Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
164 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
What is ohms law? |
The flow F of blood in a vessel is directly proportional to the pressure difference (pressure at one end P1 - pressure at other end) and indirectly proportional to the resistance R. F=◇P/R R=◇P/F ◇P=F x R |
|
|
|
What is the total blood flow in the adult circulation? |
5000ml/min |
Cardiac output |
|
|
What is Reynolds number? |
The measure of the tendency for turbulence to occur. Turbulence is directly proportional to velocity of blood flow V (cm/sec), vessel diameter D (cm) and density P. It is inversely proportional to the viscosity N (in poise) Re= V.D.P/N When >200-400 turbulence will occur. When >2000 will occur even in straight vessels |
|
|
|
Peripheral resistance unit |
= ◇P/F = approx 100mm in systemic and 14 in pulmonary/CO (100ml/sec) =1 in systemic and 0.14 in pulmonary |
|
|
|
Conductance |
1/resistance Conduction of a vessel increase in proportion to the fourth power o the diameter: conduction -(proportional)- diameter to the power 4. When pressure difference = 100... Diameter of vessel 1 = flow 1ml/min Diameter 2 = 16ml/min Diameter 3 = 256ml/min |
|
|
|
Poiseuille's law |
Diameter of a blood vessel plays the bigger role in blood flow as flow is directly proportional to the fourth power of the radius due to laminar blood flow (flow in the centre of a vessel moves faster that the outside) |
|
|
|
How do parallel blood vessels affect total blood flow (CO) and PVR? |
Total conductance is the sum of conductance of each parallel pathway so more parallel pathways results in more blood flow (CO) while reducting PVR. Parallel circuits are seen in brain, kidney, muscle, GI and coronary circulations - removing a kidney/limb reduces CO and increases PVR |
|
|
|
What has the main effect on viscosity? |
Haemotocrit (proportion of blood that is RBC) Adult men =42 Adult women =38 (% of blood that is RBC) Viscosity = 3-4 (3-4x more viscous than water) |
|
|
|
Pulse pressure = |
SV/arterial compliance (PP is greater inold age due to atherosclerosis and relatively non compliant vessels) |
|
|
|
Central venous pressure |
Right atrial pressure (usually 0 = atmospheric pressure, -5-30) -right heart pumping weakly pressure increases -increase venous return - pressure increases (increased blood vol, increased large vessel tone and peripheral venous pressures, dilation of arterioles) |
|
|
|
Gravitational pressure on venous pressure |
Pressure in right atrium and above is atmospheric 0. As you go down the standing man, pressure in veins increases to +90 in feet. In a walking adult feet pressure +20 due to venous/muscle pump. The cranial cavity is closed so can have pressures below atmospheric -10. |
|
|
|
Venous reservoirs |
Can constrict to release blood into other areas of the circulation. Spleen - 100ml - higher concentrations of RBC to increase hematocrit Liver - several hundred Large abdo veins - 300mls Venous plexus beneath the skin - several hundred |
4 |
|
|
Vasomotion |
The intermittent flow through a single capillary, largely affected by oxygen concentration in the tissue. |
|
|
|
Diffusion in capillaries |
Lipid-soluble substances diffuse across all areas of capillaries (oxygen and CO2) Lipid-insoluble or water soluble substances diffuse only across pores and depend on the diameter of the substance: -water permeability = 1 -NaCl = 0.96 -Urea = 0.8 -Glucose = 0.6 -Insulin = 0.2 -Albumin = 0.001 Different tissues have different permeability -liver is very permeable -glomerular very permeable to water and electrolyte but not proteins proteins-Brain less permeable |
|
|
|
Starling forces |
Net Filtration Pressure = capillary pressure - interstitial fluid pressure - plasma colloid osmotic pressure - interstitial colloid osmotic pressure If + then net fluid filtration into interstitial fluid If - then net fluid absorption into capillaries |
|
|
|
Rate of capillary fluid filtration = |
Kf (capillary filtration coefficient- determined by number and size of pores in each capillary and number of capillaries) x NFP Net filtration rate only about 2ml/min |
|
|
|
Where does lymph from lower body, left head, arm and chest drain? |
Thoracic duct -> junction of left internal jugular vein and left subclavian vein |
|
|
|
Where does lymph from the right side of the head, neck, arm and chest drain? |
Right lymph duct -> junction if right subclavian and internal jugular |
|
|
|
Rate of lymph flow |
120ml/hr or 2-3L/day |
|
|
|
What affect does carbon monoxide have on availability of oxygen? |
Poisons the ability of haemoglobin to transport oxygen |
