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100 Cards in this Set
- Front
- Back
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Heart sounds
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Mighty Ape. Mighty (M(mitral)1, T(tricuspid)1) Ape (A(aortic)2, P(pulmonary)2)
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Carotid sinus vs carotid body function
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Carotid SinuS: measure preSSure, carotid bO2dy: measures O2
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Fick principle for determining CO
a. Formula |
CO = (O2 absorbed per minute by the lungs)\(Arteriovenous O2 difference)
(Use CVK -> pulmonary artery, arterial blood gas, and the rate of oxygen absorption by the lungs is measured by the rate of disappearance of oxygen from the respired air) (Guyton) |
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Cardiac output increase during training
a. In non-athlete b. In well-trained athlete |
a. 4-5x higher
b. 6-7x higher (In well trained athlete. normal blood flow 3-4 mL\min\100g muscle, blood flow during exercise 50-80 mL\min\100g muscle. = 15-25 x higher) (Guyton) |
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Decreased oxygen in a capillary bed cause what
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Local arteriolar vasodilation because
1. In the hypoxic state the muscle in the wall of the arteriole cannot maintain contraction 2. Production of vasodilator substances, Adenosine is the most important (Others are K+, ATP, lactic acid, CO2. Bradykinin, prostaglandins and nitric oxide has been additionally linked to the vasodilator response in coronary circulation) (Guyton) |
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Mean systemic filling pressure
a. What b. Normal value |
a. The pressure in the systemic circulation when the great vessels have been clamped
b. 7 mmHg (Guyton) |
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How is the slope of the venous return curve rotated upward
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By decreasing the resistance to venous return
(Guyton) |
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Proportion of deaths in the affluent society of the west resulting from coronary artery disease
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1\3
(Guyton) |
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Venous return of the heart
a. % through coronary sinus b. Most of the rest is drained by which chamber to where |
a. 75%
b. Right ventricle -> anterior cardiac veins -> right atrium (Guyton) |
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Under resting conditions, about 70% of the energy of cardiomyocytes is derived from?
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Fatty acids
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Is there alpha or beta receptors on the coronary circulation?
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Both
(Most alpha on epicardial vessels, most beta on intramuscular arteries. Excessive alpha sensitivity -> Prinzmetal's angina) (Overall effect of sympathetic stimulation is vasoconstriction!) (Guyton) |
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Causes of acute coronary occlusion (2)
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1. Thrombus\Embolus (where the arteriosclerotic plaque has broken through the endothelium)
2. Local muscular spasm (<- irritation of smooth muscle by edge of arteriosclerotic plaque or nervous reflex dysfunction)(secondary thrombosis) (Guyton) |
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How many percent of the normal resting coronary blood flow is needed to keep the cardiomyocytes from infarcting?
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15-30%
(Guyton) |
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Systolic stretch
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The phenomenon when the the normal portions of the ventricular muscle contracts, the ischemic portion of the muscle instead of contracting si forced outward by the pressure that develops inside the ventricle.
