Heart Failure Flashcards
1
Q
how many hospital admissions does HF account for yearly?
A
10%
2
Q
how many people die yearly from HF?
A
100K
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)
4
Q
what happens when the ventricle is stretched more?
A
greater force of contraction to pump blood out
BNP secreted
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
6
Q
what does ejection fraction approximate?
A
systolic function of LV
7
Q
what is ejection fraction measuring?
A
proportion of blood present at he end of diastole that is ejected from ventricle on contraction
8
Q
how do you calculate EF?
A
(EDV- ESV)/ EDV
9
Q
what is a normal EF?
A
> 0.5 or 50-60%
10
Q
what is n expected EF that is ‘reduced’?
A
<45%
11
Q
what does HF start with?
A
damage to myocardium that leads to neurohumoral activation - adaptive mechanisms
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)
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
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
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
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
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
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
19
Q
what is one of the main causes of HF-PEF?
A
years of hypertension
20
Q
what is HF-REF?
A
common left ventricular failure
reduced ejection fraction
21
Q
what are the main causes of HF?
A
CHD and hypertension
22
Q
apart from CHD and hypertension, what else causes HF?
A
myocardial diseases, volume overload, congenital, arrhythmias, infiltrative disease, iatrogenic, systemic stressors
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
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
25
what are the main symptoms of chronic HF?
breathlessness ( orthopnoea/ paroxysmal nocturnal dsypnoea)
fatigue
oedema
decreased exercise tolerance
26
what are less common symptoms for chronic HF?
nocturnal cough, weight gain/ weight loss, bloated, loss of appetite, confusion, depression, palpitations, syncope
27
what are clinical signs of chronic HF?
laterally displaced apex beat (hypertrophy)
raised JVP, hepatomegaly, gallop rhythm, tachycardia, lung crepitiations
28
what is usually the cause of left sided HF?
CAD
29
what are common presentations of left sided HF?
- 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
30
what is the usual causation for right sided HF?
pulmonary causation
31
what are the common presentations of right sided HF?
- Fatigue
- Increased peripheral venous pressure
- Ascites
- Enlarged liver and spleen
- Distended JVP
- Anorexia/ complaints of GI distress
- Weight gain
- Dependent oedema
32
what are the initial investigations for HF?
ECG, CXR, Bloods, echo, MI in past
33
on an ECG, what would indicate HF?
LV hypertrophy (increased amplitude and duration of QRS), evidence of prior MI, conduction defects m infiltrative cardiomyopathy
34
on a chest X ray would would indicate HF?
ABCDE
Alveolar oedema (bat wings)
kerly B lines - interstitial oedema
cardiomegaly
Dilated prominent upper lobe vessels
pleural Effusion
35
what would you look for within blood tests for HF?
FBC
U&E
BNP - secreted from heart wall when stretched
36
what does BNP do?
secreted when ventricular wall is stretched
increases renal excretion of sodium/ water
relaxes smooth vascular muscle. >400pg/ml needs urgent referral
37
what would an echo show for HF?
excluded valvular disease
assess systolic/ diastolic function
detects intracardiac shunts
measures ventricular function
38
name some loop diuretics
furosemid, bumentanide, torasemide
39
what is the action of loop diuretics?
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
what is the function of loop diuretics?
decrease ventricular filling and improve pulmonary vascular congestion
41
what are cautions with loop diuretics?
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
what is contra-indicated within loop diuretics?
hypovolemia and dehdryation, severe hypokalemia/ severe hyponatraemia. acute kidney injury and CKD
43
what needs monitoring with loop diuretics?
renal function, serum electrolytes, blood pressure - check before and after
44
what are common side effects with loop diuretics?
hyponatraemia, hypocholaraemia, hypokalemia, hypomagnesaemia, hypocalaemia, dehydration, metabolic alkalosis, hyperuricaemia, blood disorders
45
what drugs are used to treat chronic HF?
loop diuretics, thiazide diuretics, aldosterone antagonists
ACEi, ARB, Bblockers
isosorbide dinitrate and hydralazine
ivabradine
digoxin
dapagliffloxin and aepaglififlozin
entresto
46
what might aldosterone antagonist also be kneon as?