|
|
|
What affect does cyanide have on the availability of oxygen to tissues? |
Poisons the ability of tissues to use oxygen |
|
|
|
What is vasodilator theory? |
The greater the rate of metabolism or less availability of oxygen or other nutrients, the greater the release of vasodilatir substances in the tissues for acute local blood flow regulation. Adenosine, carbon dioxide, histamine, potassium ions and hydrogen ions |
|
|
|
What is oxygen (nutrient) demand theory? |
Oxygen, along with other nutrients, is required to cause muscular contraction , therefore when oxygen is deficient, blood vessels relax and dilate , thereby regulating blood flow. |
|
|
|
What is reactive hyperemia? |
When blood supply to a tissue is blocked for secs - hours there is a subsequent increase in blood flow when unlocked to resupply the oxygen deficiency of the tissue. |
|
|
|
What is active hyperemia? |
When tissues become highly active ie exercise, mental activity, the increase in local metabolism eats up the nutrients and causes release of vasodilators which causes increase in blood flow. |
|
|
|
The metabolic theory of auto regulation of blood flow |
Aretrial pressure increase causes acute increase in blood flow which "washes out" the vasodilators produced by the tissues resulting in vasoconstriction and return of blood flow to near normal despite ongoing increase in arterial pressure. |
|
|
|
The myogenic theory of auto regulation of blood flow |
Sudden stretch of small blood vessels causes the smooth muscle of the vessel wall to contract which reduces blood flow back to normal. Vice versa. |
|
|
|
What substances are involved in endothelial derived blood flow regulation? |
Nitric oxide - activates soluble guanylate cyclases resulting in coversion of cGTP to cGMP and activation of PKG which cause blood vessels to relax. Release of NO also increases diameter of large upstream vessels whenever microvascular blood flow increases downstream, improving blood flow. Enothelin - usually released from endothelial cells of vessels under injury causing vasoconstriction i.e if torn it limits bleeding from a vessel but can also be release in damage due to hypertension. |
Vasodilator and vasoconstrictor |
|
|
Angiogensis |
If metabolism of a tissue is increased over prolonged period then the vascularity increases. If the metabolism decreases, the vascularity decreases. |
|
|
|
Role of oxygen in long-term regulation of blood flow |
A decrease in oxygen i.e. at high altitudes with increase the vascularity. |
|
|
|
Examples of angiogenic factors |
Vascular endothelial growth factor -Fibroblast growth factor -Platelet-derived groth factor -Angiogenin |
|
|
|
Examples of angiogensis inhibitors |
Steriod-hormones -Peptides such as angiostatin and endostatin |
|
|
|
Laplace's equation |
Vascular wall tension = radius of vessel x it's pressure T= r x P -When blood pressure increases, thickness of vascular wall increases over time and vice versa. |
|
|
|
Inward eutrophic remodelling |
In small vessels that constrict in response to increase in pressure, the smooth muscle and endothelial cells reaarange themselves around the smaller lumen diameter with no change in total cross-sectional area of the vessel wall. |
|
|
|
Hypertrophic remodelling |
Larger arteries do not constrict to increases in pressure so increased wall tensiom causes increase area of vascular wall. This results in larger vessels becomeing stiffer as in chronic HTN |
|
|
|
Humoral vasoconstrictors |
-Norepinephrine > epinephrine -Angiotensin II -Vasopressin (ADH) -Calcium ions - stimulate smooth muscle constraction -decrease in H ions |
|
|
|
Humoral vasodilators |
-Bradykinin - arteriolar dilation and increased capillary permeability -Histamine - released in response to tissue damage/inflammation/allergy - arteriolar dilation and capillary leakage -physiological increase in K ions - inhibit SM contraction -Mg ions - inhibit SM contraction -increase H ions -increase CO2 conc - marked vasodilation in brain |
|
|
|
What is the main regulator of circulation control in the ANS |
Sympathetic vasoconstriction - continuous firing causing vasoconstriction via norepinephrine secretion on alpha adrenergic receptors of vascular SM. Sympathetic nerves also cause increased HR and contractility which usually happens when vasoconstriction occurs. |
|
|
|
Role of the (sympathetic) nervous system in rapid (5-10secs) control of arterial BP |
-Most arterioles are constricted increasing PVR -The veins are strongly constricted - increasing preload thereby increasing SV -Direct stimulation of the heart increasing HR and contractility |
