Term
What would you listen for in each of the following ascultory regions?
1) RUSB
2) LUSB
3) LLSB
4) Apex
5) Left sternal border |
|
Definition
APT M
1) Aortic area
Systolic murmur
- Aortic stenosis
- Flow murmur
- Valve sclerosis
2) Pulmonic area (SEM)
- Pulmonic stenosis
- Flow murmor (ASD)
3) Tricuspid area
Pansystolic murmur
- Tricuspid regurgitation
- VSD
Diastolic murmur
- Tricuspid stenosis
- ASD
4) Mitral area
Systolic murmur
- Mitral regurgitation
Diastolic murmur
- Mitral stenosis
5) Diastolic
- Aortic regurgitation
- Pulmonic regurgitation
Systolic
- Hypertrophic cardiomyopathy |
|
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Term
| What diastolic murmurs could you hear in the LLSB? |
|
Definition
Tricuspid area (valve is open during diastole)
- Tricuspid stenosis
- ASD (left to right shunt) |
|
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Term
| What diastolic murmurs could you hear in the apex? |
|
Definition
Mitral area (open in diastole)
- Mitral stenosis |
|
|
Term
| What systolic murmurs could you hear in the LLSB? |
|
Definition
Tricuspid area (closed in systole)
- Tricuspid regurgitation
- VSD (left to right flow) |
|
|
Term
| What systolic murmurs could you hear in the RUSB? |
|
Definition
Aortic area (open during systole)
1) Aortic stenosis
2) Flow murmur
3) Aortic valve sclerosis |
|
|
Term
| What diastolic murmurs could you hear in the left sternal border? |
|
Definition
1) Aortic regurgitation
2) Pulmonic regurgitation
**Can hear hypertrophic cardiomyopathy here in systole** |
|
|
Term
| What systolic murmurs might you hear in the LUSB? |
|
Definition
Pulmonic area (open during systole)
- Pulmonic stenosis
- ASD flow murmur |
|
|
Term
| Why do you hear a pulmonary flow murmur in the case of an ASD? |
|
Definition
Left-to-right shunt causes
1) Increased flow across tricuspid in diastole (diastolic rumble)
2) Increased outflow from pulmonic valve (SEM)
** This SEM is like "relative stenosis" |
|
|
Term
What effect would each of the following bedside maneuvers have on a patient's heart sounds?
1) Inspiration
2) Expiration
3) Hand grip (increase systemic vascular resistance)
4) Valsalva (decrease VR by increasing intrathoracic pressure)
5) Rapid squatting (increase after-load and VR) |
|
Definition
1) Increase intensity of right heart sounds (decreased intrathoracic pressure/ increased pulmonary blood flow)
2) Increase intensity of left heart sounds
3) Increases MR and VSD systolic murmurs
4) Decrease murmur intensity EXCEPT for MVP (apex) and hypertrophic cardiomyopathy (left sternal border)
5) Decrease MVP and hypertrophic cardiomyopathy |
|
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Term
Describe the systolic murmur that you hear at the apex of the heart?
How could you increase its intensity? |
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Definition
This systolic murmur in the mitral area would be mitral regurgitation
1) Holosystolic murmur/ high-pitched "blowing"
2) Increase TPR by squatting or hand-grip or increase LA return (expiration)
**probably due to MVP, ischemic heart disease or LV dilation** |
|
|
Term
Describe the systolic murmur that you hear at the URSB of the heart that is often related to a bicuspid aortic valve.
What is the pulse like? |
|
Definition
This is Aortic area, which is open during systole. This is aortic stenosis.
1) Crescendo-decrescedone SEM followed by ejection click (abrupt halting)
2) Pulsus parvus et tardus (slow and weak) |
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Term
| Where do you hear a VSD murmur most intensely and how does it sound? |
|
Definition
1) Tricuspid area (back flow)
2) Holosystolic, harsh-sounding |
|
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Term
A patient presents with a late systolic crescendo murmur, with a mid-systolic click.
How would you increase/decrease the intensity of this murmur?
What are the common causes of this condition? |
|
Definition
1) MVP (click is due to valve leaflet snapping back)
2) Increase by reducing VR with valsalva (only other murmur increased like this is hypertrophic cardiomyopathy) and decrease with squatting
3) Rheumatic disease, Myxomatous degeneration, Chordae rupture. |
|
|
Term
| How can you tell between a murmur in aortic regurgitation from one in mitral stenosis? |
|
Definition
Both are diastolic murmurs
1) AR will be high-pitched "flowing" murmur, possibly with bounding pulses (decreased by vasodilators)
2) Delayed diastolic rumble in MS follows an opening snap (when valve leaflets halt) |
|
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Term
Why might you hear a continuous "machine-like murmur" that is loudest at S2?
What are some common causes |
|
Definition
1) PDA (aorta to pulmonary artery shunt)
- S2 is when aortic valve closes
2) Often due to congenital rubella or prematurity. |
|
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Term
A patient presents with "sawtooth" tachycardia.
How do you treat? |
|
Definition
Sounds like Atrial flutter
1) IA, IC, III (increase APD and QTc)
2) Maybe Warfarin too for embolism risk (if CHADS holds) |
|
|
Term
| How can you measure pulmonary capillary wedge pressure and what can it tell you about mitral stenosis? |
|
Definition
1) Swan-Ganz catheter- watch out for transient RBBB
2) PCWP approximates LA pressure, which will be greater than LV in mitral stenosis |
|
|
Term
| What are the major right-to-left shunts in congenital heart disease that give you "blue babies"? |
|
Definition
5 Ts
1) Tetralogy of Fallot (most common)
2) Transposition of Great Vessels
3) Truncus arteriosus (aorta gives rise to pulmonary artery)
4) Tricuspid atresia (no AV valve, so ASD and VSD required)
5) Total anomalous pulmonary venous return (TAPVR) [pulmonary veins drein into right heart (SVC, coronary sinus), because confluences does not connect to LA] |
|
|
Term
| Which left-to-right shunts can cause late cyanosis (blue kids)? |
|
Definition
1) VSD (most frequent)
2) ASD (loud S1, wide fixed split S2)
3) PDA (close with indomethacin)
VSD > ASD > PDA |
|
|
Term
| Why can uncorrected VSD, ASD or PDA ultimately cause clubbing and polycythemia? |
|
Definition
Eisenmenger's syndrome
These are left-to-right shunts that increase pulmonary pressure and lead to pulmonary vascular hypertrophy and HTN.
Increased pulmonary resistance from HTN reverses shunt an, causing late cyanosis. |
|
|
Term
| Why does squatting help patients with Tetralogy of Fallot? |
|
Definition
PROVe (displacement of infundibular septum)
1) Pulmonic stenosis
2) RVH
3) Overiding aorta
4) VSD
Pulmonic stenosis leads to right-to-left shunt across VSD. Squatting increases compression of femoral arteries, thereby increasing TPR and increasing the pressure on blood exiting the RV (less right-to-left shunting) |
|
|
Term
| Why are VSD, PDA or patent foramen ovale critical in a D-transposition of the great vessels? |
|
Definition
**parallel circuits** occurs in kids of diabetic moms
1) RV gives systemic blood to aorta
2) LV gives pulmonary blood to pulmonary arteries
Need pulmonary blood to get from left heart to right heart, so that it can be distributed to the body! |
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|
Term
| What is the difference between infantile and adult coarctation of the aorta? |
|
Definition
INfantile: IN close to the heart
ADult: Distal to Ductus
- associated with bicuspid aortic valve
**Can cause aortic regurgitation**
1) Infantile involves aortic stenosis proximal to ductus arteriosus insertion (Turner syndrome)
2) Adult involves stenosis distal to ligamentum arteriosum (notching of ribs from collateral circulation)
- HTN in upper extremities and absent pulses in legs. |
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|
Term
| Why might you check femoral pulses on a PE when worrying about congenital heart disease? |
|
Definition
| Coarctation of the aorta (normally from bicuspid aortic valve and subsequent stenosis- distal in adults and pre-ductal in infants) will cause upper extremity HTN and lower extremities pulselessness |
|
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Term
| How do you treat a Patent ductus arteriousus? |
|
Definition
Indomethacin inhibits prostaglandins
Remember, this is right-to-left in infancy (pulmonary circulation to aorta), but becomes left-to-right in adults as lung resistance decreases , causing RVH and "machine-like murmur."
** can eventually lead to cyanosis of lower extremities, because blood can't get to descending aorta** |
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Term
What congenital cardiac defects are associated with each of the following genetic syndromes?
1) 22q11 (DiGeorge)
2) Down Syndrome
3) Congenital Rubella
4) Turner's syndrome
5) Marfan's syndrome
6) Infant of diabetic mother |
|
Definition
1) Truncus arteriosus and tetralogy of Fallot (early cyanotic)
2) AVSD, ASD and VSD
3) Septal defects, PDA, pulmonary artery stenosis
4) Coarctation of aorta (bicuspid aorta)
5) Aortic insufficiency (late complication)
6) Transposition of great vessels |
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Term
A patients BP is 150/95.
What are the risk factors for this patient's condition? |
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Definition
Hypertension (90% essential/ due to increased CO and TPR and 10% secondary to renal failure)
1) Age
2) Genetics (black > white > asian)
3) Obesity
4) Diabetes
5) Smoking |
|
|
Term
| What pathological conditions does HTN dispose patients to? |
|
Definition
1) LVH
2) Stroke
3) Atherosclerosis
4) CHF
5) Renal failure (often cause of HTN)
6) Retinopathy
7) Aortic dissection |
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Term
A patient presents with plaques on their eyelids and skin, as well as deposits on their achilles tendon. You notice lipid deposits on their cornea as well, and see atheromas an blood vessel biopsy.
What is going on? |
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Definition
| Atheroma, Xanthoma (eyelids and achilles) and Corneal Arcus usually indicate Hyperlipidemia (could be herediatary hypercholesterolemia: type IIa) |
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Term
There is calcification in the media of the radial and ulnar arteries.
Is this very serious? Why or why not? |
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Definition
"Pipestem arteries"
Calcification of media probably means Monckeberg Arteriosclerosis, which does NOT obstruct flow (no intimal involvement).
