this lecture covered the herbs used to treat various cardiovascular conditions. allium sativa, or garlic, is one example; it affects the vascular system by several proposed mechanisms, including stimulating intracellular activity of nitric oxide synthase, which produces nitric oxide, a potent vasodilator. it also works to inhibit the cyclooxygenase enzyme, which produces inflammatory mediators from arachadonic acid- this effect is perhaps more pronounced with raw garlic. on the other hand, the oil produced from steaming garlic is high in sulphur compounds such as diallyl disulfide, which are thought to be antimicrobial and mucolytic. it might be helpful for diabetics by making more insulin available in circulation by competing for insulin binding sites in the liver. finally, garlic is thought to increase NK cells, thereby boosting innate immunity.
angelica sinensis, or dong quai as it is known in chinese medicine (as a blood mover / yin tonic) is another herb useful for cardiovascular conditions. it has vasodilating effects due to nicotinic acid and antispasmodic effects due to ferulic acid, which is thought to have calcium channel blocking effects. it is relaxing for uterine tissue and thus is indicated in some female hormonal conditions such as cramping and dysmenhorrea.
crataegus oxycantha, or hawthorne is an herb that is useful both in acute care as well as long term chronic management of cardiac cases. it has positive inotropic effects (increasing myocardial contractility), stabilizes capillaries via flavonoids, acts as a natural calcium channel blocker via procyanidins (which inhibits phosphodiesterase), and lowers blood pressure by inhibiting ACE and thus aldosterone.
gingko biloba is an herb commonly associated with increased mental clarity, which is thought to be due to increased cerebral artery perfusion. it also has beneficial effects on the vascular system, increasing coronary artery perfusion, enhancing peripheral vasodilation and also acting as an antioxidant via flavonoids and super oxide dismutase. because of its antioxidant effect it can be indicated in cases of hypoxic tissue damage.
one of the few herbs that is indicated specifically for hypotension rather than hypertension is selenicerues grandiflora, or cactus as it is commonly known. it is indicated in cases of weak heart muscle, as in CHF, mitral / aortic insufficiency, and even some arrhythmias. it is used more for functional, rather than organic disorders, and is especially indicated for a sensation of a heavy band in the chest.
a couple herbs with specific applications: leonurus cardiaca is a cardiotonic that is specific for the pelvic area and the vasculature, much like angelica (see above). thus it is used in cases of palpitations associated with pelvic pain, hormonal imbalances, or menstrual complaints. it might also have beta-blocking activity as well as improving blood viscosity. mentha piperita is an herb used specifically when angina occurs after a heavy meal, accompanied by digestive complaints such as gas and bloating. it is in fact part of the "glyconda formula", an eclectic formula used to treat cardiovascular complaints associated with gastrointestinal symptoms.
there are a number of herbs used to treat various pathologies of the peripheral vasculature. yarrow is an astringent that can be applied topically to wounds as well as internally; where it has vasodilatory effects in the peripheral vasculature and vasoconstrictive effects in the uterus. horse chestnuts aids in venous return and is therefore indicated in disorders such as varicose veins, and also has immune modulating effects via lectins. pineapple contains the sulfur-rich bromelain, which is thought to have thrombolytic effects, so much so that it might be used pre-surgery to reduce the risk of clots.
other peripheral vascular herbs: capsella (shepard's purse) is an herb used to stop chronic bleeding, especially uterine bleeding. stone root is a specific for constipation due to vascular engorgement of rectal mucosa and is also specific for congestion of oral, urinary, rectal mucosa. witch hazel is an astringent that can be applied topically or ingested, indicated for pale, engorged, congested tissues. hypericum is better known for its emotionally uplifting effects but also aids in venous stasis and varicosities due to the high flavonoid content. ruscus is in the lily family and contains rescogenins that have vasoconstrictive and anti-inflammatory effects. red clover is more commonly used to for female hormonal balance, but it also has circulatory actions, via the coumarins it contains, which improve blood lipids, reduce inflammation and reduce platelet aggregation. vaccinium, or bilberry contain anthocyanosides which have powerful antioxidant properties, and are stabilizing for capillaries as well. veratrum is an herb that can be used carefully in acute or severe cases of hypertension, indicated in a bounding pulse or flushed face. at higher doses, it acts as an emetic and thus must be used cautiously.
questions...
allium sativa...
1. what compounds does garlic contain that affect vascular endothelium?
2. how does garlic thin blood?
3. raw garlic has more of what effect?
4. which compounds are in garlic oil and result from steam processing?
5. how does garlic affect blood sugar?
6. garlic's effect on the immune system?
7. garlic's effect on inflammation?
angelica sinensis...
8. which family is angelica in? what compound is found in high quantities in this family?
9. antispasmodic effects due to which compound? what does this compound do?
10. vasodilating effects due to which compound?
11. used in chinese medicine for what purpose?
crataegus oxycantha, monogyna...
12. chemical consituents in crataegus?
13. describe the overall effect of hawthorne on the CV system.
14. flavonoids in hawthorne have what effect?
15. indicated for hyper or hypotension?
16. mechanism for lowering blood pressure?
17. mechanism for calcium channel blocking effects?
18. hawthorne berries are high in what compounds in the spring vs. the fall?
19. useful in CHF along with which other nutrient?
ginkgo biloba...
20. increases blood flow to...
21. main active constituent?
22. antioxidant actions via...
23. also used for what conditions due to cerebral perfusion?
24. why indicated for diabetics?
selenicereus grandiflorus...
25. indicated for hyper or hypotension?
26. indicated for functional or organic disorders?
27. specifically indicated for what chest sensation?
leonurus cardiaca...
28. what areas of the body is motherwort specific for?
29. leonurus injections were shown to improve...
30. 2 specific indications for leonurus.
mentha piperita...
31. most indicated for...
32. part of which formula?
33. contraindicated in which patients? why?
peripheral vasculature herbs...
34. yarrow's action in the peripheral vasculature?
35. yarrow's action on the uterus?
36. yarrow's topical effect?
37. horse chestnut's effect on vasculature?
38. [37] attributed to what compound?
39. horse chestnut immune effect via which compounds?
40. pineapple high in which compound?
41. pineapple used pre-surgery for...
more peripheral vasculature herbs...
42. shepard's purse used for...
43. capsella might be contraindicated in pregnancy because of...
44. capsella also contraindicated in people with...
45. stone root specific for which areas?
46. specific GI condition that might benefit from stone root?
47. witch hazel indicated in...
48. hypericum high in which compound?
49. cardiovascular indications of hypericum?
50. mechanism of action for hypericum?
51. what family is ruscus in?
52. active constituents of ruscus? actions?
53. indications for ruscus? affinity for which tissue?
54. active constituent in red clover?
55. effect of [54]?
56. active constituents in vaccinium?
57. effect of [56]?
58. why is bilberry particularly indicate for diabetics?
59. active constituents of veratrum viride?
60. effect of [59]?
61. veratrum effect at high doses?
62. black haw's effect is similar to what other herb?
answers
1. nitric oxide like compounds.
2. by inhibiting platelet aggregation.
3. it is more of a inhibitor.
4. diallyl disulfide and diallyl trisulfide.
5. competes with insulin binding sites on liver, allowing for more insulin to be in circulation, allowing for blood sugar stabilization.
6. increases NK cells.
7. COX inhibitor.
8. umble family, coumarins.
9. ferulic acid; ca-channel blocking effects.
10. nicotinic acid.
11. blood mover and blood builder.
12. flavonoids, tannins, organic acids, sterols, purines, triterpines.
13. normalize blood pressure, positive inotropic activity, diuresis.
14. stabilize capillaries to reduce permeability and fragility.
15. both.
16. inhibits ACE, which leads to a decrease in aldosterone and thus decreased water retention.
17. procyanidins inhibits phosphodiesterase, which breaks down cAMP, leaving higher calcium levels.
18. amines (spring) vs. bioflavonoids.
19. CoQ10.
20. cerebral arteries, carotid arteries.
21. flavonoids; ginkgo heterosides.
22. super oxide dismutase, flavonoids.
23. tinnitus or ear congestion.
24. to increase peripheral perfusion and prevent retinopathy, nephropathy, gangrene, etc.
25. hypotension.
26. functional.
27. band squeezing the chest.
28. pelvis and vasculature.
29. blood viscosity.
30. heart palpitations associated with pelvic pain or hormonal imbalance such as hyperthyroid.
e31. angina that occurs after eating accompanied by digestive symptoms.
32. glyconda.
33. patients with GERD, due to relaxing effects on LES.
34. peripheral vasodilator.
35. promotes constriction of uterine blood vessels.
36. astringent; aids in wound healing.
37. increases venous returns.
38. coumarins.
39. lectins have many immune modulating effects.
40. bromelain.
41. to reduce risk of clotting.
42. to stop chronic bleeding, especially from the uterus.
43. alkaloids.
44. high blood pressure.
45. oral, urinary, rectal mucosa.
46. constipation due to vascular engorgement of rectal mucosa.
47. pale, engorged, congested tissues.