most rapid mechanism for arterial pressure regulation |
|
|
Baroreceptor reflex |
Negative feedback reflex mechanism: baroreceptors located in the walls of large arteries when stretched send signals to the ANS to reduce arterial pressure by decreased PVR (dilate peripheral vessels) and decreased CO (decrease HR and constractility). Vice versa. I.E. the carotid sinus in the internal carotid artery |
|
|
|
Barorecptors role in reducsing orthostatic hypotension |
When we stand, the drop in pressure in upper body triggers to baroreceptors to ellicit an immediate reflex resulting in strong sympathetic discharge to minimize decrease in pressue in head and upper body. |
|
|
|
Chemoreceptor reflex |
Chemoreceptors are like baroreceptors as they excite the vasomotor centre in response to low arterial pressure. - located in several small chemoreceptor organs (i.e. carotid and aortic body) - repsond to low O2, excess CO2 and excess H ions (as in low arterial oressure) |
|
|
|
Where are low-pressure receptors located |
Walls of the atria and pulmonary arteries (act as stretch receptors like baroreceptors) |
|
|
|
The volume reflex |
Stretch in the atria causes reflex dilation of the afferent arterioles in the kidneys and decrease secretion of ADH from hypothalamus. This decreased resistence in afferent arterioles causes GFR to rise and decreased ADH causes reduces reabsorption of water from tubules causing increase in fluid loss. |
|
|
|
The Bainbridge reflex |
Stretch receptors in the atria trigger the Bainbridge reflex which causes increase in HR. |
|
|
|
CNS ischaemic response |
When blood flow to the vasomotor centre in the lower brainstem becomes low there is a powerful sympathetic repsonse to increase cerebral blood pressure, so much so that peripheral circulation may shut down and UO cease. |
|
|
|
Cushing reaction CNS ischaemic response |
When CSF rises to a pressure equal to aretial pressur ein the brain, it compresses the brain and arterial supply, diminishing blood flow and triggering the CNS ischaemic repsonse. |
|
|
|
Abdominal compression reflex |
When baro and chemo receptor reflexes are elicited, nerve signals are transmitted to the muscles, particularly abdo muscles to compress the venous reservoirs to translocate blood to the heart |
|
|
|
Describe respiratory waves in arterial pressure |
During inspiration, the pressure in the thoracic cavity becomes more negative, causing expansion of the vessels and reduced BP. There is usually an increase in arterial pressure at the early part if expiration and a decrease during the rest of the resp cycle. |
|
|
|
Pressure diuresis (and natriuresis) |
Increase in arterial pressure increases urine output (and also sodium output) |
|
|
|
What makes blood pressure more salt sensitive |
-Loss of functional nephrons due to kidney injury i.e. HTN, DM and kidney disease -excessive formation of anti-natriuretic hormones such as angiotensin II and aldosterone |
In healthy kidneys, increases in salt and water only have mild affects on BP |
|
|
If arterial pressure = CO x PVR - why does the pressure remain stable in increased PVR if kidneys are functioning normally? |
Because they reduce the blood vol by pressure diuresis however PVR many times will also affect intrarenal vascular resistence, altering kidney function and causes HTN by shifting the renal function curve to a higher pressure level. |
|
|
|
How does salt increase the vol of extracellular fluid, and thereby increases arterial pressure |
1. osmolality increases stimulating the thirst centre and the person drinks more water 2. osmolality increases stimulates hypothalamic-posterior pituitary gland to secrete more ADH, causing greater reabsorption of water from renal tubular fluid. |
2 |
|
|
Why does HTN cause reduced life expectancy? |
1. excess workload on heart leads to early heart failure and coronary heart disease 2. damage to major vessels in the brain leading to stroke 3. kideny injury leading to kidney failure, uremia and death |
3 |
|
|
Describe the RAS control of aterial pressure control |
Decreased arterial pressure -> renin (kidneys) -> renin substrate (angiotensiongen) -> angiotensin I -(converting enzyme from lung)> angiotension II -> renal retention of salt and water AND vasoconstriction -> increased arterial pressure |
|
|
|
Where is renin synthesized and stored? |
In the inactuve form prorenin in the juxtaglomerular cells of the kidneys (mainly in the walls of the afferent arterioles - prox to glomeruli) |
|
|
|
How does angiotensin II cause renal retention of salt and water? |
