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Cardiovascular > Pathophysiology - CV disease > Flashcards

Pathophysiology - CV disease Flashcards

1
Q

Define heart failure

A

a complex syndrome initiated by an inability of the heart to maintain a normal CO at normal filling pressures

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2
Q

How can heart failure be classified?

A

Cause
Predominantly under-perfusion or congestion (forward or backward failure)
Left or right side most affected

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3
Q

In what ways can function of the CVS be impaired sufficiently to bring about HF?

A 
Pump failure (systolic failure)
Volume overload
Pressure overload
Arrhythmias
Diastolic failure
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4
Q

How can pump failure lead to HF?

Example?

A

Intrinsic failure of contraction of the heart mm

EXAMPLE = DCM

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5
Q

How can volume overload lead to HF?

Examples?

A

Chronic increase inthe amount of blood that must be pumped by a given cardiac chamber - due to:
blood shunting (VSD, PDA)
regurgitation (mitral insufficiency)
anaemia (chronic)
increased metabolic demands on tissue (hyperthyroidism)

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6
Q

How can pressure overload lead to HF?

Examples?

A

Systemic or pulmonary hypertension or an outflow obstruction such as aortic/pulmonary stenosis results in an increased resistance to emptying of a chamber

EXAMPLES: hypertension (systemic or pulmonary), narrowing of the outflow tract (pulmonic/aortic stenosis)

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7
Q

How can arrhythmias lead to HF?

A

compromised CO because of increased/decreased HR. Tachycardias shorten diastole and impair filling thus reducing the SV and CO. Bradycardia limits CO by limiting HR.

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8
Q

How does diastolic failure lead to HF?

Examples? 3

A

impaired ventricular filling with normal systolic function such as peridcardial tamponade or HCM.

EXAMPLES: HCM, DCM (myocardial fibrosis), pericardial effusion)

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9
Q

What is the final common pathway leading to HF?

A

Initiated by underfilling of the arterial circulation which initiates a cascade of events leading to several nervous and endocrine adaptation sand eventually a chance in the structure and function of the heart.

Generally divided into ANS effects (rapid and short lived) and endocrine/paracrine effects (longer to arise but longer lasting)

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10
Q

What is the commonest cause leading to HF in vet med?

A

Volume overload.

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11
Q

What is commonly associated with myocardial disease in cats?

A

Diastolic failure –> HF

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12
Q

Mitral insufficiency pathophysiology

Prevalence?

A

Where total SV = forward SV + regurgitant SV

If you have a big leak/insufficiency, you may well have an equal forward SV and regurgitant SC putting increased demand on the heart to pump blood.

THIS IS THE MOST COMMON HEART DISEASE IN PETS.

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13
Q

MST in HCM?

A

= hypertrophic cardiomyopathy

Typical MST in dogs and cats is < 1 year.

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14
Q

What does long term adaptation of the CVS result in?

A

ventricular hypertrophy - type of hypertrophy determined by the type of abnormal load

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15
Q

Outline the autonomic changes in HF

A

Shift from PS dominance to S dominance
Reduced arterial filling detected by decreased BP by baroreceptors –> these emit less signals –> increased SNS activity which is mediated by cardiac beta-effects and vascular alpha-effects. Result = increased HR and contractility and TPR in an effort to restore BP.

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16
Q

Which endocrine systems are involved when there is increased circulating volume? 4

A

RAAS
ADH/AVP - acute hypotension
NPs (ANP and BNP) - counter-regulatory to RAAS
(Local regulators of vascular tone - NO, PGs, endothelin - overall less important)

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17
Q

What is a positive luisitrope?

A

Drugs that improves cardiac relaxation

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18
Q

RAAS - advantages - 3

A

Increased circulating fluid volume –> increased preload

Increased CO (starling)

Increased systemic vascular resistance –> improves BP

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19
Q

RAAS - disadvantages

A

Long term stimulation results in excessive fluid retention

Excessive resistance to vascular emptying

Direct and indirect deleterious effects on myocardium (modifies growth in cardiac myocytes and fibroblasts –> remodelling and hypertrophy within the myocardium)

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20
Q

Reasons for renin release

A

Renal underperfusion
Sympathetic stimulation
Decreased chloride delivery to parts of renal tubule

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21
Q

What is ADH normally involved in?

A

Regulating osmolality. Plays less of a role in regulating fluid volume. But in HF, there are increased levels of ADH probably due to a marked drop in BP in late/severe HF.

22
Q

Effects of ADH - 2

A

Increases vascular resistance to protect BP but ultimately deleterious.

Increases fluid retention (without sodium) –> dilutional hyponatraemia (correlation between this and poor survival)

23
Q

What is the main site of manufacture, storage and release of NPs?

A

Myocardium

ANP and BNP - atrial myocardium

In disease states, BNP is manufactured predominanlty in the ventricular myocardium.

Both are released in response to increased cardiac chamber wall stress so increase with increased filling pressures. Used as biomarkers.

24
Q

Effects of NPs?