(explain why the overall pumping strength is decreased more than one might expect) (Guyton) |
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Cardiac shock almost always occurs when more than ... of the left ventricle is infarcted
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40%
(Guyton) |
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Development of pulmonary edema following MI is often delayed a few days because
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1. ↓CO -> ↓Renal blood flow
2. ↓Renal blood flow -> diminished urine production 3. Progressive congestive symptoms (Patients who develop acute pulmonary edema in this manner can die within a few hours after appearance of the initial pulmonary symptoms) (Guyton) |
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Two risk periods for fibrillation post-MI
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1. The first 10 minutes post-MI
2. After the first hour and continuing for a few hours (Guyton) |
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Fibrillation post-MI, 4 contributing factors
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1. Intracellular K+ depletion. ↑K+ in ECF increase the irritability of cardiac musculature
2. Injury current 3. Powerful sympathetic reflexes -> ↑irritability 4. Cardiac muscle weakness -> ↑dilation -> ↑conduction pathway -> Circus movements (Guyton) |
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Current of injury
a. What b. Causes (3) c. EKG |
a. Some different cardiac abnormalities can cause the heart to remain partially\totally depolarized constantly. When this occurs, current flows between the pathological depolarized areas (which is - outside) and the normally polarized areas (which is + outside) even between heartbeats
b. 1. Mechanical trauma (increased membrane permeability) 2. Infectious processes (damage membranes) 3. Ischemia (insufficient energy to repolarize) c. Can localize the area of ischemia by using J point for reference and vector analysis (Guyton) |
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Circus movements
a. What b. Causes c. Associated pathologies |
a. A excitation wave traveling continuously in circular fashion around a ring of muscle (Stedman)
b. 1. ↑Length of pathway (dilation, ie post MI) 2. ↓Velocity of conduction (blockage of Purkinje system, ischemia, ↑serum K+) 3. ↓Refractory period of the muscle (drugs: epinephrine, repetitive electric stimuli as in AC current) c.Atrial flutter, atrial fibrillation, ventricular fibrillation (Guyton) |
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Rupture of infarcted area
a. How b. When c. How to measure\follow progression of |
a. Dead muscle fibers degenerate -> heart wall become stretched and very thin -> rupture -> cardiac tamponade
b. A few days c. See status of systolic stretching by cardiac imaging (Guyton) |
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Large coronary ischemic area - components
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1. Center of infarcted dead fibers (no collaterals, within 1-3h)
2. Around is nonfunctional area with failure of contraction and usually failure of impulse conduction 3. Around is mild ischemic area (Guyton) |
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Development of ischemic coronary area
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1. 1-3h -> central area die
2. Few days -> part of surrounding nonfunctional area die due to prolonged ischemia 3. Few days-3weeks -> part of the nonfunctional area become functional again due to collateral circulation 4. Meantime infarcted area is replaced by fibrous tissue 5. Fibrous tissue contract and dissolve and is replaced by hypertrophy of surrounding tissue (Guyton) |
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Coronary steal syndrome
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During ischemia the ischemic area is supplied partly by anastomotic collaterals. When the workload of the heart is increased for whatever reason, the coronary vessels become dilated and a lesser proportion of the blood flow go to the ischemic area via the anastomotic connections and more to the part it originally supplies
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Cardiac reserve
a. What b. Amount |
a. The CO the heart is capable of producing above resting conditions
b. 300-400% (Guyton) |
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Pain in coronary artery disease - postulated cause
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Excessive accumulation of acidic substances (Lactic acid) or
pain-promoting substances: histamine, kinins, cellular proteolytic enzymes (Guyton) |
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Compensation for acute cardiac failure by sympathetic nervous reflexes - 3 reflexes
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1. Baroreceptor reflex
2. Chemoreceptor reflex 3. Central nervous system ischemic response (4. Reflexes that originate in the damaged heart) (Maximized within 30 seconds, double CO & mean systemic filling pressure (14 mmHg) (Guyton) |
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Recovery of the myocardium post-MI - when is most of its final state of recovery achieved
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5-7 weeks
(Most rapid the first few weeks, can be some continuing improvement after 7 weeks) (Guyton) |
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How does decompensated cardiac failure develop
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1. CO is decreased to a point where the kidneys cannot re-establish normal fluid balance (equate output with input)
2. Progressive fluid retention 3. ↓CO due to heart stretching & cardiac edema -> vicious circle (Guyton) |
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Indicator dilution method for measuring cardiac output
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CO = (Mg of dye injected to right atrium x 60)\((Average concentration of dye in each mL of blood for the duration of the curve) x (duration of the curve in seconds))
(Dye: cardio-green Measure in arterial tree) (Guyton) |
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In severe, acute left heart failure, pulmonary edema occasionally occurs so rapidly that it can cause death by suffocation in …..
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20 minutes (Guyton)
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Vicious circle of cardiac deterioration in cardiogenic shock
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↓CO -> ↓Arterial pressure -> ↓Coronary blood flow -> ↓↓CO -> ↓↓ Arterial pressure .....
(Is initiated at higher MAP in patients with already stenosed\occluded coronary vessels) (Guyton) |
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When and why can we see peripheral edema after right heart failure?
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After the first day or so. Due to long-term fluid retention by the kidneys
(Guyton) |
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How low does the CO has to fall for anuria to arise?
