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Medicine 1 > Anatomy - Heart Failure > Flashcards

Anatomy - Heart Failure Flashcards

1
Q

What are the origins of the first and second heart sounds?

A

First = AV valves closing = low pitched ‘lub’

Second = closing of aortic/pulmonary valve = high pitched ‘dup’

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2
Q

What are the properties of the jugular venous pulse?

A
  • Pulsations in internal jugular vein reflect changes in right atrial pressure
  • Visible 2cm above clavicle
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3
Q

What are the third and fourth heart sounds?

A

Third heart sound = vibration of ventricular wall when filling (hard to hear)

Fourth heart sound = ventricular filling during atrial systole (hard to hear)

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4
Q

When do the aortic and mitral valves open and close?

A

Aortic:

  • Opens during systole
  • Closes at start of diastole

Mitral:

  • Opens during diastole
  • Closes at start of systole
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5
Q

What are the types of abnormal heart sounds?

A

Murmurs –> excessive noise (high flow or flow in different directions)

Stenosis –> narrowing, creating steep pressure gradient so murmur when valve opens

Leaky valve –> flow can occur in different directions, so murmur when valves should be closed

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6
Q

What drives the intrinsic heart rate?

A

Pacemaker (SA node) and conduction (AV node)

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7
Q

What things influence heart rate?

A

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

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

Hormones – e.g. adrenaline acting on b-adrenoceptors causes an increase in heart rate

Extra/intracellular ions – alterations in membrane potential (e.g. potassium)

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8
Q

What is the ESV and EDV?

A

ESV = end systolic volume = blood remaining in ventricle after ventricular contraction

EDV = end diastolic volume = blood in ventricle before contraction

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9
Q

How do you work out cardiac output?

What are the normal values at rest and during exercise?

A

Cardiace output (litres/min) = stroke volume (litres/beat) X heart rate (b/min)

Rest = 5 L/min

Exercise = 22 L/min

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10
Q

What 3 things determine stroke volume?

A
  • Pre-load –> blood coming back into heart from veins
  • Cardiac contractility –> determined by blood present in heart
  • After-load –> pressure to push blood out of heart
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11
Q

What is stroke volume?

What influences cardiac output?

A

Blood ejected from each ventricle in a single heartbeat = difference between EDV and ESV

Influenced by venous return, alongside filling time and atrial contractility

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12
Q

What to remember about cardiac muscle and stretch?

What does the Frank-starling curve show and look like?

A

Force of contraction of cardiac muscle fibres is proportional to degree of stretch

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13
Q

What factors affect stroke volume and what increases and decreases stroke volume?

A
  • Cardiac contractility
  • Aortic pressure and after-load

Increase:

    • SNS activity
  • Calcium
  • Positive inotropic drugs (digoxin)

Decrease:

    • SNS activity
  • Hypoxia
  • Acidosis
  • Heart failure
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14
Q

What does the graph of velocity against load look like?

A
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15
Q

What is happening at and between each letter?

A
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16
Q

What happens once baroreceptors detect fall in blood pressure?

A
    • Sympathetic outflow from CNS for minute by minute response
  • Kidney determines long-term bp restoration
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17
Q

What are all the functions of the kidney?

A
  • Regulation of pH (H+ and HCO3-)
  • Removing metabolic waste products
  • Production of hormones (e.g. erythropoeitin)
  • Activation of vitamin D
  • Regulation of osmolarity (control of solute concentrations)
  • Regulation of salt concentrations
  • Regulation of extracellular fluid volume
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18
Q

What are the properties of the kidneys?

A
  • Receive about 20% of the cardiac output at rest
  • Shows good autoregulation i.e. the blood flow stays relatively constant over a wide range of arterial pressures.
  • About 20% of the fluid arriving in the kidney is filtered into the renal tubule but then 99% of this is reclaimed.
  • This process is intimately linked with sodium reabsorption and is under hormonal control.
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19
Q

What are the functions of the granular and lacula densa and what is the importance of them?

A

Granular = regulate bp and volume by detecting stretch

Macula densa = monitor salt concentrations

These factors influence first part of renin-angiotensin system

Low volume = renin release

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20
Q

What 3 things trigger renin release?

A
  • Decreased renal perfusion pressure (detected by granular cells)
  • Decrease NaCl concentration (detected at the macula densa)
  • Increased sympathetic nerve activity (via activation of beta-1 adrenoceptors)
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21
Q

What is the cascade of reactions that happen once renin is released?

