Wake Cardio

Front 1

What valves are open during systole?

Back 1

The aortic and pulmonary valves

Front 2

What valves are open during diastole?

Back 2

The tricuspid and mitral (bicuspid) valves

Front 3

What is the steady state equilibrium voltage for a myocyte

Back 3

-90 mV

Front 4

What ion is passively leaking out of the all myocyte while at rest? Do any special parts of the heart leak any other ions in or out at rest?

Back 4

Cardiac myocytes passively leak K+ (maintaining their -90mV charge). The myocytes of the sinus and AV nodes, the His bundle, and Purkinje fibers leak Na+ inward decreasing their polarity and leading to their automaticity and pacemaker properties.

Front 5

What ion is responsible for rapid depolarization of myocytes?

Back 5

Na+ is responsible for phase 0. The opening of the ion channels is voltage-gated and occurs when the cell reaches a specific membrane threshold

Front 6

What are the three possible states of Na+ ion channels during the cardiac cycle?

Back 6

* Na+ channels start closed. * When a threshold potential is reached (obtained from neighboring cells), the voltage-gated channels open, allowing Na+ to rush into the cell.
* The channel will spontaneously inactivate, while depolarization is still occurring. The channel will remain inactive until the cell membrane is repolarized, returning the channel to the closed (resting) state.

Front 7

How does the action potential get transmitted from cell to cell?

Back 7

One myocyte gets depolarized to the point of its threshold, triggering the opening of its Na+ channels, rapidly depolarizing that cell. Gap junctions that connect cell to its neighbors and allows the depolarized cell to pass some positive charge to its neighbor until the neighbor reaches its threshold and opens its Na+ channels, pushing the neighbor cell to depolarize as well.

Front 8

What ion is responsible for the transient partial repolarization of the myocyte?

Back 8

The transient outward current of K+ ions (similar to what normally maintains the -90mV charge). This is phase 1 of the cardiac action potential

Front 9

What ion is responsible for phase 2 of the cardiac action potential?

Back 9

Phase 2 is the plateau phase, maintained by Ca2+ ions. Depolarization of the myocyte, in phase 0, triggers the opening of Ca2+ channels in the membrane. A slow, sustained influx of Ca2+ prolongs depolarization of the myocyte and triggers release of Ca2+ from the Sarcoplasmic Reticulum.

Front 10

What ion is responsible for phase 3 of the cardiac action potential?

Back 10

The voltage-gated K+ channels that remain open are responsible for the rapid repolarization of the myocyte. This repolarization is also what is required to turn the Na+ channels from an inactive to a resting state.

Front 11

Which portion of the EKG represents the rapid depolarization of the heart?

Back 11

The QRS segment

Front 12

Which portion of the EKG represents the influx of Ca2+ into the heart?

Back 12

The ST segment or the plateau

Front 13

Which portion of the EKG represents the repolarization of the heart?

Back 13

The T wave

Front 14

Graphically, how does a Na+ channel blocker affect the cardiac action potential and EKG

Back 14

* Slow the upstroke of phase 0
* Prolongs QRS

Front 15

Graphically, how does a K+ channel blocker affect the cardiac action potential and EKG

Back 15

* Prolongs the plateau of phase 2, delaying phase 3
* Prolongs the QT

Front 16

What is the response to a premature beat during ERP?

Back 16

The cell can provide no response

Front 17

What is the response to a premature beat after the RRP?

Back 17

The cell will produce a completely normal action potential

Front 18

What is the response to a premature beat in between the ERP and the RRP?

Back 18

The cell will produce an action potential with a slower-onset, but propagation to neighboring cells is normal

Front 19

What cells normally have automaticity and how does it work?

Back 19

The sinus node, AV node, His bundle, and Purkinje fibers all maintain a slow, inward leak of positive ions (mostly Na+) during phase 4, leading to a "pacemaker current".

Front 20

How does automaticity differ between the sinus and AV nodes and the His bundle and Purkinje fibers?

Back 20

The sinus and AV nodes are very leaky during phase 4. These cells never repolarize to -90mV, they only make it to -60mV rendering the Na+ channels irrelevant. Slow, steady Ca+ channels are responsible for phase 0 in these cells.

Front 21

How do autonomics affect the normal cardiac action potential?

Back 21

* Sympathetic influence increases the slope (leakiness) during phase 4, pushing the cell past threshold quicker, producing a quicker "pacemaker current".
* Parasympathetic stimulation decreases the slope (leakiness) during phase 4, slowing the cell's ability to overcome it's threshold, producing a slower "pacemaker current".

Front 22

What neurotransmitters are responsible for a sympathomimetic/catecholaminergic response?

Back 22

Epinephrine and Norepinephrine

Front 23

What neurotransmitters are responsible for a parasympathomimetic/cholinergic response?

Back 23

Acetylcholine

Front 24

What are Ryanodine receptors?

Back 24

They are the calcium-dependent calcium release channels found in the sarcoplasmic reticulum

Front 25

Differentiate the distribution of L- v. T-type Ca2+ channels in the heart

Back 25

* L-type (long-acting) are found in every heart cell and contribute to phase 2 (the plateau of depolarization) of the cardiac action potential
* T-type (transient) are concentrated in the SA and AV nodes, but are also found in the atria and Purkinje cells. T-type Ca2+ channels are involved in the automaticity of the nodes.

Front 26

How does the funny current (If) in the heart and what type of channel regulates it?

Back 26

The funny current is the slow, inward leak of Na+ that pushes the cell towards phase 0, and results in the pacemaker current. Positive ions flow in through Hyperpolarization-activate, Cyclic Nucleotide-gated (HCN) channels, which are open when the cell is polarized (phase 4)

Front 27

How do autonomics, ß-blockers, and Ca2+ channel blockers interact with HCNs and what are the physiologic results?

Back 27

* Sympathetics: Increases cAMP, which increases HCN activity, which increases the heart rate
* Parasympathetics: decreases cAMP, which decreases HCN activity, and slows the heart rate
* ß-blockers: decrease sympathetic stimulation, slowing the heart rate
* Ca2+ channel blockers: decrease HCN responsiveness to cAMP, slowing the heart rate

Front 28

What are the components that make up thin filaments of muscle?

Back 28

* G-actin (globular) polymerizes into f-actin (filamentous)
* Tropomyosin helps to hold f-actin together
* Troponin-T: binds tropomyosin, anchoring the troponin complex
* Troponin-C: binds Ca2+, initiating contraction
* Troponin-I: binds actin, inhibiting the actin-myosin interaction

Front 29

What is the make up of thick filaments of muscle?

Back 29

Each myosin molecule has 2 heavy chains and 4 light chains. The light chains are involved in structure and regulation. The heavy chains each have a globular head, with binding sites for ATP and actin.

Front 30

What is the name of where thick and thin filaments attach and what is one contractile unit called?

Back 30

Thin filaments, actin, bind to the Z-line. Thick filaments, myosin, bind tail-to-tail along the M-line. One contractile unit, or a sarcomere, runs from Z-line to Z-line.

Front 31

Name and describe the stages of the sliding filament model.

Back 31

* Attachment: The ATP absent myosin head is bound to actin
* Release: The myosin head binds ATP and releases the actin filament
* Bending: The breakdown of ATP to ADP + Pi (in the presence of Mg) causes the myosin head to bend
* Force generation: If Ca2+ is present, myosin will bind a new actin site and return to its unbent state, moving the actin filament. ADP is released from the myosin head.

Front 32

Which portions of the sarcomere change in size with contraction

Back 32

The I (actin only) and H (myosin only) bands both shrink as the thick and thin filaments overlap. the A band (total length of myosin, tail-to-tail) doesn't shrink

Front 33

What ion is responsible for linking action potential to actual sarcomere filament interactions?

Back 33

Ca2+ which rushes into the cell from outside and from the sarcoplasmic reticulum is responsible for unbending the myosin head during force generation, allowing muscle contraction.

Front 34

How does Ca2+ regulation from the sarcoplasmic reticulum differ in skeletal muscle from cardiac muscle?

Back 34

In skeletal muscle, Ca2+ is voltage-dependent. Confirmational changes in DHP receptors opens ryanodine receptors. In cardiac muscle, Ca2+ is Ca2+ activated. Ca2+, released by the DHP receptors binds the ryanodine receptors, triggering Ca2+ release.

Front 35

How are cardiac cells coupled together?

Back 35

Intercalated disks form linear cell-to-cell attachments to form muscle fibers, allowing cardiac action potential to be propagated in many directions.

Front 36

What are the different types of junctions formed by intercalated disks?

Back 36

* Adhering junctions tightly hold adjacent cells
* Desmosomes prevent cells from pulling apart with tension
* Gap/communicating junctions provide ionic continuity among adjacent cells so information can be passed between cells

Front 37

Where are the SA and AV nodes located?

Back 37

The sinoatrial node is located in the atrial wall, close to the entrance of the SVC. The atrioventricular node is located in the right atrium, near the lower part of the interatrial septum

Front 38

What nerves regulate autonomic stimulation of the cardiac muscle?

Back 38

CNX (vagus) regulates parasympathetic conduction at the SA and AV nodes, as well as in the coronary arteries. T1-T6 sympathetically innervates the SA and AV nodes, the myocardium, epicardium, and coronary arteries

Front 39

How do autonomics affect heart contraction?

Back 39

* ACh (parasympathetic) decreases heart rate by slowing depolarization at phase 4. It also reduces force of contraction (at muscarinic receptors), and constricts coronary arteries
* NE (sympathetic) increases heart rate, increses force of contraction (ß-receptors), and inhibits constriction of coronary arteries

Front 40

What is the only electrical path from the atria to the ventricles?

Back 40

The His bundle

Front 41

How do the ERPs differ for atrial and ventricular myocytes?

Back 41

Atrial myocytes have a short ERP, allowing them to repolarize quickly and sustain rapid arrhythmias

Front 42

Why is the slow conduction through the AV node a protective mechanism?

Back 42

Atrial myocytes with much shorter ERPs can sustain very rapid arrhythmias. The AV node, with a longer refractory period (only uses Ca2+ channels) will not propagate every beat during an arrhythmia.

Front 43

What are the autonomic effects at the AV node?

Back 43

Sympathetics (NE) speed up conduction through the AV node (+dromotropy). Parasympathetics (ACh) slow conduction through the AV node (-dromotropy)

Front 44

Define chromotorpy, dromotropy, inotropy, and lusitropy

Back 44

Chromotropy: automaticity (usually of the SA node).
* Dromotropy: the propagation of impulse (usually through the AV node).
* Inotropy: the strength of contraction (usually of the ventricles)
* Lusitropy: the ability to relax

Front 45

What are two general mechanisms of bradycardia?

Back 45

Failure to generate an impulse due to abnormal automaticity (fibrosis, ischemia, drugs). Failure to propagate an impulse from SA block, AV block, or a His bundle (infranodal)/bundle brach/purkinje fiber block

Front 46

What are the normal automaticity rates for the latent pacemakers?

Back 46

* Sinus node: 60-100bpm
* AV node and His bundle ("Junctional escape"): 40-60bpm
* Bundle braches, Purkinje system ("Ventricular escape"): 30-40bpm

Front 47

What is an important difference between "pure" drugs that only work at ß1 and drugs that affect ß1 and a1 receptors.

Back 47

The pure drug will only have positive chrono and dromo effects. The dirty drug will also stimulate a1, causing vasoconstriction (elevating BP).

Front 48

What are common drugs for speeding up the heart rate?

Back 48

Isoproterenol, a ß-agonist, and Atropine, a parasympathetic blocker

Front 49

What coronary artery supplies the SA node? The AV node?

Back 49

The right coronary artery usually supplies both the SA and AV nodes

Front 50

What are the 3 primary mechanisms of tachycardia?

Back 50

Abnormal automaticity, triggered activity (early afterdepolarizations - torsades, or delayed afterdepolarizations - intracellular Ca2+ overload), and Reentry

Front 51

What are some causes of abnormal automaticity leading to tachycardia?

Back 51

Ischemia, metabolic derangement, or ion channel abnormality that leads to phase 4 activity

Front 52

What is the main cause for early afterdepolarization and what is a common result?

Back 52

Phase 3 repolarization being interrupted by a depolarizing current, usually a reactivation of Ca2+ channels. This can be self-perpetuating and cause Torsades de Pointes

Front 53

What condition, visible on an EKG, increases the likelihood of early afterdepolarization?

Back 53

A prolonged QT interval like some drugs

Front 54

What are the functional deficits found in congenital long QT syndrome and what type of arrhythmia does it predispose patients to?

Back 54

Loss of K+ channel function and an increase in Na+ channel function. Prolonged QT can cause ventricular tachycardia.

Front 55

What is Jervell & Lange-Nielsen syndrome and what is its key symptomatic association? Are there other forms of this syndrome?

Back 55

* JL-N is a very malignant autosomal recessive syndrome resulting in a very long QT on EKG and a high risk of fatal arrhythmia. It is associated with a SENSORINEURAL deafness present at birth.
* Romano Ward & Andersen-Tawil (hypokalemic periodic paralysis) syndromes are autosomal dominant and less malignant

Front 56

What are some reasons one pathway may conduct faster than another, contributing to reentry.

Back 56

* Fast pathway cells may have a higher density of Na+ channels allowing for faster depolarization
* Fast pathways may be connected with more or better gap junctions
* Anisotropic conduction: conduction may be faster in one direction than another (due to myofibril alignment)

Front 57

What direction is typical AV node reentry?

Back 57

A slow pathway causes reentry into a fast pathway that has unidirectional block

Front 58

What is the mechanism of Wolff-Parkinson-White syndrome?

Back 58

These patients have a fast accessory pathway down the wall of a ventricle. A SA impulse can propagate through the AV node (slow) and reenter through the accessory pathway (fast) causing an Atrioventricular Reciprocating Tachycardia (AVRT)

Front 59

What is AVNRT?

Back 59

AV nodal reentry tachycardia where the impulse reenter within the AV node

Front 60

Why is VT so bad following an MI?

Back 60

The VT occurs because the the impulse is using mostly dead, scar tissue as slow pathways for reentry. The partial dead cardiac tissue cannot maintain necessary cardiac output.

Front 61

Does the endocardium or the epicardium depolarize first? Repolarize?

Back 61

The endocardium depolarizes first, the epicardium repolarizes first.

Front 62

What is the general reason for a wide QRS?

Back 62

Premature ventricular contraction (PVC). If the impulse originates outside the specialized conduction system, it will take longer to activate all of the ventricular cells

Front 63

What is the EKG manifestation of WPW?

Back 63

A delta wave and a very short PR interval

Front 64

What portion of the EKG represents atrial contraction and which represents ventricular contraction?

Back 64

Atria: The P wave
Ventricles: Onset of the QRS segment until the end of the T wave

Front 65

Which are the inferior leads?

Back 65

II, III, and aVF

Front 66

Which are the lateral leads?

Back 66

I and aVL

Front 67

What does a deep pathologic Q wave represent?

Back 67

Cell death like from an old MI

Front 68

Differentiate ST elevation vs. ST depression

Back 68

ST elevation represents a transmural injury. ST depression can represent subendocardial ischemia and NSTEMI or just reciprocal changes during an ST elevation

Front 69

What are the numbers used to determine HR from an EKG?

Back 69

300, 150, 100, 75, 60, 50

Front 70

How is the 10-second rule used?

Back 70

In EKG reading, to determine the HR if the rate is somewhat variable. Count the beats over the 10 second strip and multiple by 6.

