Term
Cardiac Output (CO) vs. Cardiac Index (CI) |
|
Definition
CO=vol. of blood pumped by L per unit time (min) Normal=5 L/min CI=CO in proportion to body size (surface area); CO/m^2 Normal=3 L/min/m^2 Hence, average body SA=1.67 m^2 |
|
|
Term
Factors affecting normal/basal CI (4): |
|
Definition
1. Body surface area (different slide)
2. AGE: Birth=2.4, 10y/o=4-4.5 (max), then slow decline back to ~2.4 by 80 y/o (this decline can be slowed significantly in very active people) (see graph, p. 280)
3. Metabolic rate of individual (thyroid, fever, etc.) 4. Exercise
|
|
|
Term
Relationships between CO and: 1. Venous return (VR)
2. Tissue oxygen consumption |
|
Definition
Tissue oxygen demand-->VR-->CO 1. Increased tissue oxygen demand drives arteriolar vasodilation (local control; oxygen theory)-->decreased Total peripheral resistance (TPR)
2. VR increases b/c TPR decreases while CO is constant or elevated (blood shifts: arterial to venous circulation) 3. Increased VR drives incrased CO (heart ALWAYS pumps out what it receives...up to a limit) Hence, VR=CO always unless there is damming up of blood somewhere in the circulation, or volume is being added to/extracted from total (conservation of mass idea) |
|
|
Term
Starling Law of the Heart: |
|
Definition
The heart pumps all blood returned to it up to a limit (VR=CO). |
|
|
Term
CO and/or CI directly related to: (2)
|
|
Definition
1. Work output of heart 2. Tissue oxygen demand (whch determines VR) Hence, CO is determined almost ENTIRELY by the sum of factors affecting peripheral resistance to blood flow /VR. |
|
|
Term
Notes on Starling curves: |
|
Definition
1. Initial steep slope means: a small change in right atrial (filling) pressure (RAP) translates into a LARGE change in CO (this is good) 2. Increased VR-->RAP-->diastolic end pressure-->CO 3. Also: heart fibers exhibit the same Length-Tension (L-T) relationship as skeletal mm. (in terms of a single sarcomere), however, the heart muscle does not stretch to the point of actin-myosin non-overlap like skeletal... |
|
|
Term
1. BE ABLE TO DRAW A NORMAL STARLING CURVE FROM MEMORY 2. Limits of Starling curve affected by neural control, physical control/modification |
|
Definition
1. Start: -2mmHg, 0 L/min, normal max=13 L/min, limit reached by ~+2mmHg, (x, y=0 mmHg, 5 L/min) 2. Super-athletes: max=30-40 L/min (hypereffective; achieved by combined changes discussed in #3 below)
Heart failure: max~5 L/min (less than this=death) 3. Sympathetic stimulation: HR (180 bpm), contractility 2X (inotropic effect), hypertrophic heart (150-175% normal size) |
|
|
Term
Factors causing a hypoeffective heart: (7) |
|
Definition
1. Inhibited nervous excitation (sympathetic) 2. Abnormal rhythms or rates/decreased effectiveness
3. Hypertension (increased arterial pressure (Pa)) 4. Congenital defects 5. Cardiac hypoxia or anoxia (extreme hypoxia) 6. Infections: myocarditis, diptheria, botulism, tetanus 7. Abnormal wear (tamponade, etc.) |
|
|
Term
Experimental example: importance of neural control on Pa regulation (dinitrophenol; DNP)
|
|
Definition
1. Symp control + DNP: arterial dilation-->decreased TPR leads to a drop in Pa, which is compensated for by increased 4X CO (HR and contractility mainly). 2. No control +DNP: arterial dilation-->decreased TPR: leads to decreased Pa b/c CO only increases 1.6X w/o sympathetic innerv. (CO increases 1.6X based on increased VR; blood running from arterial to venous circulation with lowered TPR) |
|
|
Term