48. hypericin, a bright red flavonoid.
49. venous stasis, varicosities.
50. hypericin and other flavonoids strengthen venous wall integrity, prevent free radical damage and enzymatic breakdown of collagen.
51. lily family.
52. ruscogenins: vasoconstrictive and anti-inflammatory effects.
53. peripheral vasculature, varicosities and hemorrhoids.
54. coumarin.
55. improve blood lipids, reduce inflammation and platelet aggregation.
56. flavonol glycosides-- anthocyanosides.
57. antioxidant and capillary stabilization.
58. because of its specificity for the eyes, fighting the effects of diabetic retinopathy.
59. veratrine.
60. potent hypotensive; circulatory depressant.
61. emesis.
62. cramp bark: uterine relaxant, relaxes peripheral blood vessels.
Showing posts with label cardiovascular. Show all posts
Showing posts with label cardiovascular. Show all posts
Tuesday, October 19, 2010
Sunday, October 17, 2010
pharmacology: cardiovascular drugs
the lecture about the conventional medications used to treat cardiac arrhythmias. the electrical conduction system of the heart can be affected in many different ways and there are several classes of drugs, each with a unique mechanism that targets different portions of the cardiac cycle [see questions 4-9]. quinidine is in class Ia, which works to slow the phase 0 depolarization, thereby prolonging action potential and slowing conduction. it is indicated in atrial fibrillation, atrial flutter, and some other arrhythmias, but tends to be avoided due to its high side effect profile; GI upset, cinchonism (a host of symptoms including nausea/vomiting, tinnitus, headache, disorientation), and torsade de pointes (an abnormal heart rhythm normally found in ventricular tachycardia where the peaks and troughs of the Q wave are equidistant from the baseline).
mexiletine is indicated in ventricular arrhythmias and recurrent ventricular tachycardia post-MI. it is class 1b; still a sodium channel blocker like quinidine but acts upon phase 3 repolarization instead of phase 0. side effect include drowsiness, confusion, and pro-arrhythmic potential. flecainide is used for supra-ventricular arrhythmias; arrhythmias that have an origin above the ventricles. the main side effect is its pro-arrhythmic potential; thus it is contraindicated in patients with a history of an MI or ventricular arrhythmia related to an acute ischemic event.
atenolol is a drug in class II anti-arrhythmics, drugs which diminish phase 4 repolarization by acting as beta-adrenergic blockers, thus decreasing sympathetic tone in the myocardium. it is indicated in tachyarrhythmias, a-flutter, a-fib, hypertension, angina, among other conditions, and stabilizes heart rate by the mechanism mentioned above; resulting in decreased automaticity in the various pacemaker cells in the heart. side effects might include drowsiness, bradycardia, dizziness, hypotension.
amiodarone is a typical class III anti-arrhythmic drug, causing a K+ channel blockade that results in prolonged phase 3 repolarization. it is indicated for arrhythmias with a ventricular origin and contains high amounts of iodine, which can cause blue-gray discoloration of the skin as a side effect. other side effects include dizziness / light headedness and pulmonary fibrosis.
the last class of anti arrhythmic, class IV, is represented by verapamil; these are drugs that block calcium channels, resulting in slowed phase 0 depolarization, which results in decreased AV conduction and a slower heart rate. side effects might include flushing, dizziness, hypotension.
there are other drugs that do not fall into the 6 major classes; one such drug is adenosine, which is produced endogenously from the breakdown of ATP. pharmacologically, adenosine has the effect of lengthening the refractory period and decreasing automaticity in the AV node by acting directly on the sinus pacemaker cells and vagal nerve terminals. it is administered by IV and can work as quickly as 15 seconds. it is the drug of choice for patients with PSVT (paroxysmal supraventricular tachycardias).
atropine is a drug derived from the nightshade belladonna which is used in cases of severe bradycardia with hypotension. it works by competitively inhibiting muscarinic acetylcholine receptors, thus blocking parasympathetic activity. thus it can also be used orally to treat diarrhea due to its effect of slowing peristalsis. it is also an effective antidote to organophosphate poisoning; these pesticides work by inhibiting acetylcholinesterase, leaving an abundance of acetylcholine-- while atropine works to block the effects of acetylchoine in the synapse.
digoxin is an anti-arrhythmic derived from the plant digitalis lanata and is classified as a cardiac glycoside. it both increases cardiac contractility as well as lowering conductivity, leading to a more stable, stronger heart beat. it works by inhibiting the Na/K ATPase and allowing for more intracellular influx of Na and Ca, as well as increasing the AV node's sensitivity to vagal stimulation. an overdose can cause "digitalis intoxication" which has a host of symptoms which might include bradycardia, fatigue, nausea, vomiting, blurred vision. digibind is used in such cases, an antibody formulated against digoxin (harvested IgG from sheep that are immunized with digoxin) which forms complexes that can be excreted via the kidneys.
questions
1. what are the five phases of the cardiac rhythm?
2. how does the origin of the arrhythmia correspond with prognosis?
3. common causes of arrhythmias?
4. describe the mechanism for the anti-arrhythmic drug class Ia.
5. describe the mechanism for the anti-arrhythmic drug class Ib.
6. describe the mechanism for the anti-arrhythmic drug class Ic.
7. describe the mechanism for the anti-arrhythmic drug class II.
8. describe the mechanism for the anti-arrhythmic drug class III.
9. describe the mechanism for the anti-arrhythmic drug class IV.
quinidine...
10. what class is quinidine?
11. indications?
12. mechanism of action?
13. side effects?
14. what is cinchonism?
15. what is torsade de pointes?
mexiletine...
16. what class is mexiletine? what is the mechanism?
17. indications?
18. side effects?
flecainide...
19. class? mechanism?
20. indications?
21. side effects?
22. contraindicated for which patients?
atenolol...
23. class?
24. indications?
25. mechanism of action?
26. side effects?
amiodarone...
27. indicated for...
28. mechanism of action?
29. contains high amounts of...
30. [29] results in what side effect?
31. other side effects?
verapamil...
32. which class? mechanism?
33. side effects?
adenosine...
34. drug of choice for which disorder?
35. breakdown product of...
36. mechanism of action?
37. acts directly on...
38. increases vagal tone by...
39. method of administration? onset of action?
atropine...
40. derived from...
41. cardiac use is for treatment of...
42. mechanism of action?
43. oral atropine can be used for...
44. can act as an antidote for...
45. symptoms of organophosphate poisoning?
46. specific antidote for atropine overdose? mechanism?
digoxin...
47. belongs to which family of drugs?
48. derived from which plant?
49. difference between digoxin and digitoxin?
50. mechanism of action?
51. effect on AV node?
52. effect on kidneys?
53. effect on EKG?
54. what is digitalis intoxication?
55. what is digibind?
answers
1. sodium channels open
sodium channels close, potassium channels begin to open
calcium and potassium channels open
calcium channels close
return to resting membrane potential
[Na, Na/K, Ca/K, Ca, return]
2. arrhythmias that originate in the atrias are generally more benign while ventricular arrhythmias are generally fatal within minutes.
3. ischemic damage
electrolyte disturbances
pH imbalance
4. sodium channel blockade: slow phase 0 depolarization-- prolong action potential and slow conduction.
5. sodium channel blockade: shorten phase 3 repolarization and decrease action potential duration by blocking sodium channels.
6. sodium channel blockade: markedly slow phase 0 depolarization.
7. diminish phase 4 repolarization, thus depressing automaticity.
8. prolong phase 3 repolarization without altering phase 0.
9. slow phase 4 depolarization and slow conduction, particularly at the AV node.
10. class Ia.
11. a-flutter, a-fib, AV and ventricular arrhythmias.
12. diminished inward flow of sodium at phase 0 results in decreased automaticity and a longer refractory period.
13. arrhythmias
GI symptoms: nausea, diarrhea, vomiting
cinchonism
torsade de pointes
14. nausea / vomiting
tinnitus
headache / disorientation
psychosis.
15. abnormal rhythm of ventricular tachycardia; peaks and troughs of Q wave are equidistant from baseline.
16. class 1b: blocks open sodium channels and shortens phase 3 repolarization.
17. ventricular arrhythmias, recurrent v-tach post MI.
18. drowsiness, confusion, pro-arrhythmias.
19. class Ic- sodium channel blocker.
20. supraventricular arrhythmias, WPW syndrome.
21. pro-arrhythmic.
22. patients with history of MI or ventricular arrhythmia due to acute ischemic event.
23. class II.
24. tachyarrhythmias
a-flutter, fib
PSVT
hypertension
angina
25. reduced sympathetic myocardial tone.
26. bradycardia, hypotension, fatigue, dizziness.
27. ventricular arrhythmias.
28. potassium channel blockade; prolong phase 3 repolarization.
29. iodine.
30. blue-gray skin discoloration.
31. dizziness, light headedness, pulmonary fibrosis.
32. class IV-- calcium channel blocker, slows phase 0 depolarization resulting in slowed AV conduction.
33. dizziness, flushing, hypotension, headaches.
