Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
144 Cards in this Set
- Front
- Back
|
Pregnant women in 3rd trimester has normal Bp when standing and sitting. When supine, Bp drpos to 90/50, DX?
|
Compression of the IVC
|
|
|
35-yr-old man has hihg BP in his arms and low BP in his legs, DX
|
Coarctation of the Aorta
|
|
|
5-yr-old boy presents w/ systolic murmur and side, fixed split S2, Dx
|
ASD
|
|
|
During a football game , a young football player collagses and dies immediately, what is the most likley type of cardiac disease?
|
Hypertrophic cardiomyopathy
|
|
|
Pateint has a stroke after incurring multiple long bone fractures in trauma stemming from a motor vehicle accident, what caused the infart
|
Fat emboli
|
|
|
Elderly women presents w/ headache and jaw pain the labs show elevated ESR (erythrocyte sedementation rate), Dx
|
Temporal arteritis
|
|
|
80-yr-old presents w/ systolic cresendo-decrescendo murmur, What is the most likely cause?
|
Aortic stenosis
|
|
|
Man starts a medication of rhyperlipidemia, He then develops a rash, pruritus and GI upset, what was the drug
|
Niacin
|
|
|
Patient develops a cough and must discontinue captopril, what is a good replacement drug, and why?
|
Losartan, an angiotensin II receptor antoagnoist, does not increase bradykinin as captopril does
|
|
|
What are the components to the carotid sheath?
|
VAN
1. Internal jugular vein (lateral) 2.Common carotid artery (medial) 3. Vegus nerve (posterior) |
|
|
The SA and AV node are usually supplied by the...
|
RCA
|
|
|
What are the two major branches of the right coronary artery (RCA)
|
Acute marginal
Posterior descending artery (PD) |
|
|
What are the are the two major branches of the Left main coronary artery (LCA)
|
LAD - left anterior descening artery
circumflex artery (CFX) |
|
|
In a right dominant heart what coronary artery supplies inferior portion of the left ventricle?
|
80% of the time the RCA does via the PD
|
|
|
What Coronary artery is most commonly occluded?
|
LAD
|
|
|
What part of the heart does the the LAD (left anterior descending artery) supply?
|
Anterior interventricular septum
|
|
|
When do the coronary arteries fill?
|
During diastole
|
|
|
What is the most posterior aspect of the heart?
What can happen when it becomes enlarged? |
Left atrium
dysphagia can result |
|
|
Cardiac output (CO) =
|
Stroke volume (SV) x (Heart rate (HR)
|
|
|
What happens to CO during excercise, explain why?
|
increases first becuase of Inc. SV but after prolonged excercise it inc. due to Inc. HR.
|
|
|
What happens to CO if HR is too high? What is an example of this?
|
diastolic filling is incomplete and CO decreases (e.g. of tachycardia)
|
|
|
What is the fick principle
|
CO = (Rate of O2 consumption)/(arterial O2 content - Venous O2 content)
|
|
|
Mean arterial pressure =
|
CO x TPR
|
|
|
What proportion of MAP is diastolic and which is sytolic?
|
systolic - 1/3
diastolic - 2/3 |
|
|
Pulse pressure =
|
systolic - diastolic
|
|
|
Pulse pressure is equivilant to?
|
stroke volume
|
|
|
Stroke volume =
|
CO/HR
or EDV - ESV |
|
|
What is stroke volume affected by?
|
Contractility, afterload, and preload
|
|
|
An increase in preload, a dec. in afterload and an increase in contractility would have what effect on Stroke volume?
|
increase stroke volume
|
|
|
When does Contractility (and SV) increase (4)?
|
1.Catecholamines (inc. activity of the Ca2+ pump in the sarcoplasmic reticulum)
2.Inc. intracelllular Calcium 3. Dec. Extracellular calcium 4. Digitalis (inc. intracellular Na+, resulting in inc. Ca2+) |
|
|
When does contractility (and SV)decrease (5)?
|
1. Beta1 blockade
2. Heart failure 3. Acidosis 4. Hypoxia/hypercapnea 5. Ca2+ channel blockers |
|
|
In what three scernarios does SV increase?
|
anxiety, excercise, and pregnancy
|
|
|
WHat is the effect of a failing heart on Stroke volume?
|
decreases
|
|
|
Myocardial oxygen demand is increased by (4)
|
1. Inc. afterload (diastolic BP)
2. Inc. in contractility 3. Inc. in HR 4. Inc. in heart size (inc. wall tension) |
|
|
Ventricular End diastolic volume is the same thing as...
|
Preload
|
|
|
Systolic arterial pressure (proportional to peripheral resistance) is equal to?
|
Afterload
|
|
|
What is the physiological affect of Venos dilators?
