Term
| What are the 2 ways the two ways in which nervous transmission is continually occurring for cerebral fxn? |
|
Definition
-stimulation of background neuronal activity
-activation of neurohormonal systems |
|
|
Term
| How does neurohormonal control of brain activity occur? |
|
Definition
-pumps ach up and back (keeps CNS awake)
-excitatory or inhib. NT hormonal agents secreted by neurons in pons and mesencephalon
-can last mins-hours
-occurs by 4 main systems... |
|
|
Term
| What are the 4 main systems of neurohormonal control of brain activity? |
|
Definition
Norepinephrine system
Dopamine system
Serotonin System
Ach System |
|
|
Term
| Where is the Norepinephrine system? what are its effects? |
|
Definition
-locus cerelus
-generally excitatory
-important for dreams and sleep |
|
|
Term
| Where is the Dopamine system? what are its effects? |
|
Definition
-substantia nigra (basal ganglia)
-inhib or stimulatory |
|
|
Term
| Where is the serotonin system? What are its effects? |
|
Definition
-raphe nuclei
-pain relief, inhibitory role
-facilitates sleep |
|
|
Term
| Where is the Ach system? What are its effects? |
|
Definition
-gigantocellular neurons of reticular excitatory center
-excitatory, awakens CNS, amy activate REM sleep. |
|
|
Term
| Fxns of limbic system through neuronal circuitry |
|
Definition
-majorly controlled by hypothalamus:
-controls emotional behavior
-regulation of vegetative function (blood composition, temperature, body fluids, satiety, weight control)
-other: septum pellucidum, hippocampus, paraolfactory area, amegdala, ant. nucleus of thalamus. |
|
|
Term
|
Definition
-EVERYTHING almost
-control center of limbic system
-CONTROLS vegetative and endocrine fxns
-CONTROLS behavior and motivaiton
-3 outputs:
-brainstem reticular formation (to autonomic system)
-anterior thalamus and limbic cerebrum
-hypothalamic infindibulum (to pituitary) |
|
|
Term
| Vegetative Hypothalamic Fxns (What keps you alive in a vegetative state!) |
|
Definition
-Arterial pressure and heart rate
-temp. regulation
-body fluid reg.
-thirst center
-ADH secretion (via pituitary)
-Uterine contraction and milk ejection
-Hunger and satiety centers
-regulation of pituitary hormones |
|
|
Term
| behavioral influences of hypothalamus |
|
Definition
-level of general activity, rage and fighting
-satiety and tranquility
-fear and punishment rxn
-sexual drive |
|
|
Term
Reward Center
-location?
-effects if stimulated? |
|
Definition
-mainly in hypothalamus
-sense of pleasure ad satisfaction (preferable to food)
-if strong enough, causes rage
-important in limbic system fxn!!!
-influence what we learn!!!/way you react with the world. |
|
|
Term
Punishment Center
-location?
-effects if stimulated? |
|
Definition
-primarily in central gray area surrounding aquaduct of Sylvius (midbrain)
-fear, terror and pain, can inhibit reward centers.
-important in limbic system fxn!!!
-influence what we learn!!!/ay you react with the world |
|
|
Term
| Effect of tranquilizers on reward and punishment centers. |
|
Definition
|
|
Term
| How does the hippocampus play a critical role in learning? |
|
Definition
-provides drive that translates short term memory into long term
-without, consolidation of long-term memory does not exist. |
|
|
Term
| What are the 2 stages of sleep that can alternate nightly? |
|
Definition
-Slow wave sleep
-REM sleep |
|
|
Term
| Describe Slow wave sleep. |
|
Definition
-strong, low frequency brain waves
-majority of night
-deep and restful
-decreased vegetative fxn (BP, resp)
-dreams-but not remembered
-no excess muscular activity |
|
|
Term
|
Definition
-brain highly active (metabolism increased 20 %)
-25% of sleep, harder to wake from this.
-every 90 min
-vivid dreams with frequent irregular movement |
|
|
Term
| What is the physiologic value of 2 stages of sleep? |
|
Definition
| restoration of balance among neuronal centers. |
|
|
Term
| Contributing factors of sleep mechanisms. |
|
Definition
-result from active inhibition by brainstem.
-occurs by activating one of following in brain:
raphe of the caudal pons and medulla.
-NT= serotonin
- other important factors: muramyl peptide, hypothalamic and thalamic nuclei
-ACH activate REM sleep |
|
|
Term
| How do sleeping pills work? |
|
Definition
| -They go into the limbic system and prevent reuptake of serotonin (serotnin will have bigger effect) |
|
|
Term
| What are brain waves and how are they read? |
|
Definition
-electrical potentials that originate near surface of brain and are recorded from outside as an EEG
-INTENSITY-determined by synchronus neuronal filling (NT activity)
-mental activity causes asynchronous activity (lowers voltage) |
|
|
Term
| What are the brain wave readings on an EEG used for? |
|
Definition
| to evaluate seizure, coma or brain death. |
|
|
Term
| What are the 4 main types of brain waves? How are they characterized? |
|
Definition
alpha- awake adults with quiet cerebration
beta- replace alpha waves with directed mental activity (taking a test)
theta- normal children and emotionally stressed adults- seen in degenerative brain disease
delta- during sleep and infancy (seen in serious brain disease) |
|
|
Term
| What activates the autonomic nervous system? |
|
Definition
-brainstem, spinal cord and hypothalamus
-also by subconscious visceral reflexes |
|
|
Term
| what is the path along the sympathetic nervous system? |
|
Definition
visceral motor neurons located in intermediolateral horn of spinal cord--> leave spinal cord vis ventral root--> then follows 1 of 3 paths"
1. enter symp. chain via white ramus and termimante at level of origin
2. enter symp chain via white ramus and ascend or descend chain to terminate at different level
3. enter sympathetic chain through white ramus and exit without synapse via a SPHLANCHNIC NERVE |
|
|
Term
| To what organ do preganglionics pass through the chain without synapse? |
|
Definition
adrenal medulla!