A

Counteract many hormone systems. Lead of vasorelaxation and increase sodium loss (hence their name). This system is overwhelmed in HF by other vasconstrictive and sodium-retaining mechanisms.

25
Q

How can NPs be used prognostically?

A

Consistent elevations of ANP, proANP, BNP and NTproBNP have been found in canine, feline and human patients with HF.

26
Q

What happens to local flow regulators in HF?

A

Their ‘paracrine’ regulation dysfunctions.

27
Q

Define myocardial hypertrophy

A

Increase in cell size

28
Q

Factors implicated in cardiac hypertrophy - 4

A 
Adrenergic stimulation
Angiotensin 2 
Increased IC calcium
Aldosterone
(i.e. increased volume or pressure)
29
Q

What happens to pressure loaded ventricles?

A

Concentric hypertrophy (increase in wall thickness, decrease in internal diameter, no overall change in external diameter of chamber)

30
Q

What happens to volume loaded ventricles?

A

Eccentric hypertrophy (increased internal diameter of the chamber and an approximately normal wall thickness). Leads to an overall increase in the external diameter of the chamber.

31
Q

Why might ventricular hypertrophy be bad?

A

Bad after the initial adaptation which is good. Since increased myocardial mass –> increases myocardial oxygen demand –> outstrips ability of coronary circulation –> ischaemia and regional hypoxia and fibrosis –> myocardial dysfunction –> cardiac dysfunctiion –> viscious circle with perpetuation of cardiac dysfunction.

32
Q

What is HF characterised by?

A

Short term - altered autonomic tone (increased SNS and decreased PNS)
Medium term - stimulation of endocrine systems
Long term - hypertrophy

Mechanisms initially assist in compensation but ultimately contribute to the deterioration.

33
Q

What is seen when cardiac compensation becomes HF? 3

A

Congestion due to excessive fluid retention.

Increased cardiac work (increased afterload, increased HR and contractility)

Worse myocardial performance (due to pathological hypertrophy)

34
Q

CS - HF

A

Tachycardia (increased SNS tone)
Poor peripheral perfusion (vasoconstriction)
Fluid retention (RAAS and ADH)
LCHF and/or RCHF

35
Q

Signs of LCHF

A

Due to elevated filling pressures in left heart. Retained fluid found in pulmonary circulation

36
Q

Signs of RCHF

A

Diseases result in elevation in filling pressures in right side of heart –> fluid retained in systemic veins

37
Q

Reasons for oedema (excessive ECF) - 4

A
  • Increased vascular hydrostatic pressures (RCHF or venous occlusion)
  • Increased vascular permeability (vasculitis)
  • Decreased plasma oncotic pressures (hypoproteinaemia)
  • Decreased lymphatic drainage (lymphoedema)
38
Q

What are the broad diseases of the vasculature? 5

A
  1. Thrombosis and embolism
  2. Vasculitis
  3. Degenerative vascular disease
  4. Malformations of the vasculature
  5. Hypertension (arterial or venous and systemic or pulomary)
39
Q

Thrombosis risk factors 4

Species?

A

Diseases that result in blood stasis, increased coagulation, decreased fibrinolysis and/or endothelial damage.

Commonly occurs in cats secondary to cardiac disease and in horses secondary to some parasites. Numerous other causes too.

40
Q

Name 2 degenerative vascular diseases

A

Arteriosclerosis (common in dogs) and atherosclerosis (rare in dogs, common in humans).

41
Q

In what circumstances may a arteriovenous fistula develop as an acquired malformation?

A

Secondary to trauma, neoplasia or surgery.

42
Q

Secondary problems of systemic hypertension in elderly cats - 4

A

Ocular
Renal
Cerebrovascular
Cardiac

43
Q

Signs of vascular disease -4

A
  • Underperfusion (vascular obstruction - partial or complete, causes loss of function, ischaemia, necrosis)
  • Increased vascular permeability (oedema or haemorrhage)
  • Abnormal flow
  • Abnormal pressures
44
Q

What is needed for thromboembolism to occur?

A 
One or more of the following present:
Disturbance of flow
Disturbance of endothelial integrity
Disturbance of haemostasis
Disturbance of fibrinolysis
45
Q

Causes of thromboembolism - 6

A 
Cardiac disease
Cushings (hyperadrenocorticism)
Parasitic disease
PLN
Neoplasia
AIHA
46
Q

Define forward failure (HF)

A

Inadequate output at normal pressures

47
Q

Define backward failure (HF)

A

Adequate output at abnormal pressures (backward of CHF)

48
Q

What is inadequate output at abnormal pressures?

A

Forward and backward failure

49
Q

List stimuli for renin release

A

Renal SNS stimulation (beta effect)
Reduced pressure in afferent arteriole
Reduced NaCL in distal tubules (macular densa)

50
Q

What is ACE?

A

Converts Ang 1 (decapeptide) to Ang 2 (octapeptide)

It is a non-specific carboxypeptidase which also breaks down bradykinin.

Cardiovascular (22 decks)

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