A
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22
Q

What are the 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 (anti-diuretic hormone) from posterior pituitary
  • Trophic effects in heart and blood vessels (? Sustain hypertension, cardiac hypertrophy)
  • Increase in oxidative stress (? Endothelial cell damage)
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23
Q

What are the actions of vasopressin in CV system?

A
  • Direct vasoconstriction
  • Increases number of aquaporin-2 channels in the distal tubules/collecting duct of the kidney – increases fluid retention (produces a more concentrated urine)
  • Hence vasopressin is also known as Anti-Diuretic Hormone (ADH)
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24
Q

What are the actions of aldosterone?

A
  • Increase expression of sodium channels
  • Activates the sodium potassium pump
  • This results in retention of sodium (and water) in the body
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25
Q

What are pathological causes of decreased blood flow?

A
  • Decrease in cardiac output – heart failure
  • Renal stenosis or aortic stenosis (narrowing of the renal artery or aorta), produces renin-induced hypertension.
  • Hypotensive shock –> a condition in which blood pressure is below the autoregulatory range for maintenance of cerebral and renal perfusion, such that consciousness is lost and vital organ perfusion critically impaired
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26
Q

What are general causes of decreased blood pressure?

A
  • BP = Cardiac Output x Total Peripheral Resistance
  • Therefore, low BP can be due to low CO and/or peripheral vasodilatation
  • Haemorrhagic shock – blood loss, low CO
  • Cardiogenic shock – myocardial infarction causing loss of myocardial power
  • Endotoxic shock – bacterial toxins cause marked peripheral vasodilatation
  • Anaphylactic shock – allergic reaction, histamine release causes vasodilatation and increased capillary permeability
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27
Q

What are the types of heart failure?

A
  • Chronic heart failure
  • Congestive heart failure
  • Congestive cardiac failure
  • May be valve or muscle failure
  • Chronic or acute
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28
Q

What are the 3 main causes of heart failure?

A
  • Ischaemic heart disease
  • Hypertension
  • Cardiomyopathies
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29
Q

What things precipitate heart failure?

A
  • Pregnancy
  • Anaemia
  • Hyper and hypothyroidism
  • Fluid retaining drugs (i.e. NSAIDs and glucocorticoids)
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30
Q

What happens during neurohormonal adaptation?

A
  • Compensation for circulatory failure
  • Sympathetic nervous system activation (worsen)
  • Renin-angiotensin-aldosterone system activation (worsen)
  • Antidiuretic hormone (worsen)
  • Atrial natriuretic peptide –> + sodium excretion, + fluid excretion (better)
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31
Q

What does neurohormonal adaptation lead to?

A
  • Increased afterload
  • Increased circulating volume (increased preload & afterload)
  • Increased resistance will lead to impaired renal function, more salt/water retention with further activation of RAAS
  • A vicious cycle develops which further impairs the pump activity of the heart.
  • Myocyte dysfunction
  • Makes heart failure worse
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32
Q

What are the properties of left-sided heart failure?

A
  • Secondary to hypertension usually
  • Impairment of left ventricle = pulmonary oedema
  • Dyspnoea
  • Cough
  • Orthopnoea
  • Inspiratory crepitations
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33
Q

What are the properties of right-sided heart failure?

A
  • Failure of right ventricle output
  • Due to lung disease, pulmonary valvular stenosis
    • venous pressure
    • jugular venous pressure
  • Enlarged liver
  • Peripheral oedema (ankles)
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34
Q

What is biventricular heart failure?

A
  • Both chambers affected by disease
  • Left ventricular failure = pulmonary congestion = right ventricular failure
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35
Q

What are the symptoms of heart failure?

A
  • Fatigue, listless
  • Poor exercise tolerance (determines grade)
  • Cold peripheries
  • Low blood pressure
  • Reduced urine flow
  • Weight loss
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36
Q

How do you diagnose heart failure?

A
  • Symptoms
  • Examination
  • Echocardiogram –> ejection fraction < 45%
  • B-type natriuretic peptide levels (BNP elevated = heart failure indication)
  • Chest X-ray –> enlarged heart, pulmonary oedema
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37
Q

How is atrial fibrillation relevant to heart failure?

A
  • Complication of heart failure
  • LV failure = + left atrial pressure = distention = AF
  • Stasis of blood –> thrombus formation
  • Need prophylaxis, warfarin or DOAC
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38
Q

What is the prognosis of heart failure?

A
  • Dependent on stage (i – iV)
  • Poor
  • Median survival rate = 5 years
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39
Q

What are the goals of the treatment of heart failure?