-goes through but does NOT synapse at celiac ganglion |
|
|
Term
| Preganglionic (shouldn’t even be called this bc go to effector cells or tissues) fibers exit CNS via |
|
Definition
|
|
Term
| What is the preganglionic NT of parasymp and sympathetic NS? |
|
Definition
always Ach because both systems are cholinergic.
-Therefore, Ach and Ach-like substances excite both. |
|
|
Term
| What do cholinergic autonomic neurons secrete? adrenergic? |
|
Definition
|
|
Term
| What is the postganglionic NT of parasymp and sympathetic NS? |
|
Definition
symp: E, NE, sometimes dopamine (adrenergic)
parasymp: Ach (cholinergic
EXCEPTIONS: symp to sweat glands, piloerectors and some blood vessels are cholinergic (important vasovagal syncope) |
|
|
Term
| NT secretion by Autonomic nervous system |
|
Definition
| postganglionic nerves terminate in varacosities where NTs are stored--> terminate on parenchymal cells or nearby connective tissue--> AP increases Ca permeability in terminal-->NT releases |
|
|
Term
| how is Ach synthesized? destroyed? |
|
Definition
-choline acetyl transferase enzymatically combines acetyl-CoA and choline
-after release, acetylcholinesterase degrades Ach |
|
|
Term
| How is NE and E synthesized? destroyed? |
|
Definition
-from dopamine
-removed after release by: diffusion, reuptake and degradation of by MAO or COMT |
|
|
Term
| What are the 2 types of Ach receptors? |
|
Definition
Muscarinic- on all effector cells, stim by cholinergic postganglionic nerves
Nicotinic- in autonomic ganglia at synapses bw pre- and postganglionic nerves |
|
|
Term
| Adrenergic receptor types |
|
Definition
| Tables to know--- different flashcards! |
|
|
Term
| What are stimulatory effects of autonomic NS? |
|
Definition
symp and parasymp stimulation excites some organs and inhibits others
-act in reciprocal fashion
-normal continuous background activity generates 'tone'. (maintains basal rate of activity of autonomic system) |
|
|
Term
Mass organ stimulation
-when occurs and how? |
|
Definition
"Fight or Flight"
-increased BP
-increased blood glucose, glycolysis &BMR
-increased strength, coagulation and alertness |
|
|
Term
| Discrete organ stimulation |
|
Definition
don't need as dramatic a response during rest and digest
-organ specific parasympathetic effects |
|
|
Term
| Sympathetic autonomic pharmacology: What are the effects of General Sympathomimetic Drugs? |
|
Definition
-E & NE- As therapeutic drugs.
ex: Methoxamine |
|
|
Term
| Sympathetic autonomic pharmacology: What are the effects of Sympathomimetics |
|
Definition
-isolated receptor response
examples: a. phenylepherine (alpha agonist)
b. isoproterinol- (beta agonist)
c. albuterol- beta2 agonist |
|
|
Term
| Sympathetic autonomic pharmacology: What are the effects of indirect sympathomimetrics? |
|
Definition
Induce NE release
-ephedrine- makes you release more NT
-amphetamine
-tyramine |
|
|
Term
| Sympathetic autonomic pharmacology: What are the effects of adrenergic blockers? |
|
Definition
blocks NE
-RESPERINE- blocks synthesis and storage of NE
-GUANETHIDINE- blocks NE release
-PHENOXYBENZAMINE, PHENTOLAMINE- alpha blocker
-PROPANOL, METOPROLOL- beta blockers. |
|
|
Term
| Parasympathetic autonomic pharmacology: 5 types and examples |
|
Definition
1. Ach- not used as drug bc so plentiful
2. Direct parsympathomimetics- pilocarpine, metacholine
3. Anticholinesterase drugs- neostigmine, pyridostigmine
4.Cholinergic blockers- atropine, scopolamine (only influence muscarinics
5. Nicotine- simultaneous stim of sympathetic and parasympathetic postganglionics |
|
|
Term
| Factors that increase cerebral blood flow |
|
Definition
-excess [CO2] (forms hydrogen ions which induces vasodilation)
-excess [H] (because increases acidity)
-reduced PO2 tissue
-atrocyte secretions (NO, adenosine, K) (increases vasoactive metabolites in response to neuronal activity such as in reading) |
|
|
Term
| Describe the circulation of CSF? |
|
Definition
-Fills ventricles, cisterns & subarachnoid space
-500 ml formed daily from CHOROID PLEXUS in lateral ventricle (this secretion depends on active Na transport)
-absorbed by arachnoid villi into venous system to maintain normal pressure (65-195 mmHg) |
|
|
Term
| What does the brain lack? |
|
Definition
|
|
Term
| Describe brain metabolism. |
|
Definition
-7.5 times that of nonneural tissue due to high energy needed for active transport.
-not capable of much anaerobic metabolism
-most energy is from glucose, this transport is not dependent on insulin
-Dr. Ghoulson saying how dark venous return from vein is! |
|
|
Term
| How is cardiac muscle a hybrid of smooth and skeletal muscle? |
|
Definition
-striated (like skeletal) AND is arranged in latticework which contain actin and myosin
-fxns as atrial and ventricular syncitum (like smooth muscle)
-intercolated discs with gap jxns facilitate flow of ions and AP |
|
|
Term
| What is the mechanism of the plateau of the AP which is not present in skeletal muscle? |
|
Definition
-this plateau prompts depolarization
*AP caused by fast Na channels (do not remain open long)
*then, slow Ca channels open later but stay open longer.