Give an example? |
Decrease preload
nitroglycerin |
|
|
What is the physiological mechanism behind vasodilators?
Give and example of a vasodilator? |
decrease afterload
hydralazine |
|
|
what three things increase preload?
|
excercise (slight)
increase blood volume (overtransfusion) excitment (sympathetics) |
|
|
What are the 7 common congenital birth defects?
|
1. Heart defects
2. Hypospadias 3. Cleft lip (w/ or w/o the cleft palate) 4. Congenital hip dislocation 5. Spina bifida 6. Anencephaly 7. Pyloric stenosis (projectile vomiting) |
|
|
What are teh congenital heart diseases that have right-to-left shunts and result in early cyanois ("blue babies)
|
1. Tetralogy of Fallot (most common cause of early cyanosis)
2.Transposition of the great vessels 3.Truncus arteriosus (All start w/ T) |
|
|
What are the congenital heart diseases that have Left-right-shunts and result in late cyanosis ("blue kids")
|
1. VSD
2. ASD 3. PDA |
|
|
What drug can be used to close a PDA?
|
indomethacin
|
|
|
What is the most common congential anomaly?
|
VSD>ASD>PDA
|
|
|
What effect does a left-to-right shunt have on the lungs
|
increase pulmonary resistance due to arteriolar thickening
progressive pulmonary HTN |
|
|
Patient present w/ a lound S1 and a fixed split S2, Dx?
|
ASD
|
|
|
Patient has had progressive pulmonary HTN. The pulmonary resistance has gotten so great that the left-to-right shunt has now become a Right-to-left shunt, the child is cyanotic, has clubbing and polycythemia, Dx and cause?
|
Eisenmengers syndrome
From a VSD, ASD or PDA...the right ventricle will hypertrophy from the pulmonary resistance |
|
|
Pulmnary stenosis, right ventricular hypertorphy, overriding aorta and VSD. The patient suffers from cyanotic spells, Dx?
|
Tetralogy of Fallot
pneumonic: PROVe |
|
|
What is the most important determinant for prognosis in Tetralogy of Fallot?
What does the heart look like on x-ray? |
pulmonary stenosis
boot shaped from RVH |
|
|
What went wrong during development to cause tetralogy of Fallot?
|
anterior superior discplacement of the infundibular septum
|
|
|
What is the difference between subacute and acute bacterial endocarditis?
|
Subacute - vegetations occur on damaged prosthetic heart valves VS acute where they occur on healthy
|
|
|
endocartits affecting vavles of the left side of the heart is suggestive of?
|
intravenous drug abuse
|
|
|
What is the risk of dental procedures and a prothestic heart valve?
|
may cause transient bacterimia which may be seen as vegetations on the heart valve
|
|
|
patient with a prosthetic heart (seen on X-ray) presents w/ fever, weight loss, weakness, hematuria, splenomegaly, cardiac murmur, splinter hemorrhages, Roth spots on the retina (hemorrhageic lesions), and anemia what is the most likley diagnosis?