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About one-half of normal
(Guyton) |
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3 Causes of reduced renal output during hypotension\shock
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1 ↓Glomerular filtration (reduced arterial pressure, sympathetic constriction of the afferent arterioles of the kidney)
2. RAS (ATII -> constrict renal arterioles (reduce pressure in peritubular capillaries -> ↑reabsorption)) 3. ↑Aldosterone (<- RAS & ↑K+. Take up Na+ (bring with it Cl- & water, ↑Osmotic level cause ADH release) (Guyton) |
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Which hormone increase beside catecholamines increase 5-10 fold during heart failure
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ANF
(Guyton) |
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Acute pulmonary dema in late-stage heart failure -vicious cycle
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1. Temporary overload of heart
2. Vicious cycle coronary blood flow & CO\arterial pressure 3. Stagnation of blood in lungs -> transudation 4. ↓O2-saturation 5. Weakens heart, weakens arterioles -> peripheral vasodilation 6. Peripheral vasodilation -> ↑venous return 7. ↑Venous return -> ↑pulmonary transudation -> ↓O2-saturation ..... (Guyton) |
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Transudate
a. What b. Result of c. Characteristics |
a. Any fluid (solvent and solute) that has passed through a presumably normal membrane, such as the capillary wall,
b. As a result of imbalanced hydrostatic and osmotic forces c. Characteristically low in protein unless there has been secondary concentration. (Stedman) |
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Exudate
a. What b. Characteristics |
a. Any fluid that has exuded out of capillaries because of injury or inflammation (e.g., peritoneal pus in peritonitis, or the exudate that forms a scab over a skin abrasion)
b. Characteristically high in protein and white blood cells (Stedman) |
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Normal right atrial pressure?
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0 mmHg
(Guyton) |
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Avitaminosis causing high-output cardaic failure
a. Which? b. How? |
a. Beriberi (thiamine\Vitamin B1)
b. Cause 1. Weakening of heart 2. Increased venous return due to dilation of peripheral blood vessels (Guyton) |
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Under normal conditions, is it closing or opening of the heart valves that cause audible sounds?
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Closing
(Guyton) |
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"Lub dub, Lub dub" - associated with which valves at which stage of the cardiac cycle
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Lub\1st heart sound -> closure of AV valves at beginning of systole.
Dub\2nd heart sound -> Closure of semilunar valves at the end of systole (Guyton) |
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Cause of the normal heart sounds
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Vibration of the taut valves immediately after closure, along with vibration of the adjacent walls of the heart and major vessels (mostly with the semilunar valves) around the heart
(Guyton) |
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Heart sounds
a. Pitch levels b. Peak at c. Which part is audible d. Does the AV or the semilunar valves have higher frequency? |
a. 4-500 Hz
b. 20 Hz c. 40-500 Hz d. The semilunar (More taut, the elastic arterial wall provide a better vibrating chamber) (Guyton) |
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Heart sound, points of auscultation
a. Pulmonic valve b. Aortic valve c. Mitral valve d. Tricuspid valve |
a. Left parasternal line in 2nd intercostal space
b. Right parasternal line in 2nd intercostal space c. Left miclavicular line in 5th intercostal space d. Left parasternal line in 4th intercostal space (Guyton) |
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Third heart sound
a. Signify b. When c. Frequency |
a. (Hypothesized) To be from oscillation of blood back and forth between the walls of the ventricles initiated by inrushing of blood from the atria (at end of first phase of rapid ventricular filling)
b. Beginning of middle third of diastole c. Frequency is usually below what can be heard (Detected in 1\3-1\2 of healthy hearts with phonocardiogram, esp. normal in children and younger people) (Guyton) |
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Fourth heart sound
a. Signify & associated clinical state b. When c. Frequency |
a. Occurs when the atria contract (similar sound mechanism as 3rd heart sound) and related to reduced ventricular compliance <- ventricular hypertrophy, acute MI
b. Late diastole c. Usually unaudible (Detected in 1\4 of healthy hearts with phonocardiogram) (Guyton & Stedman) |
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Valvular lesion
a. Greatest cause b. Affect |
a. Rheumatic fever
b. 1st mitral, 2nd aortic (related to degree of exposed "trauma") |
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Rheumatic fever
a. What b. <- c. Other associated diseases |
a. Autoimmune disease
b. Streptococcal toxin from group A hemolytic anemia, usually following Sore throat, Scarlet fever or middle ear infection c. Acute glomerular nephritis & valvular lesions |
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How does the valves become stenosed after rheumatic fever?