1. acting directly on the kidneys to constriuct the renal arterioles, reducing flow through kidneys, reducing pressure in peritubular capillaries and causing rapid reabsorption of fluid from tubules. Also acts directly on tubular cells to increase reabsorption. 2. acting on the adrenal glands to secrete aldosterone which increases reabsorption of salt and therefore water by the kidney tubules. |
2 |
|
|
How does obesity cause HTN |
1. CO increased to supply demand 2. Increased sympathetic nerve activity possibly from action of leptin on vasomotor centres and reduced sensitivity of baroreceptors. 3. Angiotensin II and aldosterone levels are increased (increase sympathetic stimulation increases release of renin) 4. Impaired renal-pressure natriuresis means the kidneys will not excrete adequate amounts of salt and water unless high arterial pressure. |
|
|
|
Resting cardiac output in young, healthy men and women Calculation |
-Men: 5.6L/min -Women: 4.9L/min Average adult CO = 5L/min =SV x HR |
|
|
|
Cardiac index |
CO/square meter of body surface area -for a 70kg body surface area = 3L/min/m squared |
|
|
|
Frank-Starling law of the heart |
increased quantity of blood flow into the heart stretched the walls of the heart resulting in increased contraction to empty the extra blood from venous return. |
|
|
|
How is cardiac output varied with change in PVR when arterial pressure is equal? |
CO is inversely proportional to PVR (increase in PVR results in reduced CO) Ohms law: CO = arterial pressure/PVR |
Ohms law |
|
|
Factors that cause a hypereffective heart (increase CO) |
1. nervous stimulation (symopathetic stimulation and parasympatheic inhibition) - increased HR and contractility 2. hypertrophy from increased workload (so long as not in excess that will damage the heart) |
2 |
|
|
Factors that cause a hypoeffective heart (reduced CO) |
-increased arterial pressure against which the heart must pump -inhibition of nervous excitation of the heart -arrhythmias -coronary artery blockage (MI) -valvular heart disease -congenital heart disease -myocarditis -cardiac hypoxia |
|
|
|
What affect do the following disease states have on CO: 1. beriberi 2. MI 3. pagets disease 4. pulminary disease 5. AV shunts 6. shock 7. anxiety 8. Valvular disease 9. HTN 10. anaemia 11. hyperthyroidism |
1. increase 2. decrease 3. I 4. I 5. I 6. D 7. I 8. D 9. D 10. I |
|
|
|
What effect does increased intrapleural pressure (pressure in the chest cavity) have on CO? |
Shifts the curve to the right as increased external pressure on the heart means you need increased right atrial pressure to overcome this. |
|
|
|
Venous return = |
Mean systemic filling pressure (the pressure in the circulation when blood has stopped) - right arterial pressure/resistence to venous return In healthy adults: 5L/min = 7mmHg - 0mmHg/1.4mmHg/L/min of blood flow |
|
|
|
compensatory effects initiated in response to increased blood vol and thereby increased CO |
1. increased capillary pressure and fluid into tissues reducing blood vol 2. increased pressur ein veins causes continued gradual distension in veins (stress-relaxtion) and distension of venous reservoirs. 3. excess blood flow in peripheries causes autoregulatory increae in PVR, thus increasing resistence to venoud return. |
|
|
|
Acute effects of moderate cardiac failure |
-reduced cardiac output -damming of blood in veins resulting in increased venous pressure |
2 |
|
|
acute compensation for acute cardiac failure |
-baroreceptor reflex -chemoreceptor reflex -CNS ischaemic response Sympathetic nervous reflexes occur almost immediatley -increases contractility and HR -increases blood vessel tone, especially in veins, increasing the mean systemic filling pressures and therefore blood flow back to the heart |
|
|
|
chronic compensation for acute cardiac failure |
-renal retention of fluid and increase in blood vol by increasing mean systemic filling pressure (increasing venous flow to the heart) and distending veins (reducing venous resistance)....excess fluid retention can be detrimental -recovery of heart after MI (collateral vessels and hypertrophy) |
|
|
|
decompensated cardiac failure |
The heart is so damaged that no amount of compensation can make the weakened heart produce enough CO to make the kidneys excrete sufficient fluid. DUe to low CO, the kidneys still act to retain fluid and salt further increasing blood vol, mean systemic filling pressures and therefore right atrial pressure. The increase in CO is still not sufficent so the cycle continues. |
|
|
|
peripheral oedema in prolonged heart failure |
severe ACUTE heart failure often causes a fall in capillary pressure rather than a rise so peripheral oedema is only seen in prolonged heart failure |
