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Medicine 2 > RCM Week 5 (heart Failure) > Flashcards

RCM Week 5 (heart Failure) Flashcards

1
Q

3 basic components of the circulatory system

A

Heart- pump that provides the pressure gradient needed for blood to flow

Blood vessels - passageways through which blood is distributed to different parts of the body

Blood- transport medium for delivery of gases, nutrients and hormones

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2
Q

Why is the pressure generated in the left side of the heart 4x the RHS of the heart

A

Because the lungs are a low resistance system so it is relatively easy to push blood into the lungs

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3
Q

What does systole and diastole mean

A 
Systole = contraction 
Diastole = relaxation of ventricles
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4
Q

How does fluid flow in the heart

A

Fluid flows from region of high to low pressure
Direction of flow is determined by unidirectional valves
Valves open / close due to pressure differences across them

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5
Q

Describe the steps of the heart alternately contracting to empty and relaxing to fill

A

1) atrial systole : rise in atrial pressure (A-V valves open) and atria empty blood into ventricles
2) isovolumetric ventricular contraction: increase in ventricular pressure closes A-V valves. Ventricular pressure < aortic pressure so aortic valves shut. Pressure generated but no blood ejected
3) ventricular ejection: ventricular pressure > aortic pressure so aortic valves open and blood is ejected
4) isovolumic ventricular relaxation: ventricular pressure < aortic pressure so aortic valve closes. Ventricular pressure still > atrial pressure so A-V valve still shut. Pressure falls but no filling
5) ventricular filling : ventricular pressure< atrial pressure so A-V valve opens and blood enters ventricle

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6
Q

What is the jugular venous pulse

A

Pulsation in the internal jugular vein reflect right atrial pressure changes (no valves)

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7
Q

What are heart sounds

A

Closing / opening of valves briefly causes blood to stop / start. Sudden changes in blood movement heard as vibrations are heart sounds

1st heart sound - low pitched ‘lub’ associated with A -V valve closure
2nd heart sound- brief high pitched ‘dup’- associated with aortic ‘ pulmonary valve closure
3rd heart sound - vibration of ventricular wall when filling
4th heart sound - associated with ventricular filling during atrial systole

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8
Q

When do aortic and mitral valve open / close

A

Aortic valve opens during systole and closes at start of diastole

Mitral valve opens during diastole and closes at start of systole

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9
Q

2 causes of abnormal heart sounds (murmurs)

A

Abnormal sounds can be due to high flow or flow in different directions

Stenosis : narrowing of valve which creates steep pressure gradient - high flow across the valve (murmur when valve opens)

Leaky / incompetent valve: which means that flow can occur in different directions (murmur when valve should be closed)

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10
Q

Equation for cardiac output

A

Cardiac output (L/min) = stroke volume (L/beat) x heart rate (beat / min)

At rest: 5L/min = 70ml x 70 beats / min
During exercise: 22L/min = 110ml x 200 beats / min

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11
Q

Factors that affect heart rate

A

Sympathetic nervous system: activation of B-adrenoceptors causes an increase in heart rate

Parasympathetic nervous system : activation of muscarinic receptors causes decrease in heart rate

Hormones: adrenaline acting on B adrenoceptors causes an increase in heart rate

Extra/ intracellular ions : alterations in membrane potential (eg potassium)

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12
Q

What is stroke volume

A

The volume of blood ejected by each ventricle in a single heart beat

Represents the difference between end diastolic volume and end systolic volume

Determined by the interaction of :

  • pre load
  • cardiac contractility
  • after-load
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13
Q

Factors that affect stroke volume

A

EDV dependent on end diastolic pressure (pre load)
- Influenced primarily by venous return (venous tone, blood volume, posture, intrathoracic pressure)

  • also influenced by filling time : increased heart rate reduces filling time and hence can limit EDV
  • atrial contractility
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14
Q

