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178 Cards in this Set
- Front
- Back
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what is the definition of heart failure? |
the inability of a heart to maintain adequate perfusion of the tissues (co) with a normal filling pressure |
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what is systolic dysfunction? |
impaired emptying due to impaired contractility or increased afterload |
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what is impaired ventricular relaxation or obstruction to filling? |
dystolic dysfunction |
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what can cor pulmonale be caused by? |
right sided heart failure |
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what does renin convert angiotensinogen to? |
angiotensin 1 |
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what does ACE convert? |
angiotensin 1 to angiotensin 2 |
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what stimulates the production of renin from the kidney? |
reduced renal artery pressure caused by decrease in CO and increased renal sympathetic tone due to the baroreceptor reflex |
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what does angiotensin 2 do? |
vasoconstrict, stimulates adrenal glands to produce aldosterone which stimulates kidney to reabsorb NA+ |
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what is BNP (b type naturetic peptide) produced by? |
failing myocardium |
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what does vasopressin do? |
increases the retention of water and constricts blood vessels |
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what does venoconstriction cause? |
increased filling pressures |
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what does vasconstriction cause? |
increased afterload |
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what does increased RV filling pressure lead to? |
peripheral oedema |
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what does increased LV filling pressure lead to? |
pulmonary oedema |
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what does pressure overload lead to? |
concentic hypertrophy, sacromeres added in parallel |
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what does volume overload lead to? |
eccentric hypertrophy, sarcomeres added in series |
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why does heart failure lead to odoema? |
increased venous pressure leads to an increase in capillary pressure and salt and water retention leads to a decrease concentration of proteins in the blood so doesnt draw the water from the fluid back in |
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what is tachyapnea? |
increased breathing |
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what murmur do you get in left sided heart failure? |
tricuspid regurgitation |
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what causes the kidney to release renin? |
decreased renal perfusion |
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what kind of heart failure can anaemia and pagets disease cause? |
high output heart failure |
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what does pericardial constriction cause? |
diastolic dysfunction |
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is digitoxin lipophilic or hydrophilic? |
lipophilic |
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what do cardiac glycosides inhibit? |
Na/K ATPase |
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why does inhibiting the Na/K ATPase lead to increased cardiac function? |
increases Na in the cell so increases ca in the cell via the Na/Ca exchanger |
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what do cardiac glycosides deacrease? |
AV conduction and Rate |
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how are dobutamine and dopamine given? |
IV |
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what do milrinone and Amrinone inhibit? |
cAMP phosphodiesterase |
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what is fursemide? |
loop agent |
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what do amiloride and spirononlactone spare as diuretics? |
K+ |
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what do thiazides do on VSM? |
vasodilate |
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what are the side effects of thiazides? |
K loss and hypotension |
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where do loop agents work? |
thick asending loop of henle |
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what do loop agents inhibit? |
na/k/2cl transporter |
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what does spironolactone antagonise? |
aldosterone |
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what do amiloride or triamterene, the k sparing agents block? |
na channel in kidney |
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what do captopril and enalapril inhibit the production of? |
angiotensin 2 |
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what does lostartan block? |
angiotensin 2 receptor |
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what can cause a t wave inversion and a depressed ST? |
unstable angina |
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what can cause an elevated ST? |
MI |
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where is the tear in an aortic aneurysm? |
through the tunica intima into the tunica media |
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where does an aortic dissection radiate to? |
back between the shoulder blades |
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where does the air go in a collapsed lung? |
pleural space |
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where are M2 receptors found and what is their action? |
cardiac muscle, decrease HR and contractility |
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where are M3 receptors found and what is their action? |
VSM, vasodilate due to production of NO |
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what is the action of Verapamil?