|
|
|
the vicious cycle of acute pul oedmea in late-stage heart failure |
-a temporarily increased load on the already weak left ventricle initiates the vicious cycle and blood begins to dam up in the lungs -the increased pul capillary pressure leads to fluid leaking into lung tissue -the increased fluid diminishes oxygenation of the bloos -the reduced oxygen further weakens the heart and causes peripheral vasodilation -the vasodilation increases venous return of blood to the heart -this increases the damming of blood in the lungs and the cycle cont |
|
|
|
what is the cardiac reserve? |
the maximum percentage that the cardiac output can icnrease above normal (in young, healthy adult it is 300-400%, in severe heart failure it is 0) |
|
|
|
what conditions are associated with a loud second heart sound? |
Systemic hypertension (loud A2) Pulmonary hypertension (loud P2) Hyperdynamic states (e.g. tachycardia, fever, thyrotoxicosis) Atrial septal defect (loud A2) |
4 |
|
|
what conditions are associated with a soft second heart sound? |
Decreased aortic diastolic pressure (e.g. aortic regurgitation) Poorly mobile cusps (e.g. calcification of the aortic valve) Aortic root dilatation Pulmonary stenosis (soft P2) |
4 |
|
|
what conditions are associated with a splitting of S2 |
Deep inspiration Right bundle branch block Prolonged right ventricular systole (e.g. pulmonary stenosis, P.E.) Severe mitral regurgitation Atrial septal defect (fixed splitting, doesn't vary with respiration) |
5 |
|
|
what conditions are associated with reversed splitting of S2 (P2 occuring before A2) |
Deep expiration Left bundle branch block Prolonged left ventricular systole (e.g. severe aortic stenosis, hypertropic cardiomyopathy) Severe aortic stenosis Right ventricular pacing Wolff-Parkinson-White (type B) |
6 |
|
|
What are the types of WPW syndrome? |
Type A – the delta waves and QRS complexes are predominantly positive in the praecordial leads with a dominant R wave in V1. The dominant R wave in V1 can be mistaken for RBBB Type B – The delta wave and QRS complex are predominantly negative in leads V1 and V2 and positive in the other praecordial leads, resembling LBBB |
Bundle of kent AVRT |
|
|
What conditions are associated with a loud S1 |
-Increased transvalvular gradient (e.g. mitral stenosis, tricupsid stenosis) -Increased force of ventricular contraction (e.g. tachycardia, hyperdynamic states such as fever and thyrotoxicosis) -Shortened PR interval (e.g. Wolff-Parkinson-White syndrome) -Mitral valve prolapse -Thin individuals |
6 |
|
|
What conditions are associated with a soft S1 |
-Inappropriate apposition of the AV valves (e.g. mitral regurgitation, tricuspid regurgitation) -Prolonged PR interval (e.g. heart block, digoxin toxicity) -Decreased force of ventricular contraction (e.g. myocarditis, myocardial infarction) -Increased distance from the heart (e.g. obesity, emphysema, pericardial effusion) |
4 |
|
|
what conditions are associated with a split S1 |
-Right bundle branch block -LV pacing -Ebstein anomaly |
3 |
|
|
diagnostic criteria for LBBB |
-Broad QRS complex (> 120 ms) -Dominant S wave in lead V1 -Broad, monophasic R wave in lateral leads (I, AVL, V5 and V6) -Prolonged R wave peak time > 60 ms in left praecordial leads (V5-V6) -Absence of Q waves in lateral leads (I, V5 and V6) |
5 |
|
|
causes of narrow pulse pressure (less than 25% systolic) |
-Reduced cardiac output (e.g. blood loss) -Aortic stenosis -Cardiac tamponade -Congestive cardiac failure |
4 |
|
|
causes of wide pulse pressure (>60mmHg) |
-Atherosclerosis (stiffness of major arteries) -Aortic regurgitation -Arteriovenous malformation -Aortic root aneurysm -Aortic dissection -Hyperthyroidism |
6 |
|
|
P-wave duration |
0.08-0.1sec |
|
|
|
QRS duration |
0.06-0.1sec |
|
|
|
How do you calculate the corrected QT interval? |
cQT interval = QT interval/Sq root of the RR interval QT interval (start of Q to end of T)=0.35 sec |
|
|
|
PR interval |
start of P wave to start of QRS = 0.16sec |
|
|
|
PR segment |
end of P wave to start of QRS |
|
|
|
ST interval |
end of QRS to end of T wave |
|
|
|
ST segment |
end of QRS to start of T wave |
|
|
|
causes of LBBB |
-Ischaemic heart disease -Anterior myocardial infarction -Hypertension -Aortic stenosis -Dilated cardiomyopathy -Primary fibrosis of the conducting system (Lenegre’s disease) -Hyperkalaemia -Digoxin toxicity |
8 |
|
|
what are ashmans beats |
wide complex QRS complexes, usually with a RBBB morphology, that follow a short R-R interval preceded by a prolonged R-R interval. These are typically seen in atrial fibrillation and are considered benign |