Notes on transmural pressure (TMP) significance: Equation to calculate it Relation to CO |
|
Definition
1. TMP is significant in determining CO b/c the RA is VERY compliant Eq: TMP=RAP - Intrapleural Pressure (IPP) 2. Inhalation: IPP becomes (-) RAP=0 mmHg (~constant) Exhalation: (+) ITP 3. Given equal transmural pressures, 2 different compartments will have the same volume (not dependent on values of pressure in/out, just the difference between these values!), p. 285 4. Starling curves represent a constant TMP along line. Normal=-4 mmHg 5. CO is directly proportional to RAP, VR, abs. value of IPP CO is indirectly proportional to IPP |
|
|
Term
VR: 1. Factors affecting it 2. Equation 3. Normal values 4. Notes |
|
Definition
1. Mean systemic filling pressure (Psf): "degree of fullness" of the systemic circulation, RAP, and resistance to venous return (RVR): R btw. periphery and RA. 2. VR = [Psf - RAP]/[Rv + (Ra/26)] 3. Normal values: Psf=7 mmHg, RAP=0 mmHg, RVR=varies (but Rv is 26X more important than Ra!) 4. VR is a flow, so it is dependent on a pressure difference (Psf-RAP). Equilibrium nature of eq.: RAP is directly proportional to CO but indirectly proportional to VR... |
|
|
Term
VR curve: 1. Why the plateau? 2. Transitional zone 3. X-intercept meaning 4. Slope indications and VR curve shifts**
|
|
Definition
1. Plateau caused by negative pressures collapsing major veins in the intrathoracic cavity (that feed into the RA) 2. -4-->0 mmHg (transitional zone is where the plateau begins to form: cannot suck blood into the heart with negative pressure) 3. x-intercept=where RAP=Psf (so flow, i.e. VR=0) 4. Due to changing RVR: VR=dec., RVR=inc. (slope=P/RVR), VR=inc., RVR=dec. (indirect proportionality) |
|
|
Term
Note on Psf part of VR calculation: 1. Unstressed volume 2. Equation 3. Important values 4. Factors affecting Psf |
|
Definition
1. Unstressed volume=3800 mL (x-intercept of Psf vs. total blood volume curve); volume required to fill circulation (without any increase in pressure) 2. Psf=P=Vol./Compliance (C) 3. Unstressed vol=3800 mL (Normal=5000 mL @ Psf=7 mmHg) 4. Psf <=> blood volume, compliance^-1, sympathetic stimulation of vessels (decreases C) |
|
|
Term
RVR vs. TPR: 1. Difference 2. Equations
|
|
Definition
1. RVR is mostly (2/3) in the veins (due to their high compliance relative to arterial compliance), while TPR is mostly arterial side 2. RVR=CvRv + Ca(Rv+Ra)=Rv + Ra/26
TPR=Pa/CO (??? changes by the second...) |
|
|
Term
Major VR curve shifts/alterations: 1. x-intercept 2. slope |
|
Definition
1. x-intercept (Psf factor) can be increased by increasing blood volume or reducing compliance (symp tone) 2. slope affected mainly by: inc./dec. RVR |
|
|
Term
Numbers: 1. Normal transmural pressure 2. Normal Psf 3. RV contribution to RVR (total) 4. Normal CI, average body SA, max&age, min&age 5. Normal max CO, hypo max, hyper max 6. Hypertrophic heart mass increase 7. VR curve transition zone pressure range 8. Unstressed volume of entire circulatory system 9. Respiratory affect: CO fluctuation range |
|
Definition
1. -4 mmHg 2. +7 mmHg 3. 2/3 4. 3 L/min/m2, SA=1.67 m2, max=4.5 (10 y/o), min=2.4 (birth, 80 y/o) 5. 13 L/min, hypo=5, hyper=30-40 6. 150-175% normal mass 7. -4 to 0 mmHg 8. 3800 mL 9. 4-6 L/min |
|
|
Term
Numbers 2: 1. Rest vs. exercising flow to skeletal mm./mass (multiple?) 2. Percentage of total CO #1 values represent 3. Resting flow to heart (% and mL/min) vs. skeletal 4. CO, CBF & work output of heart in exercise and major implication!