Front 71

What is the normal length of a PR interval and what are some things that can cause the PR to deviate?

Back 71

Less than 1 big box but more than 3 little boxes. Short PR is caused by AVRT (WPW). Long PR is the result of a heart block.

Front 72

What is the difference between 1˚, 2˚, and 3˚ heart block?

Back 72

1˚: All P wave produce a QRS
2˚: Only one P wave at a time is blocked
3˚: No P waves are conducted

Front 73

What are the locational differences between Wenckebach and Mobitz II AV block?

Back 73

Wenkebach is almost always a problem within the AV node (drugs). Mobitz II is usually infranodal, a problem in the His bundle or a L/R BBB

Front 74

Do Wenckebach or Mobitz II blocks respond to medications?

Back 74

Wenckebach will respond to atropine, isoproterenol, or dopamine. Mobitz II needs an urgent pacemaker, rarely responds to meds

Front 75

How do the QRS complexes and PR intervals compare between Wenckebach and Mobitz II block?

Back 75

Wenckebach will have a normal QRS and an increasingly prolonged PR. Mobitz II will have a wide QRS (infranodal) but a constant, prolonged PR

Front 76

What constitutes a wide QRS?

Back 76

More than 3 small boxes

Front 77

What are the 3 characteristic EKG findings for WPW?

Back 77

A wide QRS, a delta wave, and a short PR interval

Front 78

What is the rule of thumb for determining a long QT?

Back 78

QT is prolonged if it is more than half the RR interval

Front 79

What are the septal leads?

Back 79

V1 and V2

Front 80

What are the anterior leads?

Back 80

V2, V3, and V4

Front 81

What does T wave inversion on a EKG suggest?

Back 81

Ischemia

Front 82

Name the three layers of the heart and describe their cellular makeup

Back 82

* Endocardium: Single endothelial layer and underlying connective tissue
* Myocardium: Cardiac muscle
* Epicardium: Connective tissue, blood vessels, nerve fibers, covered by mesothelial cells

Front 83

What layer of cardiac tissue do the heart valves come from?

Back 83

Valves are extensions of the endocardium. The fibrous sheet is formed by merging fibroelastic supporting layers

Front 84

What function do atrial muscle granules serve?

Back 84

Granules contained in the atrials contain a natriuretic hormone that is secreted when the atrial fibers stretch. The hormone promotes the excretion of water, K+, and Na+ by the kidneys, and inhibits renin and aldosterone secretion, all of which help lower the blood pressure

Front 85

Explain the orientation of the 3 layers of blood vessels

Back 85

* Intima is closest to the lumen and is oriented along the direction of blood flow
* Media is oriented circumferentially and is able to regulate contractility of the vessels
* Adventitia is also longitudinal

Front 86

What are some functional roles of the endothelium?

Back 86

Secrete factors that prevents clotting, maintains the vascular tone of smooth muscle, and, when cytokines are activated, express adhesion molecules and allow WBC to stick

Front 87

Which layers is the dominant layer in arteries? Which dominate veins?

Back 87

The tunica media is the largest in arteries, the tunica adventitia is predominant in veins

Front 88

Describe transport in and out of the three different types of capillaries.

Back 88

* Continuous capillaries have endothelial cell connected with tight junctions. They use pinocytotic vessels to move material.
* Fenestrated capillaries, found in the pancreas, intestines, endocrine glands, and renal glomeruli pass material through diaphragms of extracellular material.
* SInusoids are discontinuous capillaries that do not have diaphragms and or a basal lamina. These are found in the bone marrow, liver, spleen, and lymphoid tissue and allow for the most transport.

Front 89

How do you differentiate small lymphatic vessels from a venule?

Back 89

Lymphatics will contain diifuse eosinophilic proteins. Venules will contain RBCs and some WBCs

Front 90

What are the three functions of the lymphatic system?

Back 90

Collect excess ECF and return it to cardiovascular circulation, immune defense filtering blood and ECF, transport fats

Front 91

What are the 4 classes of antiarrhythmics?

Back 91

Class I: Na+ channel blocker (1A, 1B, 1C)
Class II: ß-Blockers
Class III: K+ channel blockers
Class IV: Ca2+ channel blockers

Front 92

What are the differences of ß1 v ß2 concentration?

Back 92

ß1 receptors are found in the heart. ß2 receptors are found in vascular and bronchial smooth muscle

Front 93

Which class of antiarrhythmics actually improve survival in patients with heart disease?

Back 93

ß-blockers are shown to improve survival in patients with heart disease

Front 94

What are the tropic effects of ß-blockers?

Back 94

ß-blockers are negative chronotropic, negative dromotropic (block AVNRT & AVRT), and negative inotropic

Front 95

What are the 2 categories of ß-blockers and how are they different?

Back 95

Cardioselective drugs block only ß1 receptors. Nonselective drugs block ß1 and ß2 receptors and some also block a-receptors so they can cause bronchospasm, PVD, or Raynaud's

Front 96

Are Atenolol, Metoprolol, and Esmolol cardioselective or nonselctive ß-blockers?

Back 96

Atenolol, Metoprolol, and Esmolol are cardioselective ß-blockers

Front 97

Are Popranolol, Labetalol, and Carvedilol cardioselective or nonselective ß-blockers?

Back 97

Propanolol, Labetalol, and Carvedilol are nonselective ß-blockers. Labetalol and Carvedilol are also a-blockers, which inhibits vasodilation.

Front 98

What are some common adverse effects of ß-blockers?

Back 98

Effects of them being too efficient: sinus bradycardia (negative chromotrope), AV block (negative dromotrope), can worsen acute, severe decompensated heart failure (negative inotrope)

Front 99

Which class of Ca2+ channel blocker is better for antiarrhythmia and which is for antihypertension?

Back 99

Nondihydropyridines (Diltiazem and Verapamil) are better for antiarrhythmias. Dihydropyridines (Nifedipine, Amlodipine, Felodipine) are better for antihypertension

Front 100

What type of Ca2+ channels on what type of cells do Ca2+ channel blockers work?

Back 100

Ca2+ channel blockers work on the L-type Ca2+ channel blockers mainly in the AV node, but also the SA node.

Front 101

What are the tropic effects of Ca2+ channel blockers?

Back 101

Ca2+ channel blockers are negative chromotropic, negative dromotropic (1˚ purpose, to slow ventricular response rates during atrial tachyarrhythmias, also can interrupt a reentry loop), and negative inotropic

Front 102

What are the adverse affects of dilatiazem and verapamil?

Back 102

These Ca2+ channel blockers can be too tropic. Sinus node dysfuntion or a shut down junctional escape rhythm (chromotrope), AV block (dromotrope), or systolic heart failure (inotrope). These drugs also can cause hypotension and peripheral edema

Front 103

What are some other terms used to describe Digoxin?

Back 103

DIgoxin is a form of digitalis and is a cardiac glycoside

Front 104

What is the function of digoxin?

Back 104

* Digoxin augments vagal tone (PS) and slows conduction through the AV node
* Digoxin is also mildly a positive inotrope that disrupts the Na/K pump increasing the intracellular Na+ concentration, which leads to the Na/C exchanger bringing more Ca2+ into the cell. The increase in intracellular Ca2+ enters the sarcoplasmic reticulum increasing contraction potential

Front 105

What is digoxin toxicity?

Back 105

Nausea, vomiting, visual disturbances, high-grade AV block with atrial tachycardia, ventricular tachyarrhythmia (from delayed afterdepolarization), renal dysfunction

Front 106

In what circumstance is Adenosine indicated?

Back 106

Adenosine, a natural substance with a short half-life, is given as a rapid IV push to cause AV nodal block. It also is a vasodilator.

Front 107

What are possible side effects of Adenosine?

Back 107

Bronchospasm, atrial fibrillation, compensatory sinus tachycardia, and hypotension

Front 108

What is the mechanism of Na+ channel blockers?

Back 108

They limit the Na+ channels available for conduction, raise the threshold for action potential inititation, slow the upstroke of phase 0, and decrease the slope of phase 4.

Front 109

How do Na+ channel blockers affect reentry?

Back 109

* They slow the conduction of action potentials between cells. They can slow the "slow pathway" down so much that it converts the fast pathway unidirectional block into a bidirectional block and no conduction propagates.
* They also can slow either pathway just enough to make an incessant reentry circuit. DO NOT give to patient's with prior MI!!

Front 110

What is the general effect of Quinidine, Procainamide, and Disopyramide?

Back 110

Class I Na+ channel blocker. They prolong both the QRS and the QT. They are not "clean" and have a lot of side effects (GI, CNS, lupus-like syndrome, anticholinergic)

Front 111

What is the general effect of Lidocaine and Mexiletine?

Back 111

Class 1B Na+ channel blockers. They shorten the QT, only work in the ventricles, and preferentially target ischemic cells. Lidocaine is IV, Mexiletine is PO

Front 112

What is the general effect of Flecainide and Propafenone?

Back 112

Class 1C, most potent Na+ channel blockers. They are "clean" negative inotropes (contraindicated in heart failure), prolong the QRS with no effect on the QT interval. They are use-dependent and have mild side effects (fatigue and dizziness)

Front 113

Are Na+ channel blockers use-dependent or reverse use-dependent?

Back 113

Use-dependent

Front 114

Are K+ channel blockers use-dependent or reverse use-dependent?

Back 114

Reverse use-dependent

Front 115

What is the general mechanism of K+ channel blockers and what is a major risk?

Back 115

K+ channel blockers prolong the QT interval and torsades (polymorphic VT) is a risk, except with Amiodarone

Front 116

What are the toxicities of Amiodarone?

Back 116

Amiodarone makes you "blue, blind, and cough up your liver and thyroid".
* Eyes: corneal deposits, rare optic neuropathy
* Hypo/hyperthyroidism
* Hepatic injury
* Irreversible pulmonary toxicity
* Skin photosensitivity
* Interacts with Warfarin

Front 117

What types of antiarrhythmic drugs are ok, relatively contraindicated, and definitely contraindicated in patients with systolic heart failure?

Back 117

Ok: ß-blockers, Amiodarone, Dofetilide, Sotalol, Dronedarone, Digoxin
Relatively contraindicated: Verapamil, Diltiazem (from negative inotropy)
Definitely contraindicated: Any Class I (Na+) antiarrhythmic unless they already have an ICD

Front 118

What antiarrhythmic drugs are ok and contraindicated for use in patients with previous MI and myocardial scarring, but no systolic heart failure?

Back 118

Ok: ß-blockers, Amiodarone, Dofetilide, Sotalol, Dronedarone, Digoxin, Verapamil, Diltiazem
Contraindicated: Any Class I (Na+) antiarrhythmic unless they already have an ICD

Front 119

Which class of antiarrhythmic is safest for patients with a structurally normal ventricle?

Back 119

Class I (Na+). Especially 1C (Flecainide and Propafenone)

Front 120

What are the 3 main mechanisms of peripheral artery occlusions?

Back 120

Stenosis (atherosclerosis), thrombosis (underlying plaque or stenosis), and embolism (from thrombus in the heart)

Front 121

How do the 3 main mechanisms of peripheral artery occlusions differ in their final presentation?

Back 121

* Stenosis leads to chronic occlusion which happens slowly, allowing for bridging, collateral arteries to develop.
* Embolism leads to acute occlusion that can result in end-organ ischemia because there is no time to develop compensatory collateral blood flow

Front 122

What are some common chief complaints referring to peripheral vascular disease?

Back 122

Leg pain with or without ambulation, toe ulcers or gangrene, leg swelling, recent CVA or TIA, bruits in the neck, pulsatile abdominal mass, AAA

Front 123

What are some risk factors or conditions associated with vascular disease?

Back 123

Atherosclerosis and its risk factors (HD, stroke, smoking, DMII), altered exercise, clotting disorders, family history

Front 124

What are the hallmark signs of acute limb ischemia?

Back 124

6 "P's".
Pulselessness, pain, pallor, poikilothermia, paresthesia, paresis

Front 125

What types of skin changes are associated with arterial pathology?

Back 125

Decreased temperature, pallor, mottling, hair loss, ulceration, gangrene

Front 126

What types of skin changes are associated with venous pathology?

Back 126

Edema, varicositites, dermatitis, thickened skin, ulceration, gaiter distribution

Front 127

Name 5 modalities commonly used to assess peripheral vascular disease

Back 127

Ankle brachial index, duplex ultrasound, CT angiography, MR angiography, digital subtraction angiography

Front 128

What is the normal cut-off for a normal ABI?

Back 128

>0.9

Front 129

What is the gold standard modality for screening carotid occlusive disease?

Back 129

Duplex ultrasonography

Front 130

What is the gold standard for screening Deep Venous Thrombosis?

Back 130

Duplex ultrasound

Front 131

What conditions are digital subtraction angiography used to diagnose, what are its risks, benefits, and contraindications?

Back 131

Artery occlusive disease. It requires an artery puncture and so it carries a risk of bleeding. Since you are physically in the artery you can do an angioplasty or place a stent.

Front 132

What are the different types of claudication?

Back 132

* Intermittent is an arterial problem
* Spinal is a neurologic problem
* Venous is a postphlebitic or venous insufficiency problem
* Arthritis is a varying problem where you have good days and bad days

Front 133

What are the 3 symptomatic characteristics necessary for intermittent claudication?

Back 133

Exertional aching or cramping, that resolves with rest, and is reproducible over a consistent distance or level of exertion

Front 134

What are some diagnoses that you need to rule out for intermittent claudication?

Back 134

* Atherosclerosis
* Thrombangiitis obliterans (smokers, affects distal limbs)
Popliteal artery entrapment syndrome (cyclers)
* Fibromuscular dysplasia (beads on a string)
* Cystic adventitial disease of the popliteal artery (hypolucent tunica media outpouching into lumen)
* Cocaine-abuse
* Peripheral neuropathy, lumbar stenosis, degenerative hip or spine disease

Front 135

How does smoking affect the arterial wall?

Back 135

* Vasoconstriction, increased ACE activity
* Increased platelet aggregability, fibrinogen levels, secretion of adhesion molecules, growth of atherosclerotic plaques
* Atherosclerotic plaque stabilization decreases

Front 136

What are the methods and indications for revascularization in PAD?

Back 136

The two methods of revascularization are endovascular (arterial dilation ± stent placement, atherectomy) or surgical (endarterectomy or arterial bypass). Indications are symptomatic lifestyle limiting claudication or critical leg ischemia

Front 137

What is the common combination therapy to improve claudication symptoms?

Back 137

Medication + exercise + smoking cessation

Front 138

Describe the believed pathogenesis of atherosclerotic plaque formation.

Back 138

When there is an excess of plasma LDL/VLDL it can pass through the endothelial layer where it will interact with matrix proteoglycans. Those PGs facilitate LDL oxidation and aggregation, which upregulates the expression of adhesion molecules on the endothelium for circulating monocytes, promoting monocyte movement into the matrix and differentiation into macrophages. Those macrophages ingest the ox-LDL, recruiting more macrophages, and all of these macrophages necrose and release inflammatory cytokines. This process leads to endothelial damage which is repaired, creating a plaque

Front 139

How do T-cells affect plaque formation?

Back 139

T-cell cytokines inhibit smooth muscle proliferation and collagen production, promoting plaque rupture and thrombosis

Front 140

What is the mechanism for plaque rupture?

Back 140

Macrophage foam cells migrate towards the shoulders of plaques where they secrete matrix metalloproteinases (MMP) which breaks down collagen. T-cell cytokines also inhibit smooth muscle proliferation and collagen production. These all make plaques susceptible to rupture. When a plaque ruptures it exposes TF, causing platelet aggregation and thrombosis

Front 141

How does lowering plasma LDL levels alter the progression of atherosclerotic plaques?

