CV Part 4 Flashcards
Primary HTN
No identifiable cause
Secondary HTN
Uncontrolled BP despite optimal medications
Abrupt onset
There is a cause
Angiotensin (4)
Potent vasoconstrictor
Stimulates aldosterone secretion
Can block HP baroceptors
Stimulate release of norepi from post-ganglionic SNS fibers
Aldosterone
Na reabsorption from the forming urine
Leads to H2O retention
What are some possible treatments for HTN?(5)
ACE inhibitor Renin inhibitor B blocker Ca channel blocker Diuretic
Concentric LVH (5)
Systolic wall stress Pressure overload Thick wall Thin cavity Sarcomeres in parallel
What can cause concentric LVH? (2)
HTN
Aortic stenosis
Eccentric LVH (5)
Diastolic wall stress Volume overload Thin wall Thick cavity (dilated) Sarcomeres in series
What can cause eccentric LVH? (2)
Aortic insufficiency
Arteriovenous fistula
Conductance is
Blood flow
What’s the relationship between velocity and area?
Inversely proportional
What happens to FLOW if the difference between arterial and venous pressure increases, while resistance is constant?
Increases
Laminar flow
Streamlined movement
Predominant in vasculature under normal conditions
Turbulent flow
Random flow
How does exchange occur between capillaries and the interstitial space?
Diffusion
What are Starling forces?
Forces in the lumen and interstitium of the capillary that determines what direction the fluid will move
What is the movement of the fluid on the arterial end of a capillary?
Outward (known as filtration)
What is the movement of fluid on the venous end of a capillary?
Inward (reabsorption)
Edema
Build up of interstitial fluid
2 possible causes for edema
Increased arterial pressure → inc capillary pressure so too much fluid is pushed out
Decreased venous return → back pressure exerted so you inc capillary pressure and too much fluid pushed out
lymphatic is overwhelmed
What do we do with the extra fluid in the interstitium that isn’t picked back up by the capillaries?
Picked up and sent to the lymphatic system so that it can go back to venous circulation
Capillary allows for exchange of:
H2O soluble molecules → pores
Lipid soluble molecules → blood gases via plasma membrane
3 components of the vascular networks
Resistance (arteries and arterioles)
Exchange (capillaries)
Capacitance (veins)
Important vasodilator (4)
Adenosine
CO2
H+
lactic acid
Anything that obstructs CO can lead to
Elevations in RAP → compromise venous return
What can happen if you have right heart failure?
Elevated RAP → increased venous pressure in jugular and hepatic portal circulations
Pulse pressure
Systolic - Diastolic pressure
When does the majority of myocardial O2 uptake occur?
During diastole
How does adenosine work?
Block Ca entry into VSM
Induce vasodilation
How is the myocardium supplied with O2?
Coronary arteries
What are some factors that modulate coronary vascular tone?
Vasodilators (NO, H+, CO2)
What’s the order of myocardial O2 demand?
- Ventricular wall stress
HR
Inotropy (contractility)
What is ischemia?
Localized anemia due to reduced blood supply