If this was Atherosclerosis, the intima would be involved. |
|
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Term
| What are the 2 major types of Arteriolosclerosis and when are they seen? |
|
Definition
1) Hyaline- Essential HTN and diabetes ( Non-enzymatic glycosylization)
2) Hyperplastic "onion skinning"- Malignant hypertension |
|
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Term
| What is the pathogenesis of the disease of elastic and large and medium-sized muscular arteries that leads to fibrous plaques and atheromas in vessel intima? |
|
Definition
"Response to Injury Hypothesis**
1) Endothelial cell dysfunction
2) Macrophage and LDL accumulation (oxidized LDL)
3) Foam cell formation
4) Fatty streaks
5) Smooth muscle migration (PDGF and TGF-b)
6) Fibrous plaque and complex atheroma formation. |
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|
Term
| What is the pathogenesis of the disease of elastic and large and medium-sized muscular arteries that leads to fibrous plaques and atheromas in vessel intima? |
|
Definition
"Response to Injury Hypothesis**
1) Endothelial cell dysfunction
2) Macrophage and LDL accumulation
3) Foam cell formation
4) Fatty streaks
5) Smooth muscle migration (PDGF and TGF-b)
6) Fibrous plaque and complex atheroma formation. |
|
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Term
Which of the following is not a common complication of Atherosclerosis?
1. Thrombus/embolism
2. MI
3. Transient Visual disturbances
4. Peripheral vascular disease
5. Aneurysm |
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Definition
| 3. Not commonly, unless plaque was specifically in optic artery, in which case disturbances would not be transient. |
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|
Term
| Where does atherosclerosis most commonly occur? |
|
Definition
| **Abdominal Aorta** > Coronary artery (MI) > Popliteal Artery (diabetic dry gangrene)> Internal common carotid> Circle of Willis |
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|
Term
| What are the major risk factors for Atherosclerosis? |
|
Definition
1) Smoking
2) HTN
3) Diabetes
4) Hyperlipidemia
5) Family h/x |
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Term
A patient with Marfan's syndrome presents with tearing chest pain radiating to the back. CXR shows mediastinal widening.
What is going on? |
|
Definition
Fibrillin-1 defect in Marfan's predisposes to Aortic dissection (most commonly thoracic aorta), because of cystic medial necrosis and HTN.
In dissection, false lumen forms and occupies most of the descending aorta (can result in rupture and death) |
|
|
Term
In what population should you be most concerned about abdominal aortic aneurysms?
What about thoracic aorta aneurysms |
|
Definition
1) Most common type- In Male smokers >50 years old who have atherosclerosis
2) Hypertension is most important, with cystic medial necrosis (Marfan's) |
|
|
Term
| What are the 5 major manifestations of Ischemic heart disease? |
|
Definition
1) Angina (CAD narrowing >75%)
2) Coronary steal syndrome (vasodilator aggravates ischemia by shunting blood from critical stenosis to area of higher perfusion)
3) MI (acute thrombosis due to coronary artery atherosclerosis)
4) Sudden cardiac death (due to V fib)
5) Coronary ischemic heart disease (progressive onset following chronic myocardial damage) |
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|
Term
| Why might you see ischemic heart disease following prescription of a vasodilator? |
|
Definition
**Coronary steal syndrome**
If they have a critical stenosis, vasodilator may shunt blood from stenotic location to highly perfused area |
|
|
Term
| What are the distinguishing ECG findings for different forms of Angina in Ischemic heart disease? |
|
Definition
1) ST depression can indicate either
- Stable (secondary to atherosclerosis with chest pain on exertion ) or
- Unstable/crescendo (chest pain at rest)
2) ST elevation is Prinzmetal's variant, which is secondary to coronary artery vasospasm. |
|
|
Term
What important structures are supplied by the following arteries?
1) RCA
2) Acute marginal
3) PDA
4) LAD
5) Circumflex |
|
Definition
1) SA/AV nodes (80% of time)
2) RV
3) Posterior septum and Inferior LV
4) Apex and anterior IV septum (majority of occlusions)
5) Posterior left ventricle |
|
|
Term
| What heart ventricle might be enlarged if your patient presents with dysphagia and hoarseness? |
|
Definition
| LA is most posterior part of heart, and LA enlargement can compress the left recurrent laryngeal nerve. |
|
|
Term
| How does Fick's principle relate to CO? |
|
Definition
CO= SV * HR & SV= EDV-ESV
Fick's Principle says that
CO= (rate of O2 consumption)/(arterial O2- venous O2)
** The arteriovenous difference refers to pulmonary circulation, where a greater venous O2 concentration means more oxygen will get to the LV to be distributed to the body** |
|
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Term
| What happens to CO during early and late stages of exercise? |
|
Definition
1) Early on, CO increases because of increased HR and then is maintained by SV (since HR is limited in order to preserve diastolic filling).
2) Late stages of exercise, CO is maintained by HR |
|
|
Term
| How does pulse pressure relate to cardiac output? |
|
Definition
PP= systolic pressure - diastolic pressure
CO= SV * HR
SV is proportional to PP (because the difference in systolic and diastolic pressure provides for force to push out blood from LV). |
|
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Term
| What effect would increasing total peripheral resistance have on mean arterial pressure? |
|
Definition
This is like vasoconstriction. Increasing TPR increases MAP.
MAP= CO * TPR= SV * HR* TPR |
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|
Term
| How does Preload, Afterload and Contractility effect CO? |
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Definition
SV CAP
Increasing Preload, Decreasing Afterload and Increasing Contractility all increase SV, thereby increasing CO. |
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Term
How might each of the following alter SV?
1) Beta 1 blockage
2) Increasing intracellular calcium
3) Increasing extracellular sodium
4) Digitalis
5) Acidosis
6) Non-dihydropyridine Ca2+ blocker
7) Hypoxia |
|
Definition
1) Decrease in Catecholamine binding to beta 1 receptors will decrease contractility by decreasing cAMP-mediated calcium effects. DECREASE
2) INCREASE SV, because of greater contractility
3) High extracellular sodium will lead to less Na/Ca exchange, leaving more Ca2+ inside the cell for contraction.
4) Inhibits Na/K ATPase, increasing intracellular sodium concentrations , resulting in more Calcium.
5) Decreases contractility (and SV)
6) Decrease contractility (and SV)
7) Decrease contractility (and SV) |
|
|
Term
| Why might acidosis decrease contractility and SV? |
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Definition
Acidosis is increases H+ extracellularly, which will be exchanged for K+ intracellularly (H+/K+ ATPase).
As extracellular K+ rises (Hyperkalemia), cells become less excitable (contraction decreases). |
|
|
Term
| How is Myocardial O2 demand determined? |
|
Definition
1) HR (***)
2) Afterload (ESP or MAP)
3) Preload (EDV: wall tension)
4) Contractility |
|
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Term
| What effect do venodilators (Nitroglycerin) and vasodilators (Hydralazine) on Myocardial O2 demand? |
|
Definition
Remember, Myocardial O2 demand depends upon Preload (EDV or Wall tension) and Afterload (MAP or ESP), as well as HR and Contractility.
1) Venodilators like Nitroglycerin will decrease venous return, thereby decreasing preload, and decreasing oxygen demand.
2) Vasodilators like Hydralazine will decrease TPR, thereby decreasing MAP and afterload (also decreasing myocardial oxygen demand). |
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Term
How do each of these factors influence starling forces acting on the heart?
1) Circulating catecholamines
2) Digitalis
3) Sympathetic stimulation
4) Loss of Myocardium (MI) |
|
Definition
Remember, Starling says force of contraction is proportional to end diastolic length of cardiac muscle fibers (preload). This is to create maximum overlap of myosin and actin, as well as increase length-dependent calcium sensitivity of Troponin C.
1) These bind B1 receptors and increase contractility and HR, increasing CO for a given preload.
2) This drug increases contractility (not HR), increasing CO for a given preload as well.
3) Same as 1
4) MI will cause less CO for a given preload. |
|
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Term
| How is Ejection fraction determined and how does it changed in systolic and diastolic heart failure, respectively? |
|
Definition
EF= SV/EDV (should be 0.66)- index of contractility
In diastolic heart failure, there is a problem filling ventricle, but the proportion that is ejected does not change.
In systolic failure, the problem is with ejection, and EF drops. |
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Term
| What does the Poisuelles Law tell us about blood flow in people with anemia and polycythemia? |
|
Definition
Remember, flow Q is determined by a change in Pressure for a given resistance.
Poisuelle shows that this flow is also proportional to the RADIUS and CHANGE IN PRESSURE, as well as being inversely proportional to VISCOSITY and LENGTH.
Therefore, since anemics have less RBCs, their blood is less viscous, which will increase the rate of flow (also increasing turbulent flow by Reynold's number) |
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|
Term
| What happens to the flow a vessel when its radius is doubled? |
|
Definition
| Resistance is proportion to 1/r^4, and doubling the radius decreases the resistance by a factor of 16! |
|
|
Term
| Under what conditions might blood viscosity increase? |
|
Definition
1. Polycythemia
2) Hyperproteinemic state (Multiple myeloma)
3) Hereditary spherocytosis.
Remember, viscosity is directly proportion to resistance, which is inversely proportional to flow. |
|
|
Term
| What is the main purpose of arterioles? |
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Definition
| To regulate capillary blood flow (they are the major resistance vessels). |
|
|
Term
| What is the total resistance of a number of vessels in series? |
|
Definition
resistance= R1 + R2 + R3
vs. in parallel= 1/R1 + 1/R2 + 1/R3 |
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|
Term
What happens to the cardiac and vascular function curves under the following conditions?
1) Exercise
2) Hemorrhage
3) Heart failure
4) Narcotic overdose |
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Definition
1) Decreases TPR, so VF curve goes to right (higher pressure for given venous return) and CO goes up (more CO for a given pressure).
2) Increases TPR because of reflex vasoconstriciton (opposite of 1)
3) Shits CF down but does not effect VF
4) Same as 3 |
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|
Term
What do each of the features of the JVP refer to?
1) A wave
2) C wave
3) V wave
4) X descent
5) Y descent |
|
Definition
ACXVY
1) A wave is atrial contraction in late diastole
2) C wave is tricuspid valve bulging into RA during RV isovolemic contraction.
3) V wave is due to increased RA pressure during filling during systole
4) X descent occurs when tricuspid valve is sucked back towards RV during atrial relaxation in ventricular contraction.
5) Y descent occurs after atrial filling (V wave) when RA fills RV. |
|
|
Term
| What are the S3 and S4 heart sounds? |
|
Definition
1) S3 in early diastole during rapid filling to high high filling pressures (MR or CHF) and volume overload (dilated ventricles).