Back 141

Lowering LDL levels decreases macrophage foam cell presence in the plaque. This will decrease the inflammatory response and increase connective tissue proliferation, leading to plaque remodeling

Front 142

What are the risk factors for atherosclerosis and vascular disease?

Back 142

Age, gender, abnormal lipid levels, HTN, smoking, DMII, obesity, sedentary life style

Front 143

How does hypertension exacerbate atherosclerosis?

Back 143

* Flow/shear mediated damage to barrier function of endothelial cells
* Damage to endothelial cells due to greater stretching

Front 144

What are some things that affect resistance?

Back 144

* Greater viscosity (increased hematocrit)
* Longer vessels mean greater resistance
* Stenosis decreases the diameter of the vessel which greatly increases the resistance (r^4)

Front 145

Name 2 things that affect turbulence and what finding they will affect.

Back 145

* Increasing velocity of flow, via stenosis, or anything else that narrows vessels
* Decreasing viscosity of blood, via anemia.
* These both increase turbulence and make you more likely to hear a murmur

Front 146

How do you calculate a mean arterial pressure?

Back 146

MAP=Diastolic BP + 1/3 pulse pressure=Cardiac output * total peripheral resistance=(SV*HR)*TPR

Front 147

How do you calculate cardiac output?

Back 147

Cardiac output=Stroke volume* heart rate

Front 148

What are some examples of patient presentation of symptomatic extracranial cerebrovascular disease?

Back 148

TIA, amaurosis fugax, stroke, vertebrobasilar symptoms

Front 149

How can someone be asymptomaticlly diagnosed with extracranial cerebrovascular disease?

Back 149

Imaging findings (screening or incidental) or physical exam findings (bruit or Hollenhorst plaque)

Front 150

What is the temporal difference between a TIA and a stroke?

Back 150

Transient Ischemic Attack (TIA) is a focal neuro deficit that lasts less than 24 hours. A stroke (CVA) is a focal neuro deficit that last greater than 24 hours, representing neuronal cell death

Front 151

What is amaurosis fugax and what is its mechanism?

Back 151

Amaurosis fugax is temporary ipsilateral monocular visual loss and is the result of an embolization of the retinal artery or its branches (Hollenhorst plaques)

Front 152

What are the two etiologies of stroke and which is most common?

Back 152

Hemorrhage (aneurysm, trauma, anticoagulation, congenital abnormality) and Ischemia. Ischemia is the etiology for 80% of strokes

Front 153

What are some risk factors for ischemic stroke?

Back 153

Hypertension, increasing age, CVD (A.fib or extracranial cerebrovascular disease), smoking

Front 154

What are two ways extracranial cerebrovascular disease can cause a stroke?

Back 154

Embolism (most common) or a thrombosis/low flow state

Front 155

How are statins believed to affect atherosclerotic plaques?

Back 155

HMG-CoA (statins) are associated with fibrous remodeling and plaques stabilization

Front 156

What are some non-atherosclerotic causes of extracranial cerebrovascular disease?

Back 156

Arteritis (Takayasu, Giant cell), Dissection (Traumatic of spontaneous), Fibromuscular dysplasia, radiation

Front 157

What is the etiology, symptoms, and treatment of giant cell arteritis?

Back 157

Is most common in older caucasian women. It can lead to temporal headaches, jaw claudication, polymyalgia rheumatica, amaurosis, constitutional symptoms, elevated sedimentation rate. It is an infection treated with corticosteroids

Front 158

What are the 2 mechanisms of carotid artery dissections and what is their common treatment?

Back 158

Sponateous (cocaine/meth use, Horner's syndrome) or Traumatic compression injury occurring high in the neck (C2). They are treated with anitcoagulation treatment

Front 159

What are the indications for procedural intervention in extracranial cerebrovascular disease?

Back 159

Based on symptoms, degree of stenosis, patient's anatomy

Front 160

What symptoms are commonly associated with vertebrobasilar disease?

Back 160

"Posterior" Symptoms: dizziness, vertigo, diplopia, blurred vision, ataxia, drop attacks, bilateral sensory disturbances

Front 161

What is the presentation of vertebrobasilar disease?

Back 161

Defined precipitating factors: positional changes such as head turning or rising from sitting or standing, usage of upper extremities

Front 162

What are 2 circulatory results of bilateral renal artery stenosis?

Back 162

CHF and peripheral edema

Front 163

Where are ATII-1 receptors distributed, what are some of their regulators, and what are their effects?

Back 163

Type 1 Angiotensin II receptors are located in the kidney, vascualr wall, adrenals, heart, brain, lung, and liver. They are G-protein coupled receptors activated by angiotensin, LDL, Insulin, Estrogen, progesterone, and IFN-g. AT1R activation is vasoconstrictive, pro-inflammatory, and promotes volume expansion and sodium retention

Front 164

What is the mainstay of treatment for renal artery stenosis

Back 164

ACE inhibitors or ARBs. They improve survival, reduce cardiovascular events, and have renoprotective effects for diabetic patients

Front 165

What are the 3 main indications for HMG-CoA inhibitors?

Back 165

Statins. Vascular disease (CVD, CHD, MI), Chronic kidney disease (declining renal function), and Atherosclerotic renal artery stenosis

Front 166

What is the common patient presentation for acute arterial mesenteric ischemia?

Back 166

>60yo in severe acute abdominal pain and often nausea and diarrhea

Front 167

What is the common patient presentation for chronic arterial mesenteric ischemia?

Back 167

40-70yf in abdominal pain, often post-prandial (10-30 min) resulting in weight loss and food fear

Front 168

What is the common patient presentation for acute venous mesenteric thrombosis?

Back 168

Insidious onset, pain, nausea, vomiting, abdominal distension, fever, slow progression of symptoms

Front 169

What is the common patient presentation for chronic venous mesenteric ischemia?

Back 169

Portal hypertension that is usually only found as an incidental CT finding

Front 170

What are risk factors of mesenteric venous thrombosis?

Back 170

Hypercoagulable states, OCPs, neoplasm, IBD, smoking

Front 171

What are the methods of treatment for acute and chronic mesenteric arterial and venous ischemia?

Back 171

Acute arterial relies on open surgical management. Chronic arterial is either surgical revascularization or an endovascular procedure. Venous ischemia is treated by anticoagulation.

Front 172

What are potential complications of infectious endocarditis?

Back 172

Tamponade, CHF, rhythmic disturbances, heart block

Front 173

What is the current epidemiology for infective endocarditis?

Back 173

Older patients (~50yo) with predisposing cardiac lesions. IV drug use, indwelling catheters, & HA bacteremia are prevalent risk factors in developed countries.

Front 174

What 2 events are necessary for infective endocarditis?

Back 174

The formation of a nonbacterial thrombus (trauma, perisurgery, metabolic changes) followed by a transient bacteremia with an organism that can adhere to a platelet-fibrin matrix (usually a GPC)

Front 175

What are the two most common pathogens responsible for infective endocarditis?

Back 175

Staph aureus and Strep viridians

Front 176

What are the most common symptoms and physical findings of infectious endocarditis?

Back 176

Fever, heart murmur (new or changing regurgitant heart murmur), embolic phenomenon (skin, viscera, organs, brain), skin manifestations (Osler nodes, splinter hemorrhages, petechiae)

Front 177

What are some major complications of infective endocarditis?

Back 177

CHF (valvular destruction/regurgitation), systemic emboli, mycotic aneurysm, renal disease

Front 178

What is the name of the criteria necessary for a definitive diagnosis of infectious endocarditis and what are the criteria?

Back 178

The Duke criteria require appropriate microbiology (GPC 2+ times) and evidence of endocardial involvement (Valvular vegetation or a new regurgitant murmur via echo)

Front 179

What is the normal treatment for infectious endocarditis and when is a higher level of intervention indicated?

Back 179

Bactericidal antibiotics often in combination and for a prolonged period to achieve optimal killing. Surgery, such as a valve replacement is indicated with defined complications (HF, multiple emboli, persistent bacteremia, fungal infection, MDR infection, heart block)

Front 180

What are the differences in common pathogens in early v. late prosthetic valve endocarditis?

Back 180

Early (<2 months): Staph, GNR, fungi
Late (>2 months): Looks like native...S.aureus, coag (-) staph, strep

Front 181

How does prosthetic valve endocarditis compare to native valve infectious endocarditis?

Back 181

Prosthetic valve endocarditis is associated with a more varied microbiology, frequent metastatic complications, and greater need for surgical intervention, and a poorer outcome

Front 182

What kind of patient is a candidate for endocarditis prophylaxis?

Back 182

Patients with cardiac lesions that are at risk risk (prosthetic valve, prior IE) that are peridental procedures

Front 183

What are common signs of infectious pericarditis?

Back 183

Fever, chest pain, pericardial friction rub (sign of tamponade &/or constriction

Front 184

What type of pathogen is most implicated in myocarditis and what are is signs?

Back 184

Viral (enterovirus). Fever and signs of CHF, often in young males with new onset unexplained cardiac abnormalities and a recent URI or enteritis

Front 185

What generates ventricular pressure during diastole? Systole?

Back 185

During diastole, ventricular pressure is generated from the blood volume filling and stretching the ventricles. In systole, the pressure is from the ventricles contracting and ejecting its load

Front 186

How does the total peripheral resistance react to a hemorrhage?

Back 186

A hemorrhage greatly decreases the venous return to the heart, the body will react to this by vasoconstricting and increasing the TPR

Front 187

How do cardiac output and venous return react to an increase in total peripheral resistance?

Back 187

An increase in arterial pressure will increase the afterload, decreasing cardiac output and venous return

Front 188

How does the total peripheral resistance react to exercise?

Back 188

An increase in catecholamines increases contractility. Muscular arterioles dilate, decreasing the TPR, but allowing for greater cardiac output and venous return

Front 189

What is preload?

Back 189

Preload is the volume of blood and thereby pressure that fills and stretches the left ventricle during diastole

Front 190

What is afterload?

Back 190

Afterload is the pressure required to be generated by the left ventricle to overcome the mean arterial pressure and force the aortic valve to open, allowing for the ejection of blood

Front 191

How do changing the preload or afterload affect the ESPVR and the EDPVR?

Back 191

They do not. Those two relationships and the lines that describe them remain the same. The intrinsic properties of the heart are not changing.

Front 192

How does changing the inotropy of the heart affect the ESPVR and the EDPVR?

Back 192

A change in inotropy will affect ESPVR but keep the EDPVR the same

Front 193

How does changing the lusitropy of the heart affect the ESPVR and the EDPVR?

Back 193

A change in lusitropy will affect the EDPVR but keep the ESPVR the same

Front 194

When does a higher HR not equal a higher cardiac output?

Back 194

If the HR is going too fast, there will not be as much preload, decreasing the stroke volume and decreasing the cardiac output

Front 195

What is the LVEF, how is it calculated, and what are clinically normal values?

Back 195

The Left Ventricular Ejection Fraction is the fraction of blood actually pumped out during systole. LVEF=Stroke volume/End diastolic volume (~55-70%)

Front 196

What are normal chamber pressures for both atria, both ventricles, the pulmonary artery, the pulmonary capillary wedge, and the aorta?

Back 196

RA=0-8
RV=15-30/0-8
Pulmonary Artery=15-30/4-12
Pulmonary capillary wedge= 1-10
LA=1-10
LV=100-140/3-12
Aorta=100-140/60-90

Front 197

What is the equation for cardiac output and where are each of the measures taken?

Back 197

Cardiac output=rate of O2 consumption/(arterial O2 content - venous O2 content)
Arterial O2 content is measured from a peripheral artery. Venous O2 content is measured from the pulmonary artery

Front 198

What are 3 major factors that affect mycardial O2 demand?

Back 198

* Contractility: If the heart is squeezing harder it is doing more work and needs more O2
* Heart Rate: If the heart is beating faster it is doing more work and needs more O2
* Ventricular wall stress: More wall stress increases its need for O2

Front 199

What are the 3 general principles of the Law of Laplace?

Back 199

For any container wall stress is proportional to ventricular pressure and ventricular radius and inversely proportional to wall thickness

Front 200

What is the general mechanism for nitroglycerine use for angina?

Back 200

Nitroglycerin decreased preload, decreasing wall stress, decreasing myocardial O2 demand

Front 201

What is the heart's physical response to chronic pressure overload?

Back 201

Concentric hypertrophy. An increase in wall thickness but not in chamber size

Front 202

What is the heart's physical response to chronic volume overload?

Back 202

Eccentric hypertrophy. An increase in wall thickness and chamber size leading to the chamber dilating

Front 203

What are some behavioral risk factors for hypertension?

Back 203

Excessive alcohol consumption, sodium consumption, obesity/dietary excess, lack of aerobic exercise

Front 204

What is the rule of 2?

Back 204

* Stage 2 hypertension gets treated with 2 antihypertensive drugs (thiazide + another class)
* An increase of 20/10 will 2x your risk of CVD

Front 205

What are some results of hypotension?

Back 205

Shock, kidney failure, anoxic encephalopathy, lactic acidosis

Front 206

What are some results of hypertension?

Back 206

Intracranial hemorrhage, stroke, vascular disease, kidney damage, hypertensive heart disease, retinopathy

Front 207

What are the systolic and diastolic cutoffs of normal BP? What treatment is indicated?

Back 207

<120/<80. Treat with drugs for compelling indications

Front 208

What are the systolic and diastolic cutoffs of prehypertension? What treatment is indicated?

Back 208

120-139/80-89. Treat with drugs for compelling indications

Front 209

What are the systolic and diastolic cutoffs of Stage 1 hypertension? What treatment is indicated?

Back 209

140-159/90-99. Thiazide diuretic. Other drugs for compelling indications.

Front 210

What are the systolic and diastolic cutoffs of Stage 2 hypertension? What treatment is indicated?

Back 210

≥160/≥100. Stage 2=2 drugs. Thiazide diuretic+ ACEI, ARB, BB, or CCB.

Front 211

Differentiate the function of Angiotensin II type 1 and type 2 receptors.

Back 211

AT1 Receptors promote vasoconstriction, cell growth and proliferation, hypertrophy, aldosterone release, sympathetic activation, Na and H2O retention, and inhibit renin release. AT2 receptors cause vasodilation, promote excretion, and limit hypertrophy

Front 212

Describe the epidemiology, presentation, and treatment of pheochromocytoma.

Back 212

Pheochromocytoma is a chromaffin tumor that secretes catecholamines. Young - middle aged females that present with intermittent sympathomimetic symptoms (HTN, palpitation, sweating, anxiety). Must be treated 1 wk prior to surgical removal with Phenoxybenzamine, an a-blocker, to inhibit catecholamine secretion during surgery

Front 213

Why is a coarctation of the aorta sometimes difficult to find?

Back 213

The intercostal arteries can dilate and compensate for less flow through the abdominal aorta. A younger person can come in a have upper extremity hypertension and have normal blood pressure with diminished lower extremity pulses. Rib notching can also be seen on CXR.

Front 214

What type of drugs are hydrochlorothiazide, chlorothiazide, metolazone, and indapamide, what is their mechanism, and what are their common side effects?

Back 214

They are thiazide-type diuretics that act by inhibiting Na+ reabsorbtion at the distal tubule. Their side effects are decreased metabolites (K+, Mg, Na+), hyperglycemia, gout, dehydration, and rash

Front 215

What type of drugs are spironolactone, eplerenone, triamterene, and amiloride, what is their mechanism, and what are their common side effects?

