23 + 24 Flashcards
normal and abnormal blood pressure
normal is 120/80
abnormal is 140/90 and higher
primary hypertension
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
secondary hypertension
cause is known, usually from some type of disease state
10 percent of cases
types of hypertension?
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
theories of hypertension?
- neurological/stress hypertension (chronic increase in TPR)
- salt imbalance/ renal (increase in TPR) (increased blood volume = increased blood pressure)
Baroreceptor response to HTN?
receptors adapt to changes in blood pressure quickly, thus they only help short-term
consequences of HTN?
cardiac failure ( increased workload)
cerebral hemorrhage and aneurysms
renal damage
coronary artery disease
Congestive heart failure?
failure of the heart to pump blood
features: exercise intolerance dyspnea fatigue peripheral edema
predisposing conditions:
hypertension
coronary artery disease
valvular heart disease
classification of heart failure?
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
systolic vs diastolic heart failure
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
Draw the P-V graph for systolic, diastolic, and both heart failure
systolic:
lower EF
higher EDV
loss of inotropy
diastolic:
decreased compliance
RV and LV heart failure and edema
RV = peripheral edema
LV = pulmonary edema
compensatory mechanisms of chronic heart failure
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
harmful consequences of compensatory mechanisms
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
treatment for heart failure?
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
effects on CVS due to age
- decreased elastin in blood vessel walls
- baroreceptor sensitivity decreases
- cardiac performance during activity decreases
volume sensors pathway
- decreased blood volume
- decreased MAP (sensed by baroreceptors)
- decreased renal perfusion
- JUXTAGLOMERULAR APPARATUS
- renin release
pathway of low volume states
- renin is released
- angiotensinogen
- angiotension I
- angiotension II
- aldosterone
- Na and water retention
hypovolemic shock
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
cardiogenic shock
cause: pump failure
due to: MI or arrhythmia
skin is cold and clammy
preload: high
CO: LOW
afterload: high
treatment is inotropes and diuresis
obstructive shock
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
septic shock
cause: decreased TPR
due to: endotoxins
skin is warm and dry
preload: low
CO: high
afterload: LOW
treatment is pressors and IV
anaphylactic shock
cause: decreased TPR
due to: allergic reaction
skin is warm and dry
preload: low
CO: high
afterload: LOW
treatment is pressors and IV fluids
neurogenic shock
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
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
response to hemorrhage
- baroreceptor reflex
a short-term response to preserve heart and brain - Renin – Angiotensin System
long-term (replace fluid loss)
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)
resuscitation with different solutions
whole blood is best; no changes occur
water decreases all concentrations