A
  • Identify / treat any cause (valvular disease; IHD)
  • Reduce cardiac workload
  • Increase cardiac output
  • Counteract maladaptation
  • Relieve symptoms
  • Prolong quality life – reduce hospitalization
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40
Q

What is backward and forward heart failure?

A

Backward = fluid congestion

Forward = less blood flow to tissues

41
Q

What are the 4 classes of heart failure?

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)

42
Q

What are the 3 types of left ventricular heart failure?

A
  • Insufficient pump power
    • Problem with the heart muscle
  • Obstruction of the blood flow outwards
    • Valve, aorta, arteries, arterioles
  • Obstruction to inflow
    • Pericardial effusion, constrictive pericarditis
43
Q

What are the causes of left ventricular heart failure?

A
  • Acute ventricular dysrhythmias (VF)
  • Myocardial infarction and ischaemic heart disease
  • Longstanding hypertension
  • Valve disease (aortic and mitral)
  • Cardiomyopathies and drugs
  • Congenital heart disease
44
Q

What is high output cardiac failure and what are its consequences?

A
  • Normal heart muscle, output can’t perfuse tissue adequately
  • Arteriovenous fistula – blood bypasses tissue
  • Septic shock – vasodilatation
  • Anaemia- oxygen requirements not met
  • Thyrotoxicosis – increased tissue demand
45
Q

What do the dark and pale areas on liver represent?

A

Dark = centrilobular congestion

Pale = periportal fatty change

46
Q

What does pulmonary oedema look like on histology slide?

A
47
Q

What are the steps of left ventricular heart failure?

A
48
Q

How do ACE inhibitors work?

A
  • e.g. ramipril
  • Reduce arterial and venous vasoconstriction (reduce after- and pre-load)
  • Reduce salt/water retention, hence reduce circulating volume
  • Inhibits RAAS, prevents cardiac remodelling
  • Also used in hypertension
49
Q

What to remember when prescribing ACE inhibitors>

A
  • Low dose then titrate up
  • Monitor creatinine / eGFR and K+ before and during treatment
  • May cause severe hypotension
  • Cause renal function deterioration with pre-existing renal disease
  • Avoid in renovascular disease
  • Dry cough in 10% of users à ACE inhibitors breakdown bradykinin, causing cough
50
Q

What happens when there’s a blockage in a renal artery?

A

+ renin release

Maintenance of blood pressure

51
Q

What are the properties of AT1 receptor antagonists?

A
  • e.g. losartan, candesartan
  • Angiotensin II acts at AT1 receptors
  • AT1 receptor antagonists block the action of AII
  • Far less likely give rise to a cough
  • An alternative to ACE Inhibitors
52
Q

What are the properties of beta blockers?

A
  • Used to be contraindicated in CHF
  • Now first line with ACEi’s
  • Beta1 selective
  • Metoprolol, bisoprolol, carvedilol (also an a-blocker/antioxidant)
  • Now known to reduce disease progression, symptoms and mortality
  • Start with very small dose, with gradual build-up
53
Q

When and how are beta blockers used in heart failure?

A
  • Of use in stable, moderate failure –> cautious with COPD
  • Reduce sympathetic stimulation, heart rate and O2 consumption
  • Antiarrhythmic: will control rate in atrial fibrillation
  • Oppose the neurohormonal activation which leads to myocyte dysfunction
  • Especially useful in failure associated with ischaemia
  • Start with a low dose
  • Symptoms may get worse at first
54
Q

What are the properties of diuretics in heart failure?

A
  • Loop diuretics (act on loop of Henley) such as furosemide (and to a lesser extent thiazides)
  • Reduce circulating volume
  • Reduces preload on the heart
  • Relieve pulmonary and peripheral oedema
  • Thiazides (esp) / loop diuretics may cause hypokalaemia (drop in potassium levels)
55
Q

What are the proeprties of digoxin?

A
  • Sometimes used in heart failure
  • Favourable in patients with AF
  • +ve inotrope (increase in contractility) by inhibiting Na+/K+ ATPase, Na+ accumulates in myocytes, exchanged with Ca2+ leading to increased contractility
56
Q

How does digoxin work and when is it used?

A
  • Impairs AV conduction and increases vagal activity (via CNS).
  • The heart block and bradycardia are beneficial in heart failure with atrial fibrillation
    • Slowing the heart rate improves cardiac filling
  • Digoxin reserved for failure with AF or when ACEI + diuretic fails
  • Titrate dose to ventricular rate>60 beats/min
57
Q

What things must you monitor on patient taking digoxin?

