Chapter 11 Cardiovascular function in pathological situation Flashcards
Pulmonary hypertension is called when mean pulmonary artery pressure is greater than **** mmHg
25mmHg
True or False?
Treatment for systemic hypertension has a fairly good effect on pulmonary hypertension
Treatment of systemic hypertension have had little or no effect on the pulmonary bed.
Explain the pharmacologic effect of phosphodiesterase-5 inhibitors such as sildenafil.
PDE5 inhibitors prevent cyclic GMP(guanosine monophosphate) breakdown, thus promoting the vasodilating effects of nitric oxide
Once hypertension is established, what are changes in peripheral resistance, cardiac output and blood volume?
Total peripheral resistance Increases
Cardiac output and blood volume may be elevated during the early phase but usually normal after the hypertension is established.
True or false?
The urinary output rate is influenced by arterial pressure.
So in the long tern, arterial pressure can stabilize only at the level that makes urinary output rate less than fluid intake rate
False
arterial pressure can stabilize only at the level that makes urinary output rate equal to fluid intake rate
4 therapeutic strategies for treating systemic hypertension
- restricting salt intake to reduce water retention
- diuretic therapy - by inhibiting renal tubular salt reabsorption, urinary output rate for a given arterial pressure is increased. It would raise the renal function curve.
- ACE inhibitors
- blocking vasoconstrictor angiotensin II - alpha adrenergic receptor blockers (prazosin)
- prevent the vasoconstriction from catecholamines - calcium channel blockers (amlodipine)
- directly decrease vascular muscle tone
Definition of shock
generalized, severe reduction in blood supply to the body tissue and the metabolic needs of the tissuse are not met
Three cardiovascular crises that precipitate shock
- depressed myocardial functional ability
- decreased preload
- decreased afterload
Types of shock presented in Chapter 11
- Cardiogenic shock
- Hypovolemic shock
- Anaphylactic shock (what mediators are involved in anaphylactic shock? 1. histamine, 2. prostaglandin, 3. leukotrine, 4. bradykinin
- septic shock
- Neurogenic shock
What is the most common substance released into circulating blood by infective agents?
lipopolysaccharide (endotoxin) released by bacteria. This induces the formation of iNOS (inducible NO synthase from where? endothelium, vascular smooth muscle, and macrophages)
What are the 2 things responsible for triggering medullary cardiovascular centers in respone to decreased mean arterial pressure?
- decreased activity of arterial baroreceptors
2. cerebral ischemic response
What is the main compensatory response from shock?
increases in sympathetic activity, decreased parasympathetic activity
What are additional compensatory processes?
- Rapid and shallow breathing (resp pump) to promote venous return
- Increase renin release from kidney from sympathetic stimulation, AG2 vasoconstriction
- Increased vasopressin from posterior pituitary gland
- increased epi and NE from adrenal meculla
- intense arteriolar constriction- reduced capillary hydrostatic pressure- promote fluid movement from the interstitial space into the vascular space
- epi/NE induced glycogenolysis in the liver- release of glucose and a rise in blood/interstitial glucose level, rise in extracellular osmolarity by 20 mOsm, induced a shift of fluid from IC into EC space
“autotransfusion” include number 5 and 7- increase 1 L into the vascular space in the first hour- decreased HCT in hemorrhagic shock, this extent of fluid shift may be limited by a reduction in colloid osmotic pressure
What are the long term effects of hypovolemic states trigger fluid retention mechanism?
- RAAS
2. ADH
What are the stages of shock in this chapter
- compensatory (inadequate perfusion to renal, hepatic, and GI)
- decompensatory
- progressive stage
- irreversible stage