Back 215

They are K+ sparing diuretics and they inhibit K+/Na+ exchange at distal renal tubules. There common side effect is hyperkalemia, spironoLACtone can cause gynecomastia, and triamterene and amiloride can cause a rash.

Front 216

What type of drugs are furosemide, bumetanide, torsemide, and ethacrynic acid, what is their mechanism, and what are their common side effects?

Back 216

They are loop type diuretics and the inhibit NaCl reabsorption at the ascending Loop of Henle. Their side effects are decreased metabolites (K+, Mg, Na+), hyperglycemia, gout, dehydration, and rash (except for ethacrynic acid because it isn't made with sulfur

Front 217

In what population are diuretics good and where should you use caution?

Back 217

Diuretics work well in the african american population and caution must be exercised when administering to the elderly

Front 218

What type of drugs are captopril, enalapril, lisinopril, and ramipril, what is their mechanism, and what are their common side effects?

Back 218

* They are ACE inhibitors, inhibiting vasoconstriction, the release of aldosterone and vasopressin, and the decrease sympathetic stimulation.
* They also inhibit the breakdown of bradykinin into inactive peptides, causing a backup of bradykinin which can bind to BK-II receptors and release NO, cause vasodilation, and produce the side effect of a dry cough.
* Side effects: Hyperkalemia, increased serum creatinine, dry cough, angioedema

Front 219

What type of drugs are losartan, valsartan, and olmesartan, what is their mechanism, and what are their common side effects?

Back 219

* They are Angiotensin II receptor blockers, inhibiting vasoconstriction, the release of aldosterone and vasopressin, and the decrease sympathetic stimulation.
* Side effects: Hyperkalemia, increased serum creatinine, angioedema

Front 220

What is important to know about Enalapril?

Back 220

It is metabolized into enalaprilat which is also an active agent and can be given IV

Front 221

What is important to know about lisinopril?

Back 221

It is indicated as an antihypertensive and for CHF

Front 222

What is important to know about ramipril?

Back 222

It is indicated as an antihypertensive and can prevent HD by increasing blood flow

Front 223

What is aliskiren indicated for and what is its mechanism?

Back 223

Aliskiren is an antihypertensive and works by inhibiting renin's catalytic ability to activate angiotensinogen

Front 224

What are contraindications for ACEI, ARBs and renin inhibitors?

Back 224

Bilateral renal artery stenosis, pregnancy, angioedema to other ACEIs, hyperkalemia

Front 225

What are some common side effects of ß-blockers used as antihypertensives?

Back 225

Drowsiness, lethargy, confusion, bronchoreactive events, AV nodal blockade

Front 226

What kind of drugs are atenolol, metoprolol, carvedilol, and labetalol, what is there mechanism, and what are their side effects?

Back 226

* They are ß-blockers that can be used as antihypertensives
* Atenolol and metoprolol are cardiosensitive (ß1), labetalol and carvedilol are nonselective (a, ß1, ß2)
* Side effects: Drowsiness, lethargy, confusion, bronchoreactive events, AV nodal blockade

Front 227

Are nondihydropyridines or dihydropyridines indicated for hypertension? Arrhythmia?

Back 227

Nondihydropyridines (dilatiazem, verapamil) are used as antiarrhythmics. Dihydropyridines (Nifedipine, Nicadipine, felodipine, amlodipine) are used as antihypertensives

Front 228

What types of antiarrhythmics are indicated for the compelling indication of heart failure?

Back 228

ß-blockers, ACEIs, and ARBS

Front 229

What types of antiarrhythmics are indicated for the compelling indication of post an MI?

Back 229

ß-blockers, ACEIs, and aldosterone antagonists (ARBs)

Front 230

What types of antiarrhythmics are indicated for the compelling indication of high coronary artery risk?

Back 230

ß-blockers, ACEIs

Front 231

What types of antiarrhythmics are indicated for the compelling indication of diabetes?

Back 231

ACEIs, ARBs

Front 232

What types of antiarrhythmics are indicated for the compelling indication of chronic kidney disease?

Back 232

ACEIs, ARBs

Front 233

What types of antiarrhythmics are indicated for the compelling indication of recurrent stroke prevention?

Back 233

Diuretics, ACEIs

Front 234

Which 2 valves are most commonly affected in Rheumatic Fever?

Back 234

Mitral valve followed by aortic valve

Front 235

What are the Jones criteria used to diagnose and what are they (11)

Back 235

* Criteria used to diagnose Rheumatic Fever
* Polyarthritis, carditis, subcutaneous nodules, erythema marginatum, chorea, fever, arthralgia, increased ESR, Leukocytosis, heart block on ECG, hx of RF

Front 236

What is the most common cause of mitral stenosis?

Back 236

Rheumatic fever

Front 237

What physiologic affects does mitral stenosis cause?

Back 237

* Mitral stenosis causes elevated LA pressures, resulting in elevated pulmonary and right heart pressures
* Chronic pressure overload LA can cause A.fib which can worsen patient's symptoms

Front 238

What are the physical exam findings with mitral stenosis?

Back 238

* Loud S1 in early stages (pressure difference held longer), soft S1 in late stages
* Opening snap (after S2): the "sooner the worser"
* Diastolic rumble (longer duration, worse stenosis)

Front 239

What are the treatments for mitral stenosis?

Back 239

* Diuretics to reduce pulmonary congestion
* If A.fib occurs: control ventricular rate & start anticoagulant
* Percutaneous balloon mitral valvuloplasty is available

Front 240

What is the most common etiology of mitral regurgitation?

Back 240

Idiopathic chordae tendinae rupture

Front 241

What is the result of acute mitral regurgitation?

Back 241

Severe pulmonary edema. The LA is unprepared to deal with the extra blood flow and backs up into the pulmonary system

Front 242

What are the physiologic changes of chronic mitral regurgitation?

Back 242

* LA dilation minimizes pulmonary edema except in cases of transient decompensation (high salt intake, uncontrolled HTN)
* LA dilation can lead to A.fib
* LV is under chronic volume overload (normal blood plus regurgitated blood) and undergoes eccentric hypertrophy.

Front 243

What is the primary symptom found in mitral regurgitation?

Back 243

Fatigue, caused by decreased cardiac output (SV remains high, but is going in two directions)

Front 244

How can mitral regurgitation sneak up on you?

Back 244

LV eccentrically hypertrophys because it is chronically volume overloaded. This dilation leads to a decrease in inotropy. The afterload is also decreased though, due to blood exiting the LV in two directions, allowing the heart to compensate and keep the stroke volume artificially high. Cardiac output will be decreased.

Front 245

When is surgery indicated for mitral regurgitation?

Back 245

Severe symptomatic mitral regurgitation

Front 246

What in the non-surgical treatment for mitral regurgitation?

Back 246

* Medical therapy doesn't affect MR progression
* Diuretics to reduce pulmonary congestion
* Vasodilators to encourage more forward blood flow

Front 247

What are the physical exam findings in mitral regurgitation?

Back 247

* Holosystolic murmur, commonly with an S3

Front 248

What are the gross and physical exam findings of mitral valve prolapse?

Back 248

* A midsystolic click
* Thickened myxomatous connective tissue replaces dense collagen of the valve

Front 249

What are the 2 most common etiologies of aortic stenosis and what age groups are affected by each?

Back 249

* 40-60 yo present with atrial stenosis from a congenital bicuspid aortic valve
* >65 yo presents with degenerative aortic stenosis (similar changes to atherosclerosis)

Front 250

What are the physiological effects of aortic stenosis?

Back 250

Chronic pressure overload in the LV leads to concentric hypertrophy and decreased lusitropy. This decreases LV filling during diastole leading to increased importance on atrial contraction and the development of A.fib and a decreased cardiac output

Front 251

What are the physical exam findings of aortic stenosis?

Back 251

* A crescendo-decrescendo systolic ejection murmur (the stenosed valve maintains the pressure gradient between the LV and aorta longer)
* Pulsus parvus et tardus (weak and delayed pulse)

Front 252

When is surgery indicated for aortic stenosis?

Back 252

Once CHF, angina, or syncope develop

Front 253

How do the afterload and stroke volume compare before and after surgery in mitral regurgitation and aortic stenosis?

Back 253

* Before surgery: AS will have a high afterload and lower SV. MR will have a low afterload (blood flows into aorta AND back into LA) which artificially maintains a high SV
* After surgery: SV for AS will be drastically improved because of the decreased afterload. In MR the dilated LV now has a much higher afterload and the SV will drop sharply

Front 254

What are the medical managements for aortic stenosis?

Back 254

* No treatment will actually slow the progression of the pathology
* Statins may help reduce risk factors
* Diuretics may help (decreases TPR) especially with coexisting MR
* Vasodilators if hypertensive to decrease afterload. Be careful to NOT induce hypotension

Front 255

What is the definition of an aneurysm and what are the two classifications?

Back 255

A focal dilation of an artery, increasing the diameter at least 50%. True aneurysms involve all layers of the vessel wall while false aneurysms have none of the vessel layers

Front 256

What are the components of vessel walls that are involved in AAA formation and how are they involved?

Back 256

Elastin, matrix metalloproteinases, and collagen. Elastin is not produced in adults. Elastin concentrations decrease while matrix metalloproteinases increase degradation as we age. This elastin degradation (especially infrarenally) decreases vessel elasticity and integrity

Front 257

What population most commonly is affected by AAA, what are common risk factors, and which one is the biggest risk factor?

Back 257

* Elderly white men are 6 times more likely to get AAA.
* Risk factors: Smoking (biggest risk), family history, hypertension, white race

Front 258

What size is necessary for surgery to be indicated in AAA?

Back 258

5.5 cm for most patients, excluding petite women

Front 259

What is the most common presentation for AAA?

Back 259

Most patients with AAA are asymptomatic

Front 260

What is the best screening/diagnostic modality for AAA?

Back 260

Ultrasound

Front 261

What are some symptoms associated with AAA at its different stages?

Back 261

Acute expansion manifests as pain. An AAA rupture will present as abdominal or back pain, hypotension, syncope, abdominal distension, shock, and/or sudden death

Front 262

What physics is responsible for AAA rupture?

Back 262

The law of Laplace states that an increase in radius increases wall stress. Eventually, the wall stress will overcome the decreased wall integrity caused by decreased elastin, and the vessel wall will rupture

Front 263

What AAA risk factors are implicated in increasing risk of AAA rupture?

Back 263

Smoking and COPD are independent risk factors for increased rate of rupture

Front 264

What treatments are indicated for AAA?

Back 264

No medical therapy is proven to reduce or slow aneurysm growth

Front 265

What are the 2 common surgical treatments for AAA?

Back 265

Endovascular repair or open surgery

Front 266

What is the pathophysiology of an aortic dissection?

Back 266

Blood enters the aortic wall through an intimal tear creating a normal (true) lumen and an abnormal (false) lumen through which blood flows

Front 267

What is the best treatment for AAA?

Back 267

Reducing risk factors: HTN, DMII, smoking

Front 268

What is the key histological finding in an aortic dissection?

Back 268

Cystic medial necrosis

Front 269

What are the 2 classifications of aortic dissection, what is their presentation,

Back 269

* Stanford type A: Ascending aorta, proximal to the trunk
* Standford type B: Descending aorta, most often at the subclavian
* They both present with sharp, ripping, tearing pain

Front 270

What congenital syndromes are associated with aortic dissection?

Back 270

Connective tissue diseases: Marfan's, Turner's, Ehler-Danlos, Coarctations

Front 271

What modality is best for picking up an aortic dissection?

Back 271

Aortic dissection is best diagnosed with a CT scan. Second best would be an ultrasound revealing a widened mediastinum

Front 272

What is the treatment for an aortic dissection?

Back 272

* Immediately lower blood pressure. ß-blocker to reduce the HR and a vasodilator (nitroprusside or labetalol) to reduce afterload.
* Control pain
* Stanford type A is always a surgical emergency. Repair dissection, preserve coronary and valve function

Front 273

Where are the most common spots for peripheral aneurysms and what other vascular problem are they commonly associated with?

Back 273

The femoral and popliteal arteries are the most common peripheral aneurysms. They are usually bilateral and are STRONGLY associated with AAA. Screen for AAA

Front 274

What is the most common site for visceral aneurysm and what medical condition puts patients at an increased risk for rupture?

Back 274

The splenic (followed by renal) artery is the most common site of visceral aneurysm and pregnancy increases the risk of rupture, so surgery is indicted at a much smaller aneurysmal size

Front 275

What is the difference between signs and symptoms?

Back 275

* Signs are objective features of illness detected by a practitioner
* Symptoms are subjective features of an illness as related by the patient

Front 276

What are the epidemiological differences between DHF and SHF?

Back 276

DHF patients are older women and SHF patients are usually middle-aged men

Front 277

What are the 4 characteristics that can be manipulated to regulate cardiac output?

Back 277

Automaticity regulates the heart rate. Contractility, preload, and afterload all affect stroke volume

Front 278

How does the heart immediately respond to an acute myocardial injury? How does it respond over time?

Back 278

* Initially, the ejection fraction will decrease because the stroke volume decreases, but the heart will reflexively increase the HR to compensate for the decreased SV.
* After a period of decreased ejection fraction, the ventricle will dilate, increasing the preload to increase the stroke volume

Front 279

How do sympathetic and parasympathetic drugs affect automaticity?

Back 279

* Sympathetics bind ß-receptors that increase Na+ and Ca2+ flow into the cell, increasing the rate of depolarization, increasing the heart rate
* Parasympathetics bind muscarinic receptors, which increase the influx of K+ and block Ca2+ influx, hyperpolarizing the cell and decreasing the rate of depolarization and slowing the HR

Front 280

What are some situations that affect preload?

Back 280

Inspiration, exercise, aortic regurgitation, and a systemic shunt all increase preload. Valsalva, dehydration, A. fib, and some medications can decrease preload

Front 281

What are the 3 hemodynamic defense systems, what organs do they regulate, what cardiac characteristics can they affect, and what would chronic upregulation result in?

Back 281

* Sympathetic: Nor/Epi binds ß- and a-receptors in the cardiovascular system and adrenal glands. It increases automaticity, afterload, and preload. Chronic stimulation would lead to myocyte death and arrhythmia
* Renin-Angiotensin: Angiotensin II binds its receptors in the kidneys, lungs, and blood vessels and can increase afterload and preload. An increased stimulation would lead to myocyte hypertrophy and ischemia
* Aldosterone: Aldosterone binds mineralcorticoid receptors in the kidney and heart and increases afterload and preload. A chronic increase will cause cardiac fibrosis

Front 282

What are the stages and classes of CHF?

Back 282

Stage A: High risk but no structural changes
Stage B: Structural changes without syndrome
Stage C: Syndrom controlled with therapy
Stage D: Syndrome uncontrolled despite therapy
Class I: No activity limitation
Class II: Mild limitation that improves by slowing down
Class II: Marked limitation improved by rest
Class III: Sever limitation or symptoms even at rest

Front 283

How is exercise handled differently by a healthy heart and a CHF heart?

Back 283

Normally, with exercise the vessels dilate to try and get more blood to the tissues and the heart increases its stroke volume to compensate and meet the body demands. In HF, the heart is unable to increase the stroke volume enough to meet the body's needs

Front 284

What is the impact of diastolic dysfunction?

Back 284

With high LV pressure the LA pressure increases. This backs blood up and causes pulmonary congestion and shortness of breath with activity

Front 285

What is the approach to acute therapy of CHF?