2) S4 in late diastole due to high atrial pressure. Associated with ventricular hypertrophy (LA pushes against stiff LV). |
|
|
Term
| Why might you see wide/paradoxical S2 splitting? |
|
Definition
1) Wide- Pulmonic stenosis or RBBB (late P2)
** Conditions that delay RV emptying
2) Paradoxical- Aortic stenosis or LBBB (late A2)
**Conditions that delay LV emptying |
|
|
Term
| What are the major differences between cardiac and skeletal muscle action potentials? |
|
Definition
1) Cardiac AP has a plateu (due to Calcium influx)
2) Cardiac nodal cells spontaneously depolarize in phase 4 diastole (funny currents from HCN)
3) Cardiac cells are electrically coupled by gap junctions |
|
|
Term
| How does an SA/AV action potential differ from an AP from a ventricular myocyte? |
|
Definition
Phase 4 slope determines HR
**Adenosine decreases slope by Catecholamine increasing slope**
1) Phase 0 is dominated by Calcium influx (slower upstroke). No sodium because resting potential is above voltage-gating.
2) No plateu phase 2
3) Rapid repolarization
4) Slow diastolic depolarization (If current with Na+) |
|
|
Term
| Describe the anatomy of the coronary artery system that supplies the heart. |
|
Definition
Left and right CA arise from base of aorta and fill during diastole
1) Right
- Gives off acute marginal artery (right ventricle) and then continues as PDA (posterior septum)
- Supplies SA and AV nodes (usually)
- Supplies posterior LV 80% of time (20% of time PDA comes off of CFX)
2) Left
- Divides into LAD (apex and anterior IV septum) and circumflex (left ventricle) |
|
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Term
| What artery is most commonly affected in an MI and what type of infarction/necrosis does the heart undergo? |
|
Definition
LAD- Anterior IV septum and Apex (mitral valve)
- Pale infarct
- Coagulation necrosis |
|
|
Term
| Hypertrophy of which cardiac area is known to cause dysphagia an hoarseness? |
|
Definition
LA is most posterior portion
Dysphagia (compression of esophagus)
Hoarseness (compression of left recurrent laryngeal nerve from CN X) |
|
|
Term
| What does it mean for a heart to be "Left Dominant" |
|
Definition
Occurs in 20% of cases
The PDA (supplying the posterior septum and inferior LV) arises from the lateral CFX artery off of the LCA, instead of from the RCA.
In these cases, a RCA thrombosis might spare the inferior left ventricle. |
|
|
Term
| How is CO calculated and how does it related to "Frick's Principle" and the calculation of MAP? |
|
Definition
CO= SV * HR= {MAP-RAP}/TPR
Q= dP/R and dP is the driving force behind SV
Frick's principle:
CO= rate of O2 consumption/ (O2a- O2v)
CO * TPR= MAP
During early exercise, CO is maintained by HR and SV, but later on it is maintained only by HR. |
|
|
Term
| How is MAP calculated? How does it relate to the concept of Pulse pressure? |
|
Definition
MAP= CO * TPR= 2/3dBP + 1/3sBP
PP= Systolic pressure - diastolic pressure, the most important determinant of which is SV (if you eject more blood, there will be greater increase in systolic pressure, thereby increasing PP) |
|
|
Term
| Describe the course of blood flow to and from the heart. |
|
Definition
1) Lungs to LA via pulmonary vein
2) LA to LV via mitral valve
3) LV to Aorta via aortic valve
4) Aorta to systemic circulation
5) Tissue to systemic veins and VC
6) VC to RA (mixed blood)
7) RA to RV via tricuspid valve
8) RV to PA via pulmonic valve
9) PA to lungs for oxygenation |
|
|
Term
| Which autonomic receptors regulate arteriolar contraction int the skin, renal and skeletal muscle systems? |
|
Definition
1) Skin, Renal and Splanchnic= Alpha 1
2) Skeletal muscle= B2 |
|
|
Term
| Which vessels have the largest cross-sectional and surface area in the circulatory system? Which vessels contribute most to resistance? |
|
Definition
1) Capillaries are surface area (thin-walled enthelium- site of exchange)
2) Arterioles are resistance vessels (Smooth muscle walls receive adrenergic innervation) |
|
|
Term
| Why are capillaries optimized for nutrient exchange? How are they different from the aorta? |
|
Definition
Large cross sectional area slows down blood velocity (V= Q/A), where Q= dP/R), allowing time for exchange.
The aorta has small cross-secitonal area and pumps blood quickly |
|
|
Term
| What does Poiseuille's equation tell us about the pathophysiology of atherosclerosis/thrombosis in MI? |
|
Definition
R= 8nl/pir^4
If radius decreases by a factor of 2, resistance increases by a factor of 16, meaning that the heart will not be perfused. |
|
|
Term
| How does the concept of parallel vs. series resistance relate to systemic and specific organ arterial supply? |
|
Definition
1) Systemic arterial supply from the aorta is organized in parallel, where 1/Rt= 1/Ra + 1/Rb.....
- The total resistance is less than the resistance of any individual artery (i.e. hepatic or renal)
2) Each organ is supplies by vessels that are in series (large artery, small artery, arteriole, ect..)
Rt= Ra + Rb + Rc
- The total resistance is equal to the sum of all the resistances in the series (largest portion is from arterioles) |
|
|
Term
Reynolds number can predict whether blood flow will be laminar or turbulent.
What factors determine the R# and how can it be applied clinically? |
|
Definition
Proportional to velocity/viscosity, and when it increases, there is more turbulence. Clinically detected as Bruits, which indicate thrombosis/clotting.
Velocity increases with narrowing of vessel (V= Q/A)
Viscosity decreases with Anemia (increases with polycythemia)
So, an anemic patient with atherosclerosis would be likely o have turbulent flow! |
|
|
Term
| What is capacitance and what happens to it with age? |
|
Definition
Distensibility
C= V/P, and it decreases with age, as vessels become more stiff.
PP will increase with age, since Capacitance determines SV and SV determines systolic pressure |
|
|
Term
| How does SV relate to EDV? |
|
Definition
SV= CO/HR= EDV- ESV
If EDV increases, then so does SV, since preload increases |
|
|
Term
How does an increase in the following variables influence SV?
1) After-load,
2) Contractility
3) Pre-load |
|
Definition
SV CAP
1) Increased after-load will increase SV
- Approximated by MAP, which is proportional to TPR
- Vasoconstriction
2) Increased contractility will increase SV
- catecholamines and digitalis
3) Increased pre-load (EDV) will increase SV
- venoconstriction |
|
|
Term
SV increases in cases of anxiety, exercise and pregnancy.
How do each of the following influence O2 demand?
1) Decreased afterload
2) Increased contractility
3) Decreased HR
4) Decreased Heart size |
|
Definition
With exercise, stress and pregnancy, you get vasodilation increased HR and increased contractility by autonomic influence.
1) Decrease demand
2) Increase demand
3) Decrease demand
4) Decrease demand (lower wall tension) |
|
|
Term
Which of the following does NOT decrease cardiac contractility?
1) B1 blockage (decreased cAMP)
2) Alkalosis
3) Hypoxia
4) Non-dihydropyridine Ca2+ channel blocker
5) Systolic dysfunction |
|
Definition
When contractility decreases, so does SV
2- Alkalosis actually would do the opposite.
Contractility decreases with Beta blockage, Acidosis, Hypoxia/Hypercapnia, NHDP calcium blockers and systolic heart failrue |
|
|
Term
How do each of the following increase cardiac contractility/SV?
1) NE
2) Digitalis |
|
Definition
SV increases with contractility and preload, and decreases with after-load
For contractility, you want calcium to flow in to depolarize cell membrane, and to keep the extracellular sodium concentration low
1) Increase activity of Ca2+ pump in SR
2) Inhibit Na/K ATPase, causing Na+ to come into the cell, depolarize it, an cause Ca2+ to rush in |
|
|
Term
| What effect do Nitroglycerin and Hydralazine have on SV, respectively, and how? |
|
Definition
1) Nitroglycerin is a venodilator, which decreases preload and decreases SV (used in angina and HF)
2) HydrAlAzine is a vasodilator, which decreases arterial after-load and increases SV. |
|
|
Term
| Explain how the Starling relationship determines the force of contraction? How is it affected by contractility? |
|
Definition
1) Describes the increase in SV and CO in response to increased venous return, or EDV (pre-load).
- Increased volume in ventricle increases fiber length and developed tension
2) Increases in contractility (Exercise) shift the curve up and vice versa (CHF) |
|
|
Term
EF is defined as an index of ventricular contractility.
How is it calculated, what is it normal value and how is it affected by systolic HF? |
|
Definition
EF= SV/EDV= (EDV- ESV)/EDV
"How much blood is pumped out divided by how much is left over"
EF > 55% is normal (usually 70%)
EF decreases in HF |
|
|
Term
| A ventricular pressure-volume loop is a common tool used to analyze cardiac function. Draw a loop and explain the 4 steps in the cycle. |
|
Definition
1) Isovolumetric contraction (Highest O2 consumption)
- The LV is filled with blood to EDV and muscle is relaxed. It then contracts and pressure increases
- when LAP < LVP, mitral valve shuts, producing S1
2) Ventricular ejection
- Blood leaves LV through aortic valve and enters Aorta (SV), decreasing LV volume and increasing LVP.
3) Isovolumetric relaxation
- Ventricle relaxes, and when LVP < Aortic valve P, the valve shuts (S2)
4) Ventricular filling
- When LVP - Volume increases from ESV to EDV |
|
|
Term
| What do S1-S4 heart sounds indicate? Where do you heart them best? |
|
Definition
S1= Closure of mitral valve during isometric contraction in the beginning of systole, prior to aortic valve opening (LVP > LAP)
- Apex
S2= Closure of aortic valve during isometric relaxation, at the beginning of diastole when LVP < aortic pressure
- Left sternal border
S3= Rapid ventricular filling during early diastole, when volume rushes against an already filled ventricle (dilated cardiomyopathy in MR and CHF)
- Normal in children and pregnant women
S4= Decreased ventricular compliance (atrial kick) in late diastole (LVH) |
|
|
Term
| In what groups of people is an S3 heart sound normal? What about S4? |
|
Definition
1) S3 is normal in kids and pregnant women
2) S4 is ALWAYS pathological (usually concentric LVH and heart failure) |
|
|
Term
| Describe the 5 major components of a JVP trace. What heart sounds to they correspond to (if any)? |
|
Definition
1) A wave= atrial contraction in late diastole
- corresponds roughly to S4 heart sound and precedes mitral valve closure.
