A

decrease ventricular filling and improve pulmonary vascular congestion

41
Q

what are cautions with loop diuretics?

A

sudden drop in LV can result in decrease CO and hypotension - start low doses and titrate up
caution in elderly, electrolyte imbalance and hypotension

42
Q

what is contra-indicated within loop diuretics?

A

hypovolemia and dehdryation, severe hypokalemia/ severe hyponatraemia. acute kidney injury and CKD

43
Q

what needs monitoring with loop diuretics?

A

renal function, serum electrolytes, blood pressure - check before and after

44
Q

what are common side effects with loop diuretics?

A

hyponatraemia, hypocholaraemia, hypokalemia, hypomagnesaemia, hypocalaemia, dehydration, metabolic alkalosis, hyperuricaemia, blood disorders

45
Q

what drugs are used to treat chronic HF?

A

loop diuretics, thiazide diuretics, aldosterone antagonists
ACEi, ARB, Bblockers
isosorbide dinitrate and hydralazine
ivabradine
digoxin
dapagliffloxin and aepaglififlozin
entresto

46
Q

what might aldosterone antagonist also be kneon as?

A

MRA - mineral receptor antagonists

47
Q

when are aldosterone antagonists useful in treating HF?

A

if patient had a previous MI
class II to IV
decrease morbidity and mortality in those with symptomatic chronic HF

48
Q

what is an alternative to ACEi/ARB?

A

isosorbride dinitrate and hydralazine

49
Q

what is the mechanism of action of ivabradine

A

inhibit I-channel at SAN to reduce heart rate

50
Q

when can digoxin toxicity occur and what can it lead to?

A

during long term therapy as well as over dose
leads to anorexia, nausea, vomiting, neurological symptoms
fatal arrhythmias

51
Q

what are enresto?

A

2 part (with ACEi component)
sacubritil/ valsartan

52
Q

when is enresto best used?

A

symptomatic chronic HF REF
prevents BNP

53
Q

when is dapaglifloxin and empaglifllxin best used?

A

symptomatic HF REF
alongside ACEi/ ARB

54
Q

what are the NICE guidelines to manage chronic HF?

A
  1. Relieve symptoms of fluid overload – diuretic (titrate dose up/ down and review)
  2. Reduce mortality/ morbidity – ACEi/ ARB and B Blocker
  3. Introduce one drug at a time
  4. Second drug to be added once patient is stable on the first
  5. Specialist help: loop and thiazide diuretic, aldosterone antagonist, digoxin, anticoagulation or surgical intervention required (implantable cardioverter-defib, heart transplantation, LVAD)
55
Q

what is patient advice with HF?

A

salt consumption, fluid restriction >2L, smoking/ alcohol consumption, physical activity (regular low intensity), nutritional status, sexual activity (if stable symptoms can resume), immunisation (flu jabs to prevent acute Hf). Travel – prepare according to PA capacity and DVLA?

56
Q

what are complications of chronic HF?

A

cardiac arrhythmias, depression, cachexia, CKD, sexual dysfunction, sudden cardiac death

57
Q

what is acute HF?

A

develops rapidly and can be immediately life threatening due to lack of time to undergo compensatory changes

58
Q

what is the pathology of acute HF?

A

sudden inability to maintain adequate cardiac output and blood pressure
- arterial and venous constriction
- rapid filling of left ventricle leading to backflow

59
Q

what is a the principle symptom of acute HF?

A

breathlessness

60
Q

how do you treat acute HF?

A
  • Oxygen
  • Diuretics – reduce fluid
  • Nitrates – vasodilate. Patients with concomitant MI, severe hypertension, regurgitation aortic/ mitral valve disease
  • Inotropes – improve contractibility
  • Vasopressors – cardiogenic shock treatment
  • Fluid management
  • Opiates – relieve dyspnoea and anxiety
61
Q

what is a common symptoms of end stage HF?

A

breathlessness, pain, anxiety, insomnia, depression, anxiety, GI issues

62
Q

how is breathlessness managed?

A

diuretics and fluid restriction

63
Q

what treatment is given to help manage anxiety/ insomnia/ depression in HF?

A

sedatives and hypnotics

64
Q

what are symptoms of left sided HF?

A
  • Paroxysmal nocturnal dyspnoea
  • Elevated pulmonary capillary wedge
  • Pulmonary congestion – cough, crackles, wheezes, blood tinged sputum (alveoli ), tachypnea
  • Restlessness
  • Confusion
  • Orthopnoea
  • Tachycardia
  • Exertional dsyponea
  • Fatigue
  • Cyanosis
65
Q

what symptoms are common in right sided heart failure?

A
  • Fatigue
  • Increased peripheral venous pressure
  • Ascites
  • Enlarged liver and spleen
  • Distended JVP
  • Anorexia/ complaints of GI distress
  • Weight gain
  • Dependent oedema
66
Q

how does DVT present?

A

immobility, prominent dilated veins, warm tender swollen lower limb/ thigh
oedema - swelling and inflammation is below blockage site

67
Q

what test is good for excluding DVT diagnosis?

A

positive D dimer test

68
Q

what is a pulmonary embolism?

A

a condition where one or more emboli arising from thrombus are formed in the veins are lodged in and obstructing the pulmonary arterial system
can be provoked or unprovoked

69
Q

how common are PE?

A

3-4 per 10,000 in the UK
costs 60,000 lives yearly

70
Q

what is a saddle embolism?

A

most concerning - use altepase to bust clot or will lead to cardiac arrest

71
Q

what are symptoms of PE?

A

breathlessness, pleuritic chest pain, pulmonary infarction - clot blcoking lungs - can be asymptomatic if small
big PE - syncope, shock, severe central chest pain

72
Q

what are signs on an ECG of a PE?

A

s waves in lead I
Q waves in lead III
inverted T waves in Lead III

73
Q

what clinical signs are seen with a PE?

A

inspection - cyanosis, raised ventricular heave, tachypnoea
palpitation - tachycardia, AF
percussion - pleural effusion
ascultation - pleural rub, gallop rhythm
pyrexia, low oxygen sats, hypotnesion

74
Q

what are risk factors for PE and DVT?

A

previous thromboembolism, cancer, age, overweight, male, HF, severe infection, acquired or familial thrombophilia, smoking

75
Q

what is standard treatment of PE?

A

do not delay if suspected
LMWH safer
DOACs - once VTE has been established
thrombolysis if haemodynamically unstable

76
Q

where are complications of PE?

A

hypoxemia, pulmonary hypertension, right heart failure, resp shock, cardiogenic shock,

77
Q

if unprovoked VTE, what investigation’s should occur?

A

possibility for cancer - abdo CT , mammogram in women
antiphospholipid testing
hereditary screening if occurred in first line relatives

78
Q

how can COVID-19 put those at risk of DVT, PE?

A

higher clot risk

79
Q

what should anticoag counselling include?

A

anticoag alert card
general info
safe use
blood tests
dosage

80
Q

what are the main points of anticoag counselling?

A

use, duration, importance of appointments, what to do with unexpected bruising/ bleeding

81
Q

what should be included within an anticoag counselling session?

A

dose - colours/ mg/ missed dose
take warfarin at same time each day
further supplies
avoid aspirin / other NSAIDs
if changes to meds - inform perosn monitoring
avoid sudden changes to diet
prevent pregnancy
yellow anticoag book
any specifics for that drug

Cardiovascular (14 decks)

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