|
|
|
where does the disorganized electrical activity in AF originate? |
the root of the pulmonary veins |
|
|
|
what is the approx pressure in the right atrium |
0-4mmHg |
varies with resp |
|
|
what is the approx pressure in the right ventricle |
25 (systolic), 4 (diastolic) |
|
|
|
what is the approx pressure in the pulmonary artery |
25 (systolic), 10 (diastolic) |
|
|
|
what is the approx pressure in the left atrium |
8-10 (varies with resp) |
|
|
|
what is the approx pressure in the left ventricle |
120 (systolic), 10 (diastolic) |
|
|
|
what is the approx pressure in the aorta |
120 (systolic), 80 (diastolic) |
|
|
|
Class I haemorrhage |
-blood loss: up to 750 -blood loss % of blood vol: up to 15% -pulse rate <100 -systolic BP: normal -pulse pressure: normal or increased -RR: 14-20 -Urine output >30 -CNS: slightly anxious |
-blood loss -blood loss % of blood vol -pulse rate -systolic BP -pulse pressure -RR -Urine output -CNS |
|
|
Class II haemorrhage |
-blood loss: 750-1500 -blood loss % of blood vol: 15-30% -pulse rate: 100-120 -systolic BP: normal -pulse pressure: decreased -RR: 20-30 -Urine output: 20-30 -CNS: mildly anxious |
-blood loss -blood loss % of blood vol -pulse rate -systolic BP -pulse pressure -RR -Urine output -CNS |
|
|
Class III haemorrhage |
-blood loss: 1500-2000 -blood loss % of blood vol: 30-40% -pulse rate 120-140 -systolic BP: decreased -pulse pressure: decreased -RR: 30-40 -Urine output: 5-15 -CNS: anxious, confused |
-blood loss -blood loss % of blood vol -pulse rate -systolic BP -pulse pressure -RR -Urine output -CNS |
|
|
Class IV haemorrhage |
-blood loss: >2000 -blood loss % of blood vol: >40% -pulse rate >140 -systolic BP: decreased -pulse pressure: decreased -RR >40 -Urine output: negligible -CNS: confused, lethargic |
-blood loss -blood loss % of blood vol -pulse rate -systolic BP -pulse pressure -RR -Urine output -CNS |
|
|
Q waves -where can they be a normal finding? -what makes them pathological? |
-can be a normal finding in leads III and aVR -pathological if greated than a quarter of the height of the subsequent R wave or greated than 0.04 seconds in duration |
|
|
|
Define shock |
Inadequate blood flow throught the body, and therefore too little oxygen and nutrients delivered to tissues, causing damage to tissues. |
|
|
|
Hypovolaemic shock |
-usually from haemorrhage (can be plasma loss from intestinal obstruction or severe burns, or dehydration) -decresed filling pressure causes decressed venous return and therefore decreased cardiac output. -compensation by sympathetic reflexes (i.e. baroreceptors) causes peripheral vasoconstriction and increasing PVR and BP, also constriction of veins causing increased venous return and CO (protects heart and brain as does not significantly constrict their vessesl). CNS ischaemic reflexes. reverse stree-relaxation. Increased renin secretion (kidney). Increased secretion on ADH (post pit). Increased secretion of eopinephrine and norepinephrine (adrenal medulla) |
Common cause (less common) -mechanism -compensation 6 |
|
|
Progressive shock |
-cardiac depression from reduced blood flow to coronary vessels, weakening myocardium and reducing CO -Vasomotor failure from reduced blood flow to brains vasomotor centre - diminishing sympathetic response -Blockage of very small vessels from sludged blood from build up of acid due to metabolic demand not being met -Increased capillary permeability - decreases blood vol further -Toxin release from ischaemic tissue - i.e. emdotoxin which causes increased metabolism and cardiac depression -cellular deterioration -tissue necrosis -acidosis causes poor delivery of O2 to tissues |
|
|
|
Neurogenic shock |
-sudden loss of vasomotor tone, vascular dilation and diminished venous return (venous pooling) -deep general anaesthesia, spinal anaethesia, brain damage |
Mechanism -Causes 3 |
|
|
Anaphylactic shock |
Histamine causes - increases vascular capacity because of venous dilation -> reduced venous return - dilation of arterioles -> reduced arterial pressure - increased capillary permeability |
mechanism 3 |
|
|
What is the action potential caused by in cadiac muscle |
-opening of voltage-activated fast sodium channels (as in skeletal muscles) -L-type calcium channels (slow clacium-sodium channels) - slower to open and remain open for several tenths of a second - maintains prolonged depolarization for longer ventricular contraction than skeletal muscles (calcium also activates contractility). -decreased potassium permeability after onset of action potential - prevents early depolarization. |