Back 285

* Reduce congestion: reduce preload (diuretic) and afterload (vasodilator)
* Improve performance (inotrope)
* Provide vital organ support as needed

Front 286

What are some signs and symptoms of cardiovascular congestion and what general therapy is used to treat it?

Back 286

* Orthopnea, paroxysmal nocturnal dyspnea, S3, rales, JVD, hepatomegaly, edema
* Reduce fluids: Diuretics (Furosemide) or vasodilators (Nitroglycerine)

Front 287

What are some signs and symptoms of low perfusion?

Back 287

* Cool extremities, hypotension with and ACEi, sleepy, obtunded, low serum sodium
* Increase contractility: Inotropes (Dobutamine, milrinone)

Front 288

What is the medical therapy for CHF?

Back 288

* ACEi to block renin vasoconstriction and fluid retention
* ß-blocker to block sympathetic increase in automaticity, kidney fluid retention, and vessel vasoconstriction

Front 289

What is the most important risk factor for sudden cardiac death?

Back 289

Left ventricular ejection fraction

Front 290

What are the different vascular responses to injury in the different vessel layers?

Back 290

* Intima: thrombi, thickening and spasm, causing pain
* Media: aneurysm and rupture, leading to hypotension and pain
* Adventitia: weakening, false aneurysms causing pain

Front 291

What are the different vascular responses to injury by different sizes of vessels?

Back 291

Large: aneurysm and rupture
Medium: thickening, stenosis, thrombosis, causing ischemia
Small: narrowing causing hypertension
Capillaries: petechial hemorrhage, microthrombi, narrowing

Front 292

What is the common site of atheroma?

Back 292

Atheromas usually develop in the intimal layer of arteries (aorta and it's major branches). Atheromas form at sites of low shear force, opposite branch sites

Front 293

What are complications of arteritis?

Back 293

Inflammation from the arteritis causes:
* Weakened vessel walls leading to aneurysm or rupture
* Narrow lumen causing ischemia
* Damage to the endothelium and leading to thrombosis

Front 294

What is the epidemiology, target vessel, presentation, and results of Kawasaki's disease?

Back 294

Muco-cutaneous lymph node syndrome causes arteritis in children less than 4 years old and it's cardiac symptoms can present years after the infection. It causes fever, RASH, conjunctival or oral erythema and erosion, erythema of palms/soles, and enlarged cervical lymph nodes. It targets coronary arteries and can lead to aneurysm, AMI, or sudden death.

Front 295

What is the epidemiology, pathophysiology, and presentation of Takayasu arteritis?

Back 295

Takayasu arteritis thickens the aortic arch of women under 40. It leads to decreased pulses in the upper extremities, cold or numb fingers, occular disturbances, HTN, and neurological defects. Microscopically it looks like giant cell arteritis.

Front 296

What is the epidemiology, pathophysiology, results, and presentation of Thrombangiitis obliterans?

Back 296

Buerger disease affects young adult males less than 35. It almost exclusively affects tobacco users and the effects resolve following cessation. Inflammation and thrombosis target small & medium sized arteries and lead to fibrosis around nerves and lymphatics. This results in pain, ischemia, and gangrene in the legs and arms

Front 297

Where is the most common site of AAA and what is the physiological reason for this distribution?

Back 297

AAAs are most commonly in the infrarenal aortic section. This is because elastin is the tissue responsible for restricting AAA development and there is a 58% decrease from suprarenal aorta to infrarenal aorta

Front 298

Aortic aneurysm secondary to what infectious disease is describe as "tree-barking"?

Back 298

Syphilis causes inflammatory destruction of the thoracic aorta. It also causes chronic inflammation around the vaso vasorum

Front 299

What is the pathophysiology of mycotic aneurysm?

Back 299

An infection causes destruction to the media, resulting in aneurysm

Front 300

In what vessel pathology is the degradation of elastin important?

Back 300

Vessel aneurysms

Front 301

What are the 3 syndromes on the spectrum of acute coronary syndrome?

Back 301

Unstable angina, non-STEMI, and STEMI

Front 302

How do an unbalanced myocardial oxygen supply and demand lead to angina?

Back 302

If the oxygen demand (heart rate and wall force) is greater than the oxygen supply (arterial PO2, Hb, coronary flow, microciirculation, O2 extraction) it leads to ischemia and pain

Front 303

What classes of drugs increase coronary flow, increasing myocardial oxygen supply, lessing angina?

Back 303

Nitroglycerin and dihydropyridines

Front 304

What classes of drugs prevent thrombus formation, increasing myocardial oxygen supply, lessing angina?

Back 304

Aspirin and thienopyridines (clopdogrel)

Front 305

What classes of drugs decrease ventricular wall force, decreasing myocardial oxygen demand, lessing angina?

Back 305

ß-blockers and ACEi/ARBs

Front 306

What classes of drugs decrease heart rate, decreasing myocardial oxygen demand, lessing angina?

Back 306

ß-blockers and Nondihydropridines

Front 307

What classes of drugs decrease preload, decreasing myocardial oxygen demand, lessing angina?

Back 307

Nitroglycerins

Front 308

Name 3 cardioselective and 3 nonselective ß-blockers and explain how they are different

Back 308

* Cardioselective: Atenolol, Metoprolol, Esmolol
* Nonselective: Labetalol, Carvedilol, Propanolol.
* Nonselectives bind ß2 receptors in the lungs causing bronchospasm

Front 309

What are contraindications for ß-blockers used to treat angina?

Back 309

Hypotension, bradycardia, decompensated HF, and active bronchoconstriction

Front 310

What is the mechanism of nitroglycerin in the treatment of angina?

Back 310

Nitroglycerin increases intracellular cGMP causing venodilation (decreasing preload) and vasodilation (increasing myocardial oxygen supply)

Front 311

What are the 3 nitrates, what is an important administrating characteristic to note, and when are nitrates contraindicated?

Back 311

Nitroglycerine, isosorbide mononitrate, and isosorbide dinitrate. There are enzymes necessary to activate the nitrate and a "nitrate tolerance" can develop when those enzymes are depleted. Patients should remove treatment for 8-10 hours every day to allow for enzyme repletion. Nitrates are contraindicated with ED drugs which are also vasodilators, with RV infarcts, and critical aortic valve stenosis

Front 312

Name some dihydropyridines. What is their mechanism, when do they have compelling indications, and what physiologic reflex can occur with admission?

Back 312

* Nifedipine, Niccardipine, Idradipine, Nisolodipine, Felodipine, Amlodipine
* They inhibit Ca2+ transport across the membrane
* They have compelling indications with chronic kidney disease
* They will elicit a reflex tachycardia and greatly decreased vascular resistance

Front 313

Are nitrates used for chronic angina treatment or for breakthrough pain?

Back 313

Breakthrough pain from their chronic ß-blocker treatment

Front 314

What is Prinzmetal's angina and how is it treated?

Back 314

Prinzmetal's angina is a vasospastic angina not associated with thrombus formation and is sometimes associated with atherosclerosis. DO NOT GIVE ß-BLOCKERS, they will trigger bronchospasm and make things worse. Give long-acting nitrates or Ca2+ channel blockers (Diltiazem, verapamil, amlodipine, felodipine)

Front 315

What anti-anginal drugs are preferred with a HTN comorbidity?

Back 315

ß-blockers and Ca2+ channel blockers

Front 316

What anti-anginal drugs are preferred with a migraine comorbidity?

Back 316

ß-blockers and Ca2+ channel blockers

Front 317

What anti-anginal drugs are preferred with an asthma comorbidity?

Back 317

Nondihydropyridines. NO ß-blockers

Front 318

What anti-anginal drugs are preferred with a hyperthyrodism comorbidity?

Back 318

ß-blockers

Front 319

What anti-anginal drugs are preferred with a diabetes comorbidity?

Back 319

ß-blockers cautiously and Ca2+ channel blockers

Front 320

What anti-anginal drugs are preferred with a SHF comorbidity?

Back 320

ß-blockers, nitrates, maybe add-on a dihydropyridine (amlodipine or felodipine). Do NOT give nondihydropyridines

Front 321

What anti-anginal drugs are preferred with a DHF comorbidity?

Back 321

ß-blocker or nondihydropyridine. Do not give dihydropyridines

Front 322

What anti-anginal drugs are preferred with an A.fib comorbidity?

Back 322

ß-blocker or nondihydropyridine

Front 323

What anti-anginal drugs are preferred with a bradyarrythmia comorbidity?

Back 323

DIhydropyridines. Do NOT give ß-blockers or nondihydropyridines

Front 324

What anti-anginal drugs are preferred with a supraventricular arrythmia comorbidity?

Back 324

ß-blockers or nondihydropyridines

Front 325

What anti-anginal drugs are preferred with a ventricular arrythmia comorbidity?

Back 325

ß-blockers

Front 326

Name some thienopyridines and explain their mechanism of action

Back 326

Thienopyridines (clopidogrel, prasugrel, ticagrelor[reversible]) irreversibly bind P2Y12 receptors on platelets, inhibiting platelet aggregation

Front 327

What is aspirin's mechanism of action?

Back 327

Aspirin irreversibly blocks cyclooxygenase, blocking arachadonic acid conversion into Thromboxane A2, inhibiting platelet aggregation

Front 328

What is the mechanism of action for GpIIb/IIIa inhibitors?

Back 328

GpIIb/IIIa inhibitors displace fibrinogen in thrombi and prevent further cross-linking and platelet activation

Front 329

What is a common side effect of oral anti-platelets that is unrelated to bleeding?

Back 329

Rash

Front 330

What are the treatment recommendations for chronic stable angina?

Back 330

* Aspirin (or clopidogrel if ASA intolerant)
* ß-blocker (metoprolol, carvedilol) to vasodilate and slow HR
* Consider adding a long-acting nitrate, long-acting Ca2+ channel blockers, or an ACEi (Lisinopril: LV dysfunction benefit, decreases diabetes comorbidities)
* Manage lipids with a statin

Front 331

What is the prominent wall layer in venous vessels?

Back 331

Tunica adventitia

Front 332

What is responsible for forcing blood out and through the venous veins?

Back 332

Calf muscles contraction increases the compartment pressure and pushes blood along the venous system

Front 333

What are some causes of increased hydrostatic pressure in the venous system?

Back 333

* Venous valve failure allows blood to flow from deep veins back into superficial veins and increases column height which increases static pressure.
* Obstruction causes distal distention which induces valve failure

Front 334

What are some effects of high venous pressure?

Back 334

* Venous flow holds valve leaflets apart longer adding to value failure
* Fluid backs up into capillary beds increasing edema, extravasation of proteins, and subsequent inflammation which induces wall and valve structural changes

Front 335

Dysfunction at which venous valves contribute to varicose veins, what are the symptoms and treatment of varicose veins?

Back 335

* The saphenofemoral and saphenopopliteal junctions and the perforators are failing
* Varicose veins present as a pain, aching sensation that is better in the morning and worsens as the day progresses
* Treat with compression stockings, elevation, and treat source of reflux

Front 336

What skin changes are associated with venous stasis?

Back 336

GAITER distribution. Lipodermatosclerosis, hemosiderin deposition causing pigmentation, eczema, and ulcerations at the site of perforators

Front 337

What is the management of venous stasis ulceration?

Back 337

Aggressive compression, elevation, antibiotics and debridement if infected or necrotic, skin grafts

Front 338

What are some causes of venous stasis?

Back 338

Immobility on auto or plane trips, valvular dysfunction, pregnancy (pelvic vein compression)

Front 339

What modality is used to diagnose DVT?

Back 339

Venous duplex

Front 340

What is phlegmasia cerulea dolens?

Back 340

A limb threatening, surgical emergency of extensive venous thrombosis often associated with cancer

Front 341

What are the most common causes of secondary lymphedema in the developing v industrialized world?

Back 341

* Developing: Wuscheria bancrofti (filariasis)
* Industrialized: Malignancy and associated treatments

Front 342

What is the flow of fetal circulation and how does it changes postpartum?

Back 342

* Oxygenated blood flows into the RA via the umbilical vein and the IVC. From the RA it flows through the foramen ovale and into the LA, down into the LV, and out the aorta. Less oxygenated blood flows from the RA to the RV, out the pulmonary valve and through the fetal pulmonary system.
* After birth, the umbilical vein is gone and the foramen ovale closes, producing a normal blood flow pattern

Front 343

How do you determine respiratory distress in infants?

Back 343

Follow up on feeding problems or changes

Front 344

What is the most common congenital heart defect, what is its pathophysiology, common presentation, and surgical indications?

Back 344

* Ventricular septal defects are the most common congenital heart defect.
* The hole in the ventricular septum causes a left to right shunt.
* Children will present as not thriving, a normal sized heart, and a holosystolic murmur of varying loudness & pitch.
* Surgery is indicated if there is a huge hole with uncontrollable CHF or pulmonary HTN.

Front 345

What cardiac defect causes a fixed widely split S2?

Back 345

Atrial septal defects because chronic right-sided volume overload decreases resistance in the pulmonary vascular system and this delays the pulmonary portion of S2 even more than normal

Front 346

Which valves is most likely to have a congenital stenosis?

Back 346

The pulmonary valve is most likely to have a congenital stenosis

Front 347

What is the pathophysiology, physical exam findings, and treatment of pulmonary stenosis?

Back 347

Pulmonary stenosis is a lack of separation of the valve cusps. It can cause a hypertrophied RV and a systolic ejection murmur can be heard at the left upper sternal border. Balloon valvuloplasty is indicated in severe stenosis or with a very sick infant

Front 348

What is acrocyanosis?

Back 348

Sluggish circulation in the periphery allows for extensive removal of oxygen in the capillary beds. Common in chilled children

Front 349

Name the 6 cyanotic heart diseases

Back 349

Hey Harry This Turkey Tastes Terrible.
* Hyperplastic Right Heart Syndrome (tricuspid/pulmonary atresia)
* Hyperplastic Left Heart Syndrome
* Transposition of the great arteries
* Transposition of pulmonary veins (Total anomalous pulmonary venous return - TAPVR)
* Tetralogy of Fallot
* Truncus arteriosus

Front 350

What is the most common cyanotic defect and what defects are associated with it?

Back 350

Tetralogy of Fallot. Ventricular septal defect, with an overriding aorta, pulmonary stenosis, and right ventricular hypertrophy

Front 351

What component of tetralogy of Fallot is the variable component responsible for severity?

Back 351

Pulmonary stenosis determines the obstruction of blood flow to the lungs. Mild PS = minimally cyanotic (pink). Severe PS = critically cyanotic (blue)

Front 352

What is the treatment for a tetralogy of Fallot?

Back 352

Palliation until the child is stable , usually a surgical shunt to get more blood to the lungs. Then repair by closing the VSD with a patch and opening the pulmonary outflow tract

Front 353

What is the big picture cause of a myocardial infarction?

Back 353

Inadequate tissue perfusion results in myocardial necrosis

Front 354

How is a myocardial infarction a chronic an acute pathology?

Back 354

Myocardial infarctions a the acute ischemia and necrosing of myocardium following the chronic progression of an atherosclerotic disease

Front 355

What is the most common cause of a vasospasm myocardial infarction?

Back 355

Cocaine use

Front 356

What are some causes of plaque rupture or fissure formation?

Back 356

Changes in intraluminal pressure, bending or twisting of arteries during heart contraction, high lipid content within plaque, the thickness of the fibrous cap, the plaque shape, and mechanical injury

Front 357

What are some risk factors for CAD and acute MI?

