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Pathophysiology > alterations of cardiovascular fx for week 10 > Flashcards

alterations of cardiovascular fx for week 10 Flashcards

1
Q

Mean arterial blood pressure

A

MAP= diastolic pressure + 1/3 of the pulse pressure

-pulse pressure = systolic - diastolic pressure

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2
Q

Cardiac output

A
  • 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)

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3
Q

cardiac output formula

A

CO = HR x SV

  • HR: heart rate is # of beats/minute
  • SV: stroke volume is ant of blood ejected in one heartbeat
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4
Q

Blood pressure regulation

A
  • 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)
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5
Q

Blood pressure formula

A
  • 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
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6
Q

Peripheral resistance

A
  • 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
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7
Q

Poiseuille’s Law

A

Q = (P1 - P2) / R

  • Q is blood flow
  • P is pressure difference
  • R is resistance
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8
Q

Poiseuille’s Formula

A

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
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9
Q

Hypertension is major risk factor for?

A
  • coronary artery disease (heart attack)
  • cerebrovascular accidents (stroke)
  • both due to atherosclerosis
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10
Q

Epidemiology of Hypertension

A
  • 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
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11
Q

Causes of hypertension

A
  • 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
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12
Q

Clinical course for hypertension

A

-both essential and secondary hypertension may be either benign or malignant

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13
Q

benign hypertension

A

remains at a modest level and fairly stable over a long period of time

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14
Q

malignant hypertension

A

severe, rapidly developing hypertension; if untreated, leads to death within one or two years

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15
Q

more on malignant hypertension

A
  • 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)
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16
Q

Factors involved in the development of hypertension

A
  • obesity
  • smoking
  • heavy consumption of salt
  • atherosclerosis
  • caffeine
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17
Q

obesity involvement in the development of hypertension

A

increases peripheral resistance and increases workload on the heart

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18
Q

smoking involvement in the development of hypertension

A

increases heart rate and stimulates vasoconstriction

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19
Q

heavy consumption of salt involvement in the development of hypertension

A

increases blood volume

20
Q

atherosclerosis involvement in the development of hypertension

A

increases peripheral resistance

21
Q

caffeine involvement in the development of hypertension

A

CV & respiratory stimulant; also leads to vasoconstriction

22
Q

possible complications of hypertension

A
  • 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
23
Q

hypertension significantly increases the workload on the heart

A
  • 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)
24
Q

hypertension also puts physical stress on the walls of the blood vessels

A
  • 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
25
Q

Hypertension also increases the risk of

A
  • 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
26
Q

hypertension increases risk for other issues aside from CHF, etc.

A
  • 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
27
Q

Aneurysm

A

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
28
Q

causes of aneurysms

A
  • 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
29
Q

false aneurysms

A
  • 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
30
Q

Aortic Dissection

A
  • 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
31
Q

Diverses of the veins

A
  • varicose veins
  • venous stasis ulcers
  • deep vein thrombosis
32
Q

Varicose vein definition

A

a vein in which blood has pooled, producing an abnormally dilated, tortuous vein

33
Q

varicose veins caused by

A
  • 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)
34
Q

what kinds of valves are most affected by varicose veins

A

-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

35
Q

valve incompetence risks

A
  • age
  • females
  • family history
  • obesity
  • pregnancy
  • standing for long periods
36
Q

Pathogenesis of varicose veins

A
  • 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
37
Q

hemhorrhoids

A

result from dilation of the veins at the anorectal junction

38
Q

esophageal varices

A

usually in patients with cirrhosis of the liver (hepatic portal hypertension)

39
Q

pregnancy

A

increased fluid volume

40
Q

venous stasis ulcers

A
  • 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
41
Q

Deep vein thrombosis

A
  • 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)
42
Q

factors which promote venous thrombosis

A
  • venous stasis
  • vessel damage
  • hypercoaguability
43
Q

venous stasis

A

cause by immobility, age, and left heart failure

44
Q

vessel damage

A

caused by trauma or IV medications

45
Q

hypercoaguability

A

caused by pregnancy, oral contraceptives, coagulation disorders, and some cancers

46
Q

clinical manifestations of deep vein thrombosis

A
  • 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

Pathophysiology (11 decks)

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