L21: Hypertension, Hypotension, Shock Flashcards

1
Q

When does venous hypertension develop

A

Impaired outflow of venous blood a.k.a passive congestion

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2
Q

Give examples of conditions that may lead to venous hypertension pls

A

Congenital/ acquired arteriovenous anastomosis e.g. congenital hepatic arterioportal fistula

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3
Q

What is a consequence of venous hypertension

A

INC plasma hydrostatic pressure in tributary veins, venues, capillary beds upstream –> oedema and diapedesis of erythrocytes

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4
Q

What is pulmonary hypertension

A

sustained increase in systolic BP in pulmonary artery

>30mm Hg dog/cat

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5
Q

What is cor pulmonale

A

R heart disease caused by pulmonary hypertension

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6
Q

Why does cor pulmonale develop

A

pressure overload on right ventricle during systole –> R sided congestive heart failure or chronic compensatory concentric hypertrophy of right ventricle

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7
Q

In which circumstances does pulmonary hypertension develop

A

Congenital anomalies –> L to R shunting blood E.g.
Patent ductus arteriosus
Atrial septal defect
Ventricular septal defect

Inc resistance in pulmonary blood flow E.g.
heart worm
pulmonary neoplasia
Severe chronic diffuse interstitial fibrosis

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8
Q

Whats systemic hypertension

A

sustained increased in systemic arterial BP

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9
Q

Which diseases can predispose animals to the development of systemic hypertension

A
Diabetes 
liver disease 
glomerular disease 
renal disease 
endocrinopathies 
NSAIDS
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10
Q

Describe how some endocrinopathies can lead to systemic hypertension in animals

A

middle aged cats can develop nodular hyperplasia of their thyroid gland, generating too much T3, T4

Low thyroid function & obesity in older dogs

Cushing’s (high adrenocortical cortisol)

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11
Q

Why can systemic hypertension be self-perpetuating if not adequately treated

A

related to underlying disease process –> must treat this to reduce hypertension

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12
Q

Which organs are most susceptible to systemic hypertension

A

eyes
brian
kiddys

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13
Q

What are some clinical signs that can develop subsequent of systemic hypertension

A

PU/PD –> reflects both diuresis and underlying primary disease process (E.g. renal failure, diabetes mellitus, hyperthoiridism, hyperadrenocorticism)

Cardiac murmur +/- galloping heart

epistaxis

strokes

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14
Q

What is systemic hypotension

A

sustained decrease in systemic arterial blood pressure (<60mm cats, dogs or <80mm Hg systolic pressure)

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15
Q

What overall cardiovascular changes can cause systemic hypotension

A

dec in CO and TPR

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16
Q

What does persistent systemic hypotension lead to

A

shock

17
Q

Define shock

A

generalised phenomenon peripheral circulatory failure, characterised by systemic hypo perfusion and systemic hypotension

18
Q

What are the types of shock

A
Cardiogenic shock 
Hypovolaemic shock 
Distributive 
Neurogenic 
Anaphylactic 
Septic
19
Q

What is cardiogenic shock

A

rapid decrease in systolic CO despite adequate blood volume

20
Q

what causes cariogenic shock

A
Severe dilated cardiomyopathy*
Myocardial infarction 
Cardiomyopathy 
Atrial fibrillation
Tachyarrhythmias 
Rupture chordae tendinae 
Rapid pericardial effusion 
Pulmonary hypertension/ severe systemic hypertension 
Heart worm
21
Q

What is hypovolaemic chock

A

significant reduction in circulating blood volume (>20-25%)

22
Q

what are some causes of hypovolaemic shock

A

haemorrhage
severe fluid loss (vomiting/ diarrhoea)
or fluid loss through increased vascular permeability
sequestration fluid (e.g. grain overload)

23
Q

What is distributive shock

A

inappropriate vasodilation arterioles, pooling of blood in capillary beds & venous channels
(total reduced peripheral vascular resistance, decreased effective circulating blood volume)

24
Q

What are the 4x types of distributive shock

A

neurogenic shock
anaphylaxis
sepsis
heat stroke

25
Q

Describe neurogenic shock

A

fear/ pain –> brain signals affect vasomotor centre of medulla –> inappropriate peripheral vasodilation/ bradycardia

26
Q

Describe anaphylactic shock

A

mass mast & basophil degranulation= mass release vasoactive amines e.g. histamine

27
Q

What is septic shock

A

e.g. endotoxin release –> endothelial release vasodilators -> systemic arteriolar vasodilation –> hypotension & decreased effective circulating blood volume

High LPS doses cause also activate platelets, activate cascade, cause widespread vascular injury & thus widespread DIC

28
Q

What are the 3 stages of shock

A
  1. Initial non-progressive stage
  2. Progressive stage of tissue hypo perfusion
  3. Irreversible stage
29
Q

Describe the initial, non progressive stage of shock

A

COMPENSATED HYPOTENSION

baroreceptors detect hypotension
chemoreceptors detect hypercapnia

Stimulation sympathetic NS

Activation RAAS

30
Q

What is the outcome of initial non progressive/ compensated shock?

A

Vasoconstriction of arterioles and venules
Maintenance of blood pressure
Conservation of fluid

31
Q

In which case is the bodies attempt to compensate for initial non-progressive shock essentially useless?

A

In cases of distributive shock, where peripheral vasoconstriction is a characteristic, therefore value of compensatory response is diminished

32
Q

Describe the progressive stage of tissue hypoperfusion as part of shock

A

sustained vasoconstriction in nonessential organs= hypoxia –> lactic acid –> reversal of vasoconstriction –> pooling of blood in microcirculation

Hypoxic injury can trigger DIC

Oliguria

33
Q

Describe the irreversible stage of shock

A

shock will eventually lead to widespread hypoxic ell necrosis, multiple organ failure +/- DIC

Death can’t be prevented in this stage, only in 2nd stage with correction of underlying haemodynamic abnormalities

34
Q

What are the clinical signs of hypovolaemic and cardiogenic shock

A
hypotension 
tachycardia 
thready pulse 
tachypnoea 
MM pallor 
inc CRT 
decreased mentation
35
Q

What are the clinical signs of cardiogenic shock

A

arrhythmia,
murmur
muffled heart sounds

36
Q

What are the clinical sings of distributive shock

A

dark red (injected) MM, rapid CRT