2) C wave= tricuspid valve bulging back into right atrium during isometric contraction of RV in early systole
- Begins at S1
3) X descent
- Tricuspid valve retracting back after pulmonic valve opens and blood rushes into the pulmonary artery during ventricular ejection
4) V wave
- Atrial filling against closed tricuspid valve in early diastole
- Overlaps with S2
5) Y descent
- Blood flow from RA to RV when tricuspid valve opens.
- may overlap with S3 |
|
|
Term
| S2 splitting is a normal phenomenon. What gives rise to it and why might you see wide or narrow splitting? |
|
Definition
Aortic valve closes before Pulmonic valve (higher pressure). It is heard best with inspiration, since intrathoracid pressure decreases and venous return increases to the right heart, prolonging P2 closure.
Wide splitting can occur with pulmonic stenosis or RBBB
Narrow/paradoxical splitting with aortic stenosis |
|
|
Term
| What conditions are associated with wide fixed S2 splitting? What does this mean? |
|
Definition
ASD (common in Down's syndrome)
Left-to-right shunt increases flow through pulmonic valve.
Aortic and Pulmonic closures are separated in time, independently of inspiration/expiration |
|
|
Term
| What is paradoxical S2 splitting and when does it occur? |
|
Definition
usually, aortic valve closes before pulmonic, producing physiological splitting.
If there is Aortic Stenosis or a LBBB, the aortic valve closure may be delayed so much that it occurs AFTER pulmonic closure |
|
|
Term
When ascultating the heart, where would you listen for each of the following?
1) Aortic stenosis murmor
2) Hypertrophic cardiomyopathy
3) Pulmonic stenosis
4) Mitral regurgitation
5) Tricuspid regurgitation |
|
Definition
1) Right sternal border in systole
- flow murmurs and valve sclerosis
2) Left sternal border in systole
- Aortic regurg (diastolic)
3) Left T2/T3 at sternal border in systole
4) Apex in systole
- MS in diastole
5) Left lower sternal border during systole |
|
|
Term
| Describe the phases (0-4) of a cardiac action potential. |
|
Definition
0) Rapid upstroke
- voltage-gated Na+ channels opening
1) Initial re-polarization
- inactivation of VG-Na channels and VG-K channels opening
2) Plateu
- Ca2_ influx through VG=Ca2_ channels balances K+ efflux and triggers Ca2+ release from SR leading to myocyte contraction
3) Rapid repolarization
- Massive K+ efflux due to VG slow K+ channels and closure of VG Ca channels
4) Resting potential
- high K+ permeability to K+ channels |
|
|
Term
| How does a cardiac ventricular action potential differ from a skeletal muscle AP? |
|
Definition
Cardiac: 5 phase AP with Na+, K+, K+/Ca2+, K+ and K+, respectively
1) Cardiac AP has plateu, due to Ca2+ influx that balances initial re-polarization due to K+ efflux.
2) Cardiac nodal cells spontaneously depolarize during diastole resulting in automaticity due to If channels
3) Cardiac myocytes are electrically coupled to each other by gap junctions (like in the uterus during birth). |
|
|
Term
| How does a pacemaker cell AP in the SA/AV nodal cells differ form a ventricular AP? |
|
Definition
Basically, Na+ regulates slow, spontaneously depolarization in pacemaker cells, and controls rapid depolarization upstroke in ventricular cells (which is controlled by calcium channels in pacemaker cells)
1) In Phase 0, upstroke is due to VG Ca2+ channels, producing a slow conduction velocity used by AV node ot prolong transmission (vs. rapid VG-Na channels in skeletal)
- Na channels are inactivated, since Vm is higher
2) No phase 1/2 re-polarization/plateaus (vs. ventricular, where Ca+ and K+ balance each other to give rise to plateau)
3) Inactivation of Ca2+ channels and increased activation of K+ channels in phase 3 is similar
4) Phase 4: Slow diastolic depolarization as Na+ conductance spontaneously inreases (If vs. INa) |
|
|
Term
| What feature of the pacemaker cells determines HR and how is it manipulated by ACh/adenosine and Catecholamines? |
|
Definition
1) Slope of phase 4 of the AP (slow, spontaneous increases in Na+ conductance) determines HR
2) ACh/adenosine decrease the rate of diastolic depolarization, and decrease HR
3) NE/Epi increase diastolic depolarization rate and increase HR
**Symp stimulation increases chane the If channels are open in phase 4** |
|
|
Term
EKGs are important tools for cardiac diagnosis. What does each component indicate?
1) P wave
2) PR interval
3) QRS complex
4) QT interval (beginning of Q to end of T)
5) T wave
6) ST segment
7) U wave |
|
Definition
1) Atrial depolarization
2) Condition delay through AV node (<200 msec)
- prolonged in AV block
3) Ventricular depolarization (normally <120msec)
4) Mechanical contraction of ventricles
5) Ventricular repolarization
- Inversion indicates MI
6) Isoelectric, ventricles depolarized
7) Caused by hypokalemia, bradycardia |
|
|
Term
Describe the pathway of conduction in the heart that is measured by EKG.
Which system has the fastest conduction speed? Which is the best pacemaker? |
|
Definition
- Speed of conduction: Purkinje > atria> ventricles> AV node
- Pacemeakers: SA> AV> BOH/Purkinje/ventricles
- Pathway
SA node (RA)...AV node...Bundle of His...
-Right bundle branch (supplies Purkinje system)
-Left bundle branch (left anterior and posterior Fascicles |
|
|
Term
| What is the function of the AV nodal delay of 100 msec during cardiac contraction? |
|
Definition
Enables ventricular filling!
If it is disrupted, then you will decrease pre-load, contractility (starling) and SV |
|
|
Term
| What is Torsades de pointes, why is it dangerous and what are the predisposing factors? |
|
Definition
Ventricular tachycardia characterized by shifting sinusoidal waveforms on ECG.
Danger is V-fib and anything that lengthens QT interval (mechanical contraction) can cause it.
QT prolongation
- Congenital (defects in cardiac Na or K channel)
- Drugs (class 1A/sodium and class III/K anti-arrhythmics |
|
|
Term
What are Jervell and Lange-Nielsen syndromes?
Why are they of cardiac concern? |
|
Definition
AR syndromes that present with sensorineural deafness and involve mutations is cardiac Na+ and K+ channels that cause congenital QT prolongation (worry for Torsades and V-fib)
Give a beta blocker |
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Term
What type of EKG tracing is described by each of the following and how would you treat?
1) Chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between irregularly space QRS complexes
2) Rapid succession of identical, back-to-back atrial depolarization waves that look like "sawtooth" patterns
3) PR interval >200 ms with regular distribution and no symptoms
4) Progressive lengthening of PR interval with "Dropped" beats that is usually asymptomatic
5) Dropped beats with no change in PR interval, with 2 P waves for every QRS response
6) Atria and ventricles beat independently with present, unrelated P and QRS complexes |
|
Definition
1) Atrial fibrillation- atrial stasis and stroke
- Treat with beta-blocker, calcium channel blocker or digoxin and give Warfarin prophylaxis.
2) Atrial flutter- get them back in sinus rhythm
- 1A , 1C or III anti-arrhythmics or Beta blockers
3) 1st degree AV block
4) 2nd degree Mobitz type 1 AV block
5) Second degree Mobitz type 2 AV block
- May progress to 3rd degree
6) Complete AV block (lymes disease)
- Pacemaker |
|
|
Term
| How do you treat the bacteia that is associated with complete AV heart block? |
|
Definition
| Lyme's- Borrelia burdorferi- Doxicycline (tetracycline) |
|
|
Term
| What is the natural function of ANP? What does it do in the kidney? |
|
Definition
Released from atria in response to increased blood volume and atrial pressure, causing generalized vascular relaxation (cGMP)
- Contracts efferent arteriole and relaxes afferent arterioles, increasing GFR, promoting diuresis and contributing to "escape from aldosterone" mechanism. |
|
|
Term
The aortic arch and carotid sinus contain receptors that respond that are important for homeostatic regulation.
What are these and how do they work? |
|
Definition
Baro and Chemoreceptors to maintain BP and HR
1) Aortic arch transmits via CN X to medulla (responding ONLY to increased BP)
2) Carotid sinus send via CN IX to solitary nucleus of medulla (decreased and increased BP) |
|
|
Term
| Describe how baroreceptors respond to changes in BP. What is a 'carotid massage"? |
|
Definition
In aortic arch and carotid body (internal carotid artery)- critical for hemoorhage.
1) Hypotension (stretch signals are inhibitory)
- decreased arterial pressure leads to decreased stretch, which decreases the afferent baroreceptor firing to the brain
- Efferent sympathetic firing increases and parasympathetic decreases, leading to vasoconstriction, increased HR, contractility and BP
2) Carotid massage
- Increased pressure in the carotid artery with signal increased stretch to the solitary nucleus of the medulla, leading to decreased HR and BP. |
|
|
Term
| How do central chemoreceptors differ from peripheral chemoreceptors? |
|
Definition
1) Peripheral (carotid and aortic bodies)
- Respond to decreased pO2 (<60 mmHg), increased PCO2 and decreased blood pH
2) Central
- Respond to changes in pH and PCO2 of brain interstitial fluid, which are influence by CO2 (NOT directly by PO2) |
|
|
Term
| What is the "Cushing reaction" to increased intracranial pressure? |
|
Definition
Cushing triad: Bradycardia, Hypertension and Respiratory depression (Baroreceptor mediated)
Constriction of arterioles in brain leads to cerebral ischemia.
- Hypertensive response to ischemia leads to reflex Bradycardia and respiratory depression |
|
|
Term
| How is CO distributed between the liver, kidney and heart? |
|
Definition
1) Liver gets largest systemic CO (portal vein and hepatic artery)
2) Kidney gets highest BF per gram of tissue (not medulla or PCT)
3) Heart gets largest AV O2 difference, because O2 extraction is always 100% |
|
|
Term
True or False:
Increased O2 demand by the heart is met by increasing O2 saturation |
|
Definition
False- it is already 100%!
You increase coronary blood flow with SV |
|
|
Term
| What is pulmonary capillary wedge pressure and what does it indicate? |
|
Definition
Measured by swan-ganz catheter in pulmonary artery and estimates left atrial pressure- should be < 12
In mitral stenosis, PCWP > LV diastolic pressure |
|
|
Term
| What are the "normal" pressure values in the chambers of the heart? |
|
Definition
1) RA- <5
2) RV- 25/5
3) PA- <25/10 (estimates LAP)
4) LA- <12
5) LV- 130/10
6) Aorta- 130/90 |
|
|
Term
Autoregulation allows blood flow to an organ to remain constant cover a wide range of perfusion pressures.