*this influx of this Na and Ca prompts contraction
At AP- K permeability decreases, which delays repolarization (until Na and Ca channels close), and prevents return of membrane potential |
|
|
Term
| What is the synergistic dual mechanism seen in cardiac excitation-contraction coupling that promotes further contraction? |
|
Definition
1. Ca diffuses into myofibrils & catalyzes actin-myosin bridging, leading to contraction
2. AP also causes extracellular Ca in t-tubule lumen to diffuse into sarcoplasm
Both activate Ca release channels in sarcoplasmic reticulum, promoting further contraction
THUS-myocardial contraction is greatly dependent on extracellular Ca. |
|
|
Term
| What happens during diastole? |
|
Definition
Overall: ventricles fill with blood
-beginning is isovolumetric relaxation (caused by ventricular relaxation)
-vent pressure decreases below that of atria, AV valves open.
-high pressure in atria pushes blood into ventricles
-75 % of filling occurs this way, last 23 % with atrial contraction ("atrial kick") |
|
|
Term
| What is the basal blood pressure? |
|
Definition
-diastolic
-period of time when ventricles have to overcome the diastolic pressure to pump to pulmonary |
|
|
Term
| What happens during systole? |
|
Definition
OVERALL: ventricular contraction
-vent contraction occurs, AV valves close, and pressure builds in ventricle.
-period of isovolumetric contraction- when no outflow of blood occurs in beginning of systole
-when left ventricle exceeds aortic pressure and right ventricle exceeds pulmonary pressure, aortic and pulmonary valves open. (period of ejection)
-ventricular pressure falls below aortic/pulm pressure with blood outflow.
-Aortic and pulmonary valves close. |
|
|
Term
| What do the EKG waves indicate (P,QRS, and T)? |
|
Definition
P- atrial depolarization
QRS- ventricular depolarization (precedes ventricular contraction (base to apex))
T- ventricular repolarization (apex to base)
Atrial T-wave- obscured by QRS complex |
|
|
Term
| what do chordae tendinae do? |
|
Definition
prevent bulging
prevent valves from bulging back to far into atria during systole |
|
|
Term
| What do the heart sounds represent (S1 and S2)> |
|
Definition
S1- AV valve closure
S2- semilunar valve closure |
|
|
Term
| what is preload? afterload? |
|
Definition
-reflects end-diastolic pressure
-reflects aortic pressure (proportional to peripheral resistance) |
|
|
Term
| What are the regulators of cardiac pressure? |
|
Definition
-Frank Starling mechanism
-Autonomic Nervous System
-extracellular K-elevation (blocks conduction and deficiency yields weak flacid heart)
-increased extracellular Ca concentration (spastic, weak, flaccid)
-temperature- rate proportional to temperature.
-arterial pressure- CO falls with pressure > 160 mmHg |
|
|
Term
| Explain the Frank Starling mechanism. |
|
Definition
-within physiological limits, heart pumps all the blood that comes to it without allowing excess accumulation of blood in the veins.
-intrinsic cardiac adaptation to variations in venous return
-filling stretch increases myocardial contracility
-CO can then be increased. |
|
|
Term
| why does ventricular output increase faster in the right side? |
|
Definition
| -goes up faster in right ventricle, bcause left ventricle pushing against a much bigger pressure than that of the right ventricle (going) to the lungs. |
|
|
Term
| How does the cardiac excitation and conduction system function? |
|
Definition
-modified muscle fibers with very little contractility but enhanced speed of conduction.
-can self excite via the SA node
-rapid conduction
-sequences atrial and ventricular contraction through AV node
-allows entire ventricle to contract nearly simultaneously |
|
|
Term
| What is the mechanism of self excitation in the sinus node? |
|
Definition
OVERALL: Controls heart rate
-membrane naturally "leaky" for Na and Ca
-resting membrane potential less negative than other cardiac muscle
-these two factors eventually build up and impulse fires.- automatic contraction |
|
|
Term
| explain the AV node's delay mechanism, and why is this crucial? |
|
Definition
- fxns by reduced gap junctions to delay impulses from atria to ventricles.
-crucial so atria and ventricles contract at different times. If contracted together, CO would fall!! |
|
|
Term
| What happens once the impulse hits the bundle of HIS? |
|
Definition
| -speeds up in one way direction allowing simultaneous ventricular contraction |
|
|
Term
| How do AV node and purkinje system take over when sinus node is pacing too fast? |
|
Definition
| they can take over and slow rates, if too delayed though Strokes-Adams syndrome is present. |
|
|
Term
| Explain the autonomic influence (para and symp) on controlling the heart rate. |
|
Definition
PARASYMPATHETIC
-reduces sinus node rate
-Ach increases K permeability, hyperpolarizes node and conduction syste,
-initiates slow impulse in AV node
SYMPATHETIC
-NE stimulates beta 1 receptors
-increases Na and ca permeability
-resting membrane potential is less negative (more excitable) |
|
|
Term
| why does the t wave have the same polarity as qrs wave? |
|
Definition
| depolarizes from base to apex, and then repolarizes from apex to base |
|
|
Term
| What is the heart rate on an ECG? |
|
Definition
|
|
Term
| What are the typical patterns of cardiac depolarization and repolarization? |
|
Definition
DEPOLARIZATION:
-cell exteriors become electronegative as depolarization spreads
-current flows from depolarized to polarized areas.
-depolarization begins in septum and spreads to inner surfaces of ventricles, then outward through myocardium towards the apex.