5. Heart's oxygen utilization (efficiency)
6. CBF extremes in systole & diastole 7. What % of metabolic energy does heart get from FAs? |
|
Definition
1. Rest: 3-4 mL/min/100 g-->80 (exercise); 20X 2. Rest=15% (large % of total body mass) vs. ?!?% 3. Rest=225 mL/min (4-5% CO) 4. Exercise: CO 4-7X, CBF 3-4X, Work 6-9X...hm, flow doesn't keep pace with work (efficiency is key) 5. 75% O2 extracted from blood in coronary aa. 6. Systole=75 mL/min, diastole=300 mL/min 7. 70% |
|
|
Term
How does the heart circumvent restricted blood flow during exercise (sympathetic stimulation)? |
|
Definition
Autoregulation (local control) dominates vascular control in the coronary aa. (also adenine produced by tissue metabolism is being studied) "Autocrine" blood flow regulation |
|
|
Term
Epicardial aa. vs. subendocardial aa.: 1. Flow (term)
2. Pressure vs. flow graph (p. 304) 3. Implications with ischemia 4. Anastomoses 5. Neural regulation differences (vs. location) (Note: not as important as autoregulation in the heart!!) |
|
Definition
1. "Phasic" flow (max-diastole, min-systole) 2. Subendocardial aa. subject to greater ΔP, so flow fluctuates the most in these 3. Subendocardial aa. more susceptible to ischemia 4. Coronary aa. can sprout anastomoses to get around blockages (good MI save) 5. Subendo=β receptors (circulating Epi-->dilation-->incrases flow; closest to circulating blood filling ventricles) vs...
α receptors: mainly affec Epicardial aa. flow Note: little/no parasympathetic innerv. |
|
|
Term
Venous drainage of heart: 1. R heart path
2. L heart path 3. Thebesian vv./venae cordis minimae
|
|
Definition
1. Anterior cardiac vv.-->RA 2. Great cardiac v. (& others)-->coronary sinus-->RA Note: blood is used mainly by ventricles, not atria 3. These small veins originate in the myocardium and empty directly into their respective heart chambers via outlets called foramina venarum minimarum - Most dense in the RV - Lest dense in the LV
|
|
|
Term
Other autocrine regulators of coronary circulation: (besides Adenosine and [O2]) (5)
|
|
Definition
1. K+ 2. CO2 3. Kinins 4. Prostaglandins (PGs) 5. NO |
|
|
Term
Notes on th Wigger's diagram valve action: 1. Aortic valve opening/closing 2. AV valve opening/closing 3. What creates the heart sounds? (4) |
|
Definition
1. Aortic valve: Opens: following isovolumic contraction Closes: prior to isovolumic relaxation
2. AV valve(s): Opens: following isovolumic relaxation
Closes: prior to isovolumic contraction
3. Valve CLOSURE creates heart sounds (S1 and S2), S3 is not valvular (early diastole, LV-assoc. in children & athletes, path in adults (CHF)). S4 is just before systole (same implications as S3). |
|
|
Term
Wigger's diagram: name the steps in order, starting with beginnning of systole: (There are 6 phases, 4 valve events) |
|
Definition
-AV valve closes (S1) 1. Isovolumic contraction -Aortic valve opens 2. Ejection -Aortic valve closes (S2) 3. Isovolumic relaxation -AV valve opens 4. Rapid inflow (passive filling)
-S3 if present (path in adults, sometimes normal in children & athletes) 5. Diastasis (passive filling stops, before atrial contraction phase) 6. Atrial systole (S4 is present, same implications as S3)-->back to #1 |
|
|
Term
Identifying genetic diseases with genomics: 1. Non-parametric linkage studies 2. Asociation studies 3. Definition: haplotype |
|
Definition