34. PVST.
35. ATP.
36. prolongs refractory period and decreases automaticity in AV node.
37. sinus pacemaker cells and vagal nerve terminals
38. working between the SA and AV nodes.
39. IV, 15 seconds.
40. belladonna.
41. bradycardia and hypotension.
42. competitive inhibitor of muscarinic AcH receptors; blocks parasympathetic pathway.
43. diarrhea due its effect of slowing peristalsis.
44. pesticides that inhibit acetylcholinesterase.
45. SLUDGE:
salivation, lacrimation, urination, diarrhea, gastric distress, emesis
46. physostigmine; a reversible acetylcholinesterase inhibitor.
47. cardiac glycosides.
48. digoxin lanata.
49. digitoxoin has a longer half life and higher potential for toxicity.
50. inhibits Na/K ATPase, leads to more influx of Na and Ca intracellularly, allowing for higher contractility while decreasing conductivity and thereby stabilizing heart rate.
51. increases sensitivity to vagal stimulation.
52. increases renal perfusion.
53. flattening or inversion of t wave.
54. cardiac symptoms such as bradycardia, heart block
GI symptoms such as N/V, anorexia and diarrhea
eye symptoms such as blurred vision, double vision
55. antibodies specific to digoxin used to clear digoxin from the body after intoxication.
mexiletine is indicated in ventricular arrhythmias and recurrent ventricular tachycardia post-MI. it is class 1b; still a sodium channel blocker like quinidine but acts upon phase 3 repolarization instead of phase 0. side effect include drowsiness, confusion, and pro-arrhythmic potential. flecainide is used for supra-ventricular arrhythmias; arrhythmias that have an origin above the ventricles. the main side effect is its pro-arrhythmic potential; thus it is contraindicated in patients with a history of an MI or ventricular arrhythmia related to an acute ischemic event.
atenolol is a drug in class II anti-arrhythmics, drugs which diminish phase 4 repolarization by acting as beta-adrenergic blockers, thus decreasing sympathetic tone in the myocardium. it is indicated in tachyarrhythmias, a-flutter, a-fib, hypertension, angina, among other conditions, and stabilizes heart rate by the mechanism mentioned above; resulting in decreased automaticity in the various pacemaker cells in the heart. side effects might include drowsiness, bradycardia, dizziness, hypotension.
amiodarone is a typical class III anti-arrhythmic drug, causing a K+ channel blockade that results in prolonged phase 3 repolarization. it is indicated for arrhythmias with a ventricular origin and contains high amounts of iodine, which can cause blue-gray discoloration of the skin as a side effect. other side effects include dizziness / light headedness and pulmonary fibrosis.
the last class of anti arrhythmic, class IV, is represented by verapamil; these are drugs that block calcium channels, resulting in slowed phase 0 depolarization, which results in decreased AV conduction and a slower heart rate. side effects might include flushing, dizziness, hypotension.
there are other drugs that do not fall into the 6 major classes; one such drug is adenosine, which is produced endogenously from the breakdown of ATP. pharmacologically, adenosine has the effect of lengthening the refractory period and decreasing automaticity in the AV node by acting directly on the sinus pacemaker cells and vagal nerve terminals. it is administered by IV and can work as quickly as 15 seconds. it is the drug of choice for patients with PSVT (paroxysmal supraventricular tachycardias).
atropine is a drug derived from the nightshade belladonna which is used in cases of severe bradycardia with hypotension. it works by competitively inhibiting muscarinic acetylcholine receptors, thus blocking parasympathetic activity. thus it can also be used orally to treat diarrhea due to its effect of slowing peristalsis. it is also an effective antidote to organophosphate poisoning; these pesticides work by inhibiting acetylcholinesterase, leaving an abundance of acetylcholine-- while atropine works to block the effects of acetylchoine in the synapse.
digoxin is an anti-arrhythmic derived from the plant digitalis lanata and is classified as a cardiac glycoside. it both increases cardiac contractility as well as lowering conductivity, leading to a more stable, stronger heart beat. it works by inhibiting the Na/K ATPase and allowing for more intracellular influx of Na and Ca, as well as increasing the AV node's sensitivity to vagal stimulation. an overdose can cause "digitalis intoxication" which has a host of symptoms which might include bradycardia, fatigue, nausea, vomiting, blurred vision. digibind is used in such cases, an antibody formulated against digoxin (harvested IgG from sheep that are immunized with digoxin) which forms complexes that can be excreted via the kidneys.
questions
1. what are the five phases of the cardiac rhythm?
2. how does the origin of the arrhythmia correspond with prognosis?
3. common causes of arrhythmias?
4. describe the mechanism for the anti-arrhythmic drug class Ia.
5. describe the mechanism for the anti-arrhythmic drug class Ib.
6. describe the mechanism for the anti-arrhythmic drug class Ic.
7. describe the mechanism for the anti-arrhythmic drug class II.
8. describe the mechanism for the anti-arrhythmic drug class III.
9. describe the mechanism for the anti-arrhythmic drug class IV.
quinidine...
10. what class is quinidine?
11. indications?
12. mechanism of action?
13. side effects?
14. what is cinchonism?
15. what is torsade de pointes?
mexiletine...
16. what class is mexiletine? what is the mechanism?
17. indications?
18. side effects?
flecainide...
19. class? mechanism?
20. indications?
21. side effects?
22. contraindicated for which patients?
atenolol...
23. class?
24. indications?
25. mechanism of action?
26. side effects?
amiodarone...
27. indicated for...
28. mechanism of action?
29. contains high amounts of...
30. [29] results in what side effect?
31. other side effects?
verapamil...
32. which class? mechanism?
33. side effects?
adenosine...
34. drug of choice for which disorder?
35. breakdown product of...
36. mechanism of action?
37. acts directly on...
38. increases vagal tone by...
39. method of administration? onset of action?
atropine...
40. derived from...
41. cardiac use is for treatment of...
42. mechanism of action?
43. oral atropine can be used for...
44. can act as an antidote for...
45. symptoms of organophosphate poisoning?
46. specific antidote for atropine overdose? mechanism?
digoxin...
47. belongs to which family of drugs?
48. derived from which plant?
49. difference between digoxin and digitoxin?
50. mechanism of action?
51. effect on AV node?
52. effect on kidneys?
53. effect on EKG?
54. what is digitalis intoxication?
55. what is digibind?
answers
1. sodium channels open
sodium channels close, potassium channels begin to open
calcium and potassium channels open
calcium channels close
return to resting membrane potential
[Na, Na/K, Ca/K, Ca, return]
2. arrhythmias that originate in the atrias are generally more benign while ventricular arrhythmias are generally fatal within minutes.
3. ischemic damage
electrolyte disturbances
pH imbalance
4. sodium channel blockade: slow phase 0 depolarization-- prolong action potential and slow conduction.
5. sodium channel blockade: shorten phase 3 repolarization and decrease action potential duration by blocking sodium channels.
6. sodium channel blockade: markedly slow phase 0 depolarization.
7. diminish phase 4 repolarization, thus depressing automaticity.
8. prolong phase 3 repolarization without altering phase 0.
9. slow phase 4 depolarization and slow conduction, particularly at the AV node.
10. class Ia.
11. a-flutter, a-fib, AV and ventricular arrhythmias.
12. diminished inward flow of sodium at phase 0 results in decreased automaticity and a longer refractory period.
13. arrhythmias
GI symptoms: nausea, diarrhea, vomiting
cinchonism
torsade de pointes
14. nausea / vomiting
tinnitus
headache / disorientation
psychosis.
15. abnormal rhythm of ventricular tachycardia; peaks and troughs of Q wave are equidistant from baseline.
16. class 1b: blocks open sodium channels and shortens phase 3 repolarization.
17. ventricular arrhythmias, recurrent v-tach post MI.
18. drowsiness, confusion, pro-arrhythmias.
19. class Ic- sodium channel blocker.
20. supraventricular arrhythmias, WPW syndrome.
21. pro-arrhythmic.
22. patients with history of MI or ventricular arrhythmia due to acute ischemic event.
23. class II.
24. tachyarrhythmias
a-flutter, fib
PSVT
hypertension
angina
25. reduced sympathetic myocardial tone.
26. bradycardia, hypotension, fatigue, dizziness.
27. ventricular arrhythmias.
28. potassium channel blockade; prolong phase 3 repolarization.
29. iodine.
30. blue-gray skin discoloration.
31. dizziness, light headedness, pulmonary fibrosis.
32. class IV-- calcium channel blocker, slows phase 0 depolarization resulting in slowed AV conduction.
33. dizziness, flushing, hypotension, headaches.
34. PVST.
35. ATP.
36. prolongs refractory period and decreases automaticity in AV node.
37. sinus pacemaker cells and vagal nerve terminals
38. working between the SA and AV nodes.
39. IV, 15 seconds.
40. belladonna.
41. bradycardia and hypotension.
42. competitive inhibitor of muscarinic AcH receptors; blocks parasympathetic pathway.
43. diarrhea due its effect of slowing peristalsis.
44. pesticides that inhibit acetylcholinesterase.