- overall average current speeds from base to apex
-current flow (and deflection of EKG) occurs only during de- or repolarization
-REPOLARIZATION OCCURS IN NEARLY OPPOSITE SEQUENCE |
|
|
Term
| explain the technical aspects of an EKG. (What you are reading on the actual print out) |
|
Definition
| -A graph of voltage (generated by current flows due to myocardial de- and repolarization) vs. time |
|
|
Term
| What are the three usual 'leads' in an EKG |
|
Definition
-Limb leads (I, II, & III)
-each is bipolar (2 electrodes on different sides of the heart)
-6 Precordial leads (V1-V6)
-one electrode on one of 6 chest postions
- the other on one indifferent electrode (arms or legs)
-3 augmented unipolar limb leads (aVR, aVL, aVF)
-various combinations of limb leads. |
|
|
Term
| What is the rapid rate estimation? |
|
Definition
| 300, 150, 100, 75, 60, 50, 40, 30 |
|
|
Term
| What is Einthoven's triangle and law? |
|
Definition
1. Triangle formed by standard limb leads around heart
2. Law: sum of potential of any standard limb lead equals sum of the other two |
|
|
Term
| What are the axes of limb leads and how do they work? |
|
Definition
-the direction from negative to positive electrode for both leads
-each limb lead's axis gives the lead's instantaneous recorded potential
-use of this with the hexagonal reference system is referred to as VECTORAL ANALYSIS
-mean axis of ventricles is direction of mean vector of ventricles
-Normal is 59 degrees. |
|
|
Term
| What does it mean if axis is deviated from 59 degrees? |
|
Definition
right axis deviation: greater than 59 degrees
left axis deviation: less than 59 degrees
axis deviates towards hypertrophied ventricle. |
|
|
Term
| 4 Pathologies that can be read through limb lead axis deviations |
|
Definition
-VENTRICULAR HYPERTROPHY
-axis deviates toward hypertrophied venrticle
-BBB
-axis deviates toward blocked bundle (bundle of his)
-Deep exhalation, lying down, obesity
-heart rotates to left
-left axis deviation
-Inspiration, long lanky body habitus, standing
-heart rotates to the right
-right axis deviation results |
|
|
Term
| What is usually the cause of increased limb lead voltages? decreased? |
|
Definition
-ventricular hypertrophy
-diminished muscle mas due to MI or pericardial & pleural effusion, COPD. |
|
|
Term
| What is current of injury and what are it's causes? |
|
Definition
- constant flow bw injured and normally polarized tissue (damage of heart muscle results in constant depolariztion (cessation of ion transport due to disease)
Causes:
-ischemia or infarction
-infection
-trauma
-emits a vector poitning away from injured tissue --altered EKG due to this depolarization |
|
|
Term
| How do you locate a current of injury on an EKG. |
|
Definition
-locate J point (ST point)
-If horizontal line thru J point & horizontal line thru TP segment differ, current of injury exists. |
|
|
Term
| Where is the lesion in an Inferior MI? Anterior MI? |
|
Definition
Inferior MI= lesion in right coronary artery
Anterior MI= lesion of left coronary artery (widow maker) |
|
|
Term
| describe the current of injury in ischemic heart disease. |
|
Definition
-ischemic/ infarcted muscle cannot repolarize
-membrane ion transport is defected
-current of injury will point away from injured area
Persistent ischemis -> muscle death -> prominent Q wave. |
|
|
Term
| Describe T-wave abnormalities |
|
Definition
1. Seen when normal repolarization sequence does not occur
2. Slow conduction thru ventricles causes T wave to have polarity opposite that of QRS
3. Repolarization of base of ventricles ahead of apex “flips” T wave
4. Ischemia can shorten ventricular repolarization, causing T wave abnormality-a clue to coronary disease on treadmill tests |
|
|
Term
| What are the 4 usual mechanisms of cardiac arrhythmias? |
|
Definition
-Abnormal rhythmicity of SA node (usual pacemaker)
-Ectopic Pacemaker (shift of SA node fxn to other parts of heart)
-Aberrant conduction pathway &/or block
-Ectopic Impulse Generation (from any part of heart) |
|
|
Term
What are the 3 abnormal sinus rhythms?
(SA node discharges abnormally, P wave present and QRS &T unchanged) |
|
Definition
-Sinus Tachycardia
>100 beats/min.
-usually compensatory rxn to some other stress in body (faver, infection, hypovolemia, hyperthyroidism, low CO and sympathetic discharge)
-Sinus bachycardia
-<60 beats/min
-normal in conditioned athletes
-follows vagal stimulation
-Sinus Arrhythmia
-varied heart rate due to aberrant autonomic input (often by altered respiration) |
|
|
Term
| What does the EKG look like for a sinus tachycardia? |
|
Definition
-QRS narrow
-segment bw P and T shortened |
|
|
Term
| What does the EKG look like for a sinus bradycardia? |
|
Definition
|
|
Term
| What are the arrhythmias with conduction system blocks? |
|
Definition
-SA node block (NO P WAVE)
-AV block
-Stokes Adams Syndrome- syncope with intermittent block |
|
|
Term
| Describe an SA node block? |
|
Definition
rare
-blocked before entering atrial muscle
-NO P WAVE |
|
|
Term
| Describe an AV node block? |
|
Definition
-usually due to AV node ischemia
3 Degrees... |
|
|
Term
|
Definition
prolonged PR interval
usually due to drugs
no therapeutics necessary |
|
|
Term
|
Definition
dropped beats
either Mobitz I (Wenckebach phenomenon)
-no or very little impulses from SA to AV
OR Mobiz II (irregular dropped off beats)
-irregular dropped beats
-usually needs a permanent pacemaker |
|
|
Term
|
Definition
Complete AV jxn block
AV dissociation
-atria and ventricles beat in a dissociated way
-P waves develop without regard to QRS waves
- can result in a Stokes Adams attack (when AV block comes and goes)
NEED PACEMAKER |
|
|
Term
| What causes premature contractions? |
|
Definition
-can originate anywhere: atria, ventricle or AV jxn
-caused by ectopic foci which initiae depolarization:
-local ischemia (common)
-plaques (irritated by pressure)
-inflamm
-toxic irritation by: drugs, nicotine or alcohol |
|
|
Term
| What often follows premature contractions? |
|
Definition
compensatory pause or pulse deficit
-to allow for time for blood to refill |
|
|
Term
| If premature contraction occurs in AV node.. |
|
Definition
| no P-wave due to lack of atrial depolarization |
|
|
Term
| Premature ventricular contractions and its EKG morphology |
|
Definition
-more significant than other premature contraction due to link with v-fib.