1.use a specific marker, compare in related individuals (known mutation(s), screening) 2. identify an allele, compare cross-families, case-control design (working with symptomatic patients (compared to population) to find mutation) 3. Haplotype=set of 2 SNPs (set of loci that are in linkage disequilibrium (LD) i.e. they are transmitted together (non-Mendelian) |
|
|
Term
Warfarin: 1. Epimers 2. Deactivation (Phase 2) 3. Action 4. Clinical uses (therapeutic dose, PT, INR) |
|
Definition
1. S-Warfarin=active, R=inactive 2. CYP 2C9 is major deactivator (liver) 3. Inhibits VKORC1 (enzyme that recycles Vit K (ox) to Vit K (red) in the liver *Factors 2, 7, 9, 10 all req. K to be carboxylated (so they can bind Ca2+ 4. Action: increases Prothrombin Time (PT)-->decreased coagulability, very narrow therapeutic dosage (and quite variable based on individual, habits, liver fxn, etc.). "Loading dose" brings [warfarin] up to desired quickly, maintenance dosaes follow |
|
|
Term
Left heart (LH) catheterization vs. right heart (RH): 1. Access 2. Risks 3. Characteristic pressures observed 4. Benefits |
|
Definition
1. R=femoral v. (most common) or jugular v. L=femoral a. (most common) or carotid a. 2. LH catheterization is more risky b/c of higher pressures (bleeding, clotting, vessel/valve damage) 3. R: RA=0±2 mmHg, RV=20/0-2, Pulm aa=20/5 L: LA=5-10 mmHg, LV=120/5, aorta=120/80 4. LH catheterization best for accurately measuring cardiac fxn, pressure, and compartment volumes |
|
|
Term
Pulmonary Wedge Pressure meaaurement: 1. How 2. Why 3. Normal value (obtained) |
|
Definition
1. Catheter with inflatable balloon passed thru RH into pulm. tree as far as it can fit, balloon inflated, pulm. circulatory system acts as a catheter extension that can sense LH BP 2. Less risky than LH catheterization 3. Normal=5-10 mmHg (this is normal LA pressure)
|
|
|
Term
CO Measurement Techniques: 1. Thermodilution 2. Dye dilution 3. Fick Principle a. 3 knowns b. EQUATION
|
|
Definition
1. Swan-Ganz catheter: injects fluid out end into circulation (something measurable either visually or thermally) 2. Known dye amt. injected, measure d[C]/dt to calculate CO 3. Calculate CO from 3 values: O2 usage rate arterial-venous) must= O2 uptake rate (lungs) EQUATION: CO=lung uptake/ [art-ven] 1. O2 uptake by lungs (volume)/min 2. [O2] in venous blood, blood flow
3. [O2] in arterial blood, blood flow
|
|
|
Term
Other CV techniques in Tx and Dx: 1. Intra-aortic balloon pump 2. Radionuclide assessment 3. Echocardiogram (ECG) 4. CT scan 5. MRI 6. Plane film (x-ray) |
|
Definition
1. Use ECG to monitor heart rhythm, insert a balloon into descending aorta, DEFLATE during SYSTOLE= suction, inflate during diastole=supplements hearts pumping efforts 2. Ex: thallium-201: inject, allow to equilibrate, assess which tissues are perfused vs. not (visualize) 3. Totally non-invasive (+), uses US (waves), M-mode=1-D vs. 2-D mode (prenatal), way to sense tissue movements based on reflected sound waves (current standard)
3. CT: extremely fast, high res (with tracer) 4. MRI: extremely high resolution, slower 5. X-ray: cheap, fast, assess a lot of problems (esp. malformations) |
|
|
Term
BP measurement: 1. Compare methods (3): which is the standard? 2. Korotkoff sounds/phases 3. How to do it the RIGHT way 4. How many mmHg does each Phase span? Time? |
|
Definition
1. Direct (catheterization)=riskier, invasive, more Dx Indirect=ascultatory (gold std.) or oscillometric (automatic ascultatory basically, uses Doppler to sense movement, transducer to interpret onto display) 2. Systolic pressure=tapping (Phase 1)