Back 357

Smoking, HTN, dyslipidemia, DMII, a positive family history, sedentary lifestyle, obesity, age

Front 358

What cardiac markers are used to detect irreversibly injured ischemic myocardium and when is their elevation detectable?

Back 358

Troponin I, Troponin T, creatine kinase, aspartate serum transaminase, lactate dehydrogenase and their peak elevation is around 24 hours post event

Front 359

What are the T wave, Q wave, and ST segment changes in an acute MI?

Back 359

* Hyper acute T waves are the earliest sign of injury. T wave inversions suggest ischemia
* ST depression in an anatomical distribution suggest ischemia. ST elevation in a consistent anatomical distribution suggests an ongoing myocardial injury
* Diagnostic Q waves in a consistent anatomical pattern suggest prior MI

Front 360

What is the physiologic difference between a STEMI and a NSTEMI?

Back 360

STEMIs result from a complete vessel obstruction. NSTEMIs result from an incomplete blockage or recanalization of a thrombotic occlusion

Front 361

What type of MI shows ST elevation in II, III, and aVF and what artery is implicated?

Back 361

II, III, and aVF detect inferior MI. The right coronary artery supplies that portion of the heart

Front 362

What type of MI shows ST elevation in V1-V3 and what artery is implicated?

Back 362

V1-V3 suggests an anterior MI which implicates the LAD artery

Front 363

How much fluid is in the pericardium and what is it's purpose?

Back 363

10-50 mL and it serves as a lubricant, minimizing frictional forces between the heart and other structures

Front 364

What radiologic finding is found with a congenitally absent pericardium?

Back 364

Pericardial cysts

Front 365

What are the main sources of infections pericarditis?

Back 365

Viral (coxsakie A&B, echovirus, mumps, adenovirus, HIV), mycobacterium tuberculosis, bacterial (Pneumococcus, strep, staph, legionella), fungal (histoplasmosis, coccidioidomycosis, candidiasis, blastomycosis)

Front 366

What are some non-infectious causes of pericarditis?

Back 366

Idiopathic, neoplasm, renal failure, irradiation, MI, hypothyroidism, aortic dissection, trauma

Front 367

What are some causes of hypersensitive pericarditis?

Back 367

Collagen vascular diseases (systemic lupus, rheumatoid arthritis, scleroderma, acute rheumatic fever), drug induced (procainamide, hydralazine, isoniazid), post-MI or cardiac surgery

Front 368

What is the presentation of acute pericarditis?

Back 368

Sudden, severe onset retrosternal or left precordial pain, low-grade fever, tachycardic, frictional rub on ausculataion, possibly pleuritic

Front 369

What are the EKG findings for acute pericarditis?

Back 369

DIFFUSE ST elevation that is anatomically inconsistent with MI and T wave inversion

Front 370

What is the pathophysiology of cardiac tamponade?

Back 370

An accumulation of fluid in the pericardial space increases pressure until cardiac compression results in impaired diastolic ventricular filling, depressing cardiac output

Front 371

What is the presentation for cardiac tamponade?

Back 371

Cardiac tamponade mimics heart failure: dyspnea on exertion, orthopnea, tachycardia, tachypnea, JVD, hypotension and poor peripheral perfusion, shock and hemodynamic collapse, pulsus paradoxus

Front 372

What is the treatment for a cardiac tamponade?

Back 372

Supportive measures (IV fluids and pressors). Remove the fluid (pericardiocentesis, surgical pericardectomy)

Front 373

What is the pathophysiology of constrictive pericarditis and what are some common causes?

Back 373

* A dense fibrosis forms and causes adhesion of the parietal and visceral layers, creating a rigid "case" around the heart. This case decreases diastolic ventricular filling because of the restraint of the thick, rigid, calcified pericardium
* Mediastinal radiation, history of cardiac surgery. Can also be neoplasm, rheumatoid arthritis, or recurrent pericarditis

Front 374

What is the presentation of constrictive pericarditis?

Back 374

Right-sided heart failure: Weakness, dyspnea, orthopnea, anorexia, peripheral edema, hepatosplenomegaly, ascites, pericardial knock, JVD with prominent y descent

Front 375

What is the treatment for constrictive pericarditis?

Back 375

Surgical stripping of the pericardium

Front 376

Name the 2 types of cardiac trauma and give examples of both

Back 376

Penetrating: Gunshot or stab wound
Non-penetrating: Blunt force, rapid deceleration, transections

Front 377

What is the presentation of stable angina?

Back 377

Substernal pain that radiates to the left arm. Often described as a dull, constrictive pressure usually precipitated by exertion. It must present as an unchanged pattern for 60 days or more

Front 378

What is the presentation of unstable angina?

Back 378

New onset angina of less than 2 months. Angina will present at low activity levels or rest and will have increased in frequency or severity from previously stable angina

Front 379

What are the big picture steps in angina therapy?

Back 379

* First, reduce myocardial oxygen demand (ß-blockers, nitrates, ACEi)
* Then stabilize the process exacerbating the problem: coronary artery spasm (Ca2+ channel blockers, nitrates), platelet activation (aspirin, clopidogrel, GpIIb/IIIa receptor blockers), thrombus formation (heparin, LMWH, or thrombolytics if indicated)

Front 380

What are some diagnostic options for diagnosing ischemic heart disease and angina?

Back 380

A good history & physical, an electrocardiogram, an exercise stress test, cardiac catheterization, or coronary angiography

Front 381

What are the 3 therapeutic goals for angina?

Back 381

Relieve the angina, prevent myocardial infarction, and promote longevity

Front 382

What are the 3 main treatment options for angina?

Back 382

Medical therapy, PCI-DES, CABG

Front 383

What veins are most often used to perform CABGs?

Back 383

Saphenous vein, internal mammary artery, radial artery, or gastroepiploic artery

Front 384

What are the options for angioplasty stents and what are 2 considerations when deciding between the 2?

Back 384

Either way the patient needs to be on life-long aspirin
* Drug-eluting stents have a lower restenosis rate (5-10%)
* Bare metal stents require less time on anti-platelet therapy (restenosis rate: 15-25%)

Front 385

What are the treatment options for 50-75% and >75% stenotic angina?

Back 385

* 50-75%: try medical therapy, if angina persists consider PCI-DES or CABG
* >75%: if 1-3 vessels, individualize PCI-DES or CABG based on morphology, LV function. if diffuse, 3 vessels with poor LV and diabetes then use CABG. If it's the left main artery then do CABG

Front 386

Describe changes in the cardiovascular system due to aging

Back 386

* Arterial and myocardial stiffness, impaired ß–adrenergic responsiveness and endothelial function, and reduced sinus node function.
* There is also decreased maximal HR and CO during exercise

Front 387

How is HTN controlled in the elderly?

Back 387

Mainly with lifestyle modification (sodium restriction, weight control, physical activity, moderation of alcohol, smoking cessation, control co-morbid risk factors). First-line therapy is a thiazide diuretic. Statin.

Front 388

What factors contribute to adverse outcomes in older patients with acute coronary syndrome?

Back 388

Age related myocardial changes, increased comorbidity, atypical symptoms & non-diagnostic ECG, extensive coronary artery disease, prevalence of prior myocardial damage, risk of complications from therapy

Front 389

What is the atypical presentation of MI in the elderly?

Back 389

More common in older women: confusion, dyspnea, lassitude, new onset CHF, new arrhythmia, syncope, stroke

Front 390

What are the population differences between DHF and SHF?

Back 390

DHF is more older women with HTN, but without CAD. SHF is associated with middle-aged men with HTN & CAD comorbidities

Front 391

What are the atypical presentations of hypo and hyperthyroidism in older adults?

Back 391

Hypothyroidism is under-diagnosed and is often confused with normal aging. Hyperthyroidism will present as a sedated, apathetic patient without a goiter

Front 392

What is the atypical presentation of acute abdominal disease in older adults?

Back 392

Patients may not feel early pain and the frequency of NSAID use in this population may mask clinical features

Front 393

What is the atypical presentation of infections in older adults

Back 393

Infections can go undetected due to a lack of fever and no leukocytosis

Front 394

What is the pathophysiology of aortic regurgitation?

Back 394

If aorta chronically regugitates, the LV will eccentrically dilate from volume overload in an attempt to lessen pulmonary edema progression

Front 395

What are the physical exam findings in aortic regurgitation?

Back 395

A diastolic "blowing" murmur, an Austin-Flint murmur (diastolic rumbling w/out and opening snap), and a widened pulse pressure (back flow increases preload and increases stroke volume)

Front 396

What is the treatment for aortic regurgitation?

Back 396

Nothing will slow progression, only help symptoms. Vasodilators to encourage forward flow

Front 397

Which valve is the most common target for stenosis from carcinoid syndrome?

Back 397

The tricuspid valve

Front 398

What are the major differences between a mechanical and bioprosthetic valves?

Back 398

Mechanical valves will last the lifespan of the patient but lifetime anti-coagulation is necessary. Bioprosthetic valves need to be replace every 10 years but do not require anti-coagulant therapy

Front 399

What are the 2 systolic ejection murmurs and how are they distinguished?

Back 399

Aortic (RUSB) and Pulmonic (LUSB) Stenosis

Front 400

What are the 2 holosystolic murmurs and how are they distinguished?

Back 400

Mitral regurgitation (apex) and Ventricular septal defect (LSB)

Front 401

How do you distinguish between mitral regurgitation and aortic stenosis?

Back 401

Ask the patient to clench their fists, increasing their afterload. An increase in afterload will increase the regurgitated volume making the murmur louder. The maneuver will have no impact on aortic stenosis

Front 402

Where are a-receptors localized and what does their stimulation do?

Back 402

* A-receptors are in the peripheral and splanchnic vasculature.
* They cause smooth muscle contraction and vasoconstriction.
* They are under negative feedback control and are located pre-synaptically.

Front 403

Where are ß1-receptors localized and what does their stimulation do?

Back 403

* ß1-receptors are located in cardiac tissue and peripheral vasculature.
* They increase cAMP effects, increasing inotropy, chromotropy and lusitropy.
* They are under positive feedback control and are located pre-synaptically.

Front 404

Where are ß2-receptors localized and what does their stimulation do?

Back 404

* ß2-receptors are located in cardiac tissue, peripheral vasculature, and bronchial smooth muscle.
* In cardiac tissue, they increase ino- chromo- and lusitropy. In the peripheral vasculature, they relax smooth muscle and are vasodilators. In the bronchial smooth muscle, they are relaxants and bronchodilators

Front 405

Where are dopamine receptors localized and what does their stimulation do?

Back 405

* Cardiac tissue: Inotropic, chromotropic
* Peripheral and splanchnic vasculature: vasodilation
* Renal: diuretic, natriuretic
* CNS

Front 406

Where are vasopressin receptors localized and what does their stimulation do?

Back 406

* Peripheral & splanchnic vasculature: marked vasoconstriction

Front 407

What classes of drugs are used to increase preload?

Back 407

Administer fluids, a-agonists in low doses

Front 408

What classes of drugs are used to decrease afterload?

Back 408

Vasodilators: ACEi, Nitroprusside, phosphodiesterase inhibitor

Front 409

What classes of drugs are used to increase contractility?

Back 409

Inotropes: ß-adrenergics (dobutamine), phosphodiesterase inhibitor (milrinone)

Front 410

What classes of drugs are used to increase heart rate?

Back 410

Chronotropes: ß-adrenergics (dobutamine), atropine (vagolytic), pacemaker

Front 411

What classes of drugs are used to increase systemic vascular resistance?

Back 411

Vasoconstrictors: a-adrenergics, vasopressin agonists

Front 412

What is epinephrine's mechanism of action and what are its indications?

Back 412

Epinephrine is a ß-agonist. It is inotrophic and chronotropic. It is indicated in cardiogenic shock, post CABG, and with sepsis

Front 413

What is dobutamine's mechanism of action and what are its indications?

Back 413

Dobutamine is a ß-agonist. It is an inotrope (increasing contractility) and chromotrope (increasing HR) and a vasodilator (reducing afterload). It is indicated in acute MI, and mild cardiogenic shock

Front 414

What is norepinephrine's mechanism of action and what are its indications?

Back 414

Norepinephrine is an a-agonist. It is a vasoconstrictor and increases systemic vascular resistance. It is indicated in sepsis and distributive shock with good CO

Front 415

What is phenylephrine's mechanism of action and what are its indications?

Back 415

Phenylephrine is a pure a-agonist. It is a vasoconstrictor and increases systemic vascular resistance. It is indicated in mild sepsis and hypotension with good CO

Front 416

What is dopamine's mechanism of action and what are its indications?

Back 416

Dopamine has dose-dependent pharmacology, at low doses it is dopamine agonist and as doses increase it moves to ß- and then a-activity. It is no longer used.

Front 417

What is vasopressin's mechanism of action and what are its indications?

Back 417

Vasopressin only binds its own receptors. It causes intense vasoconstriction and gut ischemia is a concern. It is indicated in advanced cardiac life support, severe shock, and CABG (when on ACEi)

Front 418

What are milrinone and amrinone's mechanism of action and what are their indications?

Back 418

Milrinone and amrinone are phosphodiesterase inhibitors allowing cAMP and cGMP to stay in circulation longer. They are smooth muscles relaxers, vasodilators and inotropes and augment ß-adrenergic stimulation. They are indicated in CABG and situation of vasoconstriction with low CO

Front 419

How is left atrial pressure measured?

Back 419

Directly by punching a catheter through the foramen ovale, or indirectly by using a Swan-Ganz cathetor and using the pulmonary capillary wedge pressure

Front 420

What is the problem in right sided heart failure, what are some possible causes, and what is the clinical result?

Back 420

* A decreased RV SV leads to a compensatory increase in RA pressure
* Increase in afterload (PS or pulmonary HTN) or decreased contractility (RV infarct or infiltrative disease)
* The result is peripheral edema

Front 421

What is the problem with left heart failure, what are its possible causes and what is the clinical result?

Back 421

* LV SV decreases and that leads to a pressure build up in the LA
* Caused by and increased afterload (aortic stenosis, systemic HTN, aortic coarctation) or decreased contractility (LV infarct or infiltrative disease)
* The result is pulmonary edema

Front 422

What percentage of women suffer sudden cardiac death without having any symptoms?

Back 422

2/3

Front 423

What is the temporal differences in the clinical manifestation of CHD between men and women?

Back 423

Women develop clinical manifestations 10 years later than men

Front 424

What are the risk factors associated with the Framingham RIsk Score?

Back 424

Age, gender, total cholesterol, HDL, smoking, systolic blood pressure, current HTN treatment

Front 425

What are the 2 classes of lifestyle interventions for preventing heart disease in women?

Back 425

* Class I: Smoking cessation, physical activity, diet intake, weight control
* Class II: Omega-3 fatty acids

Front 426

What are the components of metabolic syndrome?

Back 426

* Waist circumference >35in
* Fasting triglycerides >150 mg/dL
* HDL cholesterol <50 mg/dL
* HTN (≥130/≥85) or on HTN drugs
* Fasting glucose ≥100 mg/dL

Front 427

What age group currently has an increasing death rate?

Back 427

Women 35-54

Front 428

What are some potential factors affecting diagnostic accuracy of the exercise tolerance test in women?

Back 428

Hormonal influences, reduced functional capacity, resting ST-T wave abnormalitities

Front 429

How does CAD grossly look in women?