What factors determine auto-regulation in the following organs?
1) Heart
2) Brain
3) Kidneys
4) Lungs
5) Skeletal muscle
6) Skin |
|
Definition
1) Local metabolites- O2, adenosine, NO
2) Local metabolites- CO2 (pH)
3) Myogenic and tubuloglomerular feedback (Cl-)
4) Hypoxia causes vasoconstriction
5) Local metabolites- lactate, adenosine, K+
6) Sympathetic stimulation- temperature control |
|
|
Term
| What is the only organ system where hypoxia causes vasoconstriction? |
|
Definition
| The lungs, where only well-ventilated areas are perfused (shunting) |
|
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Term
Starling forces determine fluid movement through a capillary membrane.
Describe how net filtration is determined and what forces are at play. |
|
Definition
There is capillary and interstitial pressures (osmotic and hydrostatic)
Filtration or Pnet= Kf [(Pc-Pi) - {Oc - Oi)], where Kf is a filtration constant for capillary permeability.
So increasing the capillary hydrostatic pressure or decreasing the interstitial hydrostatic pressure would both cause blood to flow from capillary to interstitum |
|
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Term
What are the major features of the most common cause of right-to-left shunting and "early cyanosis"?
How can patients with this condition limit symptoms with a simple maneuver? |
|
Definition
Tetralogy of Fallot form Anterosuperior displacement of infundibular septum
1) Pulmonic stenosis
2) RVH
3) Overiding aorta
4) VSD
Knees to chest squat: Pulmonic stenosis increases TPR and causes RVH and right-to-left shunting across VSD.
Squatting compresses femoral arteries, increases TPR and limits right-to-left shunt by directing more blood to RV |
|
|
Term
Congenital rubella infections are known to cause heart defects.
What is the associated heart defect and what other symptoms do they present with? |
|
Definition
1) Sensorineural deafness (58% of patients)
2) Eye abnormalities
—especially retinopathy, cataract and microphthalmia (43% of patients)
3) Congenital heart disease
- especially patent ductus arteriosus (50% of patients) |
|
|
Term
Angina is chest pain due to ischemia from CAD narrowing >75%
What are 3 types of angina and their characteristic EKG findings? |
|
Definition
1) Stable- retrosternal chest pain on exertion
- ST depression
2) Unstable- At rest, with thrombosis, but not necrosis (vs. MI)
- ST depression
3) Prinzmetal's- coronary vasospasm
- ST elevation |
|
|
Term
Patient presents with diaphoresis, nausea, vomiting, severe retrosternal pin and shortness of breath.
What are the 3 most common locations of an acute MI and how does it evolve at the following time points?
1) 0-4h
2) 4-12h
3) 12-24h
4) 2-4d
5) 5-10d
6) 7 weeks |
|
Definition
LAD > RCA > CFX (coronary occlusion)
1) No gross or LM changes, but arrythmia risk
2) Pale infarct grossly with tetrazolium stain
- LM shows coagulative necrosis, edema, hemorrhage and wavy fibers.
3) Contraction bands and release of necrotic debris into blood
- PMNs begin to migrate
4) Extensive coagulative necrosis with acute inflammatory infiltrate around infarct
- Gross evidence of hyperemia
5) Granulation tissue appears at margions of necrosis with central yellow-brown softening grossley (Free wall rupture, atamponade, papillary muscle rupture, IV septal rupture due to phages that have eaten structural components).
6) Gray-white scar complete and risk of ventricular aneurysm |
|
|
Term
When do you see each of the following during the evolution of an anterior wall MI?
1) Contraction band necrosis
2) Granulation tissue and papillary muscle rupture risk
3) Neutrophil emigration with extensive coagulative necrosis
4) Hemorrhage with wave fibers and early signs of necrosis |
|
Definition
1) 12-24h
2) 5-10d
3) 2-4d
4) 4-12h |
|
|
Term
What are the commonly used markers for diagnosis of an MI and when do they show up temporally?
What is the gold standard of diagnosis in the 1st 6 hours? |
|
Definition
CKMB, Troponins and AST
**In 1st 6 hours, EKG is gold standard**
- ST elevation (transmural infarct), ST depression (subendocardial infarct) and pathologic Q waves (transmural)
1) Troponin 1: 1st 4 hours and elevated for 7-10 days (more specific)
2) CK-MB: Arises in first hours, but goes away after 1-2d (re-infarction)
3) AST: non-specific |
|
|
Term
| What EKG findings would suggests a sub-endocardial infarction vs. a transmural infarct? |
|
Definition
1) Sub-endocardial
- ST depression
- ISchemic necrosis of <50% of ventricular wall
2) Transmural
- ST elevation and Pathological Q waves
- Increased necrosis |
|
|
Term
How can you localize an MI using the pathological Q waves in the following leads?
1) V1-V4
2) V1-V2
3) V4-V6
4) I, aVL
5) II, III, aVF |
|
Definition
1) Anterior wall (LAD)
2) Anteroseptal (LAD)
3) Anterolateral (LCX)
4) Lateral wall (LCX)
5) Inferior wall (RCA) |
|
|
Term
| What are the important MI complications? |
|
Definition
1) Arrythmia- 1st few days/common cause of death before reach hospital
2) LV failure and Pulmonary edema
3) Cardiogenic shock (high risk)
4) Ventricular free wall rupture (tamponade); papillary muscle rupture (mitral regurgitation) and IV septal rupture (VSD)
5) Aneurysm- decreased CO, arrhythmia and embolus from mural thrombus
6) Post-infarct fibrinous necrosis- friction rub (3-5 d post-MI)
7) Dressler's- autoimmune fibrinous pericarditis (several weeks post-MI) |
|
|
Term
| What kind of infarct pre-disposes to severe mitral regurgitation? |
|
Definition
| RCA infarct of posteriomedial papillary muscle of mitral valve. |
|
|
Term
| What is Dressler's syndrome? |
|
Definition
| Post-MI autoimmune fibrinous pericarditis (weeks after, vs. friction rub that occurs 3-5d post-infarct) |
|
|
Term
| What are the common causes of Dilated (congestive) cardiomyopathy? |
|
Definition
Systolic failure due to eccentric hypertrophy (sarcomeres added in series) with S3 heart sound and dilated heart on US, with balloon appearance on chest x-ray
ABCCCD
1) Alcohol
2) Beriberi (wet thiamine deficiency)
3) Coxsackie B virus myocarditis
4) Cocaine
5) Chagas (T. cruzi)
6) Doxorubicin toxicity
**Also peripartum cardiomyopathy and hemochromatosis** |
|
|
Term
Which fo the following does NOT cause dilated congestive heart failure?
1) Coxsackie B virus
2) T. cruzi
3) Friedreich's ataxia
4) Thiamine deficinecy
5) Doxorubicin |
|
Definition
3- AD trinucleotide repeat (GAA) disorder associated with hypertrophic cardiomyopathy, where IV septum is "too close" to mitral valve leaflet and causes outflow obstruction.
- You would hear an S4 heart sound and see disoriented, tangled, hypertrophied myocardial fibers. |
|
|
Term
Young athlete suddenly drops dead on the basketball court.
A month before, you had detected an S4 heart sound on exam and a systolic ejection murmor, but had failed to follow up since.
What happened and how should you have treated? |
|
Definition
Hypertrophic cardiomyopathy: IV septum is thickened and too close to mitral valve leaflet, leading to outflow tract obstruction (ejection murmur) and syncopal episodes.
Beta blockers of non-dihydropyridine calcium channel blockers (verapamil) would have worked. |
|
|
Term
| What are the 3 major types of cardiomyopathy and how can you distinguish between them? |
|
Definition
1) Dilated (congestive)- Systolic duysfunction with eccentric hypertophy do to virus (coxsackie), parasitic (T. cruzi), drugs, ect.
- S3 with dilated heart on US and balloon appearance on CXR.
2) Hypertrophic- Diastolic failure with concentric hypertrophy that presses IV septum on mitral valve leaflet and obstructing out flow tract
- S4 and systolic ejection murmor with episodes of syncope/sudden death in young athletes.
3) Restrictive/olbliterative
- Diastolic dysfunction from sarcoidosis, amyloidosis, post-radiation fibrosis, endocardial fibroelastosis, Loffler's syndrome (endomyocardial fibrosis with prominent eosinophilic infiltrate) and hemochromatosis (dilated cardiomyopathy also possible) |
|
|
Term
| How can someone end up with restrictive cardiomyopathy? |
|
Definition
Diastolic dysfunction from
1) Sarcoidosis
2) Amyloidosis
3) Post-radiation fibrosis
4) Endocardial fibroelastosis
5) Loffler's syndrome (endomyocardial fibrosis with prominent eosinophilic infiltrate)
6) Hemochromatosis (dilated cardiomyopathy also possible) |
|
|
Term
| What syndrome causes restrictive cardiomyopathy in kids with an eosinophillic infiltrate? |
|
Definition
| Loffler's syndrome (endomyocardial fibrosis with prominent eosinophilic infiltrate)- Diastolic failure |
|
|
Term
Patient presents with DOE, fatigue, edema and pulmonary rales.
What drugs are known to reduce mortality associated with this condition? Which drugs are purely sympomatic? |
|
Definition
CHF= inherited or acquired
1) ACE-i, beta blockers, ARBs and Spironolactone reduce mortality
2) Thiazide/Loop diuretics and nitrates are used for symptomatic releaf |
|
|
Term
| Why do patients with CHF get cardiac dilation and DOE? |
|
Definition
1) Dilation
- greater ventricular end-diastolic volume (loss of SV)
- S3 heart sound
2) DOE
- Failiure of CO to increase adequately during exercise because of SV limitation |
|
|
Term
| How does LHF give rise to RHF in CHF? |
|
Definition
Isolated heart failure is rare, and due to Cor Pulmonale (chronic high pressures in PA/RV)
1) Decreased LV contractility leads to pulmonary venous congestion (edema)and decreased CO
**Congestion decreases RV output, which causes peripheral edema as well**
2) Decreased CO activates the RAAS system (directly and via sympathetic baroreceptor response), leading to renal Na+/H2O reabsorption and an increase in LV contractility, which increases pre-load and CO to compensate
3) Volume expansion increases systemic venous pressure, which increases RV pre-load and causes it to work harder and hypertrophy (with RAAS increasing PA pressure) |
|
|
Term
LHF and RHF have characteristic symptoms and signs.