-linked with PVC on T wave or prolonged QT interval
-QRS prolonged (slow ventricle conduction)
-QRS voltage high (normal conduction lost)
-T wave polarity opposite QRS |
|
|
Term
| Describe 'Long QT Syndrome'. |
|
Definition
-particularily lethal!
-REpolarization delayed (because DEpolarization takes longer.
-cause: electrolyte disorders (low Mg, K, Ca)
mutations of cation channels (drug interactions) |
|
|
Term
| What is paroxysmal tachycardia? |
|
Definition
-intermittent sudden tachycardia
-brief in duration
-due to aberrant conduction path (circus movement) with treentry
-vagal reflexes or drugs may terminate this
-supraventricular or ventricular |
|
|
Term
| Name some vagal maneuvers |
|
Definition
REDUCE HEART RATE:
carotid massage
valsalva (grunting with a closed glottis)
eye compression |
|
|
Term
| Describe circus movements |
|
Definition
abnormal
-basis for ventricular fibrillation
-in normal vent: impulse passes throughout and dies bc ventr. is in a refractory state.
-In circus movement, 2 conditions allow this movement to continue: (p.89)
-increased pathway around ventricle
-decreased velocity of conduction
-shortened refractory period of muscles
MUSCLE (atrial or ventricular) IS CONTINUOUSLY DEPOLARIZED. |
|
|
Term
| what are the characteristics of supraventricular tachycardia? |
|
Definition
Origin: AV node or atria
95-150 beats/min (regular)
P-WAVE ALTERED OR ABSENT
QRS complex narrowed
usually in normal people
terminated by drugs or vagal maneuvers |
|
|
Term
| Describe ventricular tachycardia |
|
Definition
-sudden onset
-repetitive
-wide QRS complex
-pulse present
-often deteriorates into V-fib |
|
|
Term
| Describe ventricular fibrillation |
|
Definition
-most lethal arrhyhthmia
-impulses gone berserk
-coordinated ventricular coordination lost
-NO PULSE
-prompt defribrillation is life saving (in hopes that some node will be depolarized and take over)dea |
|
|
Term
| Describe atrial fibrillation |
|
Definition
Reentrant circus movement confined to atria by fibrous septum
-Impulses pass AV node to His Bundle irregularly
-Coordinated atrial contraction lost
NO P WAVE, irregular narrow QRS
irregular pulse
20% reduction in CO
Stagnant atrial blood may clot (emboli)
Atrial Enlargement may occur in chronic cases |
|
|
Term
|
Definition
SINGLE unidirectional circus movement
-200-350/ min in atria
-AV node's conductive capacity exceeded
-rapid regular P waves |
|
|
Term
| Which conduit system are arteries a part of? veins? |
|
Definition
-pefusion conduit system
-return conduit system |
|
|
Term
| Which conduit system are arteries a part of? veins? |
|
Definition
-pefusion conduit system
-return conduit system |
|
|
Term
| Where does circulation require more flow and lower resistance? |
|
Definition
| when blood passes through the lungs, bc more blood passes through here in a shorter amount of time than anywhere else. |
|
|
Term
What are the 3 basic principles of circulatory fxn?
KNOWKKNOWKNOWNKWKNOW!!!! |
|
Definition
-tissue blood flow controlled by tissue need
-controlled by tissue microvessels and neurohormonally
-CO controlled by sum of tissue flows (venous return)
-frank-Starling and neural input enable this
-HEART IS CART, NOT HORSE.
-Arterial pressyre regulated independent of tissue flow and CO
-Acute corrections- neural
-Chronic corrections-renal and hormonal |
|
|
Term
|
Definition
-a determinant of blood flow and pressure
Flow= pressure difference/ vascular resistance |
|
|
Term
| How is compliance calculated? What is it |
|
Definition
distensibility x volume
-how much blood flow a vessel can handle
-can be delayed due to gradual adjustments to volume change (due to vascular elasticity) |
|
|
Term
| What can cause blood volume shifts and pooling? |
|
Definition
|
|
Term
|
Definition
=systolic BP-diastolic BP
VARIES regionally |
|
|
Term
|
Definition
=systolic BP-diastolic BP
VARIES regionally |
|
|
Term
|
Definition
=systolic BP-diastolic BP
VARIES regionally |
|
|
Term
| What accounts for Korotkoff sounds when taking arterial BP? |
|
Definition
-partial occlusion of brachial artery
-systloic- when sounds start (as pressure deflated)
-diastolic- when sounds disappear |
|
|
Term
| When should you not take BP of arm? |
|
Definition
-broken arm
-woman with a radical mastectomy on the same side.
-someone on hemodialysis, and have a fistula for dialysis in that arm. |
|
|
Term
| What controls the stored volume of blood in the veins? |
|
Definition
| constriction and dilation under autonomic control. |
|
|
Term
| What is the fxn of venous pump? |
|
Definition
makes flow one way, unless have varicose veins.
-does not work in legs of person standing completely still |
|
|
Term
| what is the Central Venous Pressure (CVP)? |
|
Definition
-RIGHT ATRIAL PRESSURE
-balance of RV and venous return
usually about 0 mmHg |
|
|
Term
| What can alter venous pressures? |
|
Definition
-some resistance to venous return with normal venous collapse and compression (depends on body position and gravity)
-Increased CVP is transmitted retrograde thru venous return
-increased in legs due to gravity and increased intraabdominal pressure
-muscle compression and valves in leg veins create venous pump |
|
|
Term
| Where are some venous compression points that can control venous return? |
|
Definition
These areas contribute some sort of resistance via surrounding pressures and occlusion by organs:
(resistance rises when laying down in come points)
-atmospheric pressure collapse in neck
-rib collapse
-axillary collapse
-intrthoracic pressure
-abdominal pressure collapse |
|
|
Term
| What are the blood reservoirs of the body? |
|
Definition
-60% blood volume in veins
-spleen
-venous sinuses (store whole blood)
-red pulp (stores concentrated RBCs)
-liver
-large abdominal veins
-venous plexus beneath skin
If a contraction is stimulated by sympathetic NS releases these stores into general circulation.