|
|
|
Where is the sinus node |
superior lateral wall of the right atrium near the opening of the SVC |
|
|
|
What does the P wave represent |
spread of depolarization through the atria followed by atrial contraction |
|
|
|
What does the QRS complex represent |
electrical depolarization of the ventricles which initiates contraction of ventricles |
|
|
|
What does the T wave represent |
stage of repolarization |
|
|
|
Ventricular filling |
about 80% of blood flows directly from great veins, through atria, into the ventricles. The atrial contraction fills the ventricles with the extra 20%. If artia stops working, unlikely to notice unless exercising. |
|
|
|
Stroke volume = |
volume of blood pumped from the ventricle during systole -end-diastolic vol - end-systolic vol |
|
|
|
Ejection fraction = |
SV/end-diastolic vol |
|
|
|
Preload |
end-diastolic pressure when ventricle has become filled |
|
|
|
Afterload |
Pressure in the aorta leading from the ventricle (systolic pressure) |
|
|
|
Effect of potassium ions on the heart |
potassium in ECF decreases resting membrane potential (depolarizes making it less negative), decreasing intensity of action potential and making contraction weaker. Can also block conduction through AV bundle making HR slower and conduction abnormalities. |
|
|
|
Effect of calcium ions on the heart |
(opposite of K) -increase contractility (low levels will reduce contractility) |
|
|
|
What is stokes-adams syndrome |
Sudden AV block and a delay in purkinje fibres taking up an intrinsic impulse leading to 5-20 secs of no blood pumping and the perosn collapsing. |
|
|
|
ECG - 1 big sq = - 1 small sq = |
-0.20 sec -0.04 sec |
|
|
|
What is Einthoven's triangle? What is Einthoven's law? |
AVR, AVL and AVF make up an equilateral triangle -Lead I gathers info between AVR and AVL -Lead II between AVR and AVF -Lead III between AVL and AVF Law: Lead I potential + Lead III potential = Lead II |
|
|
|
What is the sgarbossa criteria? |
> 1 mm concordant ST elevation in leads with a positive QRS complex (5 points) > 1 mm concordant ST depression in leads V1-V3 (3 points) > 5 mm discordant ST elevation in leads with a negative QRS complex (2 points) Scores > than 3 have a 90% specificity for detecting myocardial infarction. |
|
|
|
Diagnostic criteria for RBBB |
-Broad QRS complex (> 120 ms) -RSR’ pattern in leads V1-V3 (‘M’ shaped QRS complex) -Wide, slurred S wave in the lateral leads – I, AVL, V5 and V6 (‘W’ shaped QRS complex) |
|
|
|
Axis -normal -R -L -extreme |
-Normal: 0 - +90 Lead I+, AVF + -R: +90 - +180, Lead I-, AVF + -L: 0 - -90, Lead I+, AVF- -extreme: -90 - +180, Lead I-, AVF- |
|
|
|
What is a fourth heart sound? |
conditions which cause stiffness of the ventricles. These include: ventricular hypertrophy, aortic stenosis, ventricular fibrosis and heart failure. |
|
|
|
CVP -indicator of what? -increases in? -decreases in? |
-indicator of right ventricular preload -increases in: Hypervolaemia Forced exhalation Tension pneumothorax Heart failure Pleural effusion Decreased cardiac output Cardiac tamponade Mechanical ventilation (and PEEP) Pulmonary hypertension Pulmonary embolism -Decreases in: Hypovolaemia Deep inhalation Distributive shock Negative pressure ventilation |
1, 10, 4 |
|
|
Calculations of MAP |
MAP = diastolic BP + [(systolic BP – diastolic BP) / 3] MAP = (CO x SVR) + CVP (CVP usually close to 0) |
|
|
|
What is the approximate threshold membrane potential in cardiac myocytes? |
-70mV |
|
|
|
Causes of prolonged QT 1. hereditary 2. metabolic 3. drugs 4. structural heart problems |
1. -jervell-lange-neilsen syn -romano ward syn 2. -hypo: thyroid, calcium, K, Mg, thermia 3. -erythromycin -quinidine -amiodarone -TCA -terfenadine -methadone -procainamide 4. -IHD -Mitral valve prolapse -pheumatic carditis |
1. 2 2. 5 3. 8 4. 3 |
|
|
Usual resting pulse pressure |
30-40mmHg |
|
|
|
Right atrial enlargement -causes -diagnostic criteria on ECG |
Causes pf pulmonary HTN -chronic lung disease (cor pulmonale) -primary pulmonary HTN -tricuspid stenosis -congenital heart disease (tetralogy, pul stenosis) Criteria -P wave amplitude in inf leads >2.5mm; or -P wave amplitude in lead V1 and V2 >1.5mm |
|
|
|
WHat are the 3 fascicles of the left bundle branch |
-left ant fascicle: supplies the upper and ant parts of left ventricle -left post fascicle: supplies the posterior and infero-post parts of left ventricle -septal fascicle: supplies septal wall |
|
|
|
diagnostic criteria for left posterior fascicle block (LPFB) |