What is the basis for each? |
|
Definition
1) LHF
- Pulmonary edema- Low LV contractility causes pulmonary venous congestion, which leads to distention and transudation
- PND is also caused by edema
- Orthopnea (dyspnea when supine): Increased venous return in supine position exacerbates venous congestion
2) RHF
- Hepatomegaly: Increased central venous pressure leads to increased resistance to portal flow
- Ankle/sacral edema: Increased venous pressure leads to transudation
- JVD: Venous pressure |
|
|
Term
Patients with bacterial endocarditis present with a number of symptoms/signs.
What is the most common location and what are the symptoms/signs? What about IV drug users? |
|
Definition
1) Mitral valve
2) Tricuspid with IV drug use, with staph, pseudomonas and candida
3) Bacteria FROM JANE
- Fever
- Roth spot's (round white spots on retina surrounded by hemoorhage)
- Osler nodes (tender, raised lesions on fingers and toes)
- Murmur
- Janeway lesions (small erythematous lesions on palms or sole)
- Anemia
- Nail-bed hemorrhage (splinter)
- Emboli |
|
|
Term
What organisms are associated with the following lesions of bacterial endocarditis?
1) Large vegetations on previously normal valves with acute onset.
2) Small vegetations on congenitally abnormal or disease valves with insidious onset (Sometimes following dental procedure).
3) Tricuspid vegetations in an IV drug user.
4) Prosthetic valves
5) Colon cancer |
|
Definition
1) Staph aureus (high virulence)
2) S. viridans
3) Staph, Pseudomonas, Candida
4) S. epidermitis
5) S. bovis |
|
|
Term
Previously healthy patient presents with sudden-onset fever and signs of anemia.
You detect large vegetations on their mitral valve.
What complications are you concerned about? |
|
Definition
Size of lesions and previously normal valves points to Staph aureus.
Complications of bacterial endocarditis include chordae rupture, glomerulonephritis, suppurative pericarditis and Emboli.
Start penicillin or vanco for MRSA |
|
|
Term
| What are the non-bacterial causes of heart valve endocarditis? |
|
Definition
1) Malignancy
2) Hypercoagulability (factor V, AT deficiency, prothrombin variant)
3) SLE (marantic.thrombotic endocarditis) |
|
|
Term
Which of the following is NOT associated with bacterial endocarditis?
1) Nail-bed hemorrhages
2) White spots on retina with surrounding hemorrhage
3) Raised, tender lesions on finger or toe pads
4) Sub-cutaneous nodules
5) Small erythematous lesions on palms or soles |
|
Definition
Need multiple blood cultures for diagnosis!
4- This is one of Jone's criteria for Rhuematic fever (Sub Q nodules, erythema marginatum, chorea, polyarthritis, carditis)
Bacteria FROM JANE
1) Fever
2) Roth spots (retina)
3) Osler nodes (tender lesions on finger)
4) Murmur
5) Janeway lesions (erythematous lesions on palms/soles)
6) Anemia
7) Nail-bed (splinter) hemorrhages
8) Emboli |
|
|
Term
What is the organism that causes Rheumatic heart disease?
What are the features? |
|
Definition
Pharyngeal infection with group A strep can cause early death (myocarditis) or late sequele with rheumatic heart disease that involves type II hypersensitivity with antibodies against M protein (mitral > aortic >>tricupsid)
FEVERSS
- fever
- erythemia marginatum
- valve damage (vegetation and fibrosis)
- ESR increased
- Red-hot joints (migratory polyarthritis)
- Sub-Q nodules
- St. Vitus' dance (chorea) |
|
|
Term
What are Anitschkow's cells and Aschoff bodies and when are they seen?
What is the diagnostic criteria for this condition? |
|
Definition
Rheumatic heart disease
1) Anitschkow's cell: Activated histiocytes
2) Aschoff body (granuloma with giant cell)
3) Jone's criteria
- Chorea
- Migratory polyarthritis
- Erythema marginatum
- Sub-q nodules
- Valve damage (vegetation and fibrosis) |
|
|
Term
| What are the early and late lesions of rheumatic heart disease and how might you detect them clinically? |
|
Definition
1) Early is mitral regurgitation
- Pan-systolic murmor and apex
2) Late is mitral stenosis
- Diastolic rumble murmor |
|
|
Term
| True or False: Rheumatic fever is a type IV hypersensitivity type pathology |
|
Definition
False! Type II (anti-M protein antibodies against group A strep)
Type IV is like PPD, and is cell-mediated |
|
|
Term
| Which valve is most affected by rheumatic heart disease? What about bacterial endocarditis? |
|
Definition
Both are mitral valve!
RHD- Mitral > Aortic >>> Tricuspid
BE- Mitral, Tricuspid (IV drug users) |
|
|
Term
Patient presents with new, sudden onset sharp chest pain that is aggravated by inspiration and relieved by sitting up and leaning forward.
What is on your differential? |
|
Definition
Acute pericarditis
1) Fibrinous- Post-MI (3-5 days) or autoimmune Dressler's (weeks)
- Pericardial friction rub
2) Serous- RA, SLE
- Look for signs of autoimmunity
3) Suppurative/purulent
- Infectious etiology, possibly following endocarditis. |
|
|
Term
Why might you observe a systolic BP that decreases in amplitude > 10mmHg during inspiration in a patient who is hypotensive with a rapid HR and distant heart sounds?
What other signs are associated with this condition? When else can you detect the abnormal pulse finding? |
|
Definition
Cardiac Tampenade: fluid compression of heart in pericardium leading to decreased CO and equilibration of diastolic pressures in all 4 chambers
1) Tampenade
- Hypotension
- Increased venous pressure (JVD)
- Distant heart sounds
- Increased HR
- Pulsus paradoxus.
2) Pulsus paradoxus
- OSA, pericarditis, asthma and croup |
|
|
Term
| Why might the aorta have a "tree bark" like appearance? |
|
Definition
Calcification of root and ascending arch due to Tertiary syphillus.
Vasa vasorum of aorta is disrupted, causing dilation or aorta and valve ring.
Can cause aneurysm of ascending aorta or arch and aortic valve incompetence (regurgitation) |
|
|
Term
| Why might you hear a diastolic murmur at the right upper sternal border in a patient with long-standing syphillis? |
|
Definition
Obstruction of vasa vasorum in tertiary syphillus leading to dilation of ascending aorta and arch, as well as valve ring dilation, which would produce a regurgitation murmor.
Aneurysms of ascending aorta and arch are also common! |
|
|
Term
| What kinds of tumors can be found in the heart? |
|
Definition
Kussmaul's sign: Increase JVP on inspiration (not specific)
1) Myxoma (most common)
- 90% are in atria (mostly LA)
- "Ball-valve" obstruction in LA associated with syncopy
2) Rhabdomyoma (most common primary in children)
- Tuberous sclerosis
3) Metastasis from melanoma/lymphoma |
|
|
Term
True or False:
The major concern with varicose veins is thromboembolism. |
|
Definition
False- Rare compared to Deep veins
These are tortuous superficial veins due to chronically increased venous pressure. They predispose to poor wound healing and varicose ulcers. |
|
|
Term
| What is the pathophysiology of Raynaud's disease? |
|
Definition
Decreased blood flow to fingers due to arterial vasospasm under conditions of cold or stress.
Associated with SLE, mixed connective tissue disease and CREST |
|
|
Term
| What are the major large, medium and small vessel vasculitities? |
|
Definition
1) Large
- Takayasu arteritis
- Temoporal(giant cell) arteritis
2) Medium
- Polyarteritis nodosa (HBV, P-ANCA)
- Kawasaki disease (coronary aneurysm in kids)
- Buerger's disease (Smoker's fingers fall off)
3) Small
- Wegener's (granulomas and c-ANCA)
- Polyangitis (no asthma, no granulomas and p-ANCA)
- Churg-Strauss (asthma, eosinophils and p-ANCA)
- Henoch shconlein purpura (IgA immune complex) |
|
|
Term
| What does "palpable purpura" indicate and what types of diseases are on the ddx? |
|
Definition
Immune complex, small vessel vasculitis
1) Henoch-Schonlein purpura (IgA)
- Follows URI, with palpable purpura on buttocks/legs, Arthralgia and GI symptoms
2) Polyarteritis nododosa (p-ANCA)
- Young adults with HBV
- Affects renal and visceral vessels, but NOT pulmonary
3) Microscopic polyangiitis
- No granulomas and p-ANCA +
- Pauci-immune glomerulonephritis
4) Churg-strauss
- P-ANCA, eosiniphilia and granulomas in an asthmatic with Pauci-immune reaction |
|
|
Term
How would you treat each of the following vasculitities based upon pathology/lab values provided?
1) Focal granulomatous inflammation with increased ESR presenting as a unilateral headache and jaw claudication
2) Young adult with hep B presents with fever, weight loss, headache and abdonominal pain/melena. Pathology shows immune complexes in the renal and visceral vessels with transmural lesions and fibrinoid necrosis (lesions of different ages)
3) 3 year old asian male presents with fever, lymphadenitis, red lips/oral mucosa, hand-foot erythemia and you are worried about coronary aneurysms.
4) Focal necrotizing vasculitis with granulomas in the lung and upper airway, as well as signs of necrotizing glomerulonephritis. |
|
Definition
1) Temporal arteritis (giant cell)
- Treat with high-dose steroids immediately to prevent irreversible blindness
- Associated with PMR
2) Polyarteritis nodosa (p-ANCA)
- Spares pulmonary vessels
- Corticosteroids and cyclophosphamide
3) Kawasaki disease with "Strawberry tongue"
- IV IG and aspirin (prevent MI)
4) Wegener's (Lung, Kidney and Upper respiratory tract. C-ANCA)
- Cyclophosphamide and steroids |
|
|
Term
How would you treat each of the following vasculitities based upon pathology/lab values provided?
1) 35 year old heavy smoker presents with intermittent claudication and evidence of Raynaud's phenomenon. You are worried about amputation risk because of a path specifim with segmental thrombosing vasculitis
2) Glomerulonephritis and palpable pupura with + P-ANCA and without granulomatous inflammation.
3) 38 year old asian female with absent upper extremity pulses, fever, night sweats and ocular disturbances. She has an increased ESR. You order a biopsy of the aortic arch.
