23 + 24 Flashcards

(28 cards)

1
Q

normal and abnormal blood pressure

A

normal is 120/80

abnormal is 140/90 and higher

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2
Q

primary hypertension

A

can be benign (slow progression) or malignant (fast progression)

cause is not known but risk factors are:

age, weight, diabetes, activity level, salt intake, alcohol, family history

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3
Q

secondary hypertension

A

cause is known, usually from some type of disease state

10 percent of cases

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4
Q

types of hypertension?

A

pump-based hypertension: increase in CO; usually seen in younger patients

vascular resistance-based hypertension: increase in TPR; seen more in older adults

volume-based hypertension: retention of Na and water

remember:

MAP = CO x TPR

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5
Q

theories of hypertension?

A
  1. neurological/stress hypertension (chronic increase in TPR)
  2. salt imbalance/ renal (increase in TPR) (increased blood volume = increased blood pressure)
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6
Q

Baroreceptor response to HTN?

A

receptors adapt to changes in blood pressure quickly, thus they only help short-term

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7
Q

consequences of HTN?

A

cardiac failure ( increased workload)

cerebral hemorrhage and aneurysms
renal damage
coronary artery disease

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8
Q

Congestive heart failure?

A

failure of the heart to pump blood

features:
exercise intolerance
dyspnea
fatigue
peripheral edema 

predisposing conditions:
hypertension
coronary artery disease
valvular heart disease

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9
Q

classification of heart failure?

A

class I: no limitation of physical activity

class II: slight limitation of physical activity

class III: marked limitation of physical activity

class IV: inability of physical activity; not comfortable at rest

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10
Q

systolic vs diastolic heart failure

A

systolic:
reduced contractility
reduced stroke volume
more common

diastolic:
failure in filling
reduced EDV and reduced SV

systolic has a reduced EF, EF is normal in diastolic

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11
Q

Draw the P-V graph for systolic, diastolic, and both heart failure

A

systolic:
lower EF
higher EDV
loss of inotropy

diastolic:
decreased compliance

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12
Q

RV and LV heart failure and edema

A

RV = peripheral edema

LV = pulmonary edema

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13
Q

compensatory mechanisms of chronic heart failure

A

vasoconstriction and sodium/water retention

increasing TPR and blood volume

this is done by the Renin Angiotensin Aldosterone System.

initially beneficial, but is mostly more harmful

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14
Q

harmful consequences of compensatory mechanisms

A

increasing blood volume = pulmonary edema

increasing TPR = increase afterload and decreasing SV and CO

increasing HR = more metabolic demand

continuous sympathetic activity = down regulation of beta receptors

increased angiotensin II = adverse heart remodeling

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15
Q

treatment for heart failure?

A

ACE inhibitors and Ang II antagonists decrease blood volume

vasodilators: increase mechanical efficiency

Diuretics: decrease venous pressure, lower edema, lower blood volume

beta blockers: increase SC and CO; decrease overload

digoxin: increase contractility

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16
Q

effects on CVS due to age

A
  1. decreased elastin in blood vessel walls
  2. baroreceptor sensitivity decreases
  3. cardiac performance during activity decreases
17
Q

volume sensors pathway

A
  1. decreased blood volume
  2. decreased MAP (sensed by baroreceptors)
  3. decreased renal perfusion
  4. JUXTAGLOMERULAR APPARATUS
  5. renin release
18
Q

pathway of low volume states

A
  1. renin is released
  2. angiotensinogen
  3. angiotension I
  4. angiotension II
  5. aldosterone
  6. Na and water retention
19
Q

hypovolemic shock

A

cause: decreased blood volume

due to: hemorrhage, diarrhea, vomiting

skin is cold and clammy

PCWP or preload is LOW
CO is low
Afterload (SVR) is high

treatment is IV fluids

20
Q

cardiogenic shock

A

cause: pump failure

due to: MI or arrhythmia

skin is cold and clammy

preload: high
CO: LOW
afterload: high

treatment is inotropes and diuresis

21
Q

obstructive shock

A

cause: obstruction to blood flow

due to: pulmonary embolism, cardiac tamponade, pneumothorax

skin is cold and clammy

preload: high
CO: LOW
afterload: high

treatment is to relieve obstruction

22
Q

septic shock

A

cause: decreased TPR

due to: endotoxins

skin is warm and dry

preload: low
CO: high
afterload: LOW

treatment is pressors and IV

23
Q

anaphylactic shock

A

cause: decreased TPR

due to: allergic reaction

skin is warm and dry

preload: low
CO: high
afterload: LOW

treatment is pressors and IV fluids

24
Q

neurogenic shock

A

cause: disruption of vasomotor control

due to: brain or spinal injury

skin is warm and dry

preload: low
CO: low
afterload: LOW

treatment is pressors and IV

25
consequences of blood loss
5-10% = no change in MAP 15 to 20% = modest low MAP (full recovery) 20-30% = MAP 60-80mm (rarely fatal) 30-40 % = MAP 50-70 (serious shock) 50% = fatal
26
response to hemorrhage
1. baroreceptor reflex a short-term response to preserve heart and brain 2. Renin – Angiotensin System long-term (replace fluid loss)
27
decompensated shock
Severe, untreated prolonged shock can lead to decompensated shock which is fatal. occurs when 30 percent of blood volume is lost and no fluid replacement within 3-4 hours massive vasodilation will occur which will decrease contractility, CO, MAP, and tissue perfusion (sympathetic escape)
28
resuscitation with different solutions
whole blood is best; no changes occur water decreases all concentrations