What is cardiac contractility

A

The amount of force generated by cardiac muscle fibres can vary independently from the degree of stretch ie ventricular contractility can vary at any given end - diastolic volume depending upon other influences eg sympathetic nerve activation

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15
Q

What increases /. Decreases stroke volume

A

Increased by SNS activity calcium
Positive ionotropic drugs eg digoxin

Decreased by SNS activity hypoxia
Acidosis
Heart failure

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16
Q

How does aortic pressure affect stroke volume

A

Stroke volume also depends upon how large a force (aortic pressure) it has to work against (afterload)
An increase in aortic pressure (caused by increased peripheral resistance, altered aortic stiffness etc) will increase afterload which will reduce stroke volume at a constant pre load

Velocity of contraction at a fixed length is greatest at low loads and slows as afterload increases

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17
Q

What are baroreceptors

A

When blood pressure falls there is an immediate activation of sensors located in the major blood vessels (carotid arteries and aorta) and the heart (baroreceptors)
They increase sympathetic outflow from the CNS to produce immediate mechanisms to raise blood pressure

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18
Q

Functions of the kidneys

A
  • regulations of pH (H+ and HCO3-)
  • Removing metabolic waste products
  • production of hormones (eg erythropoietin- stimulated RBC production)
  • activation of Vit D
  • regulation of osmolarity (control of solute concentration)
  • regulation of salt concentrations
  • regulation of extracellular fluid volume
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19
Q

How long does long term restoration of blood pressure take

A

24-48 hours (determined by the kidney)

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20
Q

How much of the cardiac output does the kidney receive

A

20%

This blood shows good autoregulation ie the blood flow stays relatively constant over a wide range of arterial pressures

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21
Q

What happens to the fluid arriving in the kidney

A

20% of it is filtered into the renal tubule but then 99% of it is reclaimed

This process is intimately linked with sodium reabsorption and is under hormonal control

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22
Q

What does the macula densa do

A

Samples what’s contained in the kidney tubule when it comes back up to the glomerulus

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23
Q

What is the function of the juxtaglomerular apparatus

A
  • regulates salt and fluid balance

- contains special cells: granular cells and macular densa

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24
Q

3 stimuli for renin release

A

1) decreased renal perfusion pressure (detected by granular cells)
2) decrease NaCl concentration (detected at the macula densa)
3) increased sympathetic nerve activity (via activation of B1-adrenoceptros

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25
Q

Actions of angiotensin II

A
  • potent vasoconstrictor - increases peripheral resistance and hence blood pressure
  • enhances sympathetic nerve function
  • increases the release of aldosterone (adrenal gland)
  • promotes thirst
  • Release vasopressin from posterior pituitary (causes vasoconstriction)
  • trophic effects in heart and blood vessels (sustains hypertension and cardiac hypertrophy)
  • increase in oxidative stress (endothelial cell damage)
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26
Q

What is the action of vasopressin in the CV system

A
  • direct vasoconstriction
  • increases number of aquaporin- 2 channels in the distal tubules / collecting duct of the kidney - increases fluid rentention (more conc urine)
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27
Q

Describe the action of aldosterone

A

Increases expression of sodium channels
Activates the sodium potassium pump
- this results in retention of sodium (and water) in the body

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28
Q

Why is decrease in blood flow to the kidney an important stimulus for renin release

A

It can occur physiologically with normal variations in fluid intake but can also result from pathological causes :

  • decrease in cardiac output : heart failure
  • renal stenosis or aortic stenosis (narrowing of the renal artery or aorta), produces renin- induced hypertension
  • hypotensive shock
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29
Q

What is the difference between hypotension and hypotensive shock

A

Hypotension = low BP

Hypotensive shock = a condition in which BP is below the autoregulatory range for maintenance of cerebral and renal perfusion, such that consciousness is lost and vital organ perfusion is critically impaired