-BP can thus be maintained even with 20 % blood loss |
|
|
Term
| What regulates the precapillary sphincter in arterioles? |
|
Definition
|
|
Term
| What are the intercellular clefts for in capillaries? |
|
Definition
|
|
Term
| What do the caveolae of capillaries facilitate? |
|
Definition
| endocytosis and transcytosis |
|
|
Term
| What is the main regulator of vasomotion in capillary flow? |
|
Definition
tissue oxygen concentration controls:
-terminal arteriole contraction
-precapillary sphincter |
|
|
Term
| What is the most important means of exchange from capillary to interstitial fluid? |
|
Definition
diffusion
-greater for lipid solubles (CO2 and O2)
-Also: lipid soluble substances diffuse through cell membrane faster |
|
|
Term
| What are the Starling forces? IMPORTANT! |
|
Definition
-Balance of hydrostatic & oncotic pressure
-hydrostatic pressure forces fluid and solutes toward interstitium
-plasma oncotic pressures draws fluid from interstitium to blood |
|
|
Term
| What 2 things does interstitial fluid exchange with? |
|
Definition
cells and lymphatics
-lymphatics return leaked protein and excess fluid to circulation |
|
|
Term
| Where are the 3 places substance can go once gets out of capillary? |
|
Definition
-back to capillay
-to cell
-to interstitial fluid
(balance of all these is Frank-Starling) |
|
|
Term
| What is interstitial fluid? |
|
Definition
spaces bw cells
-1/6 of body fluid
-capillary filtrate w/ protein concentration < plasma
-pressure is slightly negative (bc lymphatics pumps out excess fluid) |
|
|
Term
| What is the fxn of proteoglycan filaments and collagen bundles in interstitial fluid? |
|
Definition
-provide tensional strength for tissues
-makes tissue gel
-gel promotes diffusion rather than flow. |
|
|
Term
| Why is the negative pressure of interstitial fluid a good thing? |
|
Definition
| -gives patient a safety margin to prevent swelling or edema |
|
|
Term
| Hydrostatic pressure (Frank starling) |
|
Definition
FORCE EXERTD FROM WITHIN CAPILLARY WALLS
-at arteriole end, higher than osmotic (fluid forced out)
-changes blood composition |
|
|
Term
| What are capillaries leaky for? |
|
Definition
ions, water and glucose
-tends to hold macromlcls in. |
|
|
Term
| Interstitial fluid colloid Osmotic pressure |
|
Definition
force exerted on capillary walls from interstitial fluid
-Higher than hydrostatic pressure on venous side, so fluid leaks into vessel |
|
|
Term
|
Definition
fluid filters out at arterial end and in at venous end
-net reabsorption at venous end is > 90%
-remaining fluid flows to lymphatics
-net filtration(except for kidneys)=2ml/min |
|
|
Term
| What is the only route for protein and high MW substances in interstitial fluid to be absorbed by tissues? |
|
Definition
lymphatic system
-10 % of capillary filtrates
-'flap valves' are overlapping endothelial cells that permit high MW substances |
|
|
Term
| Where is the lymphatic system absent? |
|
Definition
Brain
- tissues around have it though |
|
|
Term
| How is lymph pumped through system? |
|
Definition
lymphatic pump valves
smooth muscle in lymphatic vessel wall
external compression
-pressure increase with increased interstitial pressure |
|
|
Term
| What does lymphatics control? |
|
Definition
interstitial protein concentration
interstitial fluid volume
interstitial fluid pressure |
|
|
Term
| what are the metabolic needs that control tissue blood flow? |
|
Definition
-O2 and nutrient delivery
-CO2 and hydrogen ion removal
-proper tissue ion concentration
-transport of hormones and other messengers. |
|
|
Term
| Why does the liver receive a majority of blood flow? |
|
Definition
| filters things that are absorbed by venous circulation form gut |
|
|
Term
| How is tissue blood flow acutely controlled (in the short term)? |
|
Definition
-constriction/dilation of precapillary sphincters
-either increased metabolic rate or decreased tissue o2 increases flow (these 2 ways below):
-Vasodilator theory- vasodilators act in time of need
-Oxygen/Nutrient lack theory- vascular smooth muscle contracts when O2 and ntrients are scarce (in times of great need) |
|
|
Term
| What are some examples of vasodilators? |
|
Definition
|
|
Term
| How is tissue blood flow chronically controlled (in the long term)? |
|
Definition
-gradual changes in vascularity (angiogenesis!)
-development of collateral circulation (growth of vessels to get around a block)
-such as developments in conditioning of athletes. |
|
|
Term
|
Definition
| -vascular endothelial growth factor (such as in long term control of blood flow) |
|
|
Term
| What are the 2 ways to increase concentration of a substance? |
|
Definition
-make more
-break it down less |
|
|
Term
| What are 2 endothelial derived factors to control blood flow control? These 2 are opposites. |
|
Definition
-Nitric oxide (NO)
-Released from endothelial cells into adjacent smooth muscle.
-stimulates production of cGMP (relaxes muscle)
-vasodilation
-cGMP is degraded by cGMP phosphodiesterase
Endothelin
-released by damaged endothelial cells
-VASOCONSTRICTOR
-may limit hemorrhage (released when arteries are damaged) |
|
|
Term
| What can cGMP be used for? |
|
Definition
-relaxes smooth muscle near endothelium
-VIAGRA & CIALIS
-reduces cGMP phosphodiesterase
-increased vessel dilation--> blood can flow to penis OR hypertension can be decreased |
|
|
Term
|
Definition
can be used as intravenous nitroglycerine.
-given during MI
-opens up vessels to cardiac muscle
-if given with subsequent vessel dilaters (CIALIS AND VIAGRA), can be fatal, too much is opened |
|
|
Term
| How can organ blood flow be autoregulated? |
|
Definition
-rapid increases in arterial pressures
-immediate increase in subsequent tissue flow
-declines to normal levels after 1 minute.
