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Vascular pressure within the lungs and why
Low pressure system; we want lots of easy blood flow through the lungs
T/F: the lungs hold a large blood volume
True
Structural characteristic of alveoli that allow for gas exchange
Very thin walls
Definition of pulmonary hypertension
Systolic pressure >25 mmHg
How much of the vascular bed needs to be lost for pulmonary HT to develop
65%
Three general causes of pulmonary HT
Increased pulmonary blood flow
Increased pulmonary vascular resistance
Pulmonary venous congestion
Causes of increased pulmonary blood flow
PDA, V/ASD
Causes of increased pulmonary vascular resistance
Chronic lung disease and chronic hypoxia
Causes of pulmonary venous congestion
Classic MMVD, other chronic L sided heart disease
Primary pathophysiology of pulmonary HT
Thicker, inflamed walls
Demographic that is highly likely to have pulmonary HT from chronic hypoxia
Brachycephalics
T/F: PHT is rare in cats
Maybe, but could be that we are just overlooking it
History associated with PHT
Coughing (common!)
Syncope/collapse
Dyspnea
Exercise intolerance
DDx for “seizures” alleged by owner
Syncope and collapse
Things to evaluate to differentiate seizure and syncope
What was happening before
How did they look waking up
Limb movement
Foaming/chattering
CS associated with PHT
Nonspecific
Tachypnea and dyspnea
Weakness
R CHF
± Tachycardia, cyanosis, crackles, murmur
T/F: true, primary PHT will present with a murmur
Not usually
Radiographic findings consistent with acute PHT
Normal rads :)
Radiographic findings consistent with chronic PHT
Dilated MPA
Dilated cr/cd lobar arteries
R sided enlargement
Where is the MPA on a VD radiograph
1-2 o’clock
Indirect measurement of pulmonary pressure that we can do via echo
Measure the velocity of blood across the pulmonic valve or tricuspid valve
If there are clots in the lungs, what WILL happen
Fluid build up
Best test we can do to evaluate clotting activity
Thromboelastography
Why is thromboelastography (and other viscoelastic testing) so great
It measures all aspects of the clotting cascade: platelets, clotting factors, fibrinolysis, etc.
Meds to consider if a patient is hypercoagulable
Antiplatelet and anticoagulant drugs
THE treatment for PHT
O2
How quickly do PHT patients respond to O2
Fast, may look much better after 30-60 minutes
Go-to meds for managing PHT
Sildenafil ± pimobendan
When might we use diuretics for PHT
If there is severe cavitary fluid accumulation
When might we really not want to give diuretics for PHT
If there is R CHF
Why do we like IVF for PHT
Helps the R heart overcome the pressure in the lungs and move blood into the LV
When can you wean a PHT patient off of O2
When they are breathing normally at room air
T/F: PHT is an acute disease
F, it is chronic and progressive
Chronic management for PHT
Manage L sided heart disease
Sildenafil ± pimobendan
± Antiplatelet drugs
Avoid physical stress
At-home monitoring for PHT
RR/RE
Log syncopal episodes
HW prevention
BP
Elements of virchow’s triad
Endothelial injury
Hypercoagulability
Turbulent blood flow
Thrombus v embolus
Thrombus is an initial clot in the heart or an artery, an embolus is a piece of the clot that breaks off and lodges somewhere else
The most common cause of clots in cats
Heart disease
The most common cause of clots in dogs
Lots of things
Types of shock caused by thromboembolic disease
Obstructive ± cardiogenic shock
How do clots cause damage
Mechanical obstruction of an artery → tissue ischemia
Clots are the number one complication of which immune mediated disease
IMHA
5 P’s of feline aortic thromboembolism (FATE)
Pain
Paralysis
Pulselessness
Poikilothermy
Pallor
The best way to diagnose thromboembolic disease
CT angiogram
More accessible ways to diagnose thromboembolic disease
Paired glucose and lactate
Ultrasound
Viscoelastic testing
Treatment for thromboembolic disease
Pain meds
Clopidogrel
Anticoagulant drugs
Nursing care
T/F: surgery can increase survival rates for thromboembolic disease
Nope
Common complication of trying to treat thromboembolic disease
Reperfusion injury
Reperfusion injury
Sudden uptick in toxins and K+ from damaged/dead cells
Clinical manifestations of reperfusion injury
Hyperkalemia → bradycardia
Severe metabolic acidosis
AKI
Death