page 360-369 Flashcards
https://drive.google.com/open?id=0B8uJUY-tie8GUm5Zb0dwUFRLQkE
https://drive.google.com/open?id=0B8uJUY-tie8GcVV6R2JmN1dPRFE
ECG
Records the flow of electrical impulses through the heart.
To read ECG:
■ Remember that a single lead corresponds to an anatomic territory.
■ Look at multiple leads together for voltage abnormalities and axis
deviations.
■ Look at a single lead for arrhythmias.
https://drive.google.com/open?id=0B8uJUY-tie8GV0h3UGEwUUpadEk
https://drive.google.com/open?id=0B8uJUY-tie8GZEJRSnBnT3h6dFU
https://drive.google.com/open?id=0B8uJUY-tie8GYzRXOW52YWY0eGM
https://drive.google.com/open?id=0B8uJUY-tie8GLTJrRHMtU2lzYTA
https://drive.google.com/open?id=0B8uJUY-tie8GQUVQYm51djVYM1U
https://drive.google.com/open?id=0B8uJUY-tie8Ga3RGSHFLcV9CbHM
https://drive.google.com/open?id=0B8uJUY-tie8GaDFlaWhReks5ZDQ
https://drive.google.com/open?id=0B8uJUY-tie8GUGh6OEQ3WFhEUEE
Bainbridge Reflex
■ Stretch of atria (with ↑ blood volume) causes ↑ HR and, therefore, ↑ CO.
■ Mediated by stretch receptors in atria.
Receptor cells are sensitive to pressure and stretch.
■ Mediated by vagal (CN X) afferents to the medulla.
■ Efferent loop is slowing of vagal output
Bainbridge Reflex
Pumps more blood out of pulmonary system to the systemic system.
■ This helps prevent pulmonary edema.
Bainbridge Reflex
Baroreceptor
HR, BP
Chemoreceptor
Respiration > vasomotor
Baroreceptors
■ Modulate intravascular pressure and HR over a short time period.
■ Activated by ↑ BP.
■ Causes ↓ HR, vasodilation, ↓ BP
BARORECEPTOR REFLEX (VALSALVA )
■ ↑ BP/↑ stretch of baroreceptors → ↑ parasympathetic afferent output (CN
IX, X) → medulla → ↑ vagal efferent tone (CN X) (↓ sympathetic tone)
→↓HR, ↓ BP (vasodilation, venodilation) →↓CO.
■ Antagonist to Bainbridge reflex.
car sinus
Spindle-shaped dilation of receptors at
he common carotid artery bifurcation
(superior border of thyroid cartilage).
Afferent = CN IX.
carotid sinus
Afferent = CN X.
Aortic Arch Baroreceptora
Receptors in the aortic arch
Aortic Arch Baroreceptora
carotid sinus syndrome
Excessive stimulation of both carotid sinuses (eg, convulsive seizures) can
lead to momentary loss of consciousness because of vagal discharge, venodilation,
vasodilation.
RESPONSE TO SUDDEN STANDING
↓ BP in brain, upper body sensed by baroreceptors →
■ ↓ parasympathetic firing (CN IX, X); (sympathetic discharge → ↑HR,
↑ conduction velocity, ↑ cardiac contractility, ↑ peripheral resistance ↑
vasoconstriction), ↓ renal blood flow ↑a1 vasocontriction of afferent artery;
b1 on JGA →↑renin →↑angiotensin-II → aldosterone→↑blood back to
heart (↑preload because venoconstriction of large veins) → ↑ CO →
return/maintain BP.
HEMORRHAGE OR HYPOVOLEMIA
COMPENSATIONS :
■ Baroreceptor reflex (↑ sympathetic, ↓ parasympathetic tone).
■ ↑ epinephrine from adrenal medulla.
■ ↓ vagal output from medulla (↓ carotid sinus, ↓ aortic baroreceptor firing
RAAS (Renin-Angiotensin-Aldosterone system). See renal also.
■ AT-II, aldosterone and increase in TPR
■ AT-II: On efferent arteriole to preserve GFR.
■ Aldosterone: On cortical collecting duct, increase Na+ reabsorption,
K+ excretion, H+ secretion by intercalated cells.
HEMORRHAGE OR HYPOVOLEMIA
HEMORRHAGE OR HYPOVOLEMIA
ADH
■ Capillary fluid shift
■ Increases water reabsorption in CCD.
Chemoreceptors
■ Detect changes in blood oxygen, carbon dioxide, and hydrogen ion
concentrations.
■ Modulate respiratory center in brain (regulate respiratory activity).
Afferent CN IX
Carotid Body
Afferent CN X
Aortic Body
CHEMORECEPTOR PATHWAY
↑ CO2, ↑ H+, and/or ↓ O2 → stimulates chemoreceptors (carotid, aortic
bodies) → ↑ parasympathetic afferent output (CN IX, X) → medulla (respiratory
center) → ↑ ventilation (to breathe down CO2) → (↑ BP, ↑ HR
secondary to simultaneous secretion of catecholamines from the adrenal
medulla).
■ Increase in sensitivity to CO2 and pH when <60 mm Hg.
Mechanisms to meet ↑ demand to muscles during exercise (↑ supply).
■ ↑ CO because ↑ HR and ↑SV.
excersize
excersize
Sympathetic nervous system.
■ b2 adrenergic receptors in muscle/pulmonary tree
■ Vasodilate
■ ↑ Blood flow to muscles
excersize
b1 receptors in heart
■ ↑ HR
■ ↑ Contraction force (inotropic) (phospholumbar “releasing brake”
on SERCA pump)
■ ↑ CO
excersize
a1 in other parts of body
■ Vasoconstriction
■ ↑ Arterial pressure
excersize
Enhanced venous return (↑ preload).
■ ↓ Venous compliance
■ Pumping effect of the skeletal muscle
■ Vasoconstriction
excersize
Local metabolites (released as O2 ↓ 0).
■ Adenosine, CO2, lactic acid
■ Vasodilate: ↓vascular resistance, ↑ blood flow
AUTOREGULATION OF BLOOD FLOW
As blood flow ↑ to muscles during exercise, the adenosine is washed out.
■ ↓ adenosine → arterioles and small arteries vasoconstrict → keeping blood
flow at a normal rate (in face of ↑arterial pressure).
hematocrit
Percentage of RBCs in blood sample.
■ Normal:
■ Male: 44–46.
■ Female: 40–42.
Venous Hct is typically higher than arterial Hct because of xxx
■ More yyy in comparison to plasma. CO2 from tissues gets converted
by zzz → HCO3 in RBC increases osmotic pressure
→water rushes in →RBC greater volume
Venous Hct is typically higher than arterial Hct because of “chloride shift.”
■ More RBC mass in comparison to plasma. CO2 from tissues gets converted
by carbonic anhydrase → HCO3 in RBC increases osmotic pressure
→water rushes in →RBC greater volume
hb conc
Normal:
■ Male: 15–16 g/dL.
■ Female: 13–14 g/dL.
Severe anemia:
■ <7.5 g/dL.
■ Hct = Hb °ø 3.
anemia
↓ Hct.
■ ↓ RBC and/or ↓ Hb concentration
Consequences of Anemia
■ ↓ oxygen transport in blood.
■ Fatigue, respiratory compensation, cardiac compensation.
■ Hypoxia in the tissues.
■ Causes small arteries and arterioles to dilate (so ↑ blood return to the
heart [preload]).
■ Hypoxia in the pulmonary circulation results in vasoconstriction of those
vessels (opposite to effect on other body tissues).
https://drive.google.com/open?id=0B8uJUY-tie8GbHk3T2wxVnc1bmM
https://drive.google.com/open?id=0B8uJUY-tie8GU0JJR195MTR4QlE
https://drive.google.com/open?id=0B8uJUY-tie8GQm9Bbnl1dXZObEE
https://drive.google.com/open?id=0B8uJUY-tie8GRnowaXEtQkhxT28
Carbon Monoxide Poisoning
■ CO competes with oxygen for Hb-binding sites and changes allosterics;
CO has greater affinity (250°ø)
■ Normal Hb level
■ O2 content ↓
■ Cherry red cheeks
Cyanosise
■ Deoxygenated hemoglobin in tissues gives the skin/mucous membranes a
blue tint.
■ Does not occur in severe anemia because you need >5 g of deoxygenated
Hb per 100 mL of blood to appreciat
ERYTHROPOIETIN
■ Glycoprotein hormone produced in kidneys
■ ↑ RBC production by bone marrow
■ Acts at the hemocytoblast (pluripotent stem cell)
erythpoetin
↓ Erythropoiesis → anemia
■ ↑ Erythropoiesis → polycythemia
■ ↑ Blood viscosity, sluggish blood flow, ie, polycythemia vera (JAK2
mutation downstream of Epo Receptor)
Negative Feedback
■ ↓ O2 tension (anoxia/hypoxia) →↑erythropoietin (HIF)
■ ↑ O2→↓erythropoietin
Virchow’s Triad
■ Endothelial injury
■ Stasis
■ Hypercoaguability
hemostasis
■ Three parts:
■ Vasoconstriction
■ Platelet aggregation/plug (primary)—platelets bind wWF on damaged
endothelium
■ Coagulation (secondary)—crosslinking with fibrin meshwork
Coagulation
Intrinsic and extrinsic pathways
Prothrombin is cleaved to thrombin.
■ Converted by prothrombin activator (Factor Va).
■ Fibrinogen cleaved to fibrin.
■ Converted by thrombin.
■ Fibrin forms the clot and cross-links with the platelets.
https://drive.google.com/open?id=0B8uJUY-tie8GbWJ0Z0JSbHlCb1U
https://drive.google.com/open?id=0B8uJUY-tie8GdkpWdTRnN09ZT2c