4) Child presents with palpable purpura on his buttocks and legs, with arthralgia and GI disturbances. |
|
Definition
1) Buerger's disease (thromboangiitis obliterans)
- Smoking cessation
2) Microscopic polyangiitis
- Steroids
3) Takayasu arteritis
- Granulomatous thickening of aortic arch, proximal to great vessels
4) Henoch-schonlein purpura (most common childhood vasculitis)
- IgA association |
|
|
Term
What is the major pathological/laboratory finding of the following forms of vasculitis?
1) Giant cell arteritis
2) Takayasu arteritis
3) Polyarteritis nodosa
4) Kawasaki disease
5) Thromboangiitis obliterans
6) Wegener's granulomatosis
7) Churg-strauss syndrome
8) Microscopic polyangiitis
9) Henoch-schonlein purpura. |
|
Definition
1) Increased ESR with focal granulomatous inflammation of branches of the carotid artery (unilateral headache and jaw claudication with blindness worry)
2) Increased ESR with granulomatous thickening of aortic arch proximal to great vessels
3) Immune complex mediated transmural lesions of various ages in the renal and visceral arteries (not pulmonary), with fibrinoid necrosis and multiple aneurysms
4) Young asian child with coronary aneurysms and strawberry tongue
5) Smoker's disease with segmental thrombosing vasculitis of distal digits
6) Necrotizing granulomatous infection of Upper respiratory tract, kidney and lungs with C-ANCA
7) Granulomatous vasculitis with Asthma, P-ANCA and Eosinophilia (palpable purpura)
8) Pauci immune glomerulonephritis and palpable purpura: P-ANCA and no granulomas
9) IgA complexes in skin (same age, vs. polyarteritis nodosa), with arthralgia and GI symptoms |
|
|
Term
| What congenital vascular disorder affects capillary-sized blood vessels with port-wine stain on face, ipsilateral AVM, seizures and early-onset glaucoma? |
|
Definition
Sturge-Weber disease
1) Port wine stain (Nevus flammeus)
2) Ipsilateral leptomeningeal angiomatosis
3) Seizures
4) Early-onset glaucoma |
|
|
Term
What vascular tumor is described by each of the following?
1) Benign capillary hemangioma of infancy that appears in first few weeks of life, grows rapidly and then regresses at 5-8 years.
2) Benign capillary hemangioma of elderly that does not regress
3) Polypoid capillary hemangioma that can ulcerate and bleed and is associated with both trauma and pregnancy.
4) Cavernous lymphangioma of the neck that is associated with turner's syndrome
5) Benign painful, red-blue tumor under fingernails that arises from modified smooth muscle cells of glomus body |
|
Definition
1) Strawberry hemangioma
2) Cherry hemangioma
3) Pyogenic granuloma
4) Cystic hygroma
5) Glomus tumor |
|
|
Term
What vascular tumor is described by each of the following?
1) Benign capillary skin papules found in AIDS patients caused by Bartonella henselae infections (mistaken for Kaposi's)
2) Highly lethal malignancy of liver associated with vinyl chloride, arsenic and ThO2 (Thorotrast) exposure
3) Lymphatic malignancy associated with persistent lymphedema (e.g. post-radical mastectomy)
4) Endothelial malignancy of skin associated with HHV-8 and HIV (mistakin for bacillary angiomatosis) |
|
Definition
1) Bacillary angiomatosis
2) Angiosarcoma
3) Lymphangiosarcoma
4) Kaposi's sarcoma |
|
|
Term
| What benign skin lesion in AIDS patients is often mistaken for a dangerous endothelial malignancy? |
|
Definition
| Bacillary angiomatosis is caused by B. henselae infections and is mistaken for Kaposi's sarcoma (HHV-8) |
|
|
Term
Name that vasculitis.
1) P-ANCA
2) C-ANCA
3) Pulseless disease
4) Raynaud's and heavy smoking
5) Upper respiratory tract with granulomas
6) Follows URI with skin involvement and arthralgia/GI
7) MI in kids |
|
Definition
1) Polyarteritis nodosa (HBV), Churg-strauss (eosinophils, asthma and granulomas), and Microscopic polyangiitis (glomerulonephritis and no granulomas)
2) Wegeners
- Upper respiratory, lungs and kidney
3) Takayasu
- Increase ESR and granulomatous thickening of aortic arch in asian females
4) Buerger's (thromboangiitis obliterans)
5) Wegener's
6) Henoch-shonlein purpura (IgA)
7) Kawasaki disease (conorary aneurysms) |
|
|
Term
| What drugs should be used for essential hypertension? |
|
Definition
1) Diuretics
2) Ace inhibitors
3) ARBs
4) Calcium channel blockers |
|
|
Term
| What anti-hypertensives should be used cautiously in compensated CHF and avoided in cardiogenic shock? |
|
Definition
|
|
Term
| What are the treatments of choice for diabetic hypertension? |
|
Definition
Ace-inhibitors and ARBs
Calcium channel blockers, diuretics, beta blockers and alpha blockers will work as well |
|
|
Term
What is the mechanism of action and major toxicities associated with each of the following drugs?
1) 1st line in hypertension in pregnancy (given with methyldopa)
2) Given for Prinzmetal's angina
3) Short-acting vasodilators used for malignant hypertension |
|
Definition
1) Hydralazine (also good for severe hypertension and CHF, and given with beta blocker to prevent reflex tachycardia)
- Increases cGMP for smooth muscle relaxation (arterioles > veins) to reduce afterload
- Compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, lupus-like
2)Calcium channel blockers
- Block L-type calcium channels in cardiac and cmooth muscle to prevent contracitility (Verapamil for heart and Nifedepine for vascular smooth muscle)
- Cardiac depression, AV block, peripheral edema, flushing, dizziness and constipation.
3a) Nitroprusside
- Increase cGMP via release of NO
- Cyanide toxicity
3b) Fenoldopam
- D1 receptor agonist to relax renal vascular smooth muscle
3c) Dizoxide
- K+ channel opener and causes hyperglycemia |
|
|
Term
Malignant hypertension occurs most frequently in blacks and can cause hyperplastic arteriolosclerosis.
What drugs are used to treat it and what are their associated toxicities? |
|
Definition
1) Nitroprusside
- Increase cGMP via release of NO
- Cyanide toxicity
2) Fenoldopam
- D1 receptor agonist to relax renal vascular smooth muscle
3) Dizoxide
- K+ channel opener and causes hyperglycemia |
|
|
Term
Which calcium channel blockers are used most effectively to block cardiac tissue? What about vascular smooth muscle?
What are their toxicites? |
|
Definition
Used for HTN, prinzmetal's angina, angina, arrythmias (NOT nifedipine) and Raynaud's
1) Heart= Verapamil >Diltiazem> Nifedipine
2) VSM= Nifedipine > DIltiazem > Verapamil
3) Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation |
|
|
Term
| When is Hydralazine commonly given and why is it given with a beta blocker? |
|
Definition
Increase cGMP and smooth muscle relaxation (arterioles > venules for afterload reduction)
1) HTN in pregnancy with methyldopa
2) Prevent reflex tachycardia (this is why you don't give hydralazine in angina/CAD) |
|
|
Term
| Which drugs increase cGMP preferentially in arterioles? What about venules? |
|
Definition
1) Hydralazine for Arterioles
- afterload reduction for CHF and hypertension in pregnancy
2) Nitroglycerin, Isosorbide dinitrate for Venules
- Pre-load reduction for angina, pulmonary edema and sex |
|
|
Term
| What is "Monday disease" and what cardiovascular drug does it relate to? |
|
Definition
| Patients on Nitroglycerine or Isosorbide dinitrate venodilators for Angina or Pulmonary edema sometimes develop tolerance for the drug during the week and then lose it over the weekend and get reflex tachycardia, headache, flushing and hypotension |
|
|
Term
The goal in anti-anginal therapy is to reduce myocardial O2 consumption (MVO2) by decreasing 1 or more of its determinants.
What are these determinants and how do Nitrates affect each of them? |
|
Definition
Nitrates= cGMP-mediated decrease in pre-load
1) EDV (Decrease)
2) BP (Decrease)
3) HR (Increase-reflex)
4) Contractility (Increase-reflex)
5) Ejection time (Decrease)
**HR and Contractile will return to normal or decrease with addition of beta blocker ** |
|
|
Term
The goal in anti-anginal therapy is to reduce myocardial O2 consumption (MVO2) by decreasing 1 or more of its determinants.
What are these determinants and how do Beta blockers affect each of them? |
|
Definition
Beta blockers decrease afterload
1) EDV (increase)
2) BP (Decrease)
3) HR (Decrease)
4) Contractility (Decrease)
5) Ejection time (Increase)
Ejection time and EDV will be normalized with addition of nitrate |
|
|
Term
| How do the calcium channel blockers Nefedipine and Verapamil affect MVO2 in relation to beta blockers and nitrates? |
|
Definition
1) Nifedipine behaves like Nitrates
- Decrease EDV, BP, Ejection time and MVO2
- Increase contractility and HR
2) Verapamil behaves like beta blocker
- Decrease BP, contractility, HR and MVO2
- Increase EDV and ejection time |
|
|
Term
| Which beta blockers are contraindicated in angina and why? |
|
Definition
Pindolol and Acebutolol are partial beta-agonists
Need to DECREASE MVO2 |
|
|
Term
How do HMG-CoA reductase inhibitors like Lovastatin and Simvastatin reduce lipid levels?
How do they affect LDL, HDL and triglycerides, respectively?
What are the side effects? |
|
Definition
1) Inhibit cholesterol precursor, mevalonate
2) Lower LDL a lot, increase HDL slightly and decrease TG slightly
3) Hepatotoxicity, Rhabdomyolysis (both are rare) |
|
|
Term
How does Niacin reduce lipid levels?
How does it affect LDL, HDL and triglycerides, respectively?
What are the side effects? |
|
Definition
1) B3 Inhibits lipolysis in adipose tissue, reducing hepatic VLDL secretion into circulation
2) Decreases LDL, Increases HDL (> Statins) and decreases TG slightly
3) Red, flushed face (reduced by aspirin)
- Long term use, Hyperglycemia acanthosis nigricans- visceral malignancy) and Hyperuricemia (gout) |
|
|
Term
How do bile acid resins like Cholestyramine, colestipol and colesevelam reduce lipid levels?
How do they affect LDL, HDL and triglycerides, respectively?
