L21: Hypertension, Hypotension, Shock Flashcards

(36 cards)

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

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
Describe neurogenic shock
fear/ pain --> brain signals affect vasomotor centre of medulla --> inappropriate peripheral vasodilation/ bradycardia
26
Describe anaphylactic shock
mass mast & basophil degranulation= mass release vasoactive amines e.g. histamine
27
What is septic shock
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
What are the 3 stages of shock
1. Initial non-progressive stage 2. Progressive stage of tissue hypo perfusion 3. Irreversible stage
29
Describe the initial, non progressive stage of shock
COMPENSATED HYPOTENSION baroreceptors detect hypotension chemoreceptors detect hypercapnia Stimulation sympathetic NS Activation RAAS
30
What is the outcome of initial non progressive/ compensated shock?
Vasoconstriction of arterioles and venules Maintenance of blood pressure Conservation of fluid
31
In which case is the bodies attempt to compensate for initial non-progressive shock essentially useless?
In cases of distributive shock, where peripheral vasoconstriction is a characteristic, therefore value of compensatory response is diminished
32
Describe the progressive stage of tissue hypoperfusion as part of shock
sustained vasoconstriction in nonessential organs= hypoxia --> lactic acid --> reversal of vasoconstriction --> pooling of blood in microcirculation Hypoxic injury can trigger DIC Oliguria
33
Describe the irreversible stage of shock
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
What are the clinical signs of hypovolaemic and cardiogenic shock
``` hypotension tachycardia thready pulse tachypnoea MM pallor inc CRT decreased mentation ```
35
What are the clinical signs of cardiogenic shock
arrhythmia, murmur muffled heart sounds
36
What are the clinical sings of distributive shock
dark red (injected) MM, rapid CRT