What is the best way to diagnose this? |
subacute bacterial endocarditis
transesophageal echo and a blood culture |
|
|
Treatment of subactue bacterial endocarditis?
|
acute - antibiotics against S. aureus
Subacute- strep viridans |
|
|
Explain the steps of the myocardial action potential?
|
Phase 0 - rapid upstroke - volatage gated Na+ channels open
phase 1 - initial repolarization - inactivation of the Na+ channels and volatage gated K+ channels begin to open. phase 2 - plateau - Ca2++ influx through volatage gate Ca++ channels balances the eflux of K+ efflux. Ca2++ influx triggers another Ca2++ releease from the sarcoplasmic reticulum and myocyte contraction Phase 3 - rapid repolarization - massive efflux of K+ through slow opeing voltage gated K+ channels and closure of Ca@++ channels phase 4 - resting potential - high premeability through K+ channels |
|
|
VHY
What phase in cardiac action potential do class I antiarrhythmic effect? |
Slow or block phase 0 in fast response fibers. block voltage gated Na+ hannels
|
|
|
VHY
What phase of the cardiac action potential do class III antiarrhythmics affect |
Phase 3, K+ channel blockers
|
|
|
Desceribe the pacemaker action potential (AV and SA node)
|
phase 0 - opening of voltage gate Ca2+ channels. These cells lack fast volatge gated Na++ channels. Results in slow conduction velocity, used by AV node to prolong transmissioin from atria to the ventricles
Phase 2 = pleateau is absent phase 3 = repolarization by volatge gated K+ channels phase 4 = slow diastolic depolarizatioin, membrane spontaneously depolarizes as Na+ conductance inc., this accounts for automaticity of SA and AV node |
|
|
What determines the heart rate
|
the slope of phase 4 in the SA node
|
|
|
How do Ach and catacholamines dec. and inc. the heart rate respectivley?
|
increase or decrease the rate of diastolic depolarization (phase 4)
|
|
|
Define refractoriness
|
The inability to respond to a stimulus (property of cardiac tissue)
|
|
|
What is effective refactory perion (ERP)
What catagory of drugs can prolong ERP |
Time when no stimulus can elicit a response (lasts into end of phase 3 becauase Na channels are in inactivated state)
Blockers of K+ channels |
|
|
What is the relative refractory period (RRP)
decreases in ERP cause |
A strong stimulus can elicit a response. begin at about the end of phase 3.
Favors the formation of premature beats |
|
|
Describe the gates of the volatage gated Na+ channels functions?
|
Has 2 gates M and h. they are both volatage sensetive. M opens fast and is responsible for the typical depol. h is slower and closes the Na gate during the refractory period
|
|
|
What does an increase in the slope of phase 4 of the AP cause of an AV or SA node?
|
increase in HR
this is what happnes through beta 1 receptor stimulation by the SANS |
|
|
what does an increase in cAMP cause (what happnes after beta 1 receptor has been stimulated)
|
increase slope of phase 4 and increase phase 0 upstroke
|
|
|
What is the mechanism by how beta blockers elicit their effectivness?
|
antagnist of Beta 1 receptor causing a decrease in cAMP formation
|
|
|
What is the majority of the mechanism of action of the class I antiarrythmics?
Describe the affect on cardiac tissue |
Na channel blockers
slows or blocks conduction (especially depolarized cells), decrease the slope of phase 4 depolarization and increase in threshold firing in abnormal pacemaker cells. Are state dependent (selectivley depress tissue that is frequently depolarized, e.g.' fast tachycardia) |
|
|
What are the important class IA antiarrhythmics?
|
Queen Amy Procalims Diso's pyramid
1. Quinidint (VHY know everything about it) 2. Amiodarone 3. Procainamide 4. Disopyramide |
|
|
What is the MOA of Class IA antiarrhythmics?
What is the effect on the heart? |
1. BLock fast Na channels (especially depolarized ones)
2. ALso blocks K+ channel INCREASED - Action potential, effective refractory period, and QT interval. Affects both ventricular and atrail arrythmias |
|
|
What are the ADRs of quinidine?
|
cinchonism - headache, tinnitus and thrombocytopenia
torsades de pointes (vent. tachycardia) due to prolonged QT interval (K+ block) |
|
|
What are the ADRs of procainamide
|
Reversible SLE-like syndrome in slow acetylators
can also cause torsades de pointes |
|
|
VHY
What is the antiarrhythmic (slowing the heart)properties of quinidine or class IA drugs? What are the proarrhytmic (speedding it up)properities of the heart? |
Blocking the fast NA channels and K+ channels
can cause muscarnic receptor blockade (atropine like affects - tachycardia) and may vasodilation (reflex tachycardia) |
|
|
What can increase the absorption of quinidine and therefore its toxicity
|
it is a weak base so antacids can do this
|
|
|
What is the MOA of the clas IB antiarrhythmic drugs?
|
BLock INACTIVTED Na channels, has a preference for slow conduction in hypoxic and ischemic tissue...causes less excitability in ischemic tissue.
