Heart Failure Flashcards

1
Q

What is frank starlings law

A

The increased venous return would increase the contractility

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2
Q

How would frank starlings law change if there was heart failure

A

Would have the reduced cardiac stretch so would not have the increased contractility
so would have the higher EDV

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3
Q

What is acute heart failure

A

Rapid onset

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4
Q

What are the main causes of the acute heart failure

A

Pulmonary embolism
Drugs
Arrhythmias
Acute valvopathy

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5
Q

What is chronic heart failure

A

Progressive cardiac dysfunction
This can happen over a long time period
Normally would be die to the systolic or the diastolic issues

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6
Q

What is an ejection fraction

A

Fraction of blood that would be pumped out the heart compared to the volume of blood that would originally enter the heart

EF = SV/EDV

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7
Q

What is systolic heart failure

A

HFrEF (heart failure reduced ejection fraction)
Systolic dysfunction
Reduced contractility
MI
Dilated cardiomyopathy
So reduced ejection fraction

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8
Q

What is a dilated cardiomyopathy

A

Walls of the heart would be dilated
Could be due to viral infection
Heart cant generate enough pressure
Less blood pumped outwards

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9
Q

What is diastolic heart failure

A

HFpEF (heart failure preserved ejection fraction)
Diastolic dysfunction
Increased stiffness of the ventricle walls
Reduced preload (decreased filling)
Increased afterload (needs to work harder)
MI
Cardiac tamponade

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10
Q

Why would the EF be preserved with diastolic

A

The stroke volume would fall (less blood out) the end diastolic volume falls (less blood in to go out)
Ratio preserved

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11
Q

What happens in right sided heart failure

A

Reduced contractility (MI)
Increased afterload
Increased preload (pulmonary/tricuspid valve regurgitation)
Can develop FROM the leftsided heart failure

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12
Q

What factors would increase the afterload in right sided heart failure

A

Pulmonary stenosis
Pulmonary hypertension (From a PE)
Hypoxic vasoconstriction in pulmonary vessels (cor pulmonale)

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13
Q

What is hypoxic vasoconstriction

A

Perfusion and ventilation decreases
Preserve oxygen vessels vasoconstrict
Lead to pulmonary hypertension

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14
Q

What is low output heat failure

A

Heart cannot meet the cardiac demand of the body
Increased systematic vascular resistance to combat
Weak pulse and low BP

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15
Q

What is high output heart failure

A

CO > 8L/min
Heart cannot meet the demand of the cardiac function
Also
Increased demand due to the shunting of blood to the venous side (AV fistula, thymine deficiency)

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16
Q

What is AV fistula

A

Abnormal connection between the artery’s and the veins
Not enough time for the oxygen exchange
Can lead to heart failure

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17
Q

What happens in a thymine deficiency (chronic alcoholism)

A

Pyruvate ———— acetyl COA
Needs thymine
No thymine means no acetyl Co A
Build of lactate
Vasoconstriction
Blood goes from the artery’s to veins
Lack of oxygen transfer

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18
Q

What happens in left sided heart failure

A

Blood would normally accumulate in the left atrium

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19
Q

What are the symptoms of left sided heart failure

A

Dry cough
Dyspnea (shortness of breath)
Orthopnoea (difficulty lying flat fluid accumulation in the lungs and tissues)
Paroxysmal nocturnal Dyspnea (breathlessness that gets worse at night)

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20
Q

What are the signs of left sided heart failure

A

Bi basal crackles (both lungs on the base)
Tachycardia
Cardiomegaly
3rd and 4th heart sounds (additional due to the stiff and loose heart)

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21
Q

What are the symptoms of right sided heart failure

A

Dyspnea
Chest discomfort
Swelling

22
Q

What are the signs of right sided heart failure

A

Jugular venous distension
Hepatic congestion
Peripheral odema
Ascites
(MAINLY FLUID BUILD UP)

23
Q

What is congestive heat failure

A

The combination of the right and the left sided heart failures

24
Q

What is the N-terminal pro-B-type Natriuretic peptide level and what does it show

A

Cardiac neurohormone
Made by the ventricle cardiomyocytes when have increased stress in the ventricles walls
Released with BNP (active) when increased pressure
Degradaes slower then BNP so better

25
Q

What does a low level of NT-pro-BNP show

A

A strong negative predictive value
Levels <4000ng/L

26
Q

What does eGFR do

A

Marks kidney function
Low renal perfusion would show a low cardiac output

27
Q

What blood tests can be done to show heart failure

A

FBC and iron (shows anemias)
LFT (hepatic congestion, RSHF)
TFT (shows increased metabolic demand)
HbA1c and lipids (diabetes and hyperlipidemia shown)

28
Q

What is the main investigative measure for the heart failure

A

Echocardiogram (transthoratic echocardiogram)

29
Q

What are the three groups of heart failure

A

HFrEF = LVEF <40%
HFmrEF =LVEF 40-49%
HFpEF = LVEF >/~ 50%

30
Q

How can you classify heart failure

A

Class 1
Class 2
Class 3
Class 4

31
Q

What is class 1 heart failure

A

No symptomatic limitations to physical activity

32
Q

What is class 2 heart failure

A

Slight limitations to physical activity. No symptoms at rest

33
Q

What is class 3 heart failure (moderate)

A

Marked limitations to physical activity, no symptoms at rest

34
Q

What is class 4 heart failure (severe)

A

Inability to carry out physical activity without symptoms. May have symptoms at rest

35
Q

What do the ACE Inhibitors do

A

No conversion of Ang 1 to Ang 2
Reduced preload and afterload
Produced bradykinin
RAMIPRIL, LISIONPRIL, ENALAPRIL, CAPTOPRIL

36
Q

What do the beta blockers do

A

Reduces heart rate
Longer time for the ventricles filling
Also increased force of heart contraction
PROPRANOLOL AND ATENOLOL

37
Q

What do the mineralocorticoid receptor antagonists do

A

Reduce sodium reabsorption
reduces blood pressure and circulating volume
SPIRONOLACTONE AND EPLERENONE

38
Q

What do the loop diuretics do

A

No effect on heart failure but can help with symptoms
Secretion of water from the kidney, reduces circulating volume and peripheral odema
FUROSEMIDE, BUMETANIDE

39
Q

What are the second line treatments for heart failure

A

Digoxin (no channels working)
Hydralazine (would be able to increase the blood pressure of the system)
Ivabradine (channel blocker that would slow down the heart)
Sacubitril/valsartan

40
Q

What are the device therapy’s

A

Implantable cardiac defibrillator
Cardiac resynchronisation therapy

41
Q

What can be seen on an echocardiogram if the patient has heart failure

A

The heart would occupy more or equal to 50%of the window of view
(This could be because of the cardiomegaly in the LSHF)

42
Q

What would happen to the after load and the preload in right sided heart failure

A

Increased afterload - pulmonary hypertension, pulmonary stenosis, hypoxic vasoconstriction
Increased preload - tricuspid/pulmonary valve regurgitation

43
Q

What would happen to the preload and afterload in the HFpEF (diastolic)

A

Increased after load - cardiac tamponade, restrictive pericarditis
Decreased preload - aortic stenosis, coartication of the aorta
So would have the decrease in the stroke volume and the EDV (as less in)

44
Q

Why would there be pulmonary edema in left sided heart failure

A

The increased venous pulmonary pressure as blood would pool in the left atrium
Backflow would lead to the pulmonary edema

45
Q

What is Cor Pulmonale and when is it likely to happen

A

Respiratory disease
Most likely when have the left sided heart failure (would have the pulmonary oedema and the fluid would build in the lungs)

46
Q

What is the normal EF

A

55-70%

47
Q

What is Cor pulmonale

A

Blocked right bundle branch
This would normally come from left sided heart failure that would go to the right

48
Q

What other factors can lead to Cor pulmonale

A

If right sided heart failure is caused by a respiratory disease

49
Q

What does the stroke volume of the heart normally respond to

A

The preload of the heart
So when would have the effected stroke volume, would normally be an issue with the preload

50
Q

What are the symptoms of the ACE inhibitors

A

Dry cough (excess bradykinin)