A
  • Renal function - elderly esp. may have eGRF impairment
  • Potassium levels
  • Hypokalaemia
58
Q

What are the negatives of digoxin?

A
  • Toxicity
  • Narrow therapeutic window
  • Can lead to anorexia, nausea, visual disturbances, diarrhoea
  • Monitor pulse (> 60bpm) in AF
59
Q

How do you know when to prescribe digoxin and when are diuretics prescribed?

A

Digoxin = prescribed as last resort

Diuretics = always prescribed in heart failure

60
Q

What is arteriosclerosis, arteriolosclerosis, atheroma and atherosclerosis?

A

ARTERIOSCLEROSIS = thickening and hardening of the wall of an artery

ARTERIOLOSCLEROSIS = thickening and hardening of the wall of an arteriole

ATHEROMA = an important disease of large and medium arteries.

ATHEROSCLEROSIS = arteriosclerosis due to atheroma

61
Q

What is hypertensive arteriosclerosis?

A
  • Hypertrophy of media
  • Fibroelastic thickening of intima
  • Elastic lamina reduplication
62
Q

Where does hypertension cause arteriolosclerosis to occur?

A

In arterioles and small arteries

63
Q

What is hypertensive arteriolosclerosis?

A

Replacement of wall structures by amorphous hyaline material

64
Q

What are the properties of atheroma?

A
  • 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
65
Q

What are the stages of atheroma formation?

A
  • Fatty streak
  • Lipid plaque
  • Fibro-lipid plaque
  • Complicated atheroma
66
Q

What happens during the first stage of atheroma formation?

A

Blood lipids enter intima at site of endothelial damage

67
Q

What happens during the second stage of atheroma formation?

A

Phagocytosis of lipids by macrophages in intima, forming raised fatty streaks

68
Q

What happens during the third stage of atheroma formation?

A
  • Lipid released by macrophages (lipid plaque)
  • Macrophages secrete cytokines, stimulating myofibroblasts to secrete collagen
  • Early elastic lamina and media damage
69
Q

What happens during the fourth stage of atheroma formation?

A
  • Collagen covers plaque surface (fibro-lipid plaque)
  • Thinning of media, replacement of muscle fibres by collagen
  • Calcification of lipid intima
  • Ulceration of surface fibro-lipid plaque
  • Weakness and inelasticity from media thinning (complicated atheroma)
70
Q

What does fibro-lipid plaque look like under microscope?

A
71
Q

What does fibro-fatty plaque look like under a microscope?

A
72
Q

What are some of the complications of atheroma?

A
73
Q

What are the potential complications of atheroma in coronary, leg, mesenteric and cerebral and vertebral arteries?

A

Coronary arteries = angina

Leg arteries = intermittent claudication

Mesenteric arteries = ischaemic colitis

Cerebral and vertebral arteries = cerebral ischaemic events

74
Q

How does aneurysm form from media damage?

A
  • Enlarging intimal atheroma plaque leads to atrophy of media
  • Muscle and elastic fibres in media replaced by collagen
  • Collagen strong but neither contractile nor capable of elastic recoil
  • With each systolic pulse, wall of artery stretches and thins, PARTICULARLY WHEN BLOOD PRESSURE IS ELEVATED
  • Most common in abdominal aorta
75
Q

What is an aneurysm and the types?

A
  • Aneurysm = abnormal permanent focal dilation of artery
  • Most common = secondary to atherosclerosis in abdominal aorta
  • Other types:
    • Syphilitic
    • developmental(“berry”) in cerebral vessels
    • “dissecting aneurysms” of thoracic aorta
    • mycotic aneurysms
76
Q

What are the properties of mycotic aneurysms?

A
  • Mostly caused by endocarditis (infection of heart valve)
  • Bacterial septicaemia
  • Infection of arterial wall
  • Weakening and dilatation = aneurysm
  • Risk of bleed
77
Q

What do the 3 types of aneurysm look like?

A
78
Q

What is a thrombus?

A

Solid mass of blood constituents aggregated together in flowing blood in lumen of blood vessel

Main constituents = platelets and fibrin

79
Q

What is the function of fibrinolysis in thrombosis?

What happens when fibrinolysis isn’t functioning?

A

Limits process of thrombosis

Thrombosis becomes a pathological process

80
Q

What happens during the first stage of thrombosis?