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The lesions often occur on adjacent valve leaflets simultaneously -> stick together -> scar tissue -> permanent fusion
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Murmur of aortic stenosis
a. When b. Associated finding |
a. Loud systolic murmur, crescendo-decresendo, best heard midsystolic (vibration spread into thorax & great vessels of neck)
b. Thrill - can palpate it on neck and upper chest (Can often be loud enough to be heard several feet away) (Guyton) |
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Aortic regurgitation
a. Description b. Heard best where |
a. Diastolic murmur, high pitch & "blowing"\swishing
b. Over left ventricle (Guyton) |
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Mitral regurgitation
a. Description of sound b. Point of best auscultation |
a. Systolic, high frequency\blowing\swishing sound
b. Left ventricle (left midclavicular line in 5th intercostal space, because left atrium is deep & "hidden") |
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Mitral stenosis
a. When b. Quality |
a. Appear gradually during mid diastole
b. Low-frequency (unaudible <- atria cannot produce high pressure gradient), rumbling murmur |
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Systolic murmurs
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1. Aortic stenosis
2. Mitral regurgitation (Guyton) |
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Diastolic murmurs
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1. Aortic regurgitation
2. Mitral stenosis (Guyton) |
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What does aortic regurgitation & aortic stenosis have in common? What about regurgitation & stenosis of mitral valve?
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Aortic = net decrease in forward movement from left ventricle (-> damming, dilation, hypertrophy)
Mitral = net decrease in forward movement from left atrium (-> damming, dilation (-> AF), hypertrophy) (Guyton) |
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Murmur of patent ductus arteriosus
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Harsh, blowing murmur heard in the pulmonary artery, more pronounced during systole.
(Called machinery murmur because it waxes and wanes with each beat of the heart, can usually not be heard until the child is 1 year) (Guyton) |
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Congenital heart disease - 2 common causes
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1. Viral infection, especially German measles in the mother during the first trimester
2. Congenital (children of patients surgically treated for congenital heart disease have 10x the risk of having a heart anomaly) (Guyton) |
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Nitric oxide
a. Pathway of production b. Isoforms |
a. Nitric oxide synthase (NOS): L-arginine -> NO
b. 1. Type 1 - neural NOS (nNOS), transmitter in brain and in non-adrenergic, non-cholinergic (NANC) autonomic nerves that innervate penile erectile tissue 2. Type 2 - inducible NOS (iNOS), in vascular endothelium 3. Type 3 - constitutive NOS (cNOS), in vascular endothelium |
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NOS
a. Activation of constitutive NOS (cNOS) in vascular endothelium b. Activation of inducible NOS (iNOS) in vascular endothelium |
a. cNOS - under normal conditions
1. Shearing forces\Flow-dependent NO formation -> Ca2+ -> Calmodulin -> ↑cNOS 2. Receptor-stimulated NO formation (Bradykinin, Substance-P, adenosine) -> Ca2+ -> Calmodulin -> ↑cNOS b. Inducible NOS (iNOS) - under abnormal conditions Inflammation: bacterial endotoxins (lipopolysaccharide), cytokines (TNF), interleukins -> ↑iNOS (Can be 1000x greater than with cNOS) (CVphysiology.com) |
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NO - mechanism
a. 3 Different fates b. 3 Effects |
a.