-Metabolic theory
-Myogenic theory |
|
|
Term
| What is the metabolic theory and how does it regulate blood flow in organs? |
|
Definition
-theory that excess flow washes out vasoDILATORS
-and that nutrient influx constricts arterioles
-increases BP on flow |
|
|
Term
| What is the myogenic theory and how does it regulate blood flow in organs? |
|
Definition
theory that stretching of vessel walls causes vasoconstriction.
-increases BP on flow |
|
|
Term
| What could not be done if it were not for autoregulation? |
|
Definition
| organ transplants. -prevents ischemic reperfusions (lack of blood flow to a place that recently lost a lot of blood flow) |
|
|
Term
| Name some vasoconstrictors. |
|
Definition
NE and E
Angiotensin II
Vasopressin (ADH)-released by pituitary, produced by hypothalamus
ions: Ca |
|
|
Term
|
Definition
-bradykinin
-histamine
ions: K, Mg, H, Acetate, Citrate, CO2 |
|
|
Term
| How does autonomic circulatory control control whole body flow? |
|
Definition
Sympathetic-
-prominent role with following innervations:
-blood vessels: stimulation increases resistance and decreases venous volume.
-heart: increases rate and contractility
Parasympathetic:
-input is limited, regardless of heart rate |
|
|
Term
| What are some examples of how autonomic NS controls circulatory flow of whole body? |
|
Definition
-redistribution of blood flow
-altered myocardial contractility
-very rapid, relfexive arterial pressure control |
|
|
Term
| How does Beta 1 affect arterioles? |
|
Definition
ionotropic- squeeze harder
cronotropic- squeeze faster |
|
|
Term
| What is the main goal of sympathetic vascular innervation? |
|
Definition
|
|
Term
| What does the vasomotor center do? |
|
Definition
-in lower pons and medulla
GOVERNOR OF PARASYMP AND SYMP:
-transmits parasymp. impulses via vagus to heart
-transmits symp. impulses via cord & symp. nevres to all blood vessels.
-input from higher centers (especially hypothalamus) |
|
|
Term
| What maintains continuous sympathetic vasoconstrictor tone? |
|
Definition
-baseline vasoconstrictor signals from vasomotor center.
-maintains partial vascular constirction
NT: NE! |
|
|
Term
| What are the 5 areas of the vasomotor center? |
|
Definition
VASOCONSTRICTOR
-nerves distributed to cord, stimulate preganglionic sympathetic vasoconstrictor nerves
VASODILATOR
-inhibits vasoconstrictor area
SENSORT
-hemodynamic sensory input from CN IX & X
-output to vasoconstrictor & vasodilator areas (important for vascular reflexes)
LATERAL AREA
-stimulates HR and contractility
MEDIAL AREA
-reduces HR via vagus. |
|
|
Term
| How does the sympathetic vasodilator system work? |
|
Definition
Epinepherine is released
-results in vasodilation (by beta to cause perfusion to skeletal muscles)
-little role in day to day regulation
-may be activated by intense emotion
-can result in vasovagal syncope
-simultaneous bradycardia and vasodilation occur!!! |
|
|
Term
| Why do people faint when they are scared? |
|
Definition
vasovagal syncope
-simultaneous bradycardia and vasodilation
-so blood to heart and to muscles, not enough to brain-->faint
-helps to elevate legs |
|
|
Term
| How does the nervous system rapidly control BP? (This is a mechanism for rapidly coping with physiologic stress) |
|
Definition
-simultaneous stim. of vasoconstrictor & cardioaccelerator fxns of symp. system
-vagal inhibition
Primary for RAPID control of low BP:
-arterioles constrict-->Increased resistance and BP
-veins constrict--> increased venous return & CO
-cardiac rate and contractility increase
onset in seconds, BP may double!
common trigger: heavy exercise, fright |
|
|
Term
| What tells sympathetic system that BP is to low, to cause rapid control of it? |
|
Definition
sensory preceptors inform medulla to perform vasoconstricion
-pressure preserved
-perfusion to less essential body parts impaired (limbs)
-perfusion to heart |
|
|
Term
| What are the 2 afferent paths of the baroreceptor REFLEX once stretch receptors are stimulated by increased arterial pressure? ON TEST. |
|
Definition
carotid sinus->Herings n-CN IX->medulla
aortic arch->CN X->medulla
Medulla- through medulalry tr. solitarius inhibits vasoconstrictor area & activates vagal parasympathetic center (dilates)
This vasodilatation & reduced heart rate reduce BP |
|
|
Term
| Overall, what do neurovascular reflexes do? |
|
Definition
| a “buffer” which minimizes BP flux with daily activity, little role in long-term control |
|
|
Term
| What would happen if baroreceptors did not exist? |
|
Definition
| arterial pressure would be unregulated and all over the place. |
|
|
Term
| Besides baroreceotors, what are some other neurovascular reflexes? |
|
Definition
-chemoreceptor
-atrial and pulmonary artery reflexes
-bainbridge reflex
-CNS ischemic response
-Cushing Reflex
**usually all of these occur when have shock- and tissue response is to not get rid of waste |
|
|
Term
| What do chemoreceptors sense? What reflexive actions are then taken? |
|
Definition
-hypoxemia, hypercarbia (high CO2 levels) & acidosis associated with hypertension
-BP and respiratory rate increases |
|
|
Term
| What do stretch receptors sense in atrial and pulmonary arteries? What reflexive actions are the taken? |
|
Definition
-hypovolemia & increased blood volume via ANP & ADH
when detect low blood volume (hypovolemia):
ANP (Atrial Natiuretic Factor)- makes you pee more salt
ADH- makes kidneys retain water. |
|
|
Term
| What does the Bainbridge reflex sense? What reflexive actions are then taken? |
|
Definition
-increased atrial pressure
-increases HR & contractility |
|
|
Term
| What does the CNS ischemic response detect? What reflexive actions then occur? |
|
Definition
-reduced blood flow to vasomotor center
-induces extreme vasoconstriction |
|
|
Term
| What does the Cushing reflex sense? What reflexive actions are then taken? |
|
Definition
-elevated CSF pressure
-arterial blood pressure raised (CSF pressure needs to stay below arterial pressure)
-Preserves perfusion to the brain until absolutely need to cut off flow to brain) |
|
|
Term
| How does the renal body fluid system regulate long term BP? (basis for treating hypertension) |
|
Definition
-slow and powerful
-Renal, hormonal & neurologic factors contribute |
|
|
Term
| What is the angiotensin system? (in general) |
|
Definition
renal conservation
-do not want to lose salt and water. |
|
|
Term
| What is the renal body fluid mechanism? |
|
Definition
-compensates for nearly any change in water/salt intake with counter-regulatory change in urine/salt output to correct BP!