45. SLUDGE:
salivation, lacrimation, urination, diarrhea, gastric distress, emesis
46. physostigmine; a reversible acetylcholinesterase inhibitor.
47. cardiac glycosides.
48. digoxin lanata.
49. digitoxoin has a longer half life and higher potential for toxicity.
50. inhibits Na/K ATPase, leads to more influx of Na and Ca intracellularly, allowing for higher contractility while decreasing conductivity and thereby stabilizing heart rate.
51. increases sensitivity to vagal stimulation.
52. increases renal perfusion.
53. flattening or inversion of t wave.
54. cardiac symptoms such as bradycardia, heart block
GI symptoms such as N/V, anorexia and diarrhea
eye symptoms such as blurred vision, double vision
55. antibodies specific to digoxin used to clear digoxin from the body after intoxication.
Sunday, January 10, 2010
CPD II: cardiovascular pathologies
in the second lecture of the cardiac pathologies series we began with the different cardiac tests used to diagnose heart conditions, then went into specific cardiac pathologies. there are several different tests for diagnosing cardiac pathologies, each with their own advantages and disadvantages. the ECG is a measure of the electrical activity of the heart and is best in discerning arrhythmias, ischemia, enlarged chambers. the electrical impulse of the beating heart are manifested on a realtime graph, which can be dissected into several components: PQRST, where the P wave represents atrial depolarization, QRS represents ventricular depolarization, and T represents ventricular repolarization. deviations of shape/rhythm in the ECG wave can indicate various cardiac pathologies (for example, pericarditis induces an elevated ST wave). the echocardiogram is an ultrasound of the heart that is best for determining valvular dysfunction, chamber hypertrophy, cardiomyopathies. EBCT is electron bean computed tomography, useful in determining coronary artery dysfunction. the PET test measures myocardial perfusion by means of radionuclides such as thallium and technitium. finally, stress testing is a ECG measured concurrently with exercise or chemical stimulation of the heart; the best way to measure coronary artery dysfunction.
there are countless pathologies available to the heart and circulatory system. arterial hypertension is high blood pressure either from a multitude of factors (primary) or from a single underlying disease (secondary). atherosclerosis results from high LDL levels which causes plaque formation in arteries and is exacerbated by diabetes mellitus. angina pectoris is chest pain generally caused by ischemia caused by coronary artery dysfunction and can be stable (worse upon exertion, better with rest) or unstable (happens at rest). acute coronary syndromes result from more severe coronary artery ischemia leading to infarction and necrosis, and include unstable angina, NSTEMI, STEMI. congestive heart failure is the dysfunction of the right or left ventricle and have symptom pictures that appear as fluid overload (right) or respiratory problems (left). cor pulmonale is right ventricular hypertrophy that is secondary to a lung disorder such as COPD. finally, cardiomyopathies are dysfunctions of myocardium that are diagnosed when other main etiologies such as valvular, HTN, pulmonary are ruled out. there are three types: dilated, restrictive, hypertrophic.
questions
cardiac testing...
1. what are ECG's used to assess?
2. what do the different components of the PQRST wave represent in the ECG?
3. which test is better to assess valvular dysfunction, the ECG or echocardiography?
4. what is the echocardiogram useful for assessing?
5. describe the difference between the TTE and TEE.
6. what does the EBCT test stand for and what does it measure?
7. what are MRI/MRA tests useful in determining?
8. PET measures...
9. examples of myocardial perfusion nuclides...
10. stress testing is a good way to assess....
arterial hypertension...
11. describe the demographic / racial trends for arterial hypertension.
12. what is the most common cause of arterial hypertension in children?
13. what are some risk factors for arterial hypertension?
14. what is the difference between primary and secondary hypertension?
15. what are some possible etiologies for primary arterial hypertension?
16. what are some examples of diseases that can cause secondary hypertension?
17. arterial hypertension patients are usually...
18. describe the symptom picture of patients with arterial hypertension.
19. what is an early sign of arterial hypertension?
20. what are some signs in a patient with arterial hypertension that might indicate an emergency situation?
21. what would you ask in a medical history of a patient with arterial hypertension?
22. what are some important aspects of the physical examination of a patient with arterial hypertension?
23. how might the specific lab tests differ for a patient who was newly diagnosed with HTN vs. a patient who has left ventricular hypertrophy or ST depression?
24. what are some blood tests that one might perform to aid in the diagnosis of arterial hypertension?
atherosclerosis...
25. describe the role of LDL in the pathogenesis of atherosclerosis.
26. what are the risk factors for developing atherosclerosis?
27. relationship of diabetes and pathophysiology of atherosclerosis.
28. describe the symptom picture/timeline for a patient with atherosclerosis.
29. what are some tests to screen for atherosclerosis?
angina...
30. angina is the result of...
31. describe the general location and sensation of the symptoms in angina pectoris.
32. unique aspects of symptom picture of angina pectoris?
33. what heart sound might be heard in a patient with angina pectoris?
34. how does the way that women experience angina pectoris differ from that of men?
35. what is variant / prinzmetal angina?
36. what is microvascular angina?
37. what is a silent ischemia?
38. what are some clues from the physical exam of a patient with chest pain that indicate coronary artery disease?
39. point tenderness over the chest wall indicates...
40. angina EKG characteristics.
41. possible differential diagnoses for angina pectoris.
acute coronary syndromes...
42. what are the hallmarks of unstable angina?
43. define NSTEMI.
44. define STEMI.
45. in general what is the etiology of acute coronary syndromes?
46. describe the symptom picture of a patient with NSTEMI or STEMI.
47. what are the tests that are diagnostic of these conditions?
48. what are some sounds one might hear upon auscultation of heart in a NSTEMI or STEMI patient?
49. blood tests.
50. ECG characteristics.
51. prognosis of the three types of acute coronary syndromes.
52. complications of MI?
53. what is the "post MI syndrome"?
left congestive heart failure...
54. what is congestive heart failure?
55. what are some possible etiologies for congestive heart failure?
56. LCHF causes...
57. what is the relationship between renal failure and CHF?
58. what is the relative difference in overall presentation of LCHF and RCHF?
59. general/systemic S/SX of LCHF.
60. respiratory S/SX of LCHF.
61. cardiac S/SX of LCHF.
62. etiologies of LCHF?
63. what are some complications of LCHF?
64. what are the differential diagnoses for LCHF?
right congestive heart failure...
65. general S/SX of RCHF.
66. cardiac S/SX of RCHF.
67. what are some possible etiologies of RCHF?
68. what are some possible differential diagnoses of RCHF?
69. what are the classes of CHF as defined by the New York Heart Association?
70. what would the chest xray of a CHF patient show?
71. what is a blood test that might aid in the diagnosis of CHF?
72. what is the best test for diagnosis of CHF and what might the test show?
73. ∂escribe the utility of a stress test in congestive heart failure.
74. what are some blood markers that might be abnormal in CHF?
75. why must water intake/output be monitered in CHF patients?
cor pulmonale...
76. what is cor pulmonale?
77. what is the etiology of cor pulmonale?
78. S/SX of cor pulmonale.
79. a chest xray of a patient with cor pulmonale might show...
80. tests that aid in the diagnosis of cor pulmonale are...
cardiomyopathies...
81. when are cardiomyopathies suspected?
82. what are the three types of cardiomyopathies?
83. describe the symptom picture dilated cardiomyopathy?
84. prognosis for dilated cardiomyopathy?
85. what is hypertrophic cardiomyopathy?
86. etiology of hypertrophic cardiomyopathy?
87. describe the typical patient and symptom picture of hypertrophic cardiomyopathy.
88. hypertrophic cardiomyopathy might result in...
89. what is a typical heart sound of hypertrophic cardiomyopathy?
90. which tests aid in the diagnosis of hypertrophic cardiomyopathy?
91. what is the least prevalent form among the types of cardiomyopathies and what is it characterized by?
92. what does restrictive cardiomyopathy result in?
93. what are common symptoms of a patient with restrictive cardiomyopathy?
94. what are the cardiac symptoms of a patient with restrictive cardiomyopathy?
answers
1. arrhythmias, myocardial ischemia, enlarged chambers.
2. P=atrial depolarization, QRS=ventricular depolarization, T=ventricular repolarization
3. echocardiography-- ECG cannot assess valvular dysfunction.
4. valvular disorders, chamber hypertrophy or dilation, blood flow, cardiomyopathies, heart failure, pericarditis.
5. TTE is more common and less invasive. TEE is used for more posterior structures of the heart, pacemaker implantation, prosthetic valves.
6. electron beam computed tomography, useful for assessing coronary artery disease.
7. mediastinal evaluation, dysfunction of aorta, muscles, non-coronary vessels.
8. myocardial perfusion via radionuclides.
9. thallium and technitium.
10. coronary artery disease.
11. more prevalence in african americans (32%) than european or mexican americans.
12. kidney disease.
13. genetic predisposition, poor lifestyle, diet (high salt intake in particular), stress, obesity.
14. primary is due to multiple factors whereas secondary is caused by a single underlying disease.