-RAD -small R waves with deep S waves in leads I and AVL (rS) -small Q waves with tall R waves in leads II, III and AVF (qR) -normal or slightly prolonged QRS (80-110ms) -prolonged R wave peak time in AVF >45ms -increased QRS voltage in limb leads -no evidence of RVH -no other cause of RAD |
8 |
|
|
What is the usual axis of: Lead I Lead II Lead III aVR aVF aVL |
Lead I: 0 Lead II: 60 Lead III: 120 aVR: 210 aVF: 90 aVL: -30 |
|
|
|
Causes of LAD |
Change in position of the heart to the left: -end of deep expiration -lieing down -obesity Left ventricle hypertrophy -HTN -aortic valve stenosis/regurg -congenital heart conditions LBBB Left anterior fascicular block Inferior MI WPW syndrome Ostium primum ASD |
3,3,5 |
|
|
Causes of RAD |
Change in position of the heart to the right: -end of deep inspiration -standing up -tall, lanky people Right ventricle hypertrophy -congenital pul valve stenosis -tetralogy of fallot -intraventricular septal defect RBBB Right heart strain (PE, COPD) Left posterior fascisular block Lateral wall MI WPW syndorme Ostium secundum ASD |
3,3,6 |
|
|
High-voltage QRS -definition -causes |
When the sum of all the QRS complexes pf the 3 standard leads (I, II, III) >4 millivolts Hypertrophy |
|
|
|
Low-voltage QRS |
Diminished muscle mass -old MIs Pericardial effusion (excess fluid to pass through) Pleural effusioin Pulmonary emphysema (excess air to pass through) |
|
|
|
What is the J point on an ECG |
The exact point at the end of the QRS when all parts of the ventricles have become depolarized. The "zero potential" line. |
|
|
|
The normal P wave is... |
<120ms duration (3 small sqs) <2.5mm in amplitude in limb leads <1.5mm in amplitude in chest leads +ve in lead II and -ve in lead aVR |
4 |
|
|
Causes of prolonged QT |
Electrolyte disturbance -hypo: K, Mg, Ca, thermia -Drugs: quinidine, amiodarone, methadone, procainamide, haloperidol, TCA, erythromycin -MI -Sleep |
3, 7, 1, 1 |
|
|
How is CVP measured? |
Pt lying flat at end of expiration. Tip between SVC and right atrium (usually 4th ICS, mid-axillary line) |
|
|
|
Normal CVP |
0-8 cmH2O (0-6 mmHg) |
|
|
|
CVP is an indicator of what? |
Right ventricular preload - a vol challange of 250-500ml causing an increase in CVP that is not sustained for >10 mins suggests hypovolaemia |
|
|
|
What do the CVP waveform components represent? -a -c -v -x descent -y descent |
a: end diastole (atrial contraction) c: early systole (closing of tricuspid valve) v: late systole (systolic filling of atrium) x descent: mid systole (atrial relaxation) y descent: early diastole (early ventricular filling) |
|
|
|
When might you hear S3? |
early diastole (at the end of rapid diastolic filling - ?the sound of flowing blood against an incompliant ventricle) |
iso-electric line |
|
|
When might you hear S4? |
Atrial systole |
P wave PR interval |
|
|
When do you hear S1 |
Isovolumetric ventricular contraction |
QRS complex |
|
|
When do you hear S2? |
Isovolumetric ventricular relaxation |
iso-electric line |
|
|
Diagnostic criteria for LAFB |
-LAD -small Q waves with tall R waves in leads I and aVL (qR) -small R waves with deep S waves in leads II, III and aVF (rS) -QRS 80-110ms (normal/slightly prolonged) -prolonged R wave peak time in aVL >45 ms -increased QRS voltage in limb leads |
|
|
|
How do you calculate cerebral blood flow? |
CPP = MAP - ICP CBF = CPP/CVR |
cerebral perfusion pressure, mean arterial pressure, intracerebral pressure, cerebral blood flow, cerebrovascular resistance |
|
|
How does auto-regulation maintain CBF? |
-myogenic reflexes - at higher pressures stretch reflexes cause vasoconstriction which increase CVR and reduces CBF -metabolic feedback - at lower pressures decreased blood flow allows vasoactive metabolites to accumulate (CO2, K) to cause vasodilation and reduce CVR and increase CBF. |
Autoregulation is lost outside CPP 60-160 mmHg, or in trauma or cerebral disease |
|
|
What are cannon a waves? |
Seen in the JVP in the presence of certain arrhythmias incl complete heart block, vent tachy, junctional tachy -caused by contraction of right atrium against a closed tricuspid valve |
|
|
|
Diagnostic criteria for RVH |
-RAD -dominant R wave in V1 -deep S wave in V5 or V6 (>7mm) -normal QRS (except RBBB) |
|
|
|
Sokolow-Lyon index for LVH? |
S wave in V1 + R wave in V5/6 >35mm (7 large sq) |
|
|
|
Cornell voltage criteria for LVH |
S wave in V3 + R wave in aVL >28mm in men and >20mm in women or R wave in aVL >12mm |
|
|
|
Normal Q wave |
Is the left to right depolarization of the intraventricular septum: < 40 ms wide (1 ‘small square’) < 2 mm in amplitude < 25% of the depth of the QRS complex |
|
|
|
What does the s wave represent? |
depolarization of he purkinjie fibres |
|