What are the side effects? |
|
Definition
1) Bind BA and prevent intestinal reabsorption, forcing liver to use cholesterol to make more.
2) Decrease LDL, slightly increase HDL and TG
3) Tastes bad and causes GI discomfort, with decreased ADEK absorption and cholesterol gallstones |
|
|
Term
How do does Ezetimibe lower lipid levels?
How does it affect LDL, HDL and triglycerides, respectively?
What are the side effects? |
|
Definition
1) Cholesterol absorption blockers in small intestine brush border
2) Lowers VLDL only
3) Rare increase in LFT's |
|
|
Term
How do Fibrates like gemfibrozil, clofibrate, bezafibrate and fenofibrate reduce lipid levels?
How do they affect LDL, HDL and triglycerides, respectively?
What are the side effects? |
|
Definition
1) Upregulate LPL to increase TG clearance
2) Decrease VLDL slightly, increase HDL slightly, Dramatically lower TG
3) Myositis, hepatotoxicity and cholesterol gallstones. |
|
|
Term
Which lipid-lowering agents are the best at each of the following?
1) Decreasing VLDL
2) Increasing HDL
3) Decreasing Triglyceride |
|
Definition
1) Statins (HMG-CoA reductase inhibitors)
2) Niacin (B3) which inhibits lipolysis in adipose tissue
3) Fibrates like Gemfibrozil and Clofibrate that up-regulate LPL |
|
|
Term
Cardiac glyclosides are used to increase contractility in CHF, and to decrease conduction at AV node and depression of SA node in A fib.
How do they work and what are their toxicities? |
|
Definition
Digoxin- 75% bioavailable, 20-40% protein-bound and t 1/2 of 40 hours with urinary excretion.
1) Directly inhibit Na/K pump, leading to indirect inhibition of Na/Ca exchanger/antiport, leading to increased intracellular calcium, Inotropy and CN X stimulation
2) Cholinergic- nausea, vomiting, T-diarrhea
EKG: Increased PR, decreased QT, scooping, T wave inversion, arrhythmia, hyperkalemia |
|
|
Term
| How can you reverse Digoxin toxicity? |
|
Definition
Used for conractility in CHF and for AV conduction decrease in A fib
- Slowly normalize K+ (hyperkalemia)
- give Lidocaine
- cardiac pacer
- anti-dig Fab fragments
- Mg2+ |
|
|
Term
| What is Nesiritide and how is it used? |
|
Definition
- Recombinant B-type natriuretic peptide that causes increase in cGMP and vasodilation
- Used in Acute decompensated heart failure (when you avoid beta blockers)
- Watch out for hypotension |
|
|
Term
There are a number of anti-arrhythmic drugs. How do each of the following classes function and why are they used?
1) Class 1A
2) Class 1B
3) Class 1C
4) Class II
5) Class III
6) Class IV |
|
Definition
Class 1 drugs are Na+ channel blockers that are used as local anesthetics and to slow or block conduction. They decrease the slope of the phase O depolarization and increase the threshold for firing in abnormal pacemaker cells. They are "state dependent" and work on cells that are firing rapidly.
Class II drugs are Beta blockers
that decrease cAMP and Ca currents. They suppress abnormal pacemekaers by decreasing the slope of phase 4 and increase PR. They are used for V-tach, SVT, slowing ventrical rate during a fib and atrial flutter.
Class III drugs are K+ channel blockers that increase AP duration and ERP. They are second-line because they increase QT interval
- Class 4 drugs are calcium channel blockers that decrease conduction velocity and increase PR/ERP. They are used in prevention of nodal arrhythmias (SVT) |
|
|
Term
| What are the major class III anti-arythmics and what are their major toxicities? |
|
Definition
Remember to check PFTs, LFTs and TFTs when using amiodarone!
K IS BAD (K+ channel blockers)
Ibutilide, Sotalol, Bretylium, Amiodarone, Dofetilide
1) Sotalol (Torsades and excessive beta block)
2) Ibutilide (Torsades)
3) Bretylium (new arrythmias and hypotension)
4) Amiodarone (Pulmonary fibrosis, hepatotoxicity and hypothyroidism/hyperthyroidism because of iodine) |
|
|
Term
| What are the major side effects of using Amiodarone and an anti-arrythmic drug? |
|
Definition
All class III K+ channel blockers are second line because of QT prolongation, but Amiodarone is special (has Class I, II, III and IV effects).
Remember to check PFTs, LFTs and TFTs when using amiodarone!
1) Pulmonary fibrosis
2) Hepatotoxicity
3) Hypo/hyperthyroidism (40% iodine by weight) |
|
|
Term
Which class of anti-arythmic drugs does each of the following?
1) Decreases slope of phase 0 depolarization and increases threshold for firing
2) Decrease slope of phase 4 by decreasing cAMP/Calcium
3) Increase AP duration, ERP and QT interval
4) Decreases conduction velocity, increases ERP/PR interval |
|
Definition
1) Class 1- sodium channel blockers
2) Class II- beta blockers
3) Class III- K+ channel blockers
4) Class IV- Calcium channel blockers |
|
|
Term
| There are 3 sub-classes of sodium channel blockers that are used as anti-arythmics. What are they and what are their side effects? |
|
Definition
All can cause hyperkalemia!
1A) Quinidine, Procainamide and Disopyramide
- Can cause QT elongation
1B) Lidocaine, Mexiletine, Tocainide
- Useful in acute ventricular arrhytmias (especially post-MI) and in digitalis-induced arrhytmia
- Can cause CV/CNS depression
1C)Flecainide, Propafenone
- Last resort: Useful in V-tachs that progress to VF and in intractable SVT
- Pro-arythmic |
|
|
Term
| What anti-arrhythmics are good choices for acute ventricular arrhythmias post-MI and for digoxin-induced arrhytmias? |
|
Definition
Class 1B sodium channel blockers: Lidocaine, Mexiletine and Tocainide
They preferentially affect ischemic or depolarized purkinje and ventricular tissue |
|
|
Term
| How are Adenosine and Mg2+ used as anti-arrhythmics in CVD? |
|
Definition
1) Adenosine (short-acting)
**Drug of choice for diagnosing/abolishing supraventricular tachycardia**
- Increases K+ efflux, hyperpolarizing cell and decreasing intracellular calcium
- Can be blocked by Theophylline
2) Mg2+
- Effective in Torsades de pointes and digoxin toxicity. |
|
|
Term
| How do sodium channel blockers treat arrhythmias? |
|
Definition
Class 1a (Quinidine), 1b (Lidocaine) and 1c (Felcainamide) drugs
Decrease slope of phase 0 depolarization and increase threshold for firing in abnormal pacemaker cells (state-dependent action preferentially affects rapidly-firing cells) |
|
|
Term
What the are uses and contraindications of the following class 1 anti-arrythmics?
1) Procainamide
2) Lidocaine
3) Quinidine
4) Flecainide
5) Disopyramide
6) Mixelitine |
|
Definition
All cause Hyperkalemia
Class 1 means sodium channel blockers (decrease slope of phase 0 and raise threshold in active cells)
1) 1A- increase AP duration, ERP and QT interval
- Reversible SLE-like symptoms
- Torsades risk
2) 1B- Decrease AP duration and affect ischemic or depolarized Purkinje and ventricular tissue
- Used for post-MI and Digoxin-induced ventricular arrhythmia
- CNS/cardiac depression risk
3) 1A- Increase AP duration, ERP and QT interval
- Cinchonism (headache and tinnitus)
- Thrombocytopenia
- Torsades
4) 1C- No effect on AP duration
- Use in V tach that progresses to VF and in intractable SVT
- Last-resort for refractory tachyarrthmia (for patients with structural abnormality)
- Pro-arhythmic Post-MI
5) 1A - same as Quinidine and Procainamide
6) 1B- same as Lidocaine and Mixiletine |
|
|
Term
| What are the effects of class 1a, 1b and 1c anti-arrythmics on AP duration? |
|
Definition
Sodium channel blockers decrease phase 0 slope and increase threshold for firing.
1a= Quinidine, Procainamide, Disopyramid
- Increase AP duration and ERP, and increase QT
1b= Lidocaine, Mixiletine and Tocamide
- Decrease AP duration
1c= Flecainide and Propafenone
- No affect on AP duration |
|
|
Term
What short-acting beta blocker is used for V-tach and SVT.
Which one can cause dyslipidemia and how can you treat an overdose? |
|
Definition
Beta blockers decrease cAMP/Ca2+ and suppress abnormal pacemakers by decreasing phase 4 slope.
They cause impotence, exacerbation of asthma and CV/CNS depression
1) Esmolol is rapid-acting
2) Metoprolol gives dyslipidemia (give Glucagon) |
|
|
Term
| What aspect of the pacemaker action potential is impacted by each of the anti-arrythmic drug classes? |
|
Definition
1) Class 1 (sodium channel)
- Decrease phase 0 slope and raise threshold
- Variable effect on AP duration
2) Class 2 (beta blockers)
- Decrease phase 4 slope (resting spontaneous depolarization)
- Increase PR interval
3) Class 3 (K+ blockers)
- Decrease phase 3 (re-polarization) slope
- Increase AP duration, ERP and QT (last resort)
4) Class 4 (Ca+ channel blockers)
- Decrease Phase 0 and phase 3 slopes
- Decrease conduction velocity, increase ERP and PR interval |
|
|
Term
Which kind of anti-arrhythmic is each of the following?
1) Ibutilide
2) Verapamil
3) Esmolol
4) Quinidine
5) Mexiletine
6) Flecainide |
|
Definition
1) K+ channel blocker
- Ibutilide, Sotalol, Bretylium, Amiodarone, Dofetilide
2) Calcium channel blocker
- Verapamil and Diltiazam (Nefedipine not used in this case)
3) Rapid-acting beta blocker
- the "olols"
4) Class 1 a sodium channel blocker
- Quinidine, Procainamide, Disopyramide
5) Class 1b sodium channel blocker
- Lidocaine, Mexiletine, Tocainide
6) Class 1c sodium channel blocker
- Felcainide and Propafenone |
|
|
Term
| Which drugs are used to slow the ventricular rate during A fib and atrial flutter? |
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Definition
Beta blockers- Also used in V-tach and SVT
Esmolol is short-acting |
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Term
| What are the drugs of choice that are used int he prevention of nodal arrhytmias like SVT? |
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Definition
| Calcium channel blockers with work (Verapamil and Diltiazam) |
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