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30
Q

How is BP calculated

A

Cardiac output x total peripheral resistance

So low BP can be due to low CO and / or peripheral vasodilation

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31
Q

Examples of low BP

A

1) haemorrhagic shock- blood loss, low CO
2) cardiogenic shock- MI causing loss of myocardial power
3) endotoxic shock - bacterial toxins cause marked peripheral vasodilation
4) anaphylactic shock- allergic reaction, histamine release causes vasodilation and increased capillary permeability

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32
Q

Define heart failure

A

Failure of the heart as a pump to meet the circulatory needs

33
Q

Causes of heart failure

A 
May be due to failure of the heart muscles or heart valves (may be chronic or acute - post MI) 
Often secondary: 
- IHD (most common) 
- hypertension 
- cardiomyopathies (alcohol, viral)
34
Q

What medical conditions can precipitate heart failure

A 
Pregnancy (expansion of circulating volume by about 40%) 
Anaemia 
Hyper and hypothyroidism 
Fluid retaining drugs: 
- glucocorticoids 
- NSAIDs
35
Q

How does hypertension cause cardiac failure

A

For the increase in afterload get hypertrophy

- cardiac enlargement thus increases the work of the heart and lessens the ejection fraction

36
Q

What is the neurohormonal adaptation of heart failure

A

To compensate for circulatory failure get activation of:

  • sympathetic nervous system
  • renin-angiotensin- aldosterone system
  • antidiuretic hormone (ADH)
  • atrial natriuretic peptide (ANP)
37
Q

What is left sided heart failure

A

Often 2 degrees to hypertension

  • LV impaired (poor output) leads to :
  • increase in left atrial / pulmonary venous pressure with pulmonary oedema (fluid on the lungs)
38
Q

What is right sided heart failure

A

RV output fails
Often due to:
- lung disease
- pulmonary valvular stenosis

39
Q

What is biventricular failure

A

Both chambers
- disease eg IHD has affected both ventricles
Or
- LVF, leads to pulmonary congestion which may lead to RVF

40
Q

Heart failure signs and symptoms

A
  • fatigue
  • poor exercise tolerance
  • cold peripheries
  • low BP
  • reduced urine flow
  • weight loss
41
Q

Signs and symptoms of LV failure

A
  • pulmonary oedema
  • dyspnoea (breathlessness- sensation of drowning, cardiac asthma)
  • cough
  • orthopnoea - breathless on lying which is relieved by sitting up
  • inspiratory crepitations
42
Q

Signs and symptoms of RV failure

A
  • raised venous pressure
  • increased JVP
  • enlarged liver
  • oedema - ankles ; if lying down, rises to thighs / abdomen
43
Q

What are the risks of ACEIs

A
  • May cause severe hypotension - withdraw diuretic therapy for a few days before; give at night
  • cause deterioration of renal function in pre-existing renal disease
  • avoid in renovascular disease
  • cough
44
Q

How does digoxin affect AF

A

Impairs AV conduction and increases vagaries activity (via CNS)
- the heart block and bradycardia is beneficial in heart failure with atrial fibrillation (slowing the heart rate improves cardiac filling)
Digoxin is reserved for failure with AF or when ACEI + diuretic fails
- titration dose to ventricular rate >60 beats / min

45
Q

What is the difference between stable and unstable angina

A

Stable: atherosclerotic disease, which limits the hearts ability to respond to increased demand
- symptoms on exertion but are relieved by rest

Unstable: plaque rupture and the formation of a non-occlusive thromboembolism or vasospasm

46
Q

Outline the uses of B blockers in IHD

A
  • first choice drugs for prevention (atenolol)
  • block B-adrenoceptors
  • negative ionotropic and chronotropic effects reducing cardiac work and preventing symptoms
  • coronary flow only occurs during diastole then by slowing the heart the diastolic period will be increased, as will the time for coronary blood flow
  • anti-arrhythmic effects and reduce the risk of myocardial infarction
47
Q