RESULTS In DECREASED AP DURATION |
|
|
What are the Class IB anthiarrhythmic drugs?
|
VHY
Lidocaine - IV formula Mexiletine and tocainide - oral formulations |
|
|
VHY:
When do you use the class IB antiarrhythmic drugs? |
POST ACUTE MI
and digitalis-induced arrhythmias |
|
|
What are the important ADRs associated w/ Lidocaine mexiletine and tocainide?
|
CNS toxicity (stimulation or depression) causing seizures
and cardiovascular depression |
|
|
What other drug blocks Na channels in the inactivated state
|
Phenytoin
|
|
|
What is the MOA of the class 1C antiarrhythmic drugs?
It what situations would you use these drugs |
block fast NA channels. NO AFFECT ON AP
V-tachs that progress to VF and in intractable SVT. Last resort in refractory tachyarrhythmias |
|
|
What are the class IC antiarrhythmia drugs
What are there toxicities |
FLECAINIDE, encainide and propafenone
proarrhythmic (speeds up the heart) especially post MI (contraindicated) |
|
|
When are the CLass IC antiarrhythmias contraindicated
|
POST MI
|
|
|
Propanolol, esmolol, metoprolol, atenolol and timolol are all considered what type of antiarrhythmia drug?
MOA |
Class II
Beta blockers - decreases cAMP and Ca2+ currents...this supprresses abnormal pacemackers by dec. the slope of phase 4. |
|
|
What area of the heart is especially sensetive to class II antiarrhythmia drugs?
What is the result of this? |
AV node...caues an increase in the PR interval
|
|
|
Which of the beta blockers that is a class II antiarrhythmias drug is the shortes acting and when is it used?
|
ESMOLOL - given IV for actue SVT (suprventricular tachycardia)
|
|
|
What are the general uses for the class II antiarrhythmia drugs?
|
prophylaxis post-MI
SVT |
|
|
What are the toxicities of class II antiarrhythmia durgs
|
impotence, exacerbation of asthma (non-selective), cardiovascular effects (bradychardia, AV block, CHF), CNS effects (Sedation, sleep alterations)
NOTE: may mask hypoglycemia |
|
|
What are the class III antiarrhythmia drugs?
|
Sotalol, ibutilide, bretylium, amiodarone
|
|
|
What is the MOA of the class III antiarrhythmia drugs?
What affect does this have on the heart? |
K+ channel blockers
INCREASE AP (all affect phase 3) and increase in ERP. Also increases QT interval |
|
|
When do you use the class III antiarrhythmia drugs
|
when all other antiarrhythmics fail
|
|
|
Which of the class III antiarrhythmia drugs causes torsades de pointes (VHY) and excessive beta block as its main toxicites?
|
Satolol
|
|
|
Which of the class III antiarrhythmia drugs causes torsades de pointes as its main toxicity?
|
ibutilide
|
|
|
Which of the class III antiarrhythmia drugs causes new arrhythmias and hypotension as its main toxicities?
|
bretylium
|
|
|
VHY
This antiarrhythmia drug cuases pulmonary fibrosis, hepatotoxicity, hypo/hyperthryroidism as its main toxicities? |
AMIODARONE - Remember to check PFTs, LFTs and TFTs when using amiodarone
|
|
|
What other drug causes pulmonary fibrosis as one of its main ADRs?
|
blomycin (anti-neoplastic agent)
|
|
|
corneal deposits, skin deposits causing photodermatits, neruologic deficits and cardiovascular effects (bradycardia, heart block, CHF) are all toxicities of what antiarrhythmia drug?
|
Amiodarone - less important ones to know.
|
|
|
VHY
What phase of the cardiac AP do the class III antiarrhythmia drugs effect? |
phase 3
|
|
|
CLASS IA and CLASS III antiarrhythmia drugs increase the risk of torsades de pointes what group of patients
|
LONG QT syndrome, familial genetic condition, have inc. risk for vent. arrhythmias
|
|
|
WHat is the MOA of the class IV antiarrhythmia drugs?