Diastolic pressure=muffled (Phases 2-4) Phase 1=peak systole heard only (sharp tap) Phase 2= murmur/swish sounds
Phase 3=crisper, getting LOUDER Phase 4=distinct, abrupt muffling (getting softer) Phase 5=silence 3. Arm bare, RESTING, cuff at heart-level, cuff snug (Large if arm d≥33cm), drop 2-3 mmHg/sec, stethoscope over antecubital a., repeat 3X (official) 4. 1=14 mmHg, 2=20, 3=6, 4=5, (5=done). Note: Phase 1+2+3=40 mmHg (normal BP)
|
|
|
Term
Numbers 3: heart-related 1. RAP vs. LAP
2. RVP vs. LVP
3. Pulmonary wedge pressure 4. Pulmonary aa./trunk pressure vs. aortic pressure 5. Korotkoff phases (time in sec and mmHg) 6. Normal % body mass that is skeletal muscle 7. MAP extremes: weightlifters and runners |
|
Definition
1. RAP=0±2 mmHg, LAP=5-10 2. RVP=20/0-2, LVP=120/5 3. Wedge=LAP=5-10 (direct BP technique) 4. Pulm=20/5, aorta=120/80 5. 1=14 mmHg (7 sec), 2=20 (10), 3=6 (3), 4=5 (2) Note: based on 2-3 mmHg drop/sec proper technique 6. 50% 7. Lifters: up to +300 mmHg (during lift), ling-distance runners: +10-40 mmHg sustained |
|
|
Term
Changes during vigorous exercise: 1. Blood flow: vessels and regulation (local regulators)
2. The "muscle pump" 3. Nervous system control 4. Circulation adjustments |
|
Definition
1. 4-->80 mL/min/100g, most capillaries constricted at rest, this changes rapidly with exercise (local controls=K+, Adenosine, ATP, lactate, CO2)
2. Muscle pump: blood flows rapidly in between contractions (contraction occludes vessels temporarily) 3. Sympathetic: releases NE (α), adrenals=Epi (β) & NE α=vasoconstriction (GI, skin, kidney, muscle not in use) β=vasodilation (muscle in use & liver) Little sympathetic control=brain, heart dilation (local) overcomes symp. stimulation in exercising muscles 4. Increase: HR, contractility, global vasoconstriction, MAP (Pa), Psf (& VR), CO |
|
|
Term
Other important notes on exercising conditions: 1. How is RVR affected? 2. Since CO increases during exercise, how does increased perfusion reach specifically the tissues that need it (working muscle, liver)? |
|
Definition
1. RVR actually DECREASES due to the muscle pump action 2. Sympathetic constriction (α) blocks the increased blood flow to tissues that don't need it, while in the tissues that do, local controls overcome this block. |
|
|
Term
Neurohumeral mechanisms of heart failure: 1. Neural response 2. Humoral response |
|
Definition
1. Sympathetic stimulation: shifts VR to R and CO to L 2. Vasopressin + endothelin-1-->vasoconstriction Renin-Ang II system: fluid vol. retention |
|
|
Term
1. How does TPR change during exercise? 2. How does blood flow to tissues not involved in sympathetic response change during exercise? |
|
Definition
1. DECREASES (globally) Why: CO increases (4X: 5 L/min-->20 L/min), while Pa increases 100 mmHg-->120 mmHg (example) TPR=Pa/CO (120/20=6, 100/5=20) 2. DOES NOT CHANGE: flow to usd muscles, liver goes way up, but flow to other places remains relatively constant (why: since CO is increasing, without sympconstriction at these unused tissues, their perfusion would also go way up) |
|
|
Term
Cutaneous circulation & temperature regulation: 1. Extent within skin
2. Control of flow 3. Anastomoses 4. % of CO going to skin (basal) 5. Other functions |
|
Definition
1. Rich vascular supply! subpapillary venous plexus (dermis): large vol., low flow 2. Control=sympathetic tone constitutively (unless body is above set point), little/no autoregulation 3. Arteriovenous in subcutaneous tissue=move blood aa. <=> vv. based on "heat load" of ea. system (eq.) 4. 1/3 5. Volume reservoir (b/c constricted basal) |