-Main determinants of this:
shifts in renal fxn control curve
level of salt and water intake. |
|
|
Term
| What are 2 ways to get increased BP? |
|
Definition
-Changed kidney- reduced ability of kidney to diurese
-Increase salt intake |
|
|
Term
| How are the counterregulatory responses to chronic renal body fluid changes greater than those of acute changes? |
|
Definition
-pressure diuresis remains active
-neural and hormonal changes occur
-symp. altered
-angiotensin and aldosterone levels altered
-long term increased Na intake may cause damage to alter these responses. |
|
|
Term
| What is diminished if increased salt intake is acute rather than chronic? |
|
Definition
| -ability to compensate to maintain BP (Fig 19-5) |
|
|
Term
| How is arterial pressure calculated? |
|
Definition
CO X total peripheral resistance
(Ohm's law adapted to while body) |
|
|
Term
| When do chronic increases in total peripheral resistance NOT increase BP? |
|
Definition
| if renal vascular resistance and function are normal |
|
|
Term
|
Definition
Increased ECFV
-by increasing CO or peripheral resistance (arterial pressure)
-pressure diuresis will eventually correct |
|
|
Term
| What is altered when someone has a pathological alteration of peripheral resistance and has normally fxning kidneys? |
|
Definition
|
|
Term
| What is the flow of events from Increased ECF volume to increased urine output? |
|
Definition
increased ECF volume-->
increased blood volume-->
increased mean circulatory filling pressure-->
increased venous return to heart-->
increased CO--> (autoregulation-->increased total
peripheral resistance)--->
increased arterial pressure-->
increased urine output.----> decreases ECF volume (negative feedback!) |
|
|
Term
Why does NaCl intake raise BP more so than water?
-normal renal fxn minimizes this effect
-abnormal accelerates it. |
|
Definition
-water is rapidly and easily excreted
-NaCl activates thirst
-Na increases osmolality (ADH released, which impairs water excretion)
-accumulated NaCl is main determinant of ECFVolume |
|
|
Term
| Kidney removed, intake NaCl, what can slowly reverse this? |
|
Definition
pure water intake.
-NaCl intake raises BP.
-Peripheral resistance decreased AT FIRST to compensate for raise in BP |
|
|
Term
| How is he Goldblatt experiment a good example of Renin-Angiotensin system? |
|
Definition
If clamp on renal artery on one side(feels like normal constriction to body)
-pressure shoots up
-baroreceptors correct by lowering her heart rate (decrease at first)
-goes up, bc eventually fluids build up - -thus BP does actually go up |
|
|
Term
| What are the physiologic characteristics of hypertension? |
|
Definition
-increased CO
-increased sympathetic tone
-increased angiotensin II and aldosterone
-impaired renal pressure- natriuresis mechanism
-harder to fix, bc hypertension got to kidney |
|
|
Term
| What can cause "salt sensitivity"? |
|
Definition
-impaired renal fxn
-renin-angiotensin system |
|
|
Term
| What are the treatments of hypertension? |
|
Definition
-diet
-exercise
-diuretics
-vasodilators
-ACE inhibitors
-beta adrenergic inhibitors |
|
|
Term
| Three levels of arterial pressure (in sequential order). |
|
Definition
Immediate control mechs:
-baroreceptors
-CNS ischemic response
-chemoreceptors
Intermediate Control Mechs
-renin-angiotensin system
-stress-relaxation in arteries
-capillary fluid shift
Long Term control mechanism
-Renal body fluid control system |
|
|
Term
| What variables are closely linked with CO? |
|
Definition
-Peripheral oxygen consumption and metabolism
-varies inversely with total peripheral resistance
-Venous return is main determinant |
|
|
Term
| What are some variables that are linked to Venous Return? |
|
Definition
Right atrium pressure
sum of all blood flows thru peripheral tissues
-heart is cart, not horse |
|
|
Term
| What is a hypereffective heart? |
|
Definition
-increase upper limits of CO
-sympathetic stimulation
-myocardial hypertrophy |
|
|
Term
| What is a hypoeffective heart? |
|
Definition
Decrease the upper limits of CO.
-hypertension
-neural inhibition
-myocardial or valvular disease
-ischemia |
|
|
Term
| How does exercise effect CO? |
|
Definition
-increased muscle metabolism dilates feeding arterioles
-flow to muscles increases and peripheral resistance falls
-Sympathetic outflow
-veins constrict, VR increases, heart rate and contractility increase
-CO increases. |
|
|
Term
|
Definition
Factors reducing pump effectiveness.
Peripheral factors reducing VR (heart is normal) |
|
|
Term
| What are some factors that reduce pump effectiveness, thus lowering CO? |
|
Definition
a. Coronary occlusion & ischemia
b. Valve Stenosis & insufficiency
c. External chamber compression (tamponade)
d. Nonischemic Myocardial disease |
|
|
Term
| What are some peripheral factors that lower CO? |
|
Definition
a. Blood Loss, Hemorrhage
b. Acute venous dilatation
c. Major venous occlusion
d. Reduced metabolic rate (hypothyroidism) |
|
|