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antagonist of L type calcium channels
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why does adrenaline have more effect on cardiac force and contractility than noradrenaline? |
noradrenaline agonises alpha receptors more strongly so acts on alpha 1 causing vasoconstriction of the coronary arteries decreasign flow |
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what is the effect of serotonin on vsm? |
vasoconstricts |
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what does prazosin do? |
a1adrenoreceptor antagonist |
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what does phenylephrine do? |
a1 agonist |
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what is dobutamine? |
b 1 agonist, for cadiogenic shock |
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what does digoxin inhibit? |
na/k atpase |
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which autonmic NS dominates at rest? |
parasympathetic |
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what is the normal stroke volume at rest? |
4-8l per min |
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what is stroke volume and what is the normal amount? |
stroke volume is the amount of blood pumped out in 1 beat and the normal amount is 55-100ml |
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what are the 3 main dterminant of stroke volume? |
preload afterload and contractility |
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what is the intrinsic regulation of SV? |
starlings law |
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what is angiotensin mainly produced by |
the liver |
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what are the actions of prostacyclin and NO? |
vasodilators and inhibit platelet aggregation |
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what is myocardial stunning? |
prolonged isheamia, prolonged systolic dysfunction despite the restoration of blood flow only gradually begins to regain contractile force |
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how is heparin (anticoagulant) administered? |
IV |
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what do stretokinase and tPa cause? |
conversion of plasminogen to plasmin |
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what is the main side effect of thrombolytics? |
strokes |
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how do you estimate a patients HR form an ECG? |
300/no. of squares between the Rs |
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what does heparin inhibit? |
factor Xa |
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what does TNKtpa do? |
convert plasminogen to plasmin
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what does aminodarone and lidocaine do? |
1b antiarrhymic, na channel blocker |
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what is the central processor for the baroreceptor reflex? |
vasomotor centre in the brain stem |
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what is the effector mechanism in the baroreceptor reflex? |
TPR |
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what happens to intrathoracic pressure during inspiration? |
gets more negative which fills central veins |
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what is c wave? |
ventricular contraction |
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what is x wave? |
atrial relaxation |
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what does a chonotrophic agent affect? |
HR |
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what do endothelin and serotonin cause? |
vasoconstriction |
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how does no cause vasodilation? |
stimulates g c in VSM which increases cgmp levels |
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what activates no synthase? |
ca2+, calmodulin |
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what activates e nos without ca just by stress? |
pkb |
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what does sildedenafil inhibit? |
phosphodiesterase which converts cgmp back to GMP so promoting vasodilation |
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what does cgmp activate? |
pkg which reduces ca causing relaxation |
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what does pkg activate? |
myosin light chain phosphotase, takes of phosphate from MLCK making it inactive and activates ca pump on SR making more ca go into the SR |
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what causes inactivation of no syntase in oxidative stress? |
becomes oxidised (in hypertension etc) |
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what causes the plateau phase in the san action potential? |
ca2+ channels |
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where are the valves attached? |
endocardium |
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what does ANP act on? |
kidney |
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what is flow equal to? |
change is pressure/resistance in vessles but flow (co) is MAP/TPR in whole circulation |
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what does pressure overload lead to? |
concentric hypertrophy |
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what does volume overload lead to? |
eccentric hypertrophy |
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what is the structure of the capillaries in the kidney or gut? |
large pores and fenestrated |
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what is the structure of the capillaries like in the spleen or liver? |
discontinous, no tight junctions and wide spaces between cells |
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what is rate of diffussion proportional to? |
solute permeability x surface area x concentration gradient/ thickness |
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what parts of the autonomic NS cause a change in diastolic BP? |
only sympathetic |
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why does the cardiac tissue get less perfusion when we age? |
stiffer arteries mean reduced time in diastole |
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where is vasopressin stored? |
posterior pituatory |
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what does losartan block? |
angiotensin 2 |
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what do minoxidil and pinacidil activate? |
k+ channels, hyperpolarises cell |
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what do thiazsides block? |
na/cl- symporter, vasodilate |
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what inhibits aldosterone? |
spirolactone |
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what do guanethidine and guanabedrel inhibit? |
ganglion blockers |
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what is the effect of potassium levels with ace inhibitors? |
increases |
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what kind of blood vessels are the aortic and pulmonary vessels? |
elastic arteries |
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what does adenosine and oestrogen and progesterone cause? |
vasodilation |
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where soes vasopressin not work? |
coronary or cerebral vessels |
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what does isotartan antagonise ? |
angiotensin 2 (no cough) |
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what is the bayliss effect? |
stretch of the muscle opens a stretch activated ion channel which results the the cells becvoming depolarised which results in a ca2+ influx causing contraction |
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From which artery is blood pressure most commonly measured when using the auscultation technique?
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brachial |
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Why was the value of systolic blood pressure obtained by palpation (feeling the pulse) not considered to be sufficiently accurate?
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The correct answer is: Because the use of palpation of the pulse leads to an underestimate of systolic blood pressure
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What cardiovascular variables are adjusted by the autonomic nervous system in order to increase blood pressure in the short term, for example in the seconds after rising up from a recumbent position?
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Decreased arteriolar calibre, Increased heart rate, Venous constriction
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what are the first line drugs for heart failure? |
ace inhibitors |
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what effect do non specific b blockers have on vsm? |
vasoconstriction |
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what side effects can a1 antagonists such as prazosin cause? |
reflex tachycardia, stimulation of the kidneys |
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give some examples of potassium channel activators |
Minoxidil Pinacidil
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what drugs for hypertension can lead to hirtuism and na+ and water retention ? |
potassium channel activators |
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what are Clonindine, Guanabenz Guanfacine?
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a2 agonists |
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where is methyl dopa carboxylated? |
liver |
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Guanethidine Guanedrel are blockers of what?
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ganglion (dont cross BBB) |
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what is Verapamil used for? |
arrhymias, l type channel ca blocker |
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what is Diltazem? |
a benzothiazapine, l type channel blocker for angina |
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what are the dihydropyridines selective for? |
vascular tissue |
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what are Furosemide, Bumetamide, Etacrynic Acid?
