Lecture 21 Flashcards
In what cirucumstances does venous hypertension develop
impairment of outflow of venous blood from tissues
pulmonary hypertension
sustained inc in systolic BP in the pulmonary artery
Cor pulmonale
characterized by
right heart disease caused by pulmonary hypertension
inc work load (pressure overload) on right ventricle during systole
Some causes of pulmonary hypertension
congenital cardiac anomalies causing left to right shunting of large volumes of blood(PDA, atrial septal defect)
inc resistance to pulmonary arterial blood flow(heartworm,pulmonary thromboembolism)
What is eisenmeyers complex
pulmonary arterial pressure inc so much that shunting of blood is reversed to right to left->poorly O2 blood circulating-> hypoxia
systemic hypertension
sustained inc in systemic arterial bP
What factors contribute to systemic arterial BP
COxTPR
Some diseases responsible for hypertension in cats/dogs (5)
renal disease hypERthryroidism (cats) hypOthyroidism (dOgs) diabetes mellitus obesity
Why does systemic hypertension become self perpetuating over time if not treated(2)
dec GFR-> inc proximal tubular reabsorption of Na and H2O
dec BP within glomerular afferent arterials->activation of RAAS
Which body organs are most susceptible to damage from systemic hypertension(4)
eyes
kidneys-PU/PD
heart-aortic aneurysm
brain-stroke
Systemic hypOtension
sustained dec in systemic arterial BP
shock
general phenomenon of peripheral circulatory failure
Cardiogenic shock
most common cause
rapid dec in systolic cardiac output despite the presence of adequate blood volume
severe DCM
Hypovolemic shock
significant reduction in circulating blood volume
Distributive shock
inappropriate vasodilation of arterioles with pooling of blood in capillary beds and venous channels->dec TPR and effective circulating blood volume(heat stroke)
What circumstances can trigger neurogenic shock
what does it do
severely frightened, emotionally stressed or suffering severe pain
->inappropriate peripheral vasodilation and bradycardia
What can trigger anaphylactic shock
what does it do
bee sting, drugs, peanuts
arteriolar and venous dilation and inc vascular permeability->dec circulating blood volume
What can trigger septic shock(3)
what does it do
what contributes to poor prognosis
gram negative bacterial infections, superantigens, endotoxin
release of TNF, IL1,NO, PGI2, platelet activating->systemic arteriolar vasodilation
DIC
Compensatory neurohumoral mechanisms that are activated in the initial stage of cardiogenic or hypovolemic shock (5)
hypotension detected by baroreceptors release of glucocorticoids aldosterone release activation of RAAS ADH release from posterior pituitary
What happens during stage 2 (progressive) shock(3)
GFR dec-> oliguria (dec urine volume)
sustained vasoconstriciton in non essential organs-> hypoxia
pooling of blood in peripheral microcirculation
What has happened by stage 3 of shock(2)
widespread hypoxic cell necrosis
failure of multiple organs and maybe DIC
when do you therapy by during shock to improve outcome
stage 1 preferable or at least stage 2
Clinical signs of shock(5)
hypovolemic and cardiogenic
hypovolemic and cardiogenic: hypotension, tachycardia, weak and rapid pulse, inc resp rate, cool dry or clammy skin, prolonged capillary refill time
what form of shock has best prognosis if treatment given stage 1 or 2
hypovolemic
clinical signs of shock cardiogenic shock(3)
arrythmia, murmur, muffled heart sounds
clinical signs of shock distributive shock(2)
dark red mucous membranes (peripheral vasodilation, rapid capillary refill time