What effect does this have on cardiac tissue? |
Ca2+ channels blockers
primarily effects slow response tissue (AV nodal cells, phase 0 and 4)...results in dec. conduction velocity, inc. ERP, and inc. PR interval |
|
|
What is the major use of verapamil and diltiazem
|
prevention of nodal arrhythmias (SVT)
|
|
|
VHY
What are the major toxicities of verapamil |
Constipation and AV block (van induce heart failure)
|
|
|
What are some of the other toxicites seen w/ verapemil and diltiazem
|
flushing, edema, CV effects (CHF, AV block and sinus node depression)
|
|
|
What phase of the cardiac AP is affected by verapamila and diltiazem
|
Phase 0, of the pacemaker AP
|
|
|
WHat are two of the important drug interaction so verapamil and diltiazem
|
Additive AV block w/ beta blockers and digoxin, verpamil displaces dig. from binding sites
|
|
|
VHY
What is the DOC for paroxysmal SVT? Is also the DOC for diagnosing and abolishing AV nodal arrhthmias What is the MOA |
Adenosine
REsults in increase k+ efflux causing hyperpolarization |
|
|
What are the ADRs of adenosinie
|
flushing, sedation and dsypnea...but they are gone quickly
|
|
|
What can be used to treat ectopic pacemakers, especially in digoxin toxicity?
|
K+
|
|
|
VHY***
potassium channel blockers (IA and III), antipsychotics (thioridazine), TCA's and Digoxin all have what related drug toxicity, how do you treat it |
TORSADES DE POINTES
treat w/ Mg+ |
|
|
Which of the sympathoplegics are used as Antihypertensive drugs?
|
1.Clonidine, Methyldopa (work centrally on alpha 2 agonist)
2.Hexamtheonium 3.Reserpine (blocks storage on NE) 4.Guanethidine (inhibits release of NE) 5.Prazosin (alpha1 blocker) 6.Beta-blockers |
|
|
Which of the sympathoplegic antihypertensive durgs has the follwoing toxicities: dry mouth, sedation and SEVERE REBOUND HYPERTENSION
|
Clonidine
|
|
|
Which of the sympathoplegic antihypertensive durgs has the follwoing toxicities: sedation and has a positive coombs test (hemolytic anemia is common)
|
Methyldopa
|
|
|
This durg is used to manage HTN during an optiate withdrawl
|
Clonidine
|
|
|
VHY**
This drug is used to treat HTN during pregnancy? |
Methyldopa
|
|
|
Which of the sympathoplegic antihypertensive durgs has the follwoing toxicities: severe orthostatic hypotension, blurred vision, constipation and sexual dysfunction
|
Hexamethonium
|
|
|
Which of the sympathoplegic antihypertensive durgs has the follwoing toxicities: Sedation, DEPRESSION, nasal stuffiness and diarrhea?
|
Reserpine
|
|
|
Which of the sympathoplegic antihypertensive durgs has the follwoing toxicities: orthostatic and excercise hypotension, sexual dysfunction and diarrhea?
|
Guanethidine
|
|
|
Which of the sympathoplegic antihypertensive durgs has the follwoing toxicities: 1st dose orthostatic hypotension, dizziness and headache (take at bedtime)
|
Prazosin
|
|
|
Which of the sympathoplegic antihypertensive durgs has the follwoing toxicities: Impotence, asthma, cardiovascular affects (AV-block, CHF, bradycardia) and can increase LDL's and TG's
|
Beta-blockers
|
|
|
How does Prazosin reduce HTN (i.e. what is the MOA)
|
dec. arteriolar and venous resistance decreasing afterload and preload respectivley.
|
|
|
What antihypertensive drug would you use for SEVERE HTN?
|
Vasodilators
|
|
|
What are the antihypertensive vasodilators
|
1.Hydralazine
2.Minoxidil 3.Nifedipine, verapamil 4.Nitroprusside |
|
|
This vasodilator decreases TPR by cuasing ARTERIOLAR DILATION?