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loop diuretics, block na+/k+and 2cl- transporter so na gets lost with k |
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what do thiazides e.g Chlorthalideone block? |
the na/cl- transporter in the DCT, used for hypertension |
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what do AmilorideTriametrineSpironolactone spare? |
potassium |
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what are Cholestryamine and Colestipol? |
bile acid sequestrants |
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how do cardiac glycosides affect the heart? |
they have positive iontopism but negative chonotropism (increase heart contractility but decrease rate) inhibit the na/k exchanger so increases calcium inside the cell because less na gets extruded causing depolarisation but negative chonotropism becuase it decreases the AVN conduction rate |
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what drugs can be used for WPW syndrome? |
cardiac glycosides as decrease avn conduction rate |
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what do you treat an overdose of cardiac glycosides with? |
lidocaine (na channel blocker) |
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how are phosphodiesterase inhibitors administered? |
IV |
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what effects do phosphodiesterase inhibitors have on the heart? |
increase contractility because an increase in camp activates PKA which increases ca |
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what effects does phosphodiesterase inhibitors have on VSM? |
relaxation because it causes SR to take up more calcium |
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what does warfarin inhibit? |
carboxylation of glutamate residues |
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what does heparin activate? |
antithrombin 3 |
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what is the action of clopigrel? |
p2y12 inhibitor (ADP antagonist) |
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what do Abcximab and Tirfiban inhibit?
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2b/3a inhibitors |
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what does streptokinase activate? |
plasminogen |
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when do the av valves shut? |
ventricular depolarisation |
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when is the ejection phase? |
ST segment |
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when is atrioventricular conduction? |
pr segment |
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when is ventricular depolarisation? |
qrs |
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when is atrial depolarisation? |
p wave |
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which wave do you get with hypokalaemia? |
u wave |
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what is raised and low is cardiogeneic shock? |
cvp raised but CO low |
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what kind of shock is cardiaac tamponade? |
obstructive heart compressed by pericardial effesuion |
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what is decreased in distributive shock? |
cvp, due to decreased peripheral resistance |
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what is decreased in hypovoleamic shock? |
cvp and co |
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what does ranolazine block? |
late na entry |
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what does NO stimulate? |
gc which increases cgmp which activates PKG which activates myosin light chain phosphatase so phosphate is taken of and muscle relaxes |
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how are b blockers 241 in glaucoma? |
reduces aq humour secretion |
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what does ca bind to contract smooth muscle? |
calmodulin |
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what do fibrates do? |
increase oxidation of fats in the liver |
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what is a side effect of bile acid binding resisins? |
malabsorbtion of lipid soluble vitamins and drugs |
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what is early after depolarisation due to? |
not enough potassium current so another AP takes off |
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what is delayed after depolarisation due to? |
spontaneuos calcium release in cell because the sr has been overloaded with calcium which is pumped out by the na/ca exchanger whivh produces inward current causing depolarisation |
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what does mg block? |
calcium |
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when does quinidine bind to na channels? |
when they are inactve |
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what is amiodarone? |
k channel blocker |
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what is dilitazem? |
ca channel BLOCKER |
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what is syncope? |
interuption of conciousness |
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what causes the carboxyglutamic residues in the liver to get reduced? |
oxidation of k |
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what affect does aspirin have on warfarin? |
displaces warfarin from plasma proteins |
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what do you use anticoagulants for? |
veins as mostly fibrin in veins |
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what do you anti platelet drugs for? |
arteries |
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how do platelets bind to collagen? |
VWF |
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which factor does trauma activate? |
7 |
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what do platlets release in response to binding to colagen? |
ADP and thromboxane |
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what allows prothrombinase to bind to activated platelets? |
phosphatidyl serine produced by platlets |
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what does thrombin cleave? |
fibrinogen to fibrin |
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what cleaves prothrombin to thrombin? |
xa |
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what does TFPI compete with? |
factor xa and v11a |
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what do urokinase and TPA activate? |
the conversion of plasminogen to plasmin which breaks down fibrin |
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what charge is phsphidyl serine |
negative |
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what does tissue factor from a complex with? |
factor 7 |
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what does the intact endothelium express to discourage thrombosis? |
sulphates mucopolysaccaharides, negative charge |
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what do tje aplpha granules in platlets contain? |
pdgf and fibrinogen |
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what do the dense bodies in platlets contain? |
ADP, ca and 5ht |
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equation linking co and sv? |
co=svxhr |
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what is a thril? |
palitatable murmur, indicative of valve incompetence |
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which antiarrhymic classess of drugs target the myocardium? |
1+3 |
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which antiarrhymic class drugs taget the nodes? |
2+4 |
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is diastolic pressure higher in the ventricles or aorta? |
aorta because no elastcicity |