|
|
Term
Numbers 3: 1. Oral vs. rectal temperature vs. core temperature 2. Temperature range in which core temp. is constant 3. Temperature above which vasodilation begins 4. Heat loss via: evaporation, radiation, convection and conduction (%s)
5. Vasodilation's multiplicative affect on heat loss (maximum) 6. # calories/L sweat lost (# calories lost/hour passively & vol. of sweat this passive loss represents) |
|
Definition
1. Oral=less 1-2oF, rectal≈core (98.7oF/37oC) 2. 60-130oF (±30oF normal) 3. 78oF: sympathetic tone starts to reduce constriction
4. Evap=22% (most significant at high env't temp.), rad=60% (Infrared), conv=15% (air), cond=3% (objects) 5. 8X (@ >110oF) 6. 600 cal/L sweat; passive=16-19 kcal/hr, 600-700 mL/day) |
|
|
Term
Neural control of blood flow to cutaneous circulation: 1. Target vessels in skin (2)
2. Nervous system 3. Transmitters used (and contribution)
4. Receptors 5. Sympathetic stimulation vs. thermoreg. reflex |
|
Definition
1. Arterioles (dense α, few β)-->constriction, cholinergic receptors=dilation (ACh) Cutaneous veins (lots of α)=controlled by hypothalamus ("thermoregulatory reflex") 2. Sympathetic (adrenergic & cholinergic, no para) 3. NE mainly (constriction), ACh (dilation) 4. NE-->α-->constriction (basal), ACh-->cholinergic (muscarinic)-->vasodilation 5. symp=arterioles, thermoreg reflex=veins |
|
|
Term
Alterations in heat loss rate: 1. Wind chill (equation) 2. Water vs. air |
|
Definition
1. √Wind velocity=its effect on heat loss: a 4mph wind is 2X as effective at wisking heat away from skin than a 1 mph wind 2. Water has a WAY higher specific heat capacity than air, so it can (1) hold a lot of heat energy and (2) conduct heat energy faster (20X faster) EX: lose heat faster sweating with a shirt ON than without a shirt (b/c shirt holds moisture near skin, which steals heat from body faster than just evaporation to air)
|
|
|
Term
1. 2 determinants of rate of heat loss from body: Examples 2. 2 sources of heat for body Examples |
|
Definition
1. (1) rate of conduction deep body-->skin, (2) rate of heat transfer to env't Ex: (1) blood flow, (2) moisture, medium, temperature, wind, clothing, etc. 2. (1) metabolic rate (chemical, physical, hormonal) (2) external sources Ex: (1) symp NS, shivering, piloerection, Thyroxine/TRH |
|
|
Term
Behavioral thermoregulation: 1. What? 2. Mechanism 3. Importance (WI-style) |
|
Definition
1. Modifying behavior b/c of cold body temperature 2. Feel cold=discomfort=wear more clothes 3. Only way to regulate body temp. under EXTREMELY cold situations (WI style)
|
|
|
Term
CNS control of thermoregulation mechanisms: 1. Cutaneous vasoconstriction/vasodilation 2. Sweating 3. Thyroid gland (thyroxine) 4. Chemical thermogenesis 5. Non-chemical (physical) thermogenesis (2)
|
|
Definition
1. Posterior hypothalamic sympathetic centers/inhibition of those centers (interneurons?) 2. Preoptic area: anterior hypothalamus (1) cholinergic receptors (2) circulating catecholamines (not AChRs)
3. Preoptic area: anterior hypothalamus 4. Sympathetic stimulation (main), brown fat 5. Primary Motor Area for Shivering (reflex): hypothalamus, piloerection=symp NS |
|
|
Term
Summary: increasing body heat: 1. Sympathetic NS 2. Hypothalamic thermoregulation 3. ________? |
|
Definition