The ADRs associated w/ this drug are LUPUS-LIKE syndrome in slow acetylators, reflex tachycardia, angina and salt retantion? |
Hydralazine
|
|
|
What do you give w/ hydralazine to prevent reflex tachyardia, and salt retention
|
beta blocker and a diuretic
|
|
|
This drug acts by opening K+ channels, causing hyperpolarization of the arteerioles.
It also has the following ADR: hypertrichosis, pericardial effusion, reflex tachycardia, angina and salt retention? |
Minoxidil
|
|
|
What do you give w/ minoxidil to prevent reflex tachycardia and salt retention?
|
Beta blocker and diuretic
|
|
|
This drug is a calcium channel blocker that has the following ADRs: dizziness, flushing, constipation and nausea?
|
Nifedipine and verapamil (only one to cause constipation)
|
|
|
What is the DOC for hypertensive emergencies?
|
Nitroprusside
|
|
|
What is the MOA of nitroprusside?
|
decreases TPR via dilation of the venules and the arteries
|
|
|
VHY:
What is the treatment of cyanide posioning? |
sodium or amyl nitirte to promote formation of methemoglobin...which binds the CN- ions PREVENTING inhibitory action of CN- on COMPLEX 4 of Electron transport chain.
Cyanomethemoblobin is then reconverted to methemoglbin by thiosulfate and the less toxic thiocynate is released by NITROPRUSSIDE. |
|
|
Orthostatic hypotension only results from drugs that cause dilation of the arteries or the veins?
|
VEINS - usually from alpha 1 blockade
|
|
|
Which of the antihypertensive drugs has the following ADR's: hypokalemia, slight hyperlipidemia, hyperuricemia, lassitue, hypercalcemia and hyperglycmia
|
Hydrochlorothiazide (Diuretics)
|
|
|
Which of the anti-hypertensive drugs has the following ADRs:
potassium wasting, metabolic alkalosis, hypotension and ototoxicity |
Loop diuretics (Drug interactions)
|
|
|
VHY
Catopril (ACE inhibitors) can also be implicated in the management of the HTN patient, what common side affects do you see w/ these drugs? |
CAPTOPRIL and hyperkalemia
C - cough (ACE only, inc. bradykinin) A - Angioedema P - proteinuria T - Taste changes Hy - O - Tension P -pregancy problems (fetal renal damage) R - Rash, Acute renal failure in renal artery stenosis I - increased renin L - lower angiotensin II |
|
|
Angiotensin II can also be used in the management of HTN, what are its common ADRS
|
Hyperkalemia and Fetal renal toxicity, acute renal artery failure in renal artery stenosis
|
|
|
VHY
Which anti-hypertensive drug is contraindicated in Preganancy |
ACEI and ARB's
|
|
|
Patient taking a new anti-hypertensive drug develops swelling of the nose, mouth, throat, glottis and larynx (lips and tongue), what is the drug?
|
ACEI (captopril) - worst ADR
|
|
|
In summary what are the different classes of durgs used to treat Hypertension (i.e. antihypertensive agents)?
|
1.Diuretics (dec preload)
2.Sypathoplegics (dec. prelaod) 3. Vasodilators (dec. preload) 4. ACE inhibitors and ARBS (Dec affects of antiogtensin II, preload, remodeling and afterload) |
|
|
What are the best antihypertensive drugs to use in a patient the following co-morbitiy: angina
|
beta blockers
CCB |
|
|
What are the best antihypertensive drugs to use in a patient the following co-morbitiy: Diabetes
|
ACEI and ARB
|
|
|
What are the best antihypertensive drugs to use in a patient the following co-morbitiy: heart failure
|
ACEI and ARB
|
|
|
What are the best antihypertensive drugs to use in a patient the following co-morbitiy: POST MI
|
beta-blocker
|
|
|
What are the best antihypertensive drugs to use in a patient the following co-morbitiy: BPH
|
alpha blockers
|
|
|
What are the best antihypertensive drugs to use in a patient the following co-morbitiy: Dyslipidemias
What drugs do you not want to use |
alpha blockers, CCB, ACEI/ARBS
don't use beta-blockers or thiazides |