A
  • Vessel wall is breached
  • Circulating platelets aggregate to plug gap
  • Platelets release factors which trigger coagulation cascade
81
Q

What happens during the second stage of thrombosis?

A
  • Coagulation cascade converts fibrinogen to large molecules of insoluble fibrin
  • Long fibrin molecules bind together platelets and entrapped red & white cells
82
Q

What is fibrinolysis and what is the function of plasmin?

A

Dissolving of thrombus due to breakdown of fibrin

Is active enzyme which fragments fibrin, forming FDPs

83
Q

What are the properties of plasmin?

A
  • Plasma contains the inactive proenzyme plasminogen, which becomes plasmi
  • Plasminogen is converted to plasmin by plasminogen activators, particularly tissue plasminogen activator (t-PA) secreted by endothelial cells
  • When fibrin is formed, plasminogen and t-PA bind to it. The t-PA converts nearby plasminogen to plasmin, which begins to degrade the fibrin
  • This controls the size of the thrombus
84
Q

What is pathological thrombosis?

A

Pathological thrombosis occurs when the thrombus enlarges beyond vessel healing requirements, and continues to grow

85
Q

What happens when fibrinolysis fails?

A

Thrombus grows by accretion of layer upon layer, forming mass in vessel lumen

86
Q

What are D-Dimers?

A

Breakdown product of fibrin mesh, stabilised by factor XIII

+ blood levels in thrombosis

87
Q

What is Virchow’s Triad?

A
  • Damage to vessel wall
    • (esp. endothelium)
  • Stasis
    • (slow or turbulent blood flow)
  • Change in character of blood
    • (esp. increased platelets, increased red cell numbers, increased viscosity)
88
Q

Where does thrombosis occur and properties?

A
  • ARTERIES
    • main predisposing factors are VESSEL WALL DAMAGE
  • VEINS
    • STASIS most important
  • HEART
    • Ventricles - chamber wall damage most important
    • Atrium - stasis most important
    • Heart valves - valve surface damage most important
89
Q

What are the potential outcomes of thrombosis?

A
  • It may be lysed by intrinsic fibrinolysis - RARE
  • It may completely block the lumen (occlusion)
  • It may undergo organisation & recanalisation
  • It may extend locally (propagation)
  • It may fragment or detach completely and travel elsewhere in the circulation. This is called THROMBO-EMBOLISM
90
Q

What is infarction and congestion?

A

Infarction = blood supply cut off

Congestion = venous blockage by thrombus, preventing drainage so blood pools (+ haemorrhaging infarction)

91
Q

What happens in an organised thrombus?

A
  • New vessels grow into the thrombus
  • Vascular granulation tissue develops
  • Fibroblasts invade & deposit collagen
  • Fibrovascular granulation tissue develops
  • Recanalisation occurs if vessels link up
92
Q

What is an embolism and what are the most important matters to embolise?

A

Transfer of abnormal material by bloodstream with eventual impaction of material in vessel distal to site of origin

Cancer (metastasis) and thrombus cells

93
Q

What is a thromboembolism?

A

Where thrombus breaks off and occludes a distal vessel

94
Q

Where does thrombus in artery of left side of heart embolise to and what are the potential consequences?

A

Systemic arterial system

  • of brain arteries -> STROKE
  • of lower limb arteries -> GANGRENE OF LEGS
  • of mesenteric arteries -> BOWEL NECROSIS
  • of renal arteries -> KIDNEY INFARCT
  • of splenic artery -> SPLENIC INFARCT
95
Q

What is the outcome of a thrombus in a systemic vein?

A

Pulmonary embolus

Small embolus = small peripheral lung infarct

Large embolus = sudden death

96
Q

How does venous thromboembolism risk assessment work?

A
  • Active cancer or cancer treatment
  • Age > 60
  • Dehydration
  • Known thrombophilias
  • Obesity (BMI >30 kg/m2)
  • One or more significant medical comorbidities
    • heart disease​
    • metabolic, endocrine or respiratory pathologies
    • acute infectious diseases
    • inflammatory conditions
97
Q

What are other factors included in VTE risk assessment?

A
  • Personal history or first-degree relative with a history of VTE
  • Use of hormone replacement therapy
  • Use of oestrogen-containing contraceptive therapy
  • Varicose veins with phlebitis
  • Pregnancy or < 6 weeks post partum (see NICE guidance for specific risk factors)
98
Q

What are other important materials to embolise?

A
  • Fat and marrow
  • Air
  • Nitrogen
  • Amniotic fluid

Medicine 1 (28 decks)

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