15. alcohol, OCP's, corticosteroids, cocaine, licorice (extreme, ridiculous amounts).
16. renal disease, pheochromocytoma, cushing's, primary aldosteronism, hyperthyroidism, myxedema, aortic coarctation.
17. asymptomatic.
18. associated with very high blood pressure: dizziness, flushing, headache, fatigue, epistaxis,
19. the 4th heart sound (S4).
20. diastolic BP above 120mmHg, JVD, CNS disorders, lung crackles (might indicate the pulmonary edema associated with heart failure), severe retinopathy.
21. history of heart disease, any lifestyle risk factors, DM, hyper/dyslipidemia, salt intake, stimulant use (especially cocaine), known duration of HTN.
22. besides vitals: fundoscopic exam to assess for retinopathy, ausculation of neck and abdominal bruits, CVP and neuro exam.
23. new dx- urinalysis and resting ECG. left ventricular hypertrophy: echocardiogram.
24. creatinine, BUN, K, Na, Mg, Calcium, glucose, lipids, TSH, homocysteine, CRP-hs, fibrinogen, fractionated lipids.
25. oxidized LDL uptake into subendothelial layers of blood vessels causes inflammation and atheroma formation, increasing risk for ischemia or stenosis.
26. obesity, atherogenic dyslipidemia, HTN, insulin resistance, prothrombic states, pro-inflammatory states, smoking, hyperhomocysteinemia.
27. diabetes can increase "advanced glycation end products" which damage endothelial cells and increase inflammation.
28. might be asymptomatic for years or decades, then symptoms of ischemia (angina, TIA, IC), then progress to acute symptoms such as unstable angina, stroke, limb pain, sudden death.
29. besides history and risk factor screening: blood tests (lipid profile, blood sugar, homocysteine, CRP-hs, fibrinogen, CBC), stress testing, imaging tests (fast CT, carotid ultrasound, catheterization) can be helpful.
30. myocardial ischemia.
31. a "substernal heaviness or pressure" that may radiate to jaw, neck, left shoulder/arm.
32. pain lasts 15-30 seconds, worse in cold weather, after a meal, or contact with cold air.
33. S4 gallop.
34. various differences: for women, angina pectoris occurs more often with diabetes, is accompanied by more muscular discomfort, nausea, shortness of breath, fatigue, and is more often mistaken for indigestion.
35. angina that is due to coronary artery spasm as opposed to arteriosclerosis.
36. angina that develops from small vessel dysfunction- which results in a normal arteriogram.
37. coronary artery dysfunction that has no symptoms, most often occuring in diabetics.
38. decreased peripheral pulses, bruits in femoral/carotid arteries, xanthomas.
39. indicates that angina probably not due to CAD.
40. usually normal between attacks. during attacks: visible Q waves, T wave inversion, maybe ST depression. possible: smaller R wave, bundle branch disturbances.
41. cervicothoracic spine abnormalities, costochondral separation, Gi disease, pulmonary disease, pericarditis, mitral valve prolapse.
42. prolonged chest pain at rest, increasing/worsening symptoms, transient ECG changes.
43. Non ST Elevation MI: "myocardial necrosis without ST elevation of Q waves"
44. myocardial necrosis with ST elevation (and possible Q waves)
45. acute obstruction of an artery, usually a coronary artery thrombus.
46. deep, intense substernal pain that is not relieved by anything. restlessness, apprehension, dyspnea, diaphoresis, nausea, vomiting.
47. ECG within 10 minutes of MI and cardiac marker tests are diagnostic.
48. murmurs, S4 gallop, split S2, soft heart sounds, tachy/bradycardia, ventricular arrhythmias.
49. cardiac markers: troponin I/T, CK-MB, myoglobin, CBC, ESR.
50. inverted T wave, ST elevation, Q waves greater than 1mm wide or 1/3 QRS height.
51. unstable angina: 30% have MI in 3 months. STEMI/NSTEMI: mortality is ~30%.
52. heart failure, myocardial disorders and rupture, arrhythmias, aneuryism, cardiogenic shock, pericarditis.
53. pericarditis, pleural effusion, pneumonitis, fever. [pppf]
54. ventricular dysfunction which leads to reduced pumping action of the heart, ventricular hypertrophy and catecholamine elevation.
55. cardiomyopathies, valvular disease, MI, ischemia, CAD, HTN, PDA, VSD, arrhythmias.
56. RCHF, renal insufficiency, liver disease.
57. renal failure causes volume overload which contributes to HTN which contributes to CHF.
58. RCHF looks more like fluid buildup, whereas LCHF looks like respiratory problem.
59. dyspnea/fatigue upon exertion, intolerance to cold, cyanosis.
60. due to pulmonary edema: dyspnea, mb bronchospasm/wheezing, cough, right sided pleural effusions with basilar rales.
61. displaced apical impulse due to hypertrophy, S3 and S4.
62. CAD, ischemia, MI, HTN, aortic stenosis, cardiomyopathy, PDA, VSD, valvular dysfunction.
63. acute p. edema and associated symptoms, abnormal serum proteins (sudden onset cases).
64. p. edema, ARDS, COPD, IPF, cancer, chronic bronchitis.
65. fatigue, peripheral cyanosis, pitting edema, JVD, hepatomegaly, nocturia, light headedness. [i'm tired because my pee is swollen swollen swollen and blue]
66. tricuspid murmur, systemic HTN, low cardiac output. [tri murmuring "COHTN"]
67. LCHF, cor pulmonale, multiple p.edema, infarction, primary pulmonary HTN, stenosis of mitral valve, pulmonary valve, pulmonary artery. [look left, right: many die; one blocked]
68. edema: peripheral, idiopathic, myedema, angioneurotic, lymphedema. nephrotic syndrome, liver cirrhosis, hemiplegia, pericarditis. [edema, kidney/liver, stroke, heart protector]
69. class I: no physical activity limitation, no dyspnea/fatigue/palpitations. class II: slight limitation, dyspnea upon normal physical activity. class III: moderate limitation, dyspnea upon "less than ordinary" activities. class IV: severe limitation, dyspnea at rest.
70. enlarged cardiac silhouette, kerly-b lines, pleural effusion.
71. B natriuretic peptide, which is released in the body during excessive fluid release in general.
72. echocardiography, will show that ejection fraction less than 50%.
73. never do one of those things.
74. high BUN, creatinine, proteinuria, abnormal liver enzymes, electrolytes.
75. because excess water intake will exacerbate edema and contribute to volume overload.
76. right ventricular hypertrophy due to lung disease.
77. COPD, lung tissue loss, p. emboli, scleroderma, obesity.
78. that of underlying lung disorder, right ventricular hypertrophy or failure. in chronic cases: slight dyspnea at rest, syncope, chest pain, S3.
79. right heart and proximal pulmonary artery enlargement.
80. echocardiogram (most helpful), CXR, ECG.
81. when valve disease, HTN, lung disease are ruled out as etiologies.
82. dilated, hypertrophic, restrictive.
83. related to ventricular dilation/systolic dysfunction: dyspnea/fatigue/edema, mb atypical chest pain, tachyarrythmias.
84. poor without transplant.
85. ventricular hypertrophy with diastolic dysfunction.
86. mostly inherited.
87. aged 20-40, =pain/dyspnea/palpitation/syncope upon exertion.
88. sudden death.
89. systolic ejection murmur that is increased with Valsalva.
90. ECG/echocardiogram/chest xray. chest xray might not show hypertrophy.
91. restrictive cardiomyopathies, characterized by low ventricular compliance.
92. pulmonary hypertension.
93. exertional dyspnea, orthopnea, p. edema, JVD.
94. S4, S3, mitral/TC regurgitation murmur, quiet heart sounds, rapid carotid pulse, arrhythmias.
there are countless pathologies available to the heart and circulatory system. arterial hypertension is high blood pressure either from a multitude of factors (primary) or from a single underlying disease (secondary). atherosclerosis results from high LDL levels which causes plaque formation in arteries and is exacerbated by diabetes mellitus. angina pectoris is chest pain generally caused by ischemia caused by coronary artery dysfunction and can be stable (worse upon exertion, better with rest) or unstable (happens at rest). acute coronary syndromes result from more severe coronary artery ischemia leading to infarction and necrosis, and include unstable angina, NSTEMI, STEMI. congestive heart failure is the dysfunction of the right or left ventricle and have symptom pictures that appear as fluid overload (right) or respiratory problems (left). cor pulmonale is right ventricular hypertrophy that is secondary to a lung disorder such as COPD. finally, cardiomyopathies are dysfunctions of myocardium that are diagnosed when other main etiologies such as valvular, HTN, pulmonary are ruled out. there are three types: dilated, restrictive, hypertrophic.
questions
cardiac testing...
1. what are ECG's used to assess?
2. what do the different components of the PQRST wave represent in the ECG?
3. which test is better to assess valvular dysfunction, the ECG or echocardiography?
4. what is the echocardiogram useful for assessing?
5. describe the difference between the TTE and TEE.
6. what does the EBCT test stand for and what does it measure?