What are the effects of calcium channel blockers (dilitazem, verapamil, dihydropyridines, amlodipine)

A
  • vasodilation and improve coronary blood flow, so preventing symptoms
  • rate limiting agents eg verapamil also have myocardial depressant and bradycardic actions so reducing cardiac work
  • verapamil also exerts class IV anti-arrhythmic activity
48
Q

What effect do statins have

A

They inhibit cholesterol synthesis which leads to the up regulation of hepatic LDL receptors
- increased uptake of cholesterol from plasma by liver (where it can be metabolised and excreted)

49
Q

Define arteriosclerosis

A

Thickening and hardening of the wall of an artery

50
Q

Define arteriolosclerosis

A

Thickening and hardening of the wall of an arteriole

51
Q

Define atheroma

A

An important disease of large and medium arteries

Only occurs in high pressure systems ie systemic arterial system not venous system

Initially a disease of tunica intima but later affects tunica media

Is ubiquitous but very mild in young people, worsening with age

52
Q

Define atherosclerosis

A

Arteriosclerosis due to atheroma

53
Q

Consequences of hypertensive vascular changes

A
  • reduction of vessel lumen > reduced flow > ischaemia in supplied tissue

Increased rigidity of vessel wall > loss of elasticity and contractility > unresponsive to normal vessel control agents eg vasodilators

54
Q

4 stages of atheroma development

A

1) fatty streak
2) lipid plaque
3) fibrolipid plaque
4) complicated atheroma

55
Q

Complications of atheroma

A

1) expansion of intima - reduction of size of lumen - reduced blood flow and hence oxygenation of tissue
2) ulceration of atheromatous intima - predisposition to thrombus formation - vessel occlusion
3) plaque fissure formation and haemorrhage
4) replacement of muscle and elastic fibres in media - loss of elasticity - thinning and stretching (aneurysm)

56
Q

3 types of aneurysms

A

Saccular
Fusiform
Dissecting

57
Q

What is a mycotic aneurysm

A

(Uncommon) mostly caused by endocarditis (infection of heart valve)

  • bacterial septicaemia
  • infection of arterial wall
  • weakening and dilation = aneurysm
  • risk of bleed
58
Q

What is the difference between acute and chronic heart failure

A

Acute heart failure : events take place rapidly and consequences is forward failure (shock)

Chronic: compensatory mechanisms may be brought into play and backward failure dominates (congestion)

59
Q

Describe the process of left ventricular failure

A

1) Raised end diastolic pressure
2) raised left atrial pressure
3) raised pulmonary capillary pressure
4) increased diffusion for gas exchange or increased interstitial fluid formation (pulmonary oedema)
5) breathlessness

60
Q

What is the classification of heart failure (New York heart association)

A

Class I- no limitation of physical activity
Class II- slight limitation of activity (breathlessness / fatigue with moderate exercise)
Class III- marked limitation of activity (breathlessness with minimal exercise)
Class IV- severe limitation of activity (symptoms at rest)

61
Q

What problems does LVF cause

A

Insufficient pump power- problem with the heart muscle
Obstruction of the blood flow outwards - valve, aorta, arteries, arterioles
Obstruction to inflow- pericardial effusion, constructive pericarditis

62
Q

Causes of LVF

A
  • acute ventricular dysrhthmias
  • MI and IHD
  • longstanding hypertension
  • valve disease (aortic and mitral)
  • cardiomyopathies and drugs
  • congenital heart disease
63
Q

Describe the course of RVF

A

1) Raised end diastolic pressure
2) raised right atrial and jugular venous pressures
3) raised central venous pressure
4) liver distension (abdominal discomfort) or increased interstitial fluid formation (peripheral oedema)

64
Q

Causes of RVF

A
  • commonest cause is the failure of the left ventricle
  • acute RVF - massive pulmonary thromboembolism
  • chronic RVF due to chronic lung disease and pulmonary hypertension
  • valve disease (pulmonary / tricuspid) is rare
65
Q