MRA - mineral receptor antagonists
47
when are aldosterone antagonists useful in treating HF?
if patient had a previous MI
class II to IV
decrease morbidity and mortality in those with symptomatic chronic HF
48
what is an alternative to ACEi/ARB?
isosorbride dinitrate and hydralazine
49
what is the mechanism of action of ivabradine
inhibit I-channel at SAN to reduce heart rate
50
when can digoxin toxicity occur and what can it lead to?
during long term therapy as well as over dose
leads to anorexia, nausea, vomiting, neurological symptoms
fatal arrhythmias
51
what are enresto?
2 part (with ACEi component)
sacubritil/ valsartan
52
when is enresto best used?
symptomatic chronic HF REF
prevents BNP
53
when is dapaglifloxin and empaglifllxin best used?
symptomatic HF REF
alongside ACEi/ ARB
54
what are the NICE guidelines to manage chronic HF?
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
what is patient advice with HF?
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
what are complications of chronic HF?
cardiac arrhythmias, depression, cachexia, CKD, sexual dysfunction, sudden cardiac death
57
what is acute HF?
develops rapidly and can be immediately life threatening due to lack of time to undergo compensatory changes
58
what is the pathology of acute HF?
sudden inability to maintain adequate cardiac output and blood pressure
- arterial and venous constriction
- rapid filling of left ventricle leading to backflow
59
what is a the principle symptom of acute HF?
breathlessness
60
how do you treat acute HF?
- 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
what is a common symptoms of end stage HF?
breathlessness, pain, anxiety, insomnia, depression, anxiety, GI issues
62
how is breathlessness managed?
diuretics and fluid restriction
63
what treatment is given to help manage anxiety/ insomnia/ depression in HF?
sedatives and hypnotics
64
what are symptoms of left sided HF?
- 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
what symptoms are common in right sided heart failure?
- Fatigue
- Increased peripheral venous pressure
- Ascites
- Enlarged liver and spleen
- Distended JVP
- Anorexia/ complaints of GI distress
- Weight gain
- Dependent oedema
66
how does DVT present?
immobility, prominent dilated veins, warm tender swollen lower limb/ thigh
oedema - swelling and inflammation is below blockage site
67
what test is good for excluding DVT diagnosis?
positive D dimer test
68
what is a pulmonary embolism?
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
how common are PE?
3-4 per 10,000 in the UK
costs 60,000 lives yearly
70
what is a saddle embolism?
most concerning - use altepase to bust clot or will lead to cardiac arrest
71
what are symptoms of PE?
breathlessness, pleuritic chest pain, pulmonary infarction - clot blcoking lungs - can be asymptomatic if small
big PE - syncope, shock, severe central chest pain
72
what are signs on an ECG of a PE?
s waves in lead I
Q waves in lead III
inverted T waves in Lead III
73
what clinical signs are seen with a PE?
inspection - cyanosis, raised ventricular heave, tachypnoea
palpitation - tachycardia, AF
percussion - pleural effusion
ascultation - pleural rub, gallop rhythm
pyrexia, low oxygen sats, hypotnesion
74
what are risk factors for PE and DVT?
previous thromboembolism, cancer, age, overweight, male, HF, severe infection, acquired or familial thrombophilia, smoking
75
what is standard treatment of PE?
do not delay if suspected
LMWH safer
DOACs - once VTE has been established
thrombolysis if haemodynamically unstable
76
where are complications of PE?
hypoxemia, pulmonary hypertension, right heart failure, resp shock, cardiogenic shock,
77
if unprovoked VTE, what investigation's should occur?
possibility for cancer - abdo CT , mammogram in women
antiphospholipid testing
hereditary screening if occurred in first line relatives
78
how can COVID-19 put those at risk of DVT, PE?
higher clot risk
79
what should anticoag counselling include?
anticoag alert card
general info
safe use
blood tests
dosage
80
what are the main points of anticoag counselling?
use, duration, importance of appointments, what to do with unexpected bruising/ bleeding
81
what should be included within an anticoag counselling session?
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