1. Bind to superoxide anion with very high affinity (explains its half life of only a few seconds) 2. Diffuse to blood and binds to heme moiety of Hb 3. Diffuse to smooth muscle and bind to the heme moiety of guanylyl cyclase and activate it -> cGMP b.↑cGMP -> 1. Inhibit Ca2+ entry into cells 2. ↑K+ channels -> hyperpolarization & relaxation 3. ↑cGMP-dependent protein kinase -> ↑Myosin light chain phosphatase (cGMP is deactivated by cGMP-dependent phosphodiesterase inhibitors such as Viagra) (Also has indirect vasodilation by inhibitign ATII & sympathetic vasoconstriction) (Has anti-platelet (inhibit platelet adhesion to vascular endothelium), anti-inflammatory effect (inhibit leukocyte adhesion to vascular endothelium, scavenges superoxide), & inhibit smooth muscle hyperplasia) (Linked to hypertension, obesity, dyslipidemia, diabetes, atherosclerosis, aging, cigarette smoking) (CVphysiology.com) |
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How many percent of the blood volume can be removed in 30 minutes before the person dies?
What if the sympathetic nervous reflexes is absent? |
30-40%
Half - 15-20% (Guyton) |
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Blood flow through which two organs is spared during sympathetic stimulation?
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Cerebral and coronary blood flow
(In addition these have excellent local blood flow autoregulation) (Blood flow here is essentially normal down to 70 mmHg MAP) (Guyton) |
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Nonprogressive\Compensated shock - recovering factors (6)
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1. Baroreceptor reflexes (30s)
2. Central nervous system ischemic response (↑↑sympathetic nervous system) 3. RAS (10min-1h) 4. ADH (10min-1h) 5. Compensatory mechanisms that return the blood volume back toward normal (interstitial -> plasma, ↑thirst, ↑intestinal uptake...) (1h-48h) 6. Reverse stress-relaxation of the circulatory system ("adaptation to the decreased volume\pressure exerted by the blood) (10min-1h) (Guyton) |
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Progressive shock - factors contributing to the vicious circle
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1. Cardiac depression (low CO -> inadequate coronary blood flow -> lower CO) (The most important factor in the final lethal progression of the shock)
2. Vasomotor failure (ischemia in CNS vasomotor center, if < 30 mmHg) 3. Blockage of very small vessels \ Sludged blood (↑acids (lactic acid, carbonic acid) + other deteriorative products from the ischemic response initiate local blood agglutination) 4. Increased capillary permability (after many hours of capillary hypoxia) 5. Release of toxins by ischemic tissue (histamine, serotonin, tissue enzymes, endotoxin (from "infarcted" gram-negative bacteria in intestine -> also cause cardiac depression)) 6. Generalized cellular deterioration (↓Na+-K+-ATPase, mitochondrial activity, lysosomal lysis, ↓hormones (ie insulin)) 7. Acidosis (lactic acid, carbonic acid) 8. Shock lung syndrome 9. Patchy necrosis in tubular epithelium in kidney (kidney failure, uremic death) (Guyton) |
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What is the factor that perhaps is the most significant for development of the final state of irreversibility of shock - 1 concept, 3 components
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Depletion of high-energy phosphate reserves
1. Creatine phosphate has been degraded 2. ATP -> ADP -> AMP -> adenosine -> adenosine diffuse out -> converted to uric acid -> cannot reenter and replenish 3. Resynthesis of adenine is very slow (2%\hour) (Guyton) |
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How can intestinal obstruction cause hypovolemic shock?
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Distention of the intestine partly blocks venous blood flow in the intestinal wall -> ↑Capillary pressure -> fluid exudates into intestinal wall & lumen -> positive feedback
(Guyton) |
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Neurogenic shock - 4 causes
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1. Deep general anesthesia
2. Spinal anesthesia (especially when it extends all the way up to the spinal cord) 3. Brain damage (concussion\contusion of basal regions, prolonged ischemia of vasomoter center (>5\10min)) 4. Spinal cord damage |
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Shock - what is the 1st and 2nd most frequent cause of shock-related death in the modern hospital?
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1. Cardiogenic shock
2. Septic shock (Guyton) |
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What is the beneficial effect of glucocorticoids in patients in severe shock (3)
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1. Frequently increase the strength of the heart in the late stages of shock
2. Stabilize lysosomes and thus prevent release of lysosomal enzymes intracellularly 3. Might aid in the metabolism of glucose by severely damaged cells (Guyton) |
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How many minutes of circulatory arrest cause some degree of permanent brain damage in >50% of patients?
