case 6: hypovolemic shock Flashcards
1
Q
Case Description
A
Physical Exam
– BP – 78/48 mm Hg (MAP = ?)
– Pulse rate – 120/min (why?) bp is low so perfusion of o2 and nutrients to tissues are deficient so body compensates with increase cardiac rate
– RR – 40/min
– The central venous pressure is 6
mm Hg
– Pallor
– Lower abdominal pain
2
Q
Central Venous Pressure (CVP)
A
- a.k.a. mean venous pressure (MVP), normal = 2-8 mm Hg
- Is the pressure of blood near right atrium, often a good approximation of right atrial pressure
- Reflect the volume of venous return (why?) pressure estimates volume, the volume is total blood in body returned to vein to RA (venous return)
- Factors that increase CVP – hypervolemia (total blood volume increased, so increase of pressure, central venous pressure, and blood returning to RA ), heart failure (heart cannot pump blood out, backflow from RA to vena cava, increase in CVP) , pulmonary hypertension (backflow of blood from pulmonary artery to RV to RA to vena cava which increases CVP), pulmonary embolism (obstruction of blood somewhere in circulation, causing backflow and congestion)
3
Q
Diagnosis
A
- Diagnosis
– Acute diarrhea -> hypovolemic shock
4
Q
Immediate Treatment
A
- Immediate treatment:
– Intravenous therapy with 4 L of crystalloid fluid
– Mechanical ventilation
5
Q
Crystalloid Solution
A
- Crystalloid – substance whose particles are smaller than those of a colloid, form a true solution, and are therefore capable of passing through a semi-permeable membrane
- capillary contains pores big enough to allow electrolytes to be exchanged but small enough to limit blood cells and blood plasma proteins to exit, proteins will remain in lumen of capillary
- Examples of crystalloid solutions
– Saline (0.9% NaCl) – pH 5.7, isotonic (?) osmolarity between 270-300 milliosmo
– Balanced electrolyte solution – pH 7.4, isotonic, contains K+, may also Ca+2 & Mg+2
– D5W – 5% dextrose in water, isotonic, pH 5.0
6
Q
Physical Exam & Follow-up Treatment
A
- 1-Hr later
– BP – 85/50 (MAP = 62 mm Hg), pulse – 105 beats/min; respiratory rate – 35 /min
– The central venous pressure – 9 mm Hg (why?) bc of iv injection of crystalloid that increases total blood volume, which increases CVP
– The capillary refill time – 1 second (normal < 2”)
– The measured urine output for the past hour – 35 ml - Follow-up treatment
– 1 L of lactated saline
– Still under mechanical ventilation
7
Q
The Use of Lactated Saline
A
- Lactated saline – a.k.a. lactated Ringer’s solution
– Osmolarity – 273 mOsm/L (Na+, Cl-, lactate, K+, Ca2+) - The concept of acid anion
– HA -> H+ + A- (where HA is the acid and A- is the acid anion)
– Acid anions are conjugate base of the acid
– Acid anions are not themselves acids - Lactate is a base whereas lactic acid is an acid
- Thus, lactate (Na+-lactate-) can help correct metabolic acidosis by removing H+ from the body fluid
8
Q
ventilation
A
ventilator is used to help push air that with high partial pressure of o2 into the lung
- this patient diaphragm cannot contract well bc of lack of o2 and nutrients to diaphragm and other inspiratory muscles, due to lack of perfusion/lack of blood circulation to muscle
- positive pressure to push air into respiratory system
9
Q
Why Would the Blood Flow?
A
- Blood flow from high P to low P
- What does cardiac muscle contraction do to blood pressure & blood flow?
- During ventricular relaxation, no blood ejection, why would the systemic arterial P remain at 80 mm Hg?
pressure is higher in ventricle compared to artery, artery is higher than capillary, higher than vein, than atrium
10
Q
Cardiac Contraction and Blood Flow
A
- Flow of blood – based on pressure gradient (ΔP; P1 – P2)
– Blood flow from high blood P (BP) → low BP
– Ventricular contraction (pumping) generates ΔP → > arterial
BP > capillary BP > venular BP > atrial BP
– Blood flow in vascular circulations is continuous (not intermittent). What if it is intermittent?
11
Q
Blood Vessels (Pressure)
A
- Pressure (P) – the amount of force exerted on a given area
– Pressure = Force/Area (P = F/A) - if area is greater, then pressure will be smaller
- if area is smaller, then pressure will be high
– Examples – exert force on skin by thumb or needle - Blood pressure (BP)
– Force generated by ventricular contraction (mainly) -> increase P -> increase ∆P gradient between 2 ends -> ↑ stroke volume
– ↑ Area (vasodilation) → low resistance → ↓ BP
– ↓ Area (vasoconstriction) → high resistance → ↑ BP
12
Q
Cardiac Output – Definition
A
- Cardiac output (C.O.; Q)
– Regarding the pumping ability of the heart
– Q is the blood volume (ml or liter) pumped per min. by each ventricle (left and right)
– Cardiac output (ml/min) = cardiac rate (beat/min) x stroke vol (ml/beat, or ml/systole, or ml/ventricular contraction) - Q at resting condition:
– ~70 beats/min, stroke vol ~80 ml/beat → ~5,600 ml /min
13
Q
Regulation of Cardiac Rate
A
- Without neuronal influences, SA node will drive heart rate at its spontaneous activity (automaticity initiated by pacemaker)
* Chronotropic (time, frequency) effect – autonomic (sym & parasym) on SA node is the main controller of cardiac rate
– Original rhythm set by SA node (auto-rhythmic, or pacemaker cells)
– Symp and parasymp nerve fibers modify rate of spontaneous depolarization and conduction rate on auto-rhythmic cells
– Symp – stimulatory; parasymp – inhibitory
– The actual pace set by SA node depends on the net effect of antagonistic influences of symp + parasymp
- Without neuronal influences, SA node will drive heart rate at its spontaneous activity (automaticity initiated by pacemaker)
- The activity of autonomic innervation
of the heart is coordinated by cardiac control centers in the medulla oblongata (vital centers: inhibitory and activating)
* Chronotropic effects
– Sympathetic (NE & E) – ↑ Na+ channels open → ↑ rate of depolarization in auto-rhythmic cells of SA node → ↑ cardiac rate → “+” chronotropic effect
– Parasympathetic (ACh) – allows K+
channels open longer → hyperpolarizes auto-rhythmic cells of SA node → “-” chronotropic effect
- The activity of autonomic innervation
14
Q
Cardiac Output – Stroke Volume
A
- Factors affecting stroke volume
– Determined by contractility (strength of contraction), end-diastolic volume (EDV), and total peripheral resistance (TPR) - EDV (preload) – vol of blood in ventricles at the end of diastole
– ↑ of EDV → ↑ in stroke vol (volume of blood ejected out of ventricle each contraction, determined by contractility)
– Ejection fraction (SV / EDV) – normally 60-70% - TPR – frictional resistance or impedance to blood flow in arteries
– ↑ of TPR → ↓ in stroke vol - At a given EDV, the amount of blood ejected depends on (proportional to) contractility
– ↑ in contractility → ↑ in stroke vol
EDV- volume of blood in ventricle at end of diastole
15
Q
Regulation of Contractility
A
- Intrinsic regulation (Frank-Starling law of
heart):
– Varying degree of stretching of
myocardium by EDV
– ↑ EDV → ↑ in myocardial stretching → the
actin filaments overlap with the myosin
only at the edges of the A band → ↑ # of
interactions between actin and myosin →
↑ in contractility (contracts more
forcefully)
– ↑ EDV → ↑ cardiac contractility → ↑ Q - Extrinsic regulation:
– Sympathoadrenal system – NE, E → “+”
inotropic effect (more Ca2+ available to
sarcomeres) → ↑ contractility
16
Q
Cardiac Output – Summary
A
- Sympathetic NS (NE, E) affect Q in 2 ways:
– “+” chronotropic effect on cardiac rate
– “+” inotropic effect on contractility (contraction strength) - Parasympathetic NS (ACh)
– “–” chronotropic effect on C.R.
– No direct effect on contractility in ventricles - Factors affecting stroke volume
– End-diastolic volume (EDV), total peripheral resistance (TPR), and contractility (strength of contraction)
17
Q
Cardiac Output – Venous Return
A
- Venous return (VR)
– The volume of blood to heart via veins, driven by venous pressure
– Veins have thinner walls, hold ~60- 70% of blood in the body (capacitance vessels) - The venous return is affected by:
– The total blood volume
– The venous pressure - ↑ VR → ↑ EDV → (Frank-Starling law of heart) → ↑ Q
18
Q
Cardiac Output – Venous Pressure
A
- Factors affecting the venous pressure:
– ↑ Sympathetic activity → ↑ venous constriction → ↑ VR
– ↑ Skeletal muscle pumps → increase VR - Breathing – P difference between the thoracic and abdominal cavities
– During inspiration, ↓ in thoracic P or ↑ in abdominal P → ↑ → ↑ P gradient → ↑ VR
19
Q
Blood Pressure (BP)
A
- Arterial blood P
– Arterioles are rich in smooth muscle →
the smallest diameter → the greatest
resistance
– Capillary BP is reduced because of the
total cross-sectional area.
– Veins have the lowest BP - Q (C.O.) proportional to BP/TPR → P proportional Q x R
– Q = cardiac rate x stroke vol
– TPR is affected by vasoconstriction and vasodilation
– 3 most important variables are cardiac
rate, SV, and TPR – increase in each
of these → ↑ in BP - BP can be regulated by:
– Kidney and sympathoadrenal system
higher the pressure in bvs the lower the cardiac output
20
Q
Juxtaglomerular Apparatus
A
- Region in each nephron where the afferent arteriole comes in contact with the thick ascending limb LOH
- Contains granular cells, macula densa cells, and mesangial cells
– Granular cells secrete renin
– Macula densa – detection of flow & [NaCl]
-vascular component (afferent and efferent arteriole
-tubular component (glomerular capsule, loop of henle, PT and DT, collecting duct)
21
Q
JG Apparatus – Granular Cells
A
- Granular cells (juxtaglomerular cells):
– Modified smooth muscle cells in the wall of afferent arterioles
– Secrete renin (hormone/enzyme)
– Sympathetic (β1 adrenergic) stimulation → ↑ renin secretion
– ↓ in renal perfusion pressure (BP, detected directly by the granular cells) → ↑ renin secretion
– [NaCl] in filtrate sensed by macula densa → affects renin secretions
22
Q
Granular Cells and BP Regulation
A
- The renin-angiotensin-aldosterone
(RAA) system – (a “-” feedback response)
– ↓ in BP → detected by granular cells →
↑ renin secretion → renin converts
angiotensinogen (produced by the liver
→ angiotensin (AT) I
– Angiotensin-converting enzyme (ACE)
converts AT I → AT II (bioactive)
– AT II → vasoconstriction → ↑ BP
– ↓ In blood vol → ↓ in BP → … → ↑
aldosterone secretion (a steroid H from
adrenal cortex) → ↑ in renal Na+ re-
absorption → ↑ in water re-absorption
→ ↑ blood vol → ↑ BP
Q inverse P/R; P inverse Q x R
23
Q
Hypovolemic Shock – Definition
A
- Shock
– A medical emergency in which the organs and tissues of the body are not receiving an adequate blood flow - Hypovolemic shock
– An emergency condition in which severe blood and fluid loss make the heart unable to pump enough blood to the body
– A condition in which systemic BP is inadequate to deliver O2 and nutrients and remove wastes to support vital organs and
cellular functions.
– A physiologic state characterized by a decrease in tissue perfusion
24
Q
Hypovolemic Shock – Causes
A
- Causes – any ways to cause excessive fluid loss
– Hemorrhage from cuts, wounds, blunt trauma or internal bleeding
– Excessive diarrhea, vomiting or sweating
– Severe burn
– Polyuria (such as ketoacidosis)
25
Q
Hypovolemic Shock – Symptoms
A
- Signs and symptoms
– Thirst (1st sign)
– Dizziness, confusion, loss of consciousness
– Hypotension, weak pulse, tachycardia (early), bradycardia (late) (why?) initial tachycardia is heart muscle pumping to compensate for the not enough perfusion to body, later when there is lack of o2 to body the heart cannot function as well so pulse rate becomes slower and slower
– Chest pain, cyanosis, rapid shallow respiration (why?) to try to increase oxygen loading in pulmonary circulation
– Oliguria or anuria (<25 ml/hr) (why?) reduced filtration of renal filtrate and reduce volume of urine
– Cold feeling (shivering), profuse sweating
26
Q
Pulse P and Mean Arterial P
A
- Pulse pressure = systolic P – diastolic P
- The mean arterial blood pressure
(MAP)
– Represents the average arterial pressure during the cardiac cycle
– Venular blood pressure – VBP
– (MAP – VBP) is the force to drive blood through capillary beds of organs
– MAP = diastolic pressure + 1/3 pulse pressure (why?) systole cardiac pressure accounts for 1/3 of cardiac cycle and diastole 2/3 - For this patient:
– BP – 78/48 mm Hg (MAP = ? mm Hg)
78-48
48 + 1/3(78-48) = 57
27
Q
Reversible vs. Irreversible Shock
A
Reversible vs. Irreversible Shock
* Reversible shock – fluid loss → > 50% of original MAP→ compensatory response → patient will recover (time varies)
* Irreversible shock – fluid loss → < 50% of original MAP → transient feeble recovery → progressive toward death
28
Q
Blood Volume – Distribution of Body Fluids
A
- Intracellular compartment (2/3 of total body H2O) within the cells
- Extracellular compartment (1/3 total body H2O)
– 80% interstitial fluid
– 20% blood plasma
– Much easier to exchange fluid between extracellular compartments (why?) intracellular fluid is compartmentalized by cell membrane where the lipid bilayer does let water through, only through aqua pores. capillary contains pores that allow water between extracellular compartments - Maintained by constant balance between H2O loss and gain
29
Q
for a person at rest, where is most of blood located by volume?
A
veins and venules
systemic veins
large veins
compensation reduced consequences of hypovolemic shock
30
Q
Fluid Movement in Capillaries
A
- Fluid movement = fluid out - fluid in
= (hydrostatic P inside capillary + oncotic P of interstitial fluid ) - (hydrostatic P of interstitial fluid + oncotic P of plasma ) - Movement of solutes
– At the arteriolar end of capillary: (37 + 0) - (1 + 25) = 11 mm Hg
– At the venular end of capillary : (17 + 0) - (1 + 25) = -9 mm Hg
– Excess tissue fluid returned to venous system by lymphatic vessel
31
Q
Flow of Fluids in Capillaries
A
- Blood plasma moves into the interstitium at the arteriolar end of the capillary and mostly
returned from the venular end of the capillary - The movements of fluid in capillaries is driven by pressure (P) gradient
- The actual volume of fluid movement depends on the interactions of hydrostatic P and colloid (oncotic) osmotic P
32
Q
Compensatory Response – Capillaries
A
- In shock patients:
– ↓ MAP → ↓ (hydrostatic P inside
capillary, originally 37 mm Hg) at
the arteriolar end, no change in
[proteins] → no change in
(oncotic P of plasma) → capillary
is drawing fluid back to vessels
from interstitium → ↑ C.O. (Q) - → A re-distribution of extracellular
fluid – slowly, fluid moves from
interstitium back to blood vessels
33
Q
what would happen to the hematocrit at initial vs later phases for patient? why?
A
initial = volume of blood cells as proportion of total blood, ~40-45% of total blood volume
blood plasma ~55% of blood volume
initial = fluid comes back from interstitial to blood circulation which increases blood plasma volume but no increase of blood cell production since it’s initial produced by bone marrow
later = more and more production of blood cell production from bone marrow so hematocrit increase gradually
34
Q
Regulation of BP – Centers
A
Central integrator – vasomotor
and cardiac control centers
– Located in medulla oblongata
– Vasomotor center controls
vasoconstriction (increase restriction and bp) and vasodilation
– Cardiac control centers regulate cardiac rate
– Receive sensory nerve activity from baroreceptors (in arch of aorta and carotid artery)
– Act through vagus & sympathetic NS to control cardiac rate and TPR
35
Q
Regulation of BP – Baroreceptors
A
- Sensors – baroreceptors
– Stretch receptors
– Located in aortic arch and carotid sinuses, detect BP change - detect mechanical change of blood pressure
- Baroreceptor reflex
– More sensitive to ↓ in BP and sudden changes in BP
– A change from lying to upright
posture → ↓ BP → detected by
baroreceptors in aortic arch &
carotid sinus → info sent to
medulla → ↓ parasympathetic
and ↑ sympathetic activities →
vasoconstriction and ↑ cardiac
rate → ↑ BP
36
Q
Compensatory Response – ANS (1)
A
- Blood (fluid) loss → ↓ MAP
– Baroreceptors detect ↓ MAP → ↓ firing rate
– → ↑ sympathetic & ↓
parasympathetic discharge →↑BP - Effects ↑ sympathetic
stimulation on heart
– ↑ heart rate (SA node
activities) & ↑ cardiac
contractility - For short time, little effect on
C.O., why? first compensatory response is in capillary so it can gradually move fluid from interstitial to blood circulation but is very slow process, won’t increase blood volume fast, little effect on C.O., gradually as total blood volume increases because of capillary redistribution of extracellular fluid
37
Q
Cardiac Output – Venous Return
A
- EDV is affected by VR
- Venous return (VR)
– Veins hold 2/3 of total blood
(capacitance vessels) - Venous return is affected by:
– The total blood volume
– The venous pressure - ↑ sympathetic activity → ↑
venous constriction → ↑
venous return - ↑ skeletal muscle pumps → ↑
venous return
38
Q
Sympathetic Adrenergic R’
A
- All adrenergic R’ – G-protein-coupled R’ (GPCR’)
– G αβγ → Gα + Gβγ
– modulation of ion channel permeability
– Modulation of enzyme activity - Mechanisms of action
– β1-, β2 R’ activation → ↑ [cAMP]i - β1 R’ → EPSP → ↑ heart contractility
- β2 R’ →IPSP → smooth muscle relaxation (bronchodilation; vasodilation at skeletal muscles)
– α1-, α2 R’ activation - α1 R’ activation → ↑ [Ca2+]i → smooth muscle contraction → vasoconstriction at certain viscera (why is it beneficial? sympathetic is for fight or flight so we want blood increase to heart muscle and skeletal muscle and eliminate more co2 out of body… vasoconstriction and less blood supply to GI and reproductive tract) and veins
- α2 R activation – ↓ NE release in a form of negative feedback
39
Q
Compensatory Response – ANS (2)
A
- P = Q x R = cardiac rate x SV x R
- We want to ↑ blood pressure to ↑ hydrostatic P of the blood
→ ↑ perfusion to essential organs (brain, heart muscle, and kidneys) - ANS (sympathetic) effects on blood vessels
– Sympathetic discharge → stimulate α receptors of smooth m. in
veins (capacitance vessels) → constriction of venous vessels → ↓ venous blood volume → ↑ venous return → ↑ C.O. (Q) → ↑ P
40
Q
Blood Flow
A
- Blood flow (rate) – blood moves
through a tissue or an organ per
unit of time (ml/min) - Pattern of blood moves to each
organs is mainly parallel → blood
flow to the organ is adjustable by
R (vascular resistance) - Blood flow is due to P gradient
(ΔP) at the two ends of a vessel
– BF proportional Δ P / R
– Blood flow is proportional to Δ P
and is inversely proportional to
vascular resistance
41
Q
Blood Flow & Cardiac Output
A
- Vascular resistance determines how much blood flows through a
tissue or organ
– Vasodilation → ↓ vascular resistance → ↑ blood flow
– Vasoconstriction→ ↑vascular resistance → ↓ blood flow - Blood flow for all organs (100%) = total blood flow = cardiac output
42
Q
Vascular Resistance to Blood Flow
A
*Poiseuille’s law – vascular
resistance proportional Lη / r4
– L = length of vessel
– η = viscosity of blood
(anemia → ↓ η)
– r = radius of vessel,
vasoconstriction vs.
vasodilation
* The power of r4 – radius = 1 vs. 2 vs. ½
* R is further adjusted by compliance/elasticity
* Total peripheral resistance (TPR) – the sum of all vascular
resistance within the systemic circulation or pulmonary
circulation
43
Q
Parallel Array of Systemic Vasculature
A
- The beauty of parallel array of vascular system – allows MAP
to increase selectively, not all vascular beds respond equally to
sympathetic tone - Examples of serial array of vascular system?
- some arteries more vasoconstricted than others
44
Q
Compensatory Response –
Selective Redirection of Blood Flow
A
- Regulation of vascular bed constriction:
– Intrinsic – arteries influenced by local metabolic factors, like in heart
and brain (autoregulation)
– Extrinsic – arteries influenced more by sympathetic discharge, like gut
(splanchnic bed), striated muscle, skin, kidney - → more blood is diverted to vital organs (brain, heart & kidneys)
from non-vital organs (skin, skeletal muscle, GI tract etc.)
45
Q
Compensatory Response – ANS (3)
A
- Peripheral chemoreceptors:
– Located at carotid sinus & aortic
arch
– Directly detect changes in PO2
– Indirectly detect changes in PCO2
through pH - ↓ Blood flow → hypoxia (↓ PO2) &
hypercapnia (↑ PCO2) → stimulate
peripheral chemoreceptors →
trigger additional sympathetic firing
→ ↑ TPR → ↑ venous return→ ↑ C.O.
(Q)
46
Q
Blood Pressure
A
- C.O. (Q) = P/R → P = Q x R
- Q = cardiac rate x stroke volume (SV)
- → P = cardiac rate x SV x R
– R (total peripheral resistance, or TPR) is affected by
vasoconstriction and vasodilation - ↑ cardiac rate, SV, R → ↑ in P (blood pressure)
47
Q
Compensatory Response – ANS (4)
A
- Cerebral ischemic reflex
– ↓ MAP → ↓ perfusion → ↓
PO2 in brain → ↓trigger
autonomic response
from medullary cardiac
and vasomotor center →
send signal to additional
sympathetic firing - This results in ↑ C.O. (Q)
& redirection of blood
48
Q
Compensatory Response – RAAS
A
- ↓ MAP → ↓ renal blood flow
→ sensed by granular cells
→ ↑ renin secretion → … ↑
angiotensin II
– angiotensin II →
vasoconstriction → ↑ end
systolic volume (ESV,
afterload)
– → ↑ aldosterone secretion
→ ↑ water & salt retention
→ ↑ end diastolic volume
(EDV, preload) (increased stretch of cardiac muscle and contractility (frank starling), blood perfusion stronger bc increase of pressure gradient, contractility at cost of workload of heart)
49
Q
ADH and Medullary CD
A
- The medullary CD is permeable to
water but not to salts → the high
[NaCl] in the medullary interstitial fluid
cannot enter the medullary CD - Antidiuretic hormone (ADH) from the
posterior pituitary → ↑ incorporation of
aquaporins (water channels) into
apical epithelial cell membranes of
medullary CD → ↑ water reabsorption - reduce volume of urine
- Action of ADH – as CD pass through
the hypertonic renal medulla, water in
renal tubular lumen through
aquaporins → tubular epithelial cells
→ interstitium → carried away in
capillarie
50
Q
Compensatory Response – ADH
A
- ↓ MAP → ↓ blood volume in atria,
vena cava & pulmonary veins →
sensed by stretch (volume)
receptors → send signals to
hypothalamus → ↑ ADH
(vasopressin) secretion by posterior
pituitary - Effects of ADH
– Very responsive to ↓ MAP →
vasoconstriction → ↑ arterial BP
– ↑ Plasma osmolality in plasma → ↑
ADH (vasopressin) → ↑renal water
reabsorption → ↑ blood volume → ↑
arterial BP
51
Q
Stress Reflex of Vascular Wall
A
- Myogenic regulation of vascular P – like to remain at the
same tension - Stress relaxation
– Spring vs. blood vessels
– Arteries – a sudden vol ↑ → ↑ tension → ↑ P→ ↑ stress; however,
the pressure does not remain steady, but declines over time
due to vascular reflex relaxation
52
Q
Compensatory Response –
Reverse Stress Relaxation
A
- Reverse stress relaxation – a vein filled with blood, a
sudden vol ↓→↓ tension → smooth muscle constrict → ↑ P
gradually
– If blood vol is restored, the pressure will overshoot, then
gradually relax down → remain in the same tension - Hemorrhage → spontaneous intrinsic (myogenic, not
extrinsic) to squeeze down on the remaining vol → ↑
venous return
53
Q
Compensatory Responses – Summary (1)
A
- Loss of blood volume (by hemorrhage, diarrhea etc.) → body will
attempt to increase tissue perfusion - Redistribution of extracellular fluid – blood loss → ↓ total blood
volume → ↓ hydrostatic P of plasma → (fluid out < fluid in) → ↑ flow
of interstitial fluid back into venular end of capillaries → ↑ blood
volume - ANS regulation → ↑ sympathetic & ↓ parasympathetic firing
– → ↑Cardiac rate and ↑ contractility → ↑ C.O. (Q)
– → ↑Vascular smooth muscle contraction → vasoconstriction → ↑
venous return → ↑ C.O. (Q)
– Involvement of peripheral chemoreceptor detection → ↑ sympathetic
firing
– Cerebral ischemic reflex → ↑ medullary cardiac and vasomotor center
→ ↑ sympathetic firing
54
Q
Compensatory Responses – Summary (2)
A
Hormonal regulation
– ↓ MAP → activates renin-angiotensin-aldosterone system (RAAS)
↑ salt & water reabsorption → ↑blood vol → ↑ C.O. (Q)
– ↓ MAP → sensed by pressure receptor (volume receptors) → ↑ADH
(vasopressin) secretion → …→ ↑ C.O. (Q)
* Myogenic regulation ↓ MAP → reverse stress relaxation
vasoconstriction → …→ ↑C.O. (Q)
* If blood plasma loss > 1.5-2 L → MAP drops > 40% → compensatory efforts likely to fail → irreversible shock → death
55
Q
Shock Patients – Sweating
A
- Hypovolemic patients are typically sweating (cold sweat). Why is the patient sweating?
sympathetic system, cholinergic postganglionic nerve fibers (instead of norepinergic) uses acetylcholine as neurotransmitter to nerve ending of sweat glands
56
Q
Shock Patients – Collapse
A
- Collapse – Is it beneficial for patient’s survival? Why?
- Question – Is there any exception? Why?
57
Q
Collapse
A
- A person collapsed due to hypovolemic shock is beneficial to
be lying down. The brain tissue in supine position will be
perfused better. - Be cautious on cerebral hemorrhage
58
Q
Shock Patients – Pallor
A
Pallor – Is it beneficial for patient’s survival? Why?
59
Q
Pallor
A
- Pallor (paleness) is a consequence of body’s effort redirecting
the blood flow to vital organs.
60
Q
Shock Patients – Shivering
A
- Question 1 – Why is this patient shivering?
- Question 2 – As a health care giver, should you give the
patient a blanket? Why?
61
Q
Shivering
A
- Shivering in hypovolemic patient
is a paradoxical phenomenon. - The cold sensor in the skin
detects the coldness → send
signals to hypothalamic shivering
center → the body shivers to
generate heat - no blanket because Warming the patient with a blanket would defy the shunting
effect for blood flow.
62
Q
Shock Patients – Alcohol?
A
- Question – As the patient is shivering, should you comfort
him with a cup of wine?
63
Q
Effects of Alcohol on Hypovolemia
A
- Alcohol is a vasodilator
- Alcohol is a diuretic, works against ADH
64
Q
Hypovolemic Shock – Treatment (1)
A
- Management of blood loss
– Immediate need – stop blood loss, apply surgical repair if necessary
– The second need – replace the lost volume - Fluid therapy – the use of crystalloid solutions as volume
expanders
– Solutions of inorganic ions and small organic molecules dissolved in
water
– The main solute is either glucose or sodium chloride (saline)
– Usually isotonic (“balanced” or “physiological”)
– Significant plasma volume expansion requires large volume -> may
lead to tissue edema
65
Q
Hypovolemic Shock – Treatment (2)
A
- Fluid therapy – the use of colloid solutions as volume
expanders
– Semisynthetic colloids (gelatins, dextrans and hydroxyethyl
starches) and the naturally occurring human plasma derivatives
(human albumin solutions)
– Most colloid solutions are presented with the colloid molecules
dissolved in isotonic saline
– Create colloid osmotic P to draw fluid from interstitium back to
blood vessels
