exam 1 lecture 8 Flashcards
circulatory shock
- Hypovolemic
- Cardiogenic
- Distributive, vasodilatory
a. Neurogenic
b. Septic* - Obstructive (e.g. pulmonary
embolism, tamponade) – sometimes grouped with cardiogenic shock
hypovolemic shock
loss of extracellular fluid and electrolytes. The initial effect is a fall in MFP, a corresponding shift of the vascular function curve, a fall of preload, and a fall of cardiac output
hypovolemic shock includes
hemorrhage, burns, vomiting and diarrhea, anaphylactic shock, trauma
response to hypovolemic shock
Rapid reflexive responses aimed at restoring
cardiac output and mean arterial pressure.
Slower hormonal responses aimed at restricting fluid excretion and returning the blood volume back to normal.
Conservation of body fluid: operates mainly through the renal-body fluid system.
Replenishing lost fluid operates via drinking and metabolic water production.
Enhanced salt appetite to replace electrolytes
hormonal symptoms to hypovolemia
thirst, increased salt appetite, oliguria
sympathetic activation symptoms to hypovolemia
tachycardia, cold msot skin, pallor, oliguria
symptoms of hypovolemia b/c of lack of oxygen
increased respiratory rate, lactic acidosis, dulled perceptions
compensation baroreceptor response
Arteriolar vasoconstriction (adrenergic)
Increases systemic vascular resistance either by direct innervation or via epinephrine and norepinephrine released by the adrenal medulla.
Particularly notable in cutaneous and splanchnic circulations. In severe hemorrhage, there is renal vasoconstriction and potential renal failure.
Not in coronary or cerebral circulations
compensation baroreceptor response
Heart: Increased rate (chronotropy), myocardial conontractility (inotropy) and rate of relaxation (lusitropy). Also increased dromotropy.
compensation baroreceptor response
Venous capacitance reduced: Sympathetic venoconstriction is supplemented by reverse stress relaxation of the veins and venules as a result of reduction of intraluminal pressure.
This is “relative hypervolemia” and will tend to maintain MFP
slow compensation.
Kidneys: increased water and sodium conservation. Renin controls the renin-angiotensin-aldosterone system, and therefore the production of angiotensin II and aldosterone. There is also increased secretion of ADH and decreased secretion of ANF.
slow compensation
movement of fluids into circulation compartment, and replenishing lost fluid and salt
compensatory mechanism
operate by negative feedback (without clincial intervention, may be recovery from hemorrhage)
decompensatory mechanism
operate by positive feedback (no recovery, need clinical intervention)
examples of DC mechanism
cardiac failure (coronary flow inadequate)
acidosis (oxygen lack generates lactic acid)
reduced cerebral blood flow
blood clotting phenomena
depression of phagocytosis of monocyte-
derived cells (e.g. Kupffer cells)
intestinal ischemia/reperfusion injury
(“cardiotoxin”, endotoxic shock)
active hyperemia in exercise
Locally produced factors (such as CO2 & H+) cause vasodilation and increased blood flow in the active muscles-> Cardiac output is therefore directed toward the active muscles, where it is needed, and away from the viscera, where it is not.
changes in exercise
Sympathetic (adrenergic):
heart β1, arterioles (skin, viscera) alpha-1,
veins alpha-1 (vascular function curve)
Venous “pump”
central venous pressure increases,
increasing cardiac output according to
Starling Law
cerebral circulation unchanged
increase flow in coronary circulation, increase flow in active muscles, cutaneous circulation
during exercise
cardiac output=increases
SVR=decreases, EDV=increases, MAP=increases, atreriovenous oxygen difference= increases as does oxygen consumption
pulmonary circuit
low resistance circuit.
3 zones of blood flow in lungs
zone 1= no blood flow
zone 2=intermittent flow (flow at systole)
zone 3=continuous flow throughout systole and diastole (constant flow)
ventilation perfusion mismatch
failure to match ventilation and blood flow, occurs in pulmonary diseases
ways to determine perfusion
V/Q scan or angiography (gold standard)
PVR
PVR decreases as pulmonary arterial pressure rises-> flow through it can increase 5-6 times in response to less than doubled pulmonary arterial pressure (not proportional to pressure like in a rigid tube)
hypoxic pulmonary vascontriction
occurs in fetus, in adults: shunts poorly ventilated alveoli to regions that are better ventilated, HPV can lead to pulmonary hypertension and right ventricular hypertrophy
pulmonary hypertension
most causes are secondary to increased resistance to flow through pulmonary vascular bed, if PVR or PAW elevated, Pa will be
some cases of PHT
high altitude, hypoventilatory diseases, chronic bronchitis, asthma, CF, adult respiratory distress syndrome
consequences of PHT
right ventricular overload, right ventricular hypertrophy
treatments of PHT
infused prostacyclins, calcium channel blockers, NO, endothelin receptor blockers,
pulmonary edema
cardiogenic edema (increased LA pressure), and increased capillary permeability (from bacterial infection or toxins)
AV anastomoses (shunts)
control flow into the heat exchanging subpapillary plexuses in the hands, feet, ears, face
metabolic factors that affect cerebral blood flow
(active hyperemia) Co2, pH, potassium, adenosine, prostoglandins
splanchnic circulation
This circulation is important in the response to circulatory shock – involving both arteriolar and venous alpha-adrenergic vasoconstriction
flow rate of splanchnic circulation influenced by
sympathetic mechanical influences GI hormones such as CCK catecholamines vasopressin angiotensin II
portal hypertension
normally: pressure in portal vein is lower than hepatic veins and vena cavae, resistance to flow in liver is very low. Elevated intrahepatic resistance= portal hypertension
consequences of Portal hypertension
Formation of portosystemic shunts: bypasses develop wherever the systemic and the portal circulation have common capillary beds.
High pressure portal blood is shunted into the systemic venous system, causing dilation of veins in the rectum (hemorrhoids) and the cardioesophageal junction (esophageal varices).
consequences of portal hypertension
Abdominal edema and ascites: The rise of portal venous pressure (P1) elevates the capillary hydrostatic pressure in the gastrointestinal tract, pancreas,and spleen. Abdominal edema occurs initially, followed by fluid leaving the tissues and accumulating in the peritoneal cavity.
septic shock
ischemia caused by splanchnic vasoconstriction followed by reperfusion causes injury, allowing bacteria to invade the circulation: Myocardial depression Hypovolemia from edema caused by permeabilization of capillaries (endotoxins) Relative hypovolemia (capacity), fall of TPR from activation of inducible NOS (iNOS).