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5-8 minutes
(Most of the damage is apparently due to minute intravascular blood clotting. Experiment with circulatory arrest with heparin\streptokinase increased the time needed to produce brain damage by 2-4) (Guyton) |
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Pulmonary artery pressure - systolic & diastolic
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25\10 mmHg
(Netter flash cards) |
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Mean arterial pressure
a. Formula b. Value when 120\80 mmHg |
a. MAP = diastolic pressure (80 mmHg) + 1\3 pulse pressure (40 mmHg)
b. 93 mmHg (Netter flash cards) |
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Turbulent & laminar blood flow
a, What is the name of the variable that determines whether flow in a tube will be laminar or turbulent b. Give the formula that predicts whether flow in a tube will be laminar or turbulent |
Reynolds number
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What is the formula for wall tension in a vessel? What is this formula called?
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T = Pt x r
Pt = transmural pressure (the difference between pressure inside and outside the vessel\pressure gradient across the vascular wall) Laplace's law (Explains why aneurysms (↑r) is prone to rupture (Netter flash cards) |
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16. S3
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1. Increased preload
2. Increased contractility Force-velocity curved are altered when preload or contractility is changed. When preload is incrased, the curve is shifted upward, but Vm (the maximal velocity, occurring at zero afterload) is unchanged. Increased contractility, however, results in a shift in the curve with an increase in Vm. |
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Reactive hyperemia - mechanism
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Occlusion of blood flow -> local buildup of metabolic products.
Restored flow -> accumulated vasodilator metabolites produce increased blood flow (Netter flash cards) |
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Metarteriole
a. What b. Structural characteristics c. Function d. Precapillary sphincter |
a. The blood vessels between arterioles and venules (precapillaries, meta- = after)
b. Pass trough capillary beds with capillaries, but are not true capillaries because they have smooth muscle present in the tunica media c. Act as a bypass channel and regulate flow into capillary beds d. Rings of smooth muscle on true capillaries where they emerge from the metarteriole or arteriole (regulates blood flow) |
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Metarteriole
a. What b. Structural characteristics c. Function d. Precapillary sphincter |
a. The blood vessels between arterioles and venules (precapillaries, meta- = after)
b. Pass trough capillary beds with capillaries, but are not true capillaries because they have smooth muscle present in the tunica media c. Act as a bypass channel and regulate flow into capillary beds d. Rings of smooth muscle on true capillaries where they emerge from the metarteriole or arteriole (regulates blood flow) |
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All the blood in the circulation traverses the entire circulatory circuit an average of how many times each minute?
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Once each minute
(Up to 6 times each minute when a person is extremely active) (Guyton) |
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Few cells in the body are located more than ... um from a capillary
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50
(Guyton) |
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Negative feedback - gain
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Gain = Correction \ Error
Correction: how much did it return the system to normal Error: how much is left to reach the homeostatic values (Guyton) |
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How many cells are in the human body?
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100 trillion (1x10^12)
(Guyton) |
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Positive feedback mechanisms (6)
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1. Ferguson reflex: contraction -> ↑oxytocin -> ↑contraction (amplitude & Hz)-> ↑↑oxytocin..