1. Sympathetic stimulation: Vasoconstriction (alpha receptors) 2. Hypothalamic thermoregulation: Anterior: "set point" control center Anterior preoptic: TRH release-->Thyroxine Primary Motor Area for Shivering 3. Behavioral Thermoregulation (higher CNS ctrs?) |
|
|
Term
Summary: decreasing body temperature |
|
Definition
1. Sympathetic NS: Inhibited α stimulation + cholinergic dilation (M) =vasodilation
2. Hypothalamus:
3. Sweating=controlled by BOTH: sympathetic muscarinic cholinergic stimulation is controlled by body temperature drop sensed by the anterior preoptic area of hypothalamus |
|
|
Term
Overview summary: temperature regulation 1. Core vs. skin temp. 2. Heat gain vs. heat loss 3. Physiological control |
|
Definition
1. core is pretty constant, while skin, being eternal to insulating fat layer, fluctuates with env't extremes 2. Exercise, radiation, evap, convection, conduction, etc. 3. HYPOTHALAMUS (Anterior) temperature regulation center receives input from peripheral temperature sensors and sends efferents to various places affecting various Symp NS responses (physical, chemical) and gland targets (hormonal responses, i.e. thyroid) |
|
|
Term
Sweat characteristics: 1. 2 types 2. Composition 3. Production 4. Control
|
|
Definition
1, 2. Precursor/primary secretion: similar to plasma w/o protein (good for bacterial growth; secreted in response to stress or before true sweating) Sweat=dilute NaCl ultrafiltrate 3. Modified tubule makes primary secretion (simple cuboid), duct (stratified cuboid) reabsorbs NaCl to make dilute end-product (sweat) 4. Sympathetic control (muscarinics) |
|
|
Term
Circulatory Shock: 1. Definition
2. Hallmark Sx 3. Types (basic circulatory issue) 4. Factors Affecting (2 major)
|
|
Definition
1. Inadequate perfusion or inappropriate distribution of perfusion to tissues 2. Sympathetic compensatory mechanisms-->increased HR, resp. or decreased TPR (eventually leads to hypotension) 3. Hypovolemic (blood vol.), distributive (vessels), cardiogenic (CO), or obstructive (CO or flow) 4. Duration & severity (time & volume-dependent)
|
|
|
Term
Hypovolemic shock examples: |
|
Definition
Hemorrhage (most common hypovolemic) Any other loss of volume: Diarrhea, vomiting, polyuria Any failure to maintain appropriate volume: Dehydration Renal dysfunction Adrenal cortical insufficiency |
|
|
Term
Examples of distributive shock:
|
|
Definition
Septic shock (most common type of shock overall) Part hypovolemic, late stage: cardiogenic
Anaphylactic Neurogenic Acute adrenal insufficiency (circulating catecholamines) |
|
|
Term
Examples of cardiogenic shock:
|
|
Definition
1. MI (most common cardiogenic) 2. Arrhythmias (ion imbalance, dehydration, renal dysfunction, celiac disease (poor nutrition), etc. |
|
|
Term
Examples of obstructive shock: |
|
Definition
1. Cardiac tamponade (High CVP, low CO!) 2. Valvular stemosis 3. Cardaic tumor 4. Pulmonary embolism 5. Tension pneumothorax |
|
|
Term
Numbers (shock): 1. % blood volume loss in compensated shock 2. % " " in decompensated shock 3. Time frame, "the Golden Hour" 4. Normal urine output 5. Normal renal function indicator 6. Normal hematocrit (Ht) 7. Mixed venous O2 tension/(CVP): normal vs. shock |
|
Definition
1. up to 20% 2. 30-45% (over this and threshold of irreversible shock) 3. Golden hour=blood volume replaced, you'll probably be ok 3-4 hours=need care before this, or you will probably die 4. 30cc/hour 5. Creatinine (serum): normal=1.0, failure/shock= >1 6. Ht: normal=45%, shock= less 7. Central venous pressure(CVP)=RAP: normal=0 mmHg, shock=8-12 goal, ventilator=11-16 mmHg goal |
|
|