7. what are MRI/MRA tests useful in determining?
8. PET measures...
9. examples of myocardial perfusion nuclides...
10. stress testing is a good way to assess....
arterial hypertension...
11. describe the demographic / racial trends for arterial hypertension.
12. what is the most common cause of arterial hypertension in children?
13. what are some risk factors for arterial hypertension?
14. what is the difference between primary and secondary hypertension?
15. what are some possible etiologies for primary arterial hypertension?
16. what are some examples of diseases that can cause secondary hypertension?
17. arterial hypertension patients are usually...
18. describe the symptom picture of patients with arterial hypertension.
19. what is an early sign of arterial hypertension?
20. what are some signs in a patient with arterial hypertension that might indicate an emergency situation?
21. what would you ask in a medical history of a patient with arterial hypertension?
22. what are some important aspects of the physical examination of a patient with arterial hypertension?
23. how might the specific lab tests differ for a patient who was newly diagnosed with HTN vs. a patient who has left ventricular hypertrophy or ST depression?
24. what are some blood tests that one might perform to aid in the diagnosis of arterial hypertension?
atherosclerosis...
25. describe the role of LDL in the pathogenesis of atherosclerosis.
26. what are the risk factors for developing atherosclerosis?
27. relationship of diabetes and pathophysiology of atherosclerosis.
28. describe the symptom picture/timeline for a patient with atherosclerosis.
29. what are some tests to screen for atherosclerosis?
angina...
30. angina is the result of...
31. describe the general location and sensation of the symptoms in angina pectoris.
32. unique aspects of symptom picture of angina pectoris?
33. what heart sound might be heard in a patient with angina pectoris?
34. how does the way that women experience angina pectoris differ from that of men?
35. what is variant / prinzmetal angina?
36. what is microvascular angina?
37. what is a silent ischemia?
38. what are some clues from the physical exam of a patient with chest pain that indicate coronary artery disease?
39. point tenderness over the chest wall indicates...
40. angina EKG characteristics.
41. possible differential diagnoses for angina pectoris.
acute coronary syndromes...
42. what are the hallmarks of unstable angina?
43. define NSTEMI.
44. define STEMI.
45. in general what is the etiology of acute coronary syndromes?
46. describe the symptom picture of a patient with NSTEMI or STEMI.
47. what are the tests that are diagnostic of these conditions?
48. what are some sounds one might hear upon auscultation of heart in a NSTEMI or STEMI patient?
49. blood tests.
50. ECG characteristics.
51. prognosis of the three types of acute coronary syndromes.
52. complications of MI?
53. what is the "post MI syndrome"?
left congestive heart failure...
54. what is congestive heart failure?
55. what are some possible etiologies for congestive heart failure?
56. LCHF causes...
57. what is the relationship between renal failure and CHF?
58. what is the relative difference in overall presentation of LCHF and RCHF?
59. general/systemic S/SX of LCHF.
60. respiratory S/SX of LCHF.
61. cardiac S/SX of LCHF.
62. etiologies of LCHF?
63. what are some complications of LCHF?
64. what are the differential diagnoses for LCHF?
right congestive heart failure...
65. general S/SX of RCHF.
66. cardiac S/SX of RCHF.
67. what are some possible etiologies of RCHF?
68. what are some possible differential diagnoses of RCHF?
69. what are the classes of CHF as defined by the New York Heart Association?
70. what would the chest xray of a CHF patient show?
71. what is a blood test that might aid in the diagnosis of CHF?
72. what is the best test for diagnosis of CHF and what might the test show?
73. ∂escribe the utility of a stress test in congestive heart failure.
74. what are some blood markers that might be abnormal in CHF?
75. why must water intake/output be monitered in CHF patients?
cor pulmonale...
76. what is cor pulmonale?
77. what is the etiology of cor pulmonale?
78. S/SX of cor pulmonale.
79. a chest xray of a patient with cor pulmonale might show...
80. tests that aid in the diagnosis of cor pulmonale are...
cardiomyopathies...
81. when are cardiomyopathies suspected?
82. what are the three types of cardiomyopathies?
83. describe the symptom picture dilated cardiomyopathy?
84. prognosis for dilated cardiomyopathy?
85. what is hypertrophic cardiomyopathy?
86. etiology of hypertrophic cardiomyopathy?
87. describe the typical patient and symptom picture of hypertrophic cardiomyopathy.
88. hypertrophic cardiomyopathy might result in...
89. what is a typical heart sound of hypertrophic cardiomyopathy?
90. which tests aid in the diagnosis of hypertrophic cardiomyopathy?
91. what is the least prevalent form among the types of cardiomyopathies and what is it characterized by?
92. what does restrictive cardiomyopathy result in?
93. what are common symptoms of a patient with restrictive cardiomyopathy?
94. what are the cardiac symptoms of a patient with restrictive cardiomyopathy?
answers
1. arrhythmias, myocardial ischemia, enlarged chambers.
2. P=atrial depolarization, QRS=ventricular depolarization, T=ventricular repolarization
3. echocardiography-- ECG cannot assess valvular dysfunction.
4. valvular disorders, chamber hypertrophy or dilation, blood flow, cardiomyopathies, heart failure, pericarditis.
5. TTE is more common and less invasive. TEE is used for more posterior structures of the heart, pacemaker implantation, prosthetic valves.
6. electron beam computed tomography, useful for assessing coronary artery disease.
7. mediastinal evaluation, dysfunction of aorta, muscles, non-coronary vessels.
8. myocardial perfusion via radionuclides.
9. thallium and technitium.
10. coronary artery disease.
11. more prevalence in african americans (32%) than european or mexican americans.
12. kidney disease.
13. genetic predisposition, poor lifestyle, diet (high salt intake in particular), stress, obesity.
14. primary is due to multiple factors whereas secondary is caused by a single underlying disease.
15. alcohol, OCP's, corticosteroids, cocaine, licorice (extreme, ridiculous amounts).
16. renal disease, pheochromocytoma, cushing's, primary aldosteronism, hyperthyroidism, myxedema, aortic coarctation.
17. asymptomatic.
18. associated with very high blood pressure: dizziness, flushing, headache, fatigue, epistaxis,
19. the 4th heart sound (S4).
20. diastolic BP above 120mmHg, JVD, CNS disorders, lung crackles (might indicate the pulmonary edema associated with heart failure), severe retinopathy.
21. history of heart disease, any lifestyle risk factors, DM, hyper/dyslipidemia, salt intake, stimulant use (especially cocaine), known duration of HTN.
22. besides vitals: fundoscopic exam to assess for retinopathy, ausculation of neck and abdominal bruits, CVP and neuro exam.
23. new dx- urinalysis and resting ECG. left ventricular hypertrophy: echocardiogram.
24. creatinine, BUN, K, Na, Mg, Calcium, glucose, lipids, TSH, homocysteine, CRP-hs, fibrinogen, fractionated lipids.
25. oxidized LDL uptake into subendothelial layers of blood vessels causes inflammation and atheroma formation, increasing risk for ischemia or stenosis.
26. obesity, atherogenic dyslipidemia, HTN, insulin resistance, prothrombic states, pro-inflammatory states, smoking, hyperhomocysteinemia.
27. diabetes can increase "advanced glycation end products" which damage endothelial cells and increase inflammation.
28. might be asymptomatic for years or decades, then symptoms of ischemia (angina, TIA, IC), then progress to acute symptoms such as unstable angina, stroke, limb pain, sudden death.
29. besides history and risk factor screening: blood tests (lipid profile, blood sugar, homocysteine, CRP-hs, fibrinogen, CBC), stress testing, imaging tests (fast CT, carotid ultrasound, catheterization) can be helpful.
30. myocardial ischemia.
31. a "substernal heaviness or pressure" that may radiate to jaw, neck, left shoulder/arm.
32. pain lasts 15-30 seconds, worse in cold weather, after a meal, or contact with cold air.
33. S4 gallop.
34. various differences: for women, angina pectoris occurs more often with diabetes, is accompanied by more muscular discomfort, nausea, shortness of breath, fatigue, and is more often mistaken for indigestion.
35. angina that is due to coronary artery spasm as opposed to arteriosclerosis.
36. angina that develops from small vessel dysfunction- which results in a normal arteriogram.
37. coronary artery dysfunction that has no symptoms, most often occuring in diabetics.
38. decreased peripheral pulses, bruits in femoral/carotid arteries, xanthomas.
39. indicates that angina probably not due to CAD.
40. usually normal between attacks. during attacks: visible Q waves, T wave inversion, maybe ST depression. possible: smaller R wave, bundle branch disturbances.
41. cervicothoracic spine abnormalities, costochondral separation, Gi disease, pulmonary disease, pericarditis, mitral valve prolapse.
42. prolonged chest pain at rest, increasing/worsening symptoms, transient ECG changes.
43. Non ST Elevation MI: "myocardial necrosis without ST elevation of Q waves"
44. myocardial necrosis with ST elevation (and possible Q waves)
45. acute obstruction of an artery, usually a coronary artery thrombus.
