alterations of cardiovascular fx for week 10 Flashcards
Mean arterial blood pressure
MAP= diastolic pressure + 1/3 of the pulse pressure
-pulse pressure = systolic - diastolic pressure
Cardiac output
- a measurement of the effectiveness of the heart as a pump
- influenced by blood volume (related to body sodium) and cardiac factors (heart rate, contractility)
cardiac output formula
CO = HR x SV
- HR: heart rate is # of beats/minute
- SV: stroke volume is ant of blood ejected in one heartbeat
Blood pressure regulation
- kidneys aid in regulating blood pressure
- they influence peripheral resistance and sodium homeostasis
- renin is produced by the kidney and converts angiotensinogen to angiotensin
- angiotensin alters BP by increasing peripheral resistance and blood pressure (via aldosterone)
Blood pressure formula
- BP = CO x PR
- BP= blood pressure: the force that causes blood to flow through vessels
- CO= cardiac output: the amount of blood pumped out of one ventricle in one minute
- PR= peripheral resistance: resistance to blood flow created primarily by the arterioles
Peripheral resistance
- precapillary sphinctors
- even more important is the vasoconstriction/vasodilation of the arterioles
- w/vasoconstriction: bld flow deceases and bld velocity increases
- total in = total out
- fluid follows path of least resistance
Poiseuille’s Law
Q = (P1 - P2) / R
- Q is blood flow
- P is pressure difference
- R is resistance
Poiseuille’s Formula
R = (8nl) / pi r^4
- R is resistance
- n is viscosity of the blood
- r is lumen’s radius
- l is length of tube
- Radius is MOST important factor
Hypertension is major risk factor for?
- coronary artery disease (heart attack)
- cerebrovascular accidents (stroke)
- both due to atherosclerosis
Epidemiology of Hypertension
- 25% of the general public are hypertensive
- blacks are affected twice as often as whites (and seem more vulnerable to the complications of hypertension)
- increased prevalence with increased age
Causes of hypertension
- 90-95% of hypertension is idiopathic
- primary or essential hypertension
- two theories:
- decreased renal excretion of sodium
- increased peripheral resistance
- 5-10% is secondary to another condition
- renal disease (largest cause of secondary)
- narrowing of the renal artery (atheromas)
- adrenal or thyroid disorders (excess of thyroid hormone is bad for the heart)
- pregnancy = pre=eclampsia
Clinical course for hypertension
-both essential and secondary hypertension may be either benign or malignant
benign hypertension
remains at a modest level and fairly stable over a long period of time
malignant hypertension
severe, rapidly developing hypertension; if untreated, leads to death within one or two years
more on malignant hypertension
- diastolic pressure often > 120 mmHg
- renal failure and/or retinal hemorrhages often occur in malignant hypertension
- can lead to cerebral edema, CHF, etc.
- may develop in previously normotensive people
- more often superimposed on preexisting benign hypertension (primary or secondary)
Factors involved in the development of hypertension
- obesity
- smoking
- heavy consumption of salt
- atherosclerosis
- caffeine
obesity involvement in the development of hypertension
increases peripheral resistance and increases workload on the heart
smoking involvement in the development of hypertension
increases heart rate and stimulates vasoconstriction
heavy consumption of salt involvement in the development of hypertension
increases blood volume
atherosclerosis involvement in the development of hypertension
increases peripheral resistance
caffeine involvement in the development of hypertension
CV & respiratory stimulant; also leads to vasoconstriction
possible complications of hypertension
- hypertension significantly increases the workload on the heart
- also puts physical stress on the walls of the blood vessels throughout the body
- also increases risk of other heart issues
hypertension significantly increases the workload on the heart
- left ventricle gradually enlarges (causes hypertrophy)
- more muscle mass means a greater oxygen demand
- if coronary circulation can’t keep pace, symptoms of cardiac ischemia appear (heart attack)
hypertension also puts physical stress on the walls of the blood vessels
- promotes the development of atherosclerosis (by creating endothelial damage)
- increases the risk of stroke and/or myocardial infarction (by creating thromboembolic in response to endothelial damage)
- increases risk of aneurysms
Hypertension also increases the risk of
- congestive heart failure by increasing after load (what heart has to pump into)
- aneurysms by straining the blood vessels and causing tears in the endothelium
- renal failure since the kidney’s arterioles thicken in response to the stress of increased pressure; lumens become narrower; renal perfusion declines
hypertension increases risk for other issues aside from CHF, etc.