Back 429

Women's CAD is more often a circumferentially diffuse disease without luminal narrowing and less often obstructive plaques

Front 430

Where in the cardiac anatomy would infarcts in the LAD, LCX, and RCA affect?

Back 430

* LAD: anteroseptal LV
* LCX: lateral LV
* RCA: posteroseptal LV

Front 431

What is the time frame for an early acute MI, what does it look like grossly and microscopically?

Back 431

* 6-24 hrs
* Subtle changes, patchy pallor, slight hyperemia
* Thin wavy fibers, eosinophilia, few PMNs

Front 432

What is the time frame for an acute MI, what does it look like grossly and microscopically?

Back 432

* 1-6 days
* Obviously pale, yellow
* Necrotic myocytes, many PMNs

Front 433

What is the time frame for an organizing MI, what does it look like grossly and microscopically?

Back 433

* 1-3 weeks
* Red-brown edges around a pale center
* Granulation tissue, acute and/or chronic inflammation

Front 434

What is the time frame for an remote MI, what does it look like grossly and microscopically?

Back 434

* 3 mos+
* Firm, white scar with a contracted, thin wall
* Collagen inside a thinning wall

Front 435

What is the difference between transmural and subendocardial infarcts?

Back 435

Transmural involves an infarction of the full ventricular wall thickness. Subendocardial is limited to the inner 1/3 to 1/2 of the ventricular wall

Front 436

In what case would a complete vessel occlusion not cause an MI?

Back 436

If there was sufficient collateral blood flow

Front 437

Plaques with what type of architecture is most vulnerable to rupture?

Back 437

Plaques with a soft lipid core and a thin fibrous cap is the most vulnerable to rupture

Front 438

What is the pathogenesis for subendocardial myocardial infarcts?

Back 438

Areas of diffuse CAD & global perfusion deficit undergo periods of increased demand, vasospasm, or hypotension

Front 439

What are common complications of myocardial infarctions?

Back 439

Death, congestive heart failure, rupture (free wall, septum, papillary muscles), mural thrombus, LV aneurysm, dysrrhythmias, pericarditis, pulmonary or leg thromboembolism

Front 440

What are the major manifestations of right-sided heart failure?

Back 440

* Portal, systemic & peripheral (feet, ankles, sacrum) congestion and edema. Pleural & peritoneal effusions/ascites
* Hepatomegaly with severe hypoxia and subsequent central fibrosis
* Congestive splenomegaly with focal hemorrhage and hemosiderin deposits
* Renal congestion with acute tubular necrosis

Front 441

What are the pathological manifestations of acute rheumatic fever?

Back 441

Pancarditis. Rare endocarditis leading to stenotic murmurs. Myocarditis that causes cardiac enlargement and failure, dilation of ventricle and mitral ring. Mitral regurgitation & Aschoff bodies (focal, granulomatous inflammation) are found in the myocardium

Front 442

What are the pathological changes seen in chronic rheumatic heart disease?

Back 442

* Thickening of left-sided valve leaflets (predominantly mitral valve) especially along closure lines. Commissures fuse, chordae tendinae thicken, shorten, and fuse. Result is mitral stenosis, insufficiency, or both
* Mitral stenosis causes LA hypertrophy and dilation, a pulmonary congestion leading to RVH, and chronic L heart failure leading to R heart failure and eventually total heart failure
* Mitral regurgitation causes LV hypertrophy and dilation leading to LA dilation
* Can cause aortic stenosis and regurgitation as well

Front 443

What gross pathological finding is often associated with aortic disease from chronic RHD?

Back 443

The "fish-mouth" bicuspid deformity of the aortic valve is commonly seen in chronic RHD

Front 444

What are the 3 general pathologies of aortic stenosis and compare their epidemiology, mechanism, and murmur presentation?

Back 444

* Acquired: Middle-aged women get fused commissures and thickened closure lines at the aortic and mitral valves almost always from rheumatic fever. Murmur presents in mid-adult life
* Degenerative: Elderly men suffer hemodynamic injury and dystrophic calcification deep in sulci of only the aortic valve. Late onset of murmur.
* Congenital: Bicuspid, uneven tricuspid, or unicommissural aortic valves develop with calcium deep in sulci AND on cusps of only the aortic valve. Childhood murmur but adult stenosis

Front 445

What are the different mechanisms of aortic regurgitation?

Back 445

* Disease of the valve: rigid (rheumatic, degenerative), destruction (microbial endocarditis), collase (prolapse through VSD or with myxomatous degeneration)
* Weaking of the valve ring leading to dilation and a valve insufficient to cover increased area (Marfan, dissecting aneurysm, cystic medial degeneration, syphilitic aortitis)

Front 446

What are the infectious and non-infectious causes of endocarditis?

Back 446

* Non-infective: Verrucous (ARF), atypical verrucous (SLE), non-bacterial thromboembolism
* Infective: Viral, bacterial, fungal destruction of valve tissue. Thrombus w/ invasive organisms

Front 447

What is the natural history of subacute endocarditis?

Back 447

Enteric organismal (S. viridans) infection of previously damaged valve. An insidious onset of low grade fever, malaise, fatigue, anemia, murmur for months. Diagnosed with a series of positive blood tests and treated with IV bacteriocidal antibiotics for 4-6 weeks

Front 448

What is the natural history of acute endocarditis?

Back 448

Virulent, focally destructive infection (S. aureus, S. faecalis) that targets previously normal valves. A sudden onset of high fever, weakness, and murmur that lasts a few weeks. Death from heart failure, valve perforation, or sepsis. Treat with IV antibiotics and resect infected valve

Front 449

What organism is commonly implicated in endocarditis in drug addicts?

Back 449

S. aureus or fungi from skin, contaminated drugs or cutting materials. Mostly left-sided endocarditis, but more likely than non-addicts to get right-sided endocarditis

Front 450

What are common complications of infectious endocarditis and what is the most common cause of death?

Back 450

* Intra-cardiac: Perforated cusps or leaflets, rupture of chordae tendinae, abcess, fistula, obstruction of valve or outflow tract, embolization to coronary arteries. Above mechanisms lead to CHF which leads to death
* Extra-cardiac: Emboli to other organs, mycotic aneurysm, glomerulonephritis (Type III immune reaction)

Front 451

What is the presentation of infective endocarditis?

Back 451

FROM JANE. Fever, roth's spots, osler's nodes, murmur, janeway lesions, anemia, nail bed hemorrhage, embolism

Front 452

What is the pathophysiology of non-infective endocarditis (marantic endocarditis)?

Back 452

Small, sterile fibrin & platelet thrombi adhere to valves at closure lines of the mitral valve. Often due to systemic hypercoagulability and seen in cancer patients 2˚ to DIC. Can embolize systemically

Front 453

What valves are targeted in Libman-Sacks endocarditis and what changes are found?

Back 453

Libman-Sacks endocarditis is a valvulitis targeting the mitral and tricuspid valves in the context of SLE & anti-phospholipid syndrome. Fibrinous vegetation builds on either side of the valve leading to necrosis and valve deformations

Front 454

What is the pathophysiology of carcinoid heart disease?

Back 454

Elaboration of bioactive products (serotonin, bradykinin, histamine, prostaglandin) cause right-sided valvular lesions

Front 455

What is the epidemiology, morphology, presentation, and complications associated with mitral valve prolapse?

Back 455

Females aged 20-40 can develop stretched, redundant myxomatous valves with interchordal hooding. Mid-systolic click (atypically dyspnea, fatigue, psychologic manifestations) or asymptomatic. Complications include mitral regurgitation, 2˚ infective endocarditis, or sudden death

Front 456

What are the diagnostic criteria, morphology, and clinical features of hypertensive cardiovascular disease?

Back 456

HTCVD is diagnose when there is concentric LVH with a history of HTN and an absence of other LVH-causing lesions. It is concentric LVH and cardiomegaly enlarged by myocytes and nuclei leading to diffuse interstitial fibrosis, focal degeneration, LV dilation and thinning.

Front 457

What is cor pulmonale and what condition is it associated with?

Back 457

The right-sided counterpart of systemic HTCVD. RVH or dilation 2˚ to chronic pulmonary HTN (disorders affecting lung structure or function). Commonly caused by COPD. EXCLUDE RVH 2˚ CHD or LV disease

Front 458

What is the morphology of general myocarditis?

Back 458

Soft myocardium w/ 4 chamber dilation and matchy hemorrhagic mottling. Mural thrombi may form. Myocardial inflammation with infiltration, myocyte necrosis and degeneration. Focal lesions

Front 459

What is the natural history of hypertrophic cardiomyopathy?

Back 459

Hypertrophic cardiomyopathy is often familial. A thickening of the septum narrow the LV outflow tract leading to impaired ventricular compliance, pump failure, systolic murmur, dysrhythmia, and sudden death. Microscopic myofiber disarray

Front 460

What are common complications of infectious endocarditis and what is the most common cause of death?

Back 460

* Intra-cardiac: Perforated cusps or leaflets, rupture of chordae tendinae, abcess, fistula, obstruction of valve or outflow tract, embolization to coronary arteries. Above mechanisms lead to CHF which leads to death
* Extra-cardiac: Emboli to other organs, mycotic aneurysm, glomerulonephritis (Type III immune reaction)

Front 461

What is the presentation of infective endocarditis?

Back 461

FROM JANE. Fever, roth's spots, osler's nodes, murmur, janeway lesions, anemia, nail bed hemorrhage, embolism

Front 462

What is the pathophysiology of non-infective endocarditis (marantic endocarditis)?

Back 462

Small, sterile fibrin & platelet thrombi adhere to valves at closure lines of the mitral valve. Often due to systemic hypercoagulability and seen in cancer patients 2˚ to DIC. Can embolize systemically

Front 463

What valves are targeted in Libman-Sacks endocarditis and what changes are found?

Back 463

Libman-Sacks endocarditis is a valvulitis targeting the mitral and tricuspid valves in the context of SLE & anti-phospholipid syndrome. Fibrinous vegetation builds on either side of the valve leading to necrosis and valve deformations

Front 464

What is the pathophysiology of carcinoid heart disease?

Back 464

Elaboration of bioactive products (serotonin, bradykinin, histamine, prostaglandin) cause right-sided valvular lesions

Front 465

What is the epidemiology, morphology, presentation, and complications associated with mitral valve prolapse?

Back 465

Females aged 20-40 can develop stretched, redundant myxomatous valves with interchordal hooding. Mid-systolic click (atypically dyspnea, fatigue, psychologic manifestations) or asymptomatic. Complications include mitral regurgitation, 2˚ infective endocarditis, or sudden death

Front 466

What are the diagnostic criteria, morphology, and clinical features of hypertensive cardiovascular disease?

Back 466

HTCVD is diagnose when there is concentric LVH with a history of HTN and an absence of other LVH-causing lesions. It is concentric LVH and cardiomegaly enlarged by myocytes and nuclei leading to diffuse interstitial fibrosis, focal degeneration, LV dilation and thinning.

Front 467

What is cor pulmonale and what condition is it associated with?

Back 467

The right-sided counterpart of systemic HTCVD. RVH or dilation 2˚ to chronic pulmonary HTN (disorders affecting lung structure or function). Commonly caused by COPD. EXCLUDE RVH 2˚ CHD or LV disease

Front 468

What is the morphology of general myocarditis?

Back 468

Soft myocardium w/ 4 chamber dilation and matchy hemorrhagic mottling. Mural thrombi may form. Myocardial inflammation with infiltration, myocyte necrosis and degeneration. Focal lesions

Front 469

What is the natural history of hypertrophic cardiomyopathy?

Back 469

Hypertrophic cardiomyopathy is often familial. A thickening of the septum narrow the LV outflow tract leading to impaired ventricular compliance, pump failure, systolic murmur, dysrhythmia, and sudden death. Microscopic myofiber disarray

Front 470

What is the pathogenesis and morphology of dilated/congestive myocarditis?

Back 470

* Alcohol, peripartum, sarcoid, autoimmune, and chemotherapy
* Cardiomegaly, mural thrombi, normal valves, subtle microscopic changes of mycotic hypertorphy and interstitial fibrosis

Front 471

What is the natural history of restrictive myocarditis?

Back 471

Amyloid infiltration of the myocardium with a characteristic CONGO RED STAIN. Amyloid can sometimes be limited to heart and vessels. Can mimic ischemic heart disease (failure, EKG changes)

Front 472

What are the 3 types of obliterative myocarditis?

Back 472

* Endomyocardial fibrosis: children and young adults in Africa. Subendocardial fibrosis decreasing ventricular chamber volume
* Fibroblastic endocarditis (Loeffler's): Endomyocardial fibrosis, mural thrombi, peripheral eosinophilia, eosinophilic infiltration, rapidly fatal!
* Endocardial fibrosis: children <2 yo

Front 473

What is the pathophysiology of arrhythmogenic myocarditis?

Back 473

* Autosomal dominant: RV adipose or fibro-adipose replacement
* Autosomal recessive: RV aneurysms
* Myocarditis: LV dilation
* Causes serious dysrhythmia and sudden death

Front 474

What is the common physiological problem with dilated cardiomyopathy?

Back 474

A decreased left ventricular ejection fraction

Front 475

What are some common etiologies of non-ischemic dilated cardiomyopathy?

Back 475

Tachycardia-meidated, excessive alcohol, peripartum, chemotherapy toxicity (especially adriamycin), infectious (chagas, lyme, rocky mountain spotted fever, rheumatic fever)

Front 476

What are some risk factors for peripartum cardiomyopathy?

Back 476

Maternal age >30 yo, african descent, previous twin or triplet pregnancy, previous preeclampsia or pregnancy-induced hypertension, long term tocolytic treatment, cocaine use

Front 477

What viruses are commonly indicated in viral myocarditis and what populations are particularly at risk?

Back 477

* Coxsakievirus! parvovirus, HHV6, influenza, adenovirus, echovirus, CMV, HIV
* Infants and pregnant women

Front 478

What mutations are commonly associated with hypertrophic cardiomyopathy?

Back 478

ß-myosin heavy chain! Troponin T or a-tropomyosin

Front 479

How do the two pathological findings in hypertrophic cardiomyopathy lead to its clinical manifestations?

Back 479

* Thickened muscle decreases its ability to relax, decreasing its diastolic function and increasing the LVEDP
* Myofibrillar disarray increases risk of dangerous, deadly ventricular arrhythmia

Front 480

What is the pathogenesis and morphology of dilated/congestive myocarditis?

Back 480

* Alcohol, peripartum, sarcoid, autoimmune, and chemotherapy
* Cardiomegaly, mural thrombi, normal valves, subtle microscopic changes of mycotic hypertorphy and interstitial fibrosis

Front 481

What is the natural history of restrictive myocarditis?

Back 481

Amyloid infiltration of the myocardium with a characteristic CONGO RED STAIN. Amyloid can sometimes be limited to heart and vessels. Can mimic ischemic heart disease (failure, EKG changes)

Front 482

What are the 3 types of obliterative myocarditis?

Back 482

* Endomyocardial fibrosis: children and young adults in Africa. Subendocardial fibrosis decreasing ventricular chamber volume
* Fibroblastic endocarditis (Loeffler's): Endomyocardial fibrosis, mural thrombi, peripheral eosinophilia, eosinophilic infiltration, rapidly fatal!
* Endocardial fibrosis: children <2 yo

Front 483

What is the pathophysiology of arrhythmogenic myocarditis?

Back 483

* Autosomal dominant: RV adipose or fibro-adipose replacement
* Autosomal recessive: RV aneurysms
* Myocarditis: LV dilation
* Causes serious dysrhythmia and sudden death

Front 484

What is the common physiological problem with dilated cardiomyopathy?