46. deep, intense substernal pain that is not relieved by anything. restlessness, apprehension, dyspnea, diaphoresis, nausea, vomiting.
47. ECG within 10 minutes of MI and cardiac marker tests are diagnostic.
48. murmurs, S4 gallop, split S2, soft heart sounds, tachy/bradycardia, ventricular arrhythmias.
49. cardiac markers: troponin I/T, CK-MB, myoglobin, CBC, ESR.
50. inverted T wave, ST elevation, Q waves greater than 1mm wide or 1/3 QRS height.
51. unstable angina: 30% have MI in 3 months. STEMI/NSTEMI: mortality is ~30%.
52. heart failure, myocardial disorders and rupture, arrhythmias, aneuryism, cardiogenic shock, pericarditis.
53. pericarditis, pleural effusion, pneumonitis, fever. [pppf]
54. ventricular dysfunction which leads to reduced pumping action of the heart, ventricular hypertrophy and catecholamine elevation.
55. cardiomyopathies, valvular disease, MI, ischemia, CAD, HTN, PDA, VSD, arrhythmias.
56. RCHF, renal insufficiency, liver disease.
57. renal failure causes volume overload which contributes to HTN which contributes to CHF.
58. RCHF looks more like fluid buildup, whereas LCHF looks like respiratory problem.
59. dyspnea/fatigue upon exertion, intolerance to cold, cyanosis.
60. due to pulmonary edema: dyspnea, mb bronchospasm/wheezing, cough, right sided pleural effusions with basilar rales.
61. displaced apical impulse due to hypertrophy, S3 and S4.
62. CAD, ischemia, MI, HTN, aortic stenosis, cardiomyopathy, PDA, VSD, valvular dysfunction.
63. acute p. edema and associated symptoms, abnormal serum proteins (sudden onset cases).
64. p. edema, ARDS, COPD, IPF, cancer, chronic bronchitis.
65. fatigue, peripheral cyanosis, pitting edema, JVD, hepatomegaly, nocturia, light headedness. [i'm tired because my pee is swollen swollen swollen and blue]
66. tricuspid murmur, systemic HTN, low cardiac output. [tri murmuring "COHTN"]
67. LCHF, cor pulmonale, multiple p.edema, infarction, primary pulmonary HTN, stenosis of mitral valve, pulmonary valve, pulmonary artery. [look left, right: many die; one blocked]
68. edema: peripheral, idiopathic, myedema, angioneurotic, lymphedema. nephrotic syndrome, liver cirrhosis, hemiplegia, pericarditis. [edema, kidney/liver, stroke, heart protector]
69. class I: no physical activity limitation, no dyspnea/fatigue/palpitations. class II: slight limitation, dyspnea upon normal physical activity. class III: moderate limitation, dyspnea upon "less than ordinary" activities. class IV: severe limitation, dyspnea at rest.
70. enlarged cardiac silhouette, kerly-b lines, pleural effusion.
71. B natriuretic peptide, which is released in the body during excessive fluid release in general.
72. echocardiography, will show that ejection fraction less than 50%.
73. never do one of those things.
74. high BUN, creatinine, proteinuria, abnormal liver enzymes, electrolytes.
75. because excess water intake will exacerbate edema and contribute to volume overload.
76. right ventricular hypertrophy due to lung disease.
77. COPD, lung tissue loss, p. emboli, scleroderma, obesity.
78. that of underlying lung disorder, right ventricular hypertrophy or failure. in chronic cases: slight dyspnea at rest, syncope, chest pain, S3.
79. right heart and proximal pulmonary artery enlargement.
80. echocardiogram (most helpful), CXR, ECG.
81. when valve disease, HTN, lung disease are ruled out as etiologies.
82. dilated, hypertrophic, restrictive.
83. related to ventricular dilation/systolic dysfunction: dyspnea/fatigue/edema, mb atypical chest pain, tachyarrythmias.
84. poor without transplant.
85. ventricular hypertrophy with diastolic dysfunction.
86. mostly inherited.
87. aged 20-40, =pain/dyspnea/palpitation/syncope upon exertion.
88. sudden death.
89. systolic ejection murmur that is increased with Valsalva.
90. ECG/echocardiogram/chest xray. chest xray might not show hypertrophy.
91. restrictive cardiomyopathies, characterized by low ventricular compliance.
92. pulmonary hypertension.
93. exertional dyspnea, orthopnea, p. edema, JVD.
94. S4, S3, mitral/TC regurgitation murmur, quiet heart sounds, rapid carotid pulse, arrhythmias.
Wednesday, January 6, 2010
CPD II: cardiovascular introduction
today we began talking about the diagnosis of cardiovascular diseases in all their manifestations. we started with a review of the cardiac anatomy and physiology, the cardiac cycle and sounds, and began talking about different aspects of the physical exam and history of the patient with heart disease. we then looked at several characteristic symptoms that might arise that are indicative of different heart diseases.
questions
heart sounds...
1. S1 is the sound of...
2. S2 is the sound of...
3. what is "S2 splitting"?
4. S2 splitting is considered normal in...
5. what do fixed and parodoxical splitting represent?
6. S3 is the sound of...
7. prominent S3 sound might indicate what?
8. S4 is the sound of...
9. S4 might indicate what?
physical examination...
10. what is orthostatic hypotension?
11. what are xanthomatas?
12. what are some cardiac related conditions that could result in altered facial appearance?
13. what is the malar flush and what might it result from?
14. if the carotid pulses are different bilaterally, what might this indicate?
15. what is the hepatojugular reflex?
16. increased jugular venous pressure can indicate...
17. common fundoscopic findings for cardiac disease?
18. how might the fingernails appear in a cardiac patient?
19. describe some common PE findings for the hands of a cardiac patient.
auscultation...
20. where is the aortic area located?
21. where is the pulmonic area?
22. where is Erb's point and what is its significance?
23. where is the tricuspid area?
24. where is the mitral area?
25. why might open heart surgery interfere with auscultation?
26. what is an ejection murmur?
27. what is a regurgitant murmur?
28. describe the sound of a diastolic murmur.
29. what are mid/late diastolic murmurs caused by?
30. what does a continuous murmur indicate?
31. what does a pericardial friction rub sound like?
answers
1. mitral and tricuspid valves closing at the beginning of systole.
2. pulmonary and aortic valves closing at the beginning of diastole.
3. when S2 has two different sounds instead of one, resulting from the aortic valve closing before the pulmonary.
4. during inspiration, common under 30yo.
5. fixed: R heart overload, RBBB, ASD, pulmonic stenosis. parodoxical: cardiac disease.
6. diastolic sound from rapid ventricular filling.
7. CHF, ASD, mitral or aortic insufficiency, VSD, PDA.
8. diastolic sound due to lower ventricular compliance.
9. aortic stenosis, HTN, CAD, cardiomyopathy, mitral regurg., MI.
10. a drop in systolic BP of more than 20mmHg upon moving from a lying to standing position.
11. lipid deposits in the skin associated with high cholesterol and diabetes.
12. cushing's, acromegaly, paget's, (as well as anxiety, pain)
13. flushing of the cheeks, might be related to valvular disease such as mitral stenosis (leads to pulmonary HTN, leads to dilation of blood vessels)
14. atherosclerosis, especially with bruits.
15. pressing on the lower abdomen to see how much the jugular venous pressure rises.
16. RCHF, constrictive pericarditis, SVC obstruction.
17. Roth's spots / flame hemorrhage.
18. might have splinter hemorrhages or clubbing.
19. cyanosis, arachnodactyly, osler nodes/janeway lesions.
20. 2nd intercostal space (IS), to the right of the sternum.
21. 2nd IS, to the left of the sternum.
22. 3rd IS to the left of the sternum; useful as a point to hear the "overall" heart cycle.
23. lower half of sternum, right parasternal area.
24. 5th IS, just medial to midclavicular line.
25. sometimes as a result of open heart surgery the pericardium sticks to the myocardium and inhibits sound conduction.
26. systolic murmur: blood flowing through a stenotic valve.
27. systolic murmur: blood flowing back into the chamber from which is being pumped out of.
28. higher pitched, decrescendo.
29. forward flow through AV valves.
30. an abnormal pathology, such as a congenital shunt.
31. high pitched, squeeking; best heard if patient leans forward.
questions
heart sounds...
1. S1 is the sound of...
2. S2 is the sound of...
3. what is "S2 splitting"?
4. S2 splitting is considered normal in...
5. what do fixed and parodoxical splitting represent?
6. S3 is the sound of...
7. prominent S3 sound might indicate what?
8. S4 is the sound of...
9. S4 might indicate what?
physical examination...
10. what is orthostatic hypotension?
11. what are xanthomatas?
12. what are some cardiac related conditions that could result in altered facial appearance?
13. what is the malar flush and what might it result from?
14. if the carotid pulses are different bilaterally, what might this indicate?
15. what is the hepatojugular reflex?
16. increased jugular venous pressure can indicate...
17. common fundoscopic findings for cardiac disease?
18. how might the fingernails appear in a cardiac patient?