2. Blood clotting 3. Lactation (suckle -> ↑prolactin -> ↑milk -> ↑suckle ..) 4. Ovulation (↑estrogen -> ↑LH -> ↑↑estrogen) 5. Generation of action potentials (stimulated nerve fiber -> slight leakage of Na+ -> ↑membrane potential -> open more channels...) 6. Pathologic processes (ie shock: ↓CO -> ↓perfusion in coronary circulation -> ↓↓CO) |
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Proteins in the cell membrane (2)
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1. Integral proteins - protrude all the way through the membrane (channels\pores, transporters, receptors)
2. Peripheral proteins - attached to one side only (often attached to integral proteins, usually functions as enzymes or controllers of transport through the cell membrane "pores") (Guyton) |
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Cell menbrane - thickness
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7.5-10 nm
(Guyton) |
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Cardiopulmonary reflexes (4)
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1. Carotid and aortic chemoreceptors (2 carotid bodies -> Hering's nerve, 2-3 aortic bodies -> vagus nerve)((excite the vasomotor center, effective < 80 mmHg) (hypoxia, hypercapnia)
2. Atrial and pulmonary artery reflexes (stretch receptors called low-pressure receptors, minimize arterial pressure changes in response to changes in blood volume) 3. Atrial reflexes that activate the kidneys - the volume reflex (↓ADH, ↑ANP, reflex dilation of the afferent arterioles of the kidneys) 4. Atrial reflex control of heart rate - The Bainbridge effect (↑atrial pressure -> heart rate: partly by stretch of SA node, part via vagus nerve to medulla. Can increase heart rate up to 75%) (Guyton) |
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Central nervous system ischemic response
a. Elicited by b. Effect c. When d. Special type of CNS ischemic response |
a. The vasoconstrictor and cardioaccelerator neurons in the vasomotor center respond directly to the ischemica and become strongly excited (via CO2 probably)
b. It can elevate the MAP to 250 mmHg for as long as 10 minutes (strongest sympathetic stimulation possible, renal blood flow totally cease) c. < 60 mmHg (strongest at 15-20 mmHg) of MAP d. Cushing reaction (Elicited by ↑intracranial pressure. -> hypertension, bradycardia, hyperpnea) |
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What is the mechanism of hypertension in all vasculitis conditions
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Decreased NO production.
(USMLE) |
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What is the mechanism of hypertension in old age
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Calcification of tunica media - Monckeberg arteriosclerosis\medial calcification.
(USMLE) |
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In what systolic BP range is the overall blood flow autoregulated?
What happens when it goes below? |
60-160 mmHg.
Ischemic infarct. (USMLE) |
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Important vasodilators in different organs
a. Brain b. CV c. Lungs d. Muscle e. GI f. Skin g. Renal h. Arterioles |
a. Brain
↓PO2, ↑PCO2 (Headache at high altitude due to compensatory hyperemia) b. CV Adenosine (Ischemia is the most common cause of Supraventricular tachycardia -> explain why adenosine is important) c. Lungs ↑PO2 d. Muscle ↑PCO2, ↓pH e. GI Food f. Skin ↑Temperature, ↑PCO2 g. Renal ANP, Prostaglandins (D2), Dopamine (D2) h. Arterioles Beta-2, ↑PCO2 (USMLE) |
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Carotid reflex
a. How low is the normal drop in blood pressure when standing up, how high is the increase in heart rate normally b. Definition of dysfunction of the carotid reflex c. Three causes of dysfunction d. When is it useful to put a patient in Trendelenburg position |
a. 5-10 mmHg, 5-10 increase in heart rate.
b. <5 increase in heart rate when standing up. c. 1. Autonomic dysfunction from diabetes (Most common cause) 2. Riley-Day syndrome\Familial dysautonomia (Born without autonomic reflexes) 3. Shy-Drager syndrome - loss of this reflex in Parkinsonian patients d. In case of excessive increase in blood pressure. Stimulate carotid sinus -> decrease BP. (USMLE) |
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Heart sounds
a. Opening snap - from which two valves in which two conditions b. Ejection click - from which two valves in which two conditions |
a. Comes when valves open forcefully during diastole. Which two valves are open during diastole - mitral and tricuspid. So these must be delayed in opening to make this sound, as we see in mitral and tricuspid stenosis.
b. Made by valves opening forcefully in systole. Which two valves open in systole? pulmonary and aortic valves. -> Pulmonary and aortic stenosis. (USMLE) |
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S4 heart sound -
a. Synonym b. The 3 associations |
a. Atrial kick
(If the atria perceives that it has to kick, there has to be increased resistance in front of it.) 1. Pressure overload 2. Hypertrophy 3. Compensation (USMLE) |
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S3 heart sound
a. The 3 associations b. Mechanism of sound c. Who has S3 phyisologically |
a.
1. Dilated ventricle 2. Volume overload 3. Decompensation b. Blood fall and smack the dilated ventricle when you open the atrioventricular valves. c. Adolescent females (Due to estrogen. Estrogen is a muscle relaxant.) (USMLE) |