- impaired vision: by damaging retinal vessels
- edema: by hydrostatic mechanisms
- impaired mobility & exercise intolerance: heart is in a work overload situation even at rest, so additional work is not tolerated
Aneurysm
a bulge in the weakened wall of an artery
- most dangerous aneurysms are those involving arteries of the brain and aorta
- aneurysms in the brain can cause strokes
- ruptured aortic aneurysms will cause fatal hemorrhage in a matter of minutes
causes of aneurysms
- atherosclerosis is by far the most common cause of aneurysms
- over time atherosclerosis causes
- vessel walls to become less elastic
- plaque formation erodes the vessel wall
- underlying tunica media becomes destroyed and thus weakens the wall
false aneurysms
- actually a bruise/hematoma
- false aneurysms break in the vessel wall but blood is contained by a clot
- dissecting aneurysm is a break in vessel wall, but blood is contained by adventitia
- both often due to trauma
Aortic Dissection
- blood makes its way between the layers of the aortic wall, separating them
- can be up to 25 cm in length
- thrombi often form in the outputting area
Diverses of the veins
- varicose veins
- venous stasis ulcers
- deep vein thrombosis
Varicose vein definition
a vein in which blood has pooled, producing an abnormally dilated, tortuous vein
varicose veins caused by
- trauma to the saphenous vein that damages one or more valves
- gradual venous distention caused by a combination of standing for long periods and the pull of gravity (genetically weak valves)
what kinds of valves are most affected by varicose veins
-superficial veins of the legs are the most frequently involved since there is less muscle mass around them so they have a harder time moving up
valve incompetence risks
- age
- females
- family history
- obesity
- pregnancy
- standing for long periods
Pathogenesis of varicose veins
- blood pooling in the superficial veins leads to increased hydrostatic pressure, stretching the veins and causing edema
- venous valves are overloaded and become incompetent
- incompetent valves lead to worsened venous stasis and further increase in intraluminal pressure
- tese veins often thrombus, but because they are superficial it is uncommon that they travel to the lungs
hemhorrhoids
result from dilation of the veins at the anorectal junction
esophageal varices
usually in patients with cirrhosis of the liver (hepatic portal hypertension)
pregnancy
increased fluid volume
venous stasis ulcers
- chronic venous insufficiency
- circulation to the extremities is so sluggish that metabolic needs for oxygen, nutrients, and waste removal are barely met
- risks: immobility, obesity, age, L heart failure, varicose veins
- results in cell death and necrosis *chronic inflammation *edema, hyperpigmentation
Deep vein thrombosis
- thrombi which arise in the deep veins of the legs (more likely -> thromboemboli)
- usually are silent clinically
- have potential to give rise to pulmonary embolism and infarction
- often results as a complication of orthopedic or obstetric procedures
- up to 65% of patients w/ lower extremity trauma -> DVT
- venous thrombi are more common than arterial thrombi in the legs (due to skeletal muscle pump)
factors which promote venous thrombosis
- venous stasis
- vessel damage
- hypercoaguability
venous stasis
cause by immobility, age, and left heart failure
vessel damage
caused by trauma or IV medications
hypercoaguability
caused by pregnancy, oral contraceptives, coagulation disorders, and some cancers
clinical manifestations of deep vein thrombosis
- markedly different from those of arterial thrombosis (hypoxia is present in arterial but indirectly present in venous)
- skin is discolored - red to deep purple
- edema is prominent (hydrostatic venous back pressure)
- pain - especially at the site of the occlusion
- neuralgia if edema compresses local nerves
