Pathophysiology of cardiovascular disease

Question 1

prevalence - cardiac disease

Answer 1

11% in dogs

Less common but still significant in other domestic species

Question 2

heart failure - define

Answer 2

Heart failure is a complex syndrome initiated by an inability of the heart to maintain a normal cardiac output at normal filling pressures

Question 3

forward failure

Answer 3

Can have inadequate output at normal pressures

Question 4

backward or congestive failure

Answer 4

Adequate output at abnormal pressures

Question 5

forward and backward failure

Answer 5

Inadequate output at abnormal pressures

Question 6

pump failure

Answer 6

Failure of systolic function of the myocardium results in inadequate SV and fall in CO
Primary diseases resulting in systolic myocardial
failure – dilated cardiomyopathy, coronary vascular disease

Question 7

volume overload

Answer 7

Diseases which result in the necessity for a cardiac chamber to chronically increase output can result in overwork and eventually failure of the heart
Valvular insufficiencies (mitral, aortic)
Shunting diseases e.g. Ventricular Septal Defect + Patent Ductus Arteriosus
Chronic anaemia

Question 8

pressure overload

Answer 8

Diseases which chronically increase the pressure against which a ventricle has to pump blood can eventually result in failure of the myocardium
Hypertension - Systemic or Pulmonary
Narrowing of the outflow tract - Pulmonic stenosis, aortic stenosis

Question 9

arrythmias

Answer 9

Abnormalities of cardiac rhythm affect both cardiac filling and heart rate and can compromise output
Low HR = decr CO
At very high HR diastole is too short to allow adequate filling therefore SV + CO fall

Question 10

diastolic failure

Answer 10

An inability of the heart to relax normally can compromise filling and result in a fall in CO
Hypertrophic cardiomyopathy
Dilated cardiomyopathy (myocardial fibrosis)
Pericardial effusion

Question 11

increasing blood volume

Answer 11

RAAS
ADH
Renal autoregulation of flow

Question 12

decreasing blood volume

Answer 12

Natriuretic peptides

Renal autoregulation of flow

Question 13

autonomic influence

Answer 13

shift from parasympathetic to sympathetic dominance
decr arterial filling - decr arterial pressure
incr activity of sympathetic nervous system

Question 14

autonomic effects

Answer 14

incr heart rate, contractility, cardiac relaxation + vascular resistance restore blood pressure

Question 15

endocrine systems in heart failure

Answer 15

Renin-Angiotensin-Aldosterone system (RAAS)
Anti-diuretic hormone
Natriuretic peptides
Local regulators of vascular tone - Nitric oxide, prostaglandins, Endothelin

Question 16

Renin-Angiotensin-Aldosterone system (RAAS)

Answer 16

secreted by juxtaglomerular cells in the kidney
sodium + water retention
incr vascular resistance
angiotensin leads to modification in growth in cardiac myocytes + fibroblasts - remodeling + hypertrophy in myocardium

Question 17

renin release stimuli

Answer 17

renal underperfusion
sympathetic stimulation
decr chloride delivery to some parts of the renal tubule

Question 18

RAAS advantages

Answer 18

Increased circulating fluid volume - Increased preload - Increased cardiac output by Starling mechanism
Increased systemic vascular resistance improves blood pressure

Question 19

RAAS disadvantages

Answer 19

Long term stimulation results in excessive fluid retention.
Excessive resistance to ventricular emptying
Direct and indirect deleterious effects on myocardium

Question 20

antidiuretic hormone (ADH)

Answer 20

aka arginine vasopressin (AVP)
May only be relevant in severe heart failure
Incr vascular resistance to protect blood pressure but ultimately deleterious
Incr fluid retention
Retention of free water without sodium results in hyponatraemia

Question 21

natriuretic peptides (NPs)

Answer 21

atrial natriuretic peptide (ANP)
brain natriuretic peptide (BNP)
made, stored + released in myocardium
Counter regulatory hormones released in response to incr ventricular and atrial pressures
Beneficial effects tend to be outweighed by the “bad” endocrine systems in heart failure
vasorelaxation + incr sodium loss
Incr levels associated with heart failure. “Biomarker” of heart failure

Question 22

local regulators of flow

Answer 22

nitric oxide + endothelin

paracrine regulation

Question 23

hypertrophy

Answer 23

Long term alteration in pressure/volume loading of the ventricle causes structural adaptation of the ventricle - Hypertrophy or remodelling
type of load on the ventricle determines the type of hypertrophy that occurs.
Mediated via a number of factors - Adrenergic stimuli, Angiotensin II, Aldosterone, Intracellular calcium
incr o2 demand due to incr myocardial mass

Question 24

eccentric hypertrophy

Answer 24

volume overload
incr in internal diameter of chamber
normal wall thickness
Mitral regurgitation
Shunting disease

Question 25

concentric hypertrophy

Answer 25

pressure overload
normal internal diameter of chamber
increased wall thickness
Hypertension
Aortic stenosis

Question 26

heart failure characteristics

Answer 26

Short term alteration in autonomic tone -Increase sympathetic decreased parasympathetic
Medium term stimulation of endocrine systems
Long term hypertrophy
Mechanisms initially assist in compensation but ultimately contribute to the deterioration of the patient

Question 27

heart failure - clinical signs

Answer 27

Tachycardia (increased sympathetic tone)
Poor peripheral perfusion (vasoconstriction)
Fluid retention (RAAS and ADH)
Left sided failure (LCHF)
right sided failure (RCHF)