19. describe some common PE findings for the hands of a cardiac patient.
auscultation...
20. where is the aortic area located?
21. where is the pulmonic area?
22. where is Erb's point and what is its significance?
23. where is the tricuspid area?
24. where is the mitral area?
25. why might open heart surgery interfere with auscultation?
26. what is an ejection murmur?
27. what is a regurgitant murmur?
28. describe the sound of a diastolic murmur.
29. what are mid/late diastolic murmurs caused by?
30. what does a continuous murmur indicate?
31. what does a pericardial friction rub sound like?
answers
1. mitral and tricuspid valves closing at the beginning of systole.
2. pulmonary and aortic valves closing at the beginning of diastole.
3. when S2 has two different sounds instead of one, resulting from the aortic valve closing before the pulmonary.
4. during inspiration, common under 30yo.
5. fixed: R heart overload, RBBB, ASD, pulmonic stenosis. parodoxical: cardiac disease.
6. diastolic sound from rapid ventricular filling.
7. CHF, ASD, mitral or aortic insufficiency, VSD, PDA.
8. diastolic sound due to lower ventricular compliance.
9. aortic stenosis, HTN, CAD, cardiomyopathy, mitral regurg., MI.
10. a drop in systolic BP of more than 20mmHg upon moving from a lying to standing position.
11. lipid deposits in the skin associated with high cholesterol and diabetes.
12. cushing's, acromegaly, paget's, (as well as anxiety, pain)
13. flushing of the cheeks, might be related to valvular disease such as mitral stenosis (leads to pulmonary HTN, leads to dilation of blood vessels)
14. atherosclerosis, especially with bruits.
15. pressing on the lower abdomen to see how much the jugular venous pressure rises.
16. RCHF, constrictive pericarditis, SVC obstruction.
17. Roth's spots / flame hemorrhage.
18. might have splinter hemorrhages or clubbing.
19. cyanosis, arachnodactyly, osler nodes/janeway lesions.
20. 2nd intercostal space (IS), to the right of the sternum.
21. 2nd IS, to the left of the sternum.
22. 3rd IS to the left of the sternum; useful as a point to hear the "overall" heart cycle.
23. lower half of sternum, right parasternal area.
24. 5th IS, just medial to midclavicular line.
25. sometimes as a result of open heart surgery the pericardium sticks to the myocardium and inhibits sound conduction.
26. systolic murmur: blood flowing through a stenotic valve.
27. systolic murmur: blood flowing back into the chamber from which is being pumped out of.
28. higher pitched, decrescendo.
29. forward flow through AV valves.
30. an abnormal pathology, such as a congenital shunt.
31. high pitched, squeeking; best heard if patient leans forward.
Saturday, November 15, 2008
11.12.08 organ systems: cardiovascular development 2
this is the second lecture in the cardiovascular development series and focuses on development of prenatal circulation and the transition to post natal circulation. it starts with where we left off with the last lecture, looking at the development of the larger structures in the heart, like the aortic arch being formed from the truncus arteriosus, forming the aorta on the left. the left recurrent laryngeal nerve is underneath the aorta and the right recurrent laryngeal nerve is underneath the right subclavian artery.
then we go back to some possible defects in structural development in the BC/TA trunk. when the spiral aortic-pulmonary septum forms from the endocardial cushion, there are several possibilities for abnormal development. these are: lack of septum altogether, called persistent truncus arteriosus, lack of a spiral in the septum, causing transposition of the aorta and pulmonary trunks, and an unequal divide in the trunk, causing one of the trunks to be bigger than the other. the tetralogy of fallot is a condition that combines the unequal divide with a VSD, resulting in right ventricular hypertrophy (induced by the pulmonary stenosis) as well as "aortic override".
finally, we look at the development of fetal circulation on a larger scale, as it interacts with its placenta. the trophoblast that is embedded in the endometrium differentiates into two layers: the syncytiotrophoblast, which contains spiralling maternal blood vessels and interstitial spaces, and the cytotrophoblast, which has "choroinic villi" that extend into the interstitial spaces and contain the fetal blood vessels. we then shift over to look at the difference between pre and post natal circulation, which is mainly in prenatal's use of shunts which divert blood from the liver and lungs. the ductus venous diverts blood from the liver, the ductus arteriosus and foramen ovale divert blood from the lungs, instead going directly back into circulation, which apparently "reduces oxygenated blood" in the lower limbs. two more random facts: blood supply from umbilical cord and vena cava remain in separate streams when entering the right atrium. the right ventricle and pulmonary trunk receives more deoxygenated blood and the left ventricle receives more oxygenated blood.
then we go back to some possible defects in structural development in the BC/TA trunk. when the spiral aortic-pulmonary septum forms from the endocardial cushion, there are several possibilities for abnormal development. these are: lack of septum altogether, called persistent truncus arteriosus, lack of a spiral in the septum, causing transposition of the aorta and pulmonary trunks, and an unequal divide in the trunk, causing one of the trunks to be bigger than the other. the tetralogy of fallot is a condition that combines the unequal divide with a VSD, resulting in right ventricular hypertrophy (induced by the pulmonary stenosis) as well as "aortic override".
finally, we look at the development of fetal circulation on a larger scale, as it interacts with its placenta. the trophoblast that is embedded in the endometrium differentiates into two layers: the syncytiotrophoblast, which contains spiralling maternal blood vessels and interstitial spaces, and the cytotrophoblast, which has "choroinic villi" that extend into the interstitial spaces and contain the fetal blood vessels. we then shift over to look at the difference between pre and post natal circulation, which is mainly in prenatal's use of shunts which divert blood from the liver and lungs. the ductus venous diverts blood from the liver, the ductus arteriosus and foramen ovale divert blood from the lungs, instead going directly back into circulation, which apparently "reduces oxygenated blood" in the lower limbs. two more random facts: blood supply from umbilical cord and vena cava remain in separate streams when entering the right atrium. the right ventricle and pulmonary trunk receives more deoxygenated blood and the left ventricle receives more oxygenated blood.
11.11.08 organ systems: cardiovascular development 1
this unit covers some basic ideas in early cardiovascular development. the first section focuses on the development of blood and blood vessels: blood production starts mainly in the yolk sac and moves to the liver/spleen, then to the bone marrow during development and involves differentiation of hemangioblast cells. these cells are derived from mesenchymal cells and triggered by the growth factor FGF to differentiate into blood cell precursors, hematopoetic stem cells, or blood vessel (capillary) walls, which then converge into larger and larger vessels. VEGF is a growth factor that stimulates nearby mesenchyme cells to differentiate into smooth muscle or pericyte cells.
the next sections describe the early structural development of the heart. the formation of the heart chambers begins when the endocardial cushion forms in the middle of the heart via a fusion of projections of tissue from the anterior and posterior walls. in the atriums, the primary septum is formed with a secondary foramen, and the secondary septum is formed with a foramen ovale. in the prenatal heart, blood flows from the right atrium, into the foramen ovale, through the primary septum, directly into the left atrium, bypassing the lungs. (this is the second "shunting" we've learned about- the first being the ductus arteriosus) in the post natal heart, the pressure from the pulmonary artery in the left atrium causes the primary septum to close and fuse with the secondary, creating the fossa ovalis. the ventricles are partitioned when the muscular and the membranous aspects of the interventricular septum join, closing up the interventricular foramen. finally, the endocardial cushion projects a spiral aortic pulmonary septum that projects into the bulbus cordis / truncus arteriosus vessel and separates it into the aortic and pulmonary trunks. the points of fusion between the bulbus cordis and truncus arteriosus becomes the semilunar valves.
we then look at some defects possible in the development of these structures. in the atriums, atrial septal defect can occur, called probe patent formation, when there is an imperfect adhesion between the primary and secondary septums. in the ventricles, VSD can occur when the membranous aspect of the interventricular septum does not close completely.
the next sections describe the early structural development of the heart. the formation of the heart chambers begins when the endocardial cushion forms in the middle of the heart via a fusion of projections of tissue from the anterior and posterior walls. in the atriums, the primary septum is formed with a secondary foramen, and the secondary septum is formed with a foramen ovale. in the prenatal heart, blood flows from the right atrium, into the foramen ovale, through the primary septum, directly into the left atrium, bypassing the lungs. (this is the second "shunting" we've learned about- the first being the ductus arteriosus) in the post natal heart, the pressure from the pulmonary artery in the left atrium causes the primary septum to close and fuse with the secondary, creating the fossa ovalis. the ventricles are partitioned when the muscular and the membranous aspects of the interventricular septum join, closing up the interventricular foramen. finally, the endocardial cushion projects a spiral aortic pulmonary septum that projects into the bulbus cordis / truncus arteriosus vessel and separates it into the aortic and pulmonary trunks. the points of fusion between the bulbus cordis and truncus arteriosus becomes the semilunar valves.
we then look at some defects possible in the development of these structures. in the atriums, atrial septal defect can occur, called probe patent formation, when there is an imperfect adhesion between the primary and secondary septums. in the ventricles, VSD can occur when the membranous aspect of the interventricular septum does not close completely.
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