Back 484

A decreased left ventricular ejection fraction

Front 485

What are some common etiologies of non-ischemic dilated cardiomyopathy?

Back 485

Tachycardia-meidated, excessive alcohol, peripartum, chemotherapy toxicity (especially adriamycin), infectious (chagas, lyme, rocky mountain spotted fever, rheumatic fever)

Front 486

What are some risk factors for peripartum cardiomyopathy?

Back 486

Maternal age >30 yo, african descent, previous twin or triplet pregnancy, previous preeclampsia or pregnancy-induced hypertension, long term tocolytic treatment, cocaine use

Front 487

What viruses are commonly indicated in viral myocarditis and what populations are particularly at risk?

Back 487

* Coxsakievirus! parvovirus, HHV6, influenza, adenovirus, echovirus, CMV, HIV
* Infants and pregnant women

Front 488

What mutations are commonly associated with hypertrophic cardiomyopathy?

Back 488

ß-myosin heavy chain! Troponin T or a-tropomyosin

Front 489

How do the two pathological findings in hypertrophic cardiomyopathy lead to its clinical manifestations?

Back 489

* Thickened muscle decreases its ability to relax, decreasing its diastolic function and increasing the LVEDP
* Myofibrillar disarray increases risk of dangerous, deadly ventricular arrhythmia

Front 490

What is the difference between HCM and HOCM?

Back 490

If the ventricular septum hypertrophies asymmetrically it can cause the anterior leaflet of the mitral valve to get sucked towards it and obstruct flow into the aorta causing "Dynamic LV outflow obstruction"

Front 491

What makes dynamic LV outflow obstruction worse or better?

Back 491

* Worse: decrease LV volume (dehydration) or increased contractility (exercise or inotropic drugs)
* Better: increase volume (hydration) or decrease contractility (ß-blocker or NDHP Ca2+ channel blocker)

Front 492

What 2 exam maneuvers are important in diagnosing a HOCM?

Back 492

The squat to stand and the valsalva.
* Patient squats increasing venous return and increasing the LVEDP, keeping the mitral away from the septum and decreasing or eliminating the murmur
* When the patient stands, it decreases their venous return and LVEDP, with less volume to keep the mitral leaflet from obstructing the HOCM murmur will get louder
* With valsalva, increased intra-abdominal pressure decreases venous return and LVEDP, the murmur will get louder

Front 493

How do you distinguish between an aortic stenosis and a HOCM murmur?

Back 493

* HOCM (dynamic LV outflow obstruction) will get louder when then volume (venous return/LVEDP) decreases, Valsalva and standing back up will make HOCM murmurs get louder.
* Aortic stenosis murmurs get louder when there is an increase in venous return and LVEDP. Squatting will make an aortic stenosis murmur get louder

Front 494

What are some potential treatments for HOCM?

Back 494

* Negative inotropes (ß–blockers, NDHP Ca2+ channel blockers)
* Surgical myomectomy (cutting out part of the septum)
* Intentional septal infarct

Front 495

What are the 3 mechanisms of restrictive cardiomyopathy? Give examples

Back 495

* Fibrosis or scarring like in scleroderma
* Infiltration of myocardium by amyloid, sarcoid, or rarely, cancer
* Deposition of hemochromatosis or glycogen

Front 496

Is systole or diastole affected in a restrictive cardiomyopathy?

Back 496

Diastole, because the "cage" restricts the ventricles ability to relax

Front 497

What are the common signs and symptoms of Rheumatic fever?

Back 497

FEVERSS.
* Fever
* Erythema marginatum
* Valvular damage (vegetation and fibrosis)
* Erythocyte sedementation rate increase
* Red-hot joints (migratory polyarthritis)
* Subcutaneous nodules
* St. Vitus' dance (chorea)

Front 498

What size vessels control vascular resistance?

Back 498

Small arteries and arterioles

Front 499

Where in the circulation is the greatest cross-sectional area?

Back 499

Capillaries and venules

Front 500

What are the two systems that coordinate together to regulate global circulatory homeostasis?

Back 500

Autonomic innervation (baro and chemoreceptors) and circulating hormones (ANP, ADH, bradykinin, PG, TxA)

Front 501

Where are the three types of baroreflexes located and what do they affect?

Back 501

* Arterial baroreceptors trigger the brainstem vasomotor center to change total peripheral resistance, cardiac performance, sympathetic kidney drive, and venous compliance
* Cardiopulmonary receptors act at the brainstem vasomotor center affecting venous compliance, sympathetic kidney drive, total peripheral resistance, and cardiac performance and stimulates the hypothalamus to release antidiuretic hormone (vasopressin)
* Intrarenal baroreceptors stimulate the RAS, GFR, and salt and water reabsorption

Front 502

What affect does increasing blood pressure have at baroreceptors?

Back 502

Increasing blood pressure will increase baroreceptor firing which will increase parasympathetic stimulation to the heart and decrease sympathetic stimulation to the heart and vessels

Front 503

What do chemoreceptors monitor and how do they respond?

Back 503

Chemoreceptors in the carotid and aortic bodies monitor oxygen, hydrogen (pH), and carbon dioxide. They are stimulated by decreased blood flow or increased CO2, and decreased pH and O2. They respond by activating a sympathetic respiration response

Front 504

What catecholamine is released more by the adrenal medulla and which is released by sympathetic nerve activation at the blood vessel?

Back 504

Epinephrine is released in higher percentages by the adrenal medulla. Sympathetic nerves release more Norepinephrine

Front 505

Name 3 situations where renal renin release is stimulated

Back 505

Sympathetic stimulation, hypotension, and decreased sodium delivery to the distal tubules

Front 506

What are the effects of the RAS at the brain, the kidney, the vasculature, and the adrenal gland?

Back 506

* Brain: thirst & sympathetic activity
* Kidney: water & salt retention
* Vasculature: vasoconstriction & increased blood pressure
* Adrenal: aldosterone release

Front 507

Where is vasopressin produced and what does it do?

Back 507

Anti-diuretic hormone (vasopressin) is released by the posterior pituitary and stimulates thirst, acts at the kidneys to increase blood volume, and vasoconstricts blood vessels

Front 508

What is atrial natriuretic peptide and what does it do?

Back 508

Atrial natriuretic peptide is released by the atrial myocytes when they are stretched and counter-balance the RAAS. ANP increases GFR decreasing the blood volume, the cardiac output, and eventually the arterial pressure

Front 509

What are some common tissue factors that contribute to local blood flow regulation?

Back 509

* CO2, H+, K+, lactate, adenosine.
* Histamine, bradykinin, prostacyclin, leukotrienes
* They originate in tissue (often as metabolic products) and act as either constrictors or relaxants

Front 510

What are some common endothelial factors and how do they contribute to local blood flow regulation?

Back 510

* Nitric oxide and prostacyclins are dilators
* Endothelin, leukotrienes, and thromboxanes are constrictors
* They are released during physical stress (shear) and act via endothelial receptors or directly on smooth muscle

Front 511

Which vasodilators are receptor dependent and which are receptor independent?

Back 511

* Acetylcholine, bradykinin, serotonin, histamine, substance P are all vasodilators that circulate in the lumen, bind a receptor and trigger NO release.
* Sodium nitroprusside is a direct NO donor and does not need to bind to endothelial receptors to have a vasodilating effect

Front 512

Are prostaglandins (PGI2) vasodilators or vasoconstrictors, what is their source, and where do they have their effect?

Back 512

Prostaglandins are vasodilators that are released by endothelial cells and have their effect at vascular smooth muscle

Front 513

Is adenosine a vasodilator or vasoconstrictor, what is its source, and where does it have its effect?

Back 513

Adenosine is a vasodilator that is released by parenchymal cells and has its effect at vascular smooth muscle

Front 514

Is epinephrine a vasodilator or vasoconstrictor, what is its source, and where does it have its effect?

Back 514

Epinephrine is a vasodilator that is released by the adrenal medulla and has its effect at ß2-receptors and vascular smooth muscle

Front 515

Are H+, CO2, and K+ vasodilators or vasoconstrictors, what is their source, and where do they have their effect?

Back 515

H+, CO2, and K+ are vasodilators that are released by skeletal muscle and have their effect at vascular smooth muscle

Front 516

Is endothelium derived hyperpolarizing factor a vasodilator or vasoconstrictor, what is its source, and where does it have its effect?

Back 516

Endothelium derived hyperpolarizing factor is a vasodilator that is released by endothelial cells and has its effect at vascular smooth muscle and K+ channels

Front 517

Where is vasopressin produced and what does it do?

Back 517

Anti-diuretic hormone (vasopressin) is released by the posterior pituitary and stimulates thirst, acts at the kidneys to increase blood volume, and vasoconstricts blood vessels

Front 518

What is atrial natriuretic peptide and what does it do?

Back 518

Atrial natriuretic peptide is released by the atrial myocytes when they are stretched and counter-balance the RAAS. ANP increases GFR decreasing the blood volume, the cardiac output, and eventually the arterial pressure

Front 519

What are some common tissue factors that contribute to local blood flow regulation?

Back 519

* CO2, H+, K+, lactate, adenosine.
* Histamine, bradykinin, prostacyclin, leukotrienes
* They originate in tissue (often as metabolic products) and act as either constrictors or relaxants

Front 520

What are some common endothelial factors and how do they contribute to local blood flow regulation?

Back 520

* Nitric oxide and prostacyclins are dilators
* Endothelin, leukotrienes, and thromboxanes are constrictors
* They are released during physical stress (shear) and act via endothelial receptors or directly on smooth muscle

Front 521

Which vasodilators are receptor dependent and which are receptor independent?

Back 521

* Acetylcholine, bradykinin, serotonin, histamine, substance P are all vasodilators that circulate in the lumen, bind a receptor and trigger NO release.
* Sodium nitroprusside is a direct NO donor and does not need to bind to endothelial receptors to have a vasodilating effect

Front 522

Are prostaglandins (PGI2) vasodilators or vasoconstrictors, what is their source, and where do they have their effect?

Back 522

Prostaglandins are vasodilators that are released by endothelial cells and have their effect at vascular smooth muscle

Front 523

Is adenosine a vasodilator or vasoconstrictor, what is its source, and where does it have its effect?

Back 523

Adenosine is a vasodilator that is released by parenchymal cells and has its effect at vascular smooth muscle

Front 524

Is epinephrine a vasodilator or vasoconstrictor, what is its source, and where does it have its effect?

Back 524

Epinephrine is a vasodilator that is released by the adrenal medulla and has its effect at ß2-receptors and vascular smooth muscle

Front 525

Are H+, CO2, and K+ vasodilators or vasoconstrictors, what is their source, and where do they have their effect?

Back 525

H+, CO2, and K+ are vasodilators that are released by skeletal muscle and have their effect at vascular smooth muscle

Front 526

Is endothelium derived hyperpolarizing factor a vasodilator or vasoconstrictor, what is its source, and where does it have its effect?

Back 526

Endothelium derived hyperpolarizing factor is a vasodilator that is released by endothelial cells and has its effect at vascular smooth muscle and K+ channels

Front 527

Are angiotensin(1-7), bradykinin, and substance P vasodilators or vasoconstrictors, what is their source, and where do they have their effect?

Back 527

Angiotensin(1-7), bradykinin, and substance P are vasodilators that are released by blood and local tissue. They have their effects at NO or PG receptors and on vascular smooth muscle

Front 528

Is Angiotensin II a vasodilator or vasoconstrictor, what is its source, and where does it have its effect?

Back 528

Angiotensin II is a vasoconstrictor that is released by the kidneys, blood, and local tissue. It has its effects at ATII receptors and on vascular smooth muscle

Front 529

Is Arginine vasopressin a vasodilator or vasoconstrictor, what is its source, and where does it have its effect?

Back 529

Arginine vasopressin is a vasoconstrictor that is released by the posterior pituitary. It has its effects at vasopressin receptors and on vascular smooth muscle

Front 530

Are Norepinephrine and Epinephrine vasodilators or vasoconstrictors, what is their source, and where do they have their effect?

Back 530

Norepinephrine and Epinephrine are vasoconstrictors that are released by the adrenal medulla. They have their effects at a-receptors and on vascular smooth muscle

Front 531

Is endothelin a vasodilator or vasoconstrictor, what is its source, and where does it have its effect?

Back 531

Endothelin is a vasoconstrictor that is released by the endothelial cells and has its effects at ET receptors and on vascular smooth muscle

Front 532

What is autoregulation of blood flow and what organs have this feature

Back 532

Autoregulation is an intrinsic characteristic to the brain, kidneys, and heart and involves being able to maintain a constant blood pressure despite changes in perfusion pressure

Front 533

Do the coronary arteries have a high or low vasodilator reserve?

Back 533

The coronary arteries have a high vasodilator reserve

Front 534

When do the coronary arteries fill and the left ventricular receive its perfusion?

Back 534

The coronary arteries fill during diastole and they deliver that pulsatile perfusion to the LV

Front 535

What is the pathology behind Raynaud's Syndrome?

Back 535

Excessive sympathetic vasoconstriction in response to cold

Front 536

What are the two capillary beds in the kidneys and what are their distinct functions?

Back 536

The glomerular capillaries are at high pressure to drive filtration. The peritubular capillaries are at low pressures to facilitate reabsorption

Front 537

What are the two circulations in the lungs, what are their functions, and which side of the heart do they receive blood from?

Back 537

* The bronchial circulation provides nutritive flow to the trachea and bronchial structures from the aorta.
* The pulmonary circulation supplies blood to the alveoli for gas exchange. It pumps right ventricle blood at low resistance and pressure. Unlike other organs, hypoxia will cause vasoconstriction (body needs more O2). Sympathetic stimulation increases resistance and mobilizes blood into the systemic circulation

Front 538

What is the greatest contributor to racial disparities in life expectancy?

Back 538

Chronic heart disease

Front 539

From a population perspective, what are the leading risk factors for heart failure?

Back 539

Hypertension leading to LVH, coronary artery disease, diabetes

Front 540

What are the 4 leading risk factors for CVD in the US?

Back 540

Smoking, diabetes, high cholesterol, hypertension. Obesity, diet, physical activity, education, genetics, socioeconomic status, and public policy all play factors as well

Front 541

Are clinical interventions or risk factor reductions contributing more to the reduction in heart disease deaths?

Back 541

Both clinical intervention and risk factor reduction are both contributing about 50% to heart disease death reduction

Front 542

What are the 1˚, 2˚, and 3˚ measures for doctors trying to prevent CVD death?

Back 542

1˚: Screen for risk factors, educate and counsel patients, treat with drugs and lifestyle modifications
2˚: Manage survivors to prevent recurrence (HTN, lipids, ASA)
3˚: Treat CVD, CVA, HF acutely using evidence-based strategies

Front 543

What is the acronym for the 4 things patients should focus on to decrease their risk of CHD?

Back 543

ABCS. Aspirin, blood pressure control, cholesterol control, smoking cessation

Front 544

What is the silver bullet strategy vs the polypill strategy?

Back 544

* Silver bullet: Pick drugs that are effective, combine them into one pill, with each drug at half dose to minimize side effects and give it to all with CVD and all adults over a certain age, regardless of risk factors
* Polypill: A statin, 3 BP lowering drugs (thiazide, ß-blocker, ACEi), folic acid, and aspirin. Start at 55 or CVD.

Front 545

What are health disparities?

Back 545

Population-specific differences in the presence of a disease, health outcome or access to healthcare