Define hypertension

A

High BP aka hypertension is usually defined as having a sustained BP of 140/90 mmHg or above

66
Q

What is jugular venous pressure

A

Left ventricle pressure. It typically increases in heart failure

67
Q

What happens in hyperkalemia

A

Caused by abnormalities in potassium levels that leads to arrhythmias

Cramps, twitching, nausea
Precipitation of heart rhythm disturbances

68
Q

What are the effects of aldosterone on the heart in heart failure

A

Aldosterone causes thickening and increasing impaired relaxation and over time reduces contractility

69
Q

What can cause a patient to feel dizzy

A

Postural hypotension (associated with furosemide)

Middle ear infection

AF - to fast a heart rate meaning there is insufficient time for filling. Cardiac output falls and this reduces cerebral blood flow

Hypoglycaemia

70
Q

What is pre load

A

End diastolic volume dependent upon end diastolic pressure

Pre load influenced primarily by venous return

71
Q

What is afterload

A 
The output (stroke volume) of the heart also depends on how large a force (aortic pressure) it has to work against (afterload) 
An increas in aortic pressure (caused by increased peripheral resistance, altered aortic stiffness etc) will increase afterload which will reduce stroke volume at a constant preload

Velocity of contraction at a fixed length is greatest at low (after) loads and slows as afterload increases

72
Q

What is thrombosis

A

The process leading to the formation of a thrombus

Thrombus is a solid mass composed of blood constituents which have aggregated together in flowing blood in the lumen of a blood vessel. The main constituents are platelets and fibrin

Thrombosis is a normal mechanism to prevent bleeding when a vessel wall is breached - the process is limited by fibrinolysis
Thrombosis becomes a pathological process when it is not controlled fibrinolysis

73
Q

What are the stages of normal thrombosis

A

1) vessel wall is breached, circulating platelet aggregate to plug gap, platelets release factors which trigger coagulation cascade
2) coagulation cascade converts fibrinogen to large molecules of insoluble fibrin, long fibrin molecules bind together platelets and entrapped red and white cells

74
Q

Define embolism

A

The transference of abnormal material by the blood stream with eventual impact ion of the material in a vessel distal to its site of origin

The most important materials so embolism are thrombus and cancer cells (metastasis)

75
Q

How does an atheroma develop

A
  1. Blood lipids enter intima through damaged endothelium
  2. Lipids are phagocytosed by macrophages
  3. Some lipid is released by macrophages. Macrophages secrete cytokines which stimulate myofibroblasts to secrete collagen
  4. Early damage to elastic lamina and media
  5. Collagen covers plaque surface, media thins with replacement of muscle fibres by collagen
  6. Lipids in intima become calcified, surface of fibro-lipid plaque ulcerates, thinning of media leads to weakness and inelasticity
76
Q

Define heart failure

A

A condition caused by impairment of the hearts function as a pump

It is clinically manifested by 2 main problems:

  • fluid congestion (backward failure)
  • inadequate blood flow to tissues (forward failure)
77
Q

Compensatory mechanisms of heart failure

A

Ventricular chamber enlargement: increases amount of blood in ventricle, so ejects more, but at cost of fluid retention
- muscle mass increases - can eject more, but requires more oxygen to larger muscle

Sympathetic stimulation: increase heart rate, contractility, redistribution and retention of fluid

78
Q

What is congested cardiac failure

A

A combination of both left and right ventricular failure

- the commonest cause of CCF is ischaemic heart disease followed by other causes of LVF

79
Q

What is high output cardiac failure

A

Heart muscle essentially normal but output cannot adequately perfume tissue

Arteriovenous fistula: blood bypasses tissue
Septic shock: vasodilation
Anaemia: oxygen requirements not met
Thyrotoxicosis: increased tissue demand

Medicine 2 (16 decks)

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