Term
| Delayed Afterdepolarization (DAD) |
|
Definition
| if the SR sequesters abnormally high levels of calcium (eg. exposure to abnormally high levels of epinephrine) it will spontaneously dump its calcium into the cytoplasm during diastole. This will cause the cell to contract but most importantly the high cytoplasmic calcium acts to promote forward Na-Ca exchange (ie. 3 Na+ in exchanged for 1 Ca2+ out) as shown in the figure below. This occurs rapidly and causes transient depolarization of the cell to produce a DAD. If the DAD reaches the INa threshold an action potential will occur (triggered beat). Digoxin and high sympathetic tone can cause DADs; |
|
|
Term
| Early Afterdepolarizations (EADs) |
|
Definition
occur during action potential
repolarization and can lead to repetitive firing. mechanism
appears to be an increase in inward current, most likely ICa, or INa, or a decrease in outward current ( IK). EADs initiated during the action potential plateau appear to depend on Ca influx via ICa . Those initiated at more negative potentials are thought to depend on Na influx via sodium channels. drugs that prolong repolarization can cause EADs |
|
|
Term
|
Definition
Normal: -30 to 110
Left deviation: -30 to -90
right deviation: 90 to 180.
Bottom of pie is all + top is -. Far right is 0 far left is 180 |
|
|
Term
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
Poor Man's Guide to the upper limit of QT: @ 70 bpm, QT < 0.40s; for every 10 bpm increase above 70 bpm subtract 0.02s, and for every 10 bpm decrease below 70 bpm add 0.02s. For example:
QT < 0.38 @ 80 bpm
QT < 0.42 @ 60 bpm |
|
|
Term
| Differential Diagnosis of Short PR: < 0.12s |
|
Definition
1. Preexcitation syndromes: WPW (Wolff-Parkinson-White) Syndrome, and LGL (Lown-Ganong-Levine) Syndrome.
2. AV Junctional Rhythms with retrograde atrial activation (inverted P waves in II, III, aVF)
3. Ectopic atrial rhythms originating near the AV node
4. Normal Variant (PR 0.10 - 0.12s) |
|
|
Term
| Differential Diagnosis of Prolonged PR: >0.20s |
|
Definition
1. First degree AV block
2. Second Degree AV block
3. AV dissociation |
|
|
Term
|
Definition
(PR interval usually constant from beat to beat); possible locations for the conduction delay include:
• Intra-atrial conduction delay (uncommon)
• Slowed conduction in AV node (most common site of prolonged PR)
• Slowed conduction in His bundle (rare)
• Slowed conduction in a bundle branch (when contralateral bundle is totally blocked; i.e., 1st degree bundle branch block) |
|
|
Term
|
Definition
(PR interval may be normal or prolonged; some P waves do not conduct to ventricles and are not followed by a QRS)
• Type I (Wenckebach): Increasing PR until nonconducted P wave occurs
• Type II (Mobitz): Fixed PR intervals plus nonconducted P waves |
|
|
Term
|
Definition
| Some PR's may appear prolonged, but the P waves and QRS complexes are dissociated (i.e., not married, but strangers passing in the night). |
|
|
Term
| Differential for QRS duration 0.10 - 0.12s |
|
Definition
• Incomplete right or left bundle branch block
• Nonspecific intraventricular conduction delay (IVCD)
• Some cases of left anterior or posterior fascicular block |
|
|
Term
|
Definition
• Complete RBBB or LBBB
• Nonspecific IVCD
• Ectopic rhythms originating in the ventricles (e.g., ventricular tachycardia, accelerated ventricular rhythm, pacemaker rhythm) |
|
|
Term
| Which types of Calcium channels are located on the t-tubules and sarcoplasmic reticulum respectively. |
|
Definition
T-tubules: L -type
SR: Ryanodine (RyR) |
|
|
Term
|
Definition
| Muscle contracts but maintains constant length. The passive tension in a muscle prior to contraction is called the preload. Preload refers to the degree to which the sarcomeres are stretched just before the onset of systole. |
|
|
Term
|
Definition
| Muscle contracts and shortens against a constant load. (afterload in the heart) |
|
|
Term
|
Definition
C = Change in Vol. / Change in Press.
Compliance is high in veins low in arteries. |
|
|
Term
| Flow rate Q is proportional to the vessel radius raised to what power |
|
Definition
|
|
Term
| Law of Laplace (vessel wall tension) |
|
Definition
Vessel wall tension = transmural
(across the wall) pressure (tm) times vessel radius (r) divided by vessel wall thickness (h).
T = (tm x r) / h.
Wall tension is the tendency of the vessel to pull apart. This becomes very important clinically for dilated hearts and vessels that have thin walls (ie, an aneurysm). They are very prone to rupture. |
|
|
Term
| What vasoactive substances do endothelial cells release |
|
Definition
| Nitric Oxide (vasodilator, acts through 2nd messenger cGMP) and endothelin (vasoconstrictor) |
|
|
Term
|
Definition
| ET, produce by endothelial cells and by cardiac cells. Most potent vasoconstrictor, also has a potent positive inotropic effect on heart. promotes cell growth-thus probably important in development of cardiac hypertrophy. ET-1 probably does not play an important role in normal regulation of vascular tone and thus arterial blood pressure. However, recent evidence suggests that it may contribute to arteriolar constriction and thus TPR in hypertensive individuals. Its production and release are augmented in damaged vessels and during ischemia and are thought to exacerbate cell injury. |
|
|
Term
|
Definition
| Systolic pressure - diastolic pressure |
|
|
Term
|
Definition
| Diastolic pressure + 1/3 Pulse pressure = average driving force. |
|
|
Term
| What effect does circulating epinephrine have on coronary and skeletal muscle arterioles |
|
Definition
Dilation via Beta 2 receptors. Epinephrine causes vasodilation in low
concentrations (i.e. the normal levels produced by body) by interacting with beta 2 adrenergic receptors. This helps dilate arterioles during exercise. At higher pharmacological concentrations E binds with alpha adrenergic receptors and elicits vasoconstriction. |
|
|
Term
| What effect does circulating NORepinephrine have on coronary and skeletal muscle arterioles |
|
Definition
| Vasocontriction via Alpha 1 receptors |
|
|
Term
| Brief summary of the two mechanisms of intrinsic Control of Arteriolar Diameter. |
|
Definition
1) metabolic autoregulation: dilation of arterioles occurs when the metabolic rate of an organ or tissue increases, resulting in increased oxygen and nutrient delivery. Called active hyperemia. Vasodilation is triggered by local chemical changes in the extracellular space, including a local fall in oxygen tension, increased carbon dioxide tension, local release of adenosine, potassium and local acidosis. Prominent mechanism in skeletal and heart muscle and brain.
2) flow autoregulation: maintenance of nearly constant tissue perfusion in the face of changes in arterial pressure. This is achieved by compensatory changes in flow resistance. When pressure rises the arterioles constrict and when pressure falls they dilate. Fails at extremes of either end. prominent in the heart,
brain, kidneys, skeletal muscle, GI tract. |
|
|
Term
| precapillary sphincters are under what control |
|
Definition
|
|
Term
|
Definition
= - (D) X (surface area for diffusion) X (ΔC/ ΔX)
where D is the diffusion coefficient, (reflecting the ease with which the substance diffuses across the membrane), ΔC is the concentration gradient of the substance across the capillary and ΔX is the thickness of the capillary wall. |
|
|
Term
| Examples of conditions that cause edema |
|
Definition
1. lymphatic blockage, blocks return extra filtered fluid back to the to circulation.
2. decreased plasma protein concentration (liver failure, malnutrition) decreases
the inwardly directed concentration gradient for H20.
3. increased capillary permeability to protein, causes ΠlF to increase, thus
decreases inwardly directed concentration gradient for water. e.g. burns.
4. vasodilatation of arterioles, increases Pcap.
5. conditions which elevate venous blood pressure, increases Pcap .
eg. blood clots in veins, heart failure (blood “backs up” in veins) |
|
|
Term
| What is the most significant mechanism and important stimuli influencing blood flow to the heart |
|
Definition
blood flow is almost entirely regulated by local metabolic mechanisms. The most important local stimuli for increased flow (arteriolar dilation) are low oxygen and adenosine. The sympathetic input to arterioles can cause vasoconstriction in response to cold or anger. In individuals with narrowed coronary arteries (atherosclerosis) this may
produce angina or provoke a heart attack. |
|
|
Term
| What is the most significant mechanism and important stimuli influencing blood flow to the brain |
|
Definition
| Metabolic regulation. Important stimuli for increased flow are elevated carbon dioxide and acidity |
|
|
Term
| What is the most significant mechanism and important stimuli influencing blood flow to the skeletal muscle |
|
Definition
During exercise local mechanisms
predominate. Arterioles are richly innervated by sympathetic vasoconstrictor fibers which
contribute to vasomotor tone at rest and especially when arterial pressure falls. The baroreceptor reflex can reduce muscle flow to 1/5 normal. |
|
|
Term
| Major mechanism of blood flow control to the kidney |
|
Definition
| Prominent role for flow autoregulation (When pressure rises the arterioles constrict and when pressure falls they dilate.) Poorly developed metabolic regulation of flow. Sympathetic input causes vasoconstriction in response to fall in arterial pressure and during exercise. The former acts to divert blood flow to heart and brain the latter helps divert flow to exercising muscle. |
|
|
Term
| Major mechanism of blood flow control to the skin |
|
Definition
| Flow controlled mainly by sympathetic input. Key role in body temperature regulation |
|
|
Term
| peripheral venous pool vs. central venous pool |
|
Definition
Peripheral Venous pool is venous blood in the systemic organs, including
skeletal muscle. The central venous pool is contained in the great veins of the thorax and right atrium. When peripheral veins constrict blood is shifted into the central pool. An increase in central venous volume and thus central venous pressure increases cardiac filling (preload) and thus stroke volume. Central venous pressure can be elevated appreciably during right heart failure since the pumping ability of the heart is markedly diminished and blood “backs up” in the veins. |
|
|
Term
| Respiratory Pump (Thoraco-abdominal pump) |
|
Definition
Venous pressure in the great veins of the thorax (i.e. the central venous pressure) is influenced by inspiration and expiration. During inspiration intrapleural pressure becomes
more negative (more subatmospheric) and acts to distend these thin walled vessels . The effect is to increase the venous driving pressure (peripheral venous pressure - central venous pressure), thereby promoting venous return. Inspiration acts like a suction pump. At the same time the diaphragm moves down and abdominal pressure increases. The result is a larger pressure gradient for the flow of blood from the abdomen into the thoracic cavity. During expiration the gradient is attenuated but still favors venous return. During positive pressure ventilation if the pressure is too high it can block venous return. |
|
|
Term
| mean systemic pressure (MSP) |
|
Definition
| The blood pressure that results when the heart is stopped (+7 mm Hg). It reflects the compliance and blood volume of the entire systemic vasculature, especially the veins. The driving force for venous return is: MSP – RAP. As RAP falls the venous return increases. |
|
|
Term
| Three ways Ang II increases blood pressure |
|
Definition
a) causing systemic arterioles to contract (increases TPR), b) directly promoting sodium reabsorption by the kidneys , c) indirectly promoting sodium reabsorption by the kidneys
by stimulating aldosterone release from the adrenal cortex. |
|
|
Term
| Atrial natriuretic factor (peptide) - ANF, ANP. Response to what stimulis and has what effects? |
|
Definition
A peptide produced by atrial cells. Released into blood stream in response to stretch of atrial cells e.g, caused by increased blood volume (volume overload). Effects of ANP: a) acts on kidneys to inhibit Na reabsorption which leads to increased urinaryloss of water (diuresis) and sodium (natriuresis), b) inhibits release and/or actions of several hormones including aldosterone, angiotensin ll, endothelin and antidiuretic
hormone (ADH, vasopressin). All of these effects help reduce plasma volume and atrial blood pressure back to normal. ANF release is reduced when atrial pressure is restored to normal. |
|
|
Term
| Vasopressin ( antidiuretic hormone, ADH) is released in response to what stimulis |
|
Definition
| DECREASED atrial pressure |
|
|
Term
| Renin -Angiotensin System is activated in response to what stimulis |
|
Definition
| DECREASED arterial pressure. Carotid sinus. |
|
|
Term
| Effects of Beta blockers on cardiac action potential |
|
Definition
| Decreased rate of depolarization (decreased phase 4 slope) |
|
|
Term
| Effects of Na and Ca channel blockers on cardiac action potential |
|
Definition
| Increased threshold (takes longer to depolarize) |
|
|
Term
| Effects of K blockers on cardiac action potential |
|
Definition
| Increased action potential duration |
|
|
Term
| Effects of adenosine and muscarinic AGONISTS on cardiac action potential |
|
Definition
| Hyperpolarize (increase maximum diastolic potential) |
|
|
Term
| Drug types that prevent reentry arrhythmias |
|
Definition
Antiarrhythmic drugs that slow conduction (Na+ channel blockers) or
increase the refractory period (K+ channel blockers, Na+ channel blockers) can inhibit the formation or maintenance of a reentrant circuit. |
|
|
Term
| MEchanism of class I antiarrhythmic drugs |
|
Definition
| act by blocking the fast inward sodium channel (phase 0 of the action potential) and slowing intracardiac conduction. They are subdivided into 3 subgroups based on their potency towards blocking the sodium channel (INa) and effects on repolarization |
|
|
Term
|
Definition
High potency sodium channel blockers, and prolong repolarization (prolong
QT interval): Quinidine, procainamide. |
|
|
Term
|
Definition
Lowest potency sodium channel blockers (little effect on PR, QRS, or QT
interval): Lidocaine. |
|
|
Term
|
Definition
The most potent sodium channel blocking agents (they slow conduction the
most, therefore prolong PR and broaden QRS intervals), but have little effect on repolarization (no effect on QT interval): Flecanide. |
|
|
Term
|
Definition
act indirectly on electrophysiological parameters by blocking beta-adrenergic
receptors (slow sinus rhythm and prolong PR interval, depending on sympathetic tone): Propanolol, esmolol, sotalol, acebutolol and other β-blockers |
|
|
Term
|
Definition
prolong repolarization (increase refractoriness, prolong QT interval, no effect on QRS interval, little effect on rate of depolarization).
• Drugs that act block fast outward potassium conductance (IKr): Amiodarone, sotalol, dofetilide
• Drugs that block both fast (IKr) and slow (IKs) outward potassium currents: Azimilide (still investigational, in phase III clinical trials, primarily blocks IKs)
• Drugs that block slow inward sodium channels: Ibutilide |
|
|
Term
|
Definition
relatively selective AV nodal L-type calcium channel blockers (slow sinus
rhythm, prolong PR interval): Verapamil, diltiazem (Note: The dihydropyridines such as nifedipine and amlodipine have minimal effects on the AV node.) |
|
|
Term
|
Definition
Class IB, only used IV for treating arrhythmias because of rapid
first-pass metabolism.•
*Severe interactions can occur with co-administration of other antiarrhythmic agents, especially amiodarone.
• *The most frequent side effects are CNS including tinnitus and seizures, and occasionally hallucinations, drowsiness, and coma. |
|
|
Term
|
Definition
| lidocaine's orally active congener. does not prolong QT interval and can be used in patients with a history of torsades or DILQTs |
|
|
Term
|
Definition
Class IA, Effective against both supraventricular and ventricular
arrhythmias. major metabolite, N-acetylprocainamide (NAPA), has
predominantly Class III antiarrhythmic actions. *Between 15 and 20% of patients develop a lupus-like
syndrome, which usually begins as mild arthralgia, but can be fatal if allowed to progress. 40% of patients discontinue within 6 months due to side effects. |
|
|
Term
|
Definition
(Class IA)Useful for supraventricular arrhythmias, and ventricular arrhythmias only in patients with good ventricular function because of its negative inotropic effects. has anticholinergic effects which may be
useful in some patients with vagally mediated paroxysmal supraventricular tachycardias, but the limits therapy in many patients |
|
|
Term
|
Definition
(Class IA)Useful in treating supraventricular and ventricular
arrhythmias, but there are significant risks of ventricular arrhythmias and other side effects esp. Torsades de point, do not use in a patient w a history of Long QT, Torsades, or hypokalemia. *Patients with heart failure can have
proarrhythmias and digoxin interactions.
• *Common side effects include hypotension, GI problems (diarrhea and vomiting), and cinchonism (tinnitus, blurred vision, and headaches).
• *potent inhibitor of hepatic CYP2D6 and is associated with more drug interactions than any other antiarrhythmic drug. |
|
|
Term
|
Definition
(Class IC)
• Used to treat symptomatic supraventricular arrhythmias and suppress life-threatening ventricular arrhythmias.
• It is structurally similar to propranolol and has beta-blocking activity in addition to its sodium channel blocking activity. At therapeutic concentrations it can have significant beta-blocking activity which must be considered in patients with heart failure. |
|
|
Term
|
Definition
(Class IC)
• A potent fast inward sodium channel blocker used to treat symptomatic supraventricular arrhythmias and documented life-threatening ventricular arrhythmias.
• Because of the risks of proarrhythmias identified in
the CAST trials, the drug is not considered a firstline agent and should not be used in patients with impaired ventricular function, myocardial ischemia, or recurrent myocardial infarctions.
• The agent lowers ventricular function in most patients. It also raises the threshold of pacing and cardiac defibrillators and should be used with caution in patients with pacemakers or ICDs. |
|
|
Term
|
Definition
(Class IV)
• Useful in treating a variety of arrhythmias of atrial or supraventricular origin. They are also more effective than digoxin in controlling ventricular rate in patients with atrial fibrillation.
*High doses can cause AV block or suppression of SA node,
particular when used in combination with beta-blockers, digoxin
or other drugs that inhibit the SA and AV nodes.
• *The most common side effect of verapamil is constipation. |
|
|
Term
|
Definition
| Class IV, about the same as Verapamil |
|
|
Term
|
Definition
Class III, • The only Class III agent that is a relatively pure potassium channel blocker
• Used for the conversion and maintenance of normal sinus rhythm in highly symptomatic patients with atrial fibrillation or flutter
• Fewer non-cardiac toxicities than amiodarone and has no negative inotropic effects
• *Because of its effects on the potassium channel, it should not be used in combination with other drugs that prolong QT interval
• Because of the risks of torsades, ECG and renal function must be assessed prior to initiation of therapy; therapy must be initiated in a hospital setting by a trained prescriber |
|
|
Term
|
Definition
Class III, • This drug blocks outward potassium (IKr), but unlike
other Class III agents, ibutilide also prolongs repolarization by increasing inward sodium flux through the slow inward sodium channels.
• It is used IV to rapidly convert atrial arrhythmias to
normal sinus rhythm; it is the only agent indicated
for this purpose
• *Class IA or Class III drugs should not be used
concurrently, or within 4 hours of ibutilide dosing, to
avoid the possibility of DILQTS and torsades
• *Ibutilide is contraindicated in patients with
prolonged QT, torsades or other polymorphic
ventricular arrhythmias, or who are taking drugs
that prolong QT or are associated with torsades |
|
|
Term
|
Definition
(Class III and II)only used to treat
life-threatening ventricular arrhythmias.
• The racemic d,l mixture of sotalol has both Class II and Class
III effects. The l-isomer causes the beta-blocking effects,
while the d-isomer causