case 6: hypovolemic shock Flashcards
Case Description
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
Central Venous Pressure (CVP)
- 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)
Diagnosis
- Diagnosis
– Acute diarrhea -> hypovolemic shock
Immediate Treatment
- Immediate treatment:
– Intravenous therapy with 4 L of crystalloid fluid
– Mechanical ventilation
Crystalloid Solution
- 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
Physical Exam & Follow-up Treatment
- 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
The Use of Lactated Saline
- 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
ventilation
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
Why Would the Blood Flow?
- 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
Cardiac Contraction and Blood Flow
- 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?
Blood Vessels (Pressure)
- 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
Cardiac Output – Definition
- 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
Regulation of Cardiac Rate
- 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
Cardiac Output – Stroke Volume
- 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
Regulation of Contractility
- 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
Cardiac Output – Summary
- 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)
Cardiac Output – Venous Return
- 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
Cardiac Output – Venous Pressure
- 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
Blood Pressure (BP)
- 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
Juxtaglomerular Apparatus
- 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)
JG Apparatus – Granular Cells
- 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
Granular Cells and BP Regulation
- 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
Hypovolemic Shock – Definition
- 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
Hypovolemic Shock – Causes
- 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)
Hypovolemic Shock – Symptoms
- 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
Pulse P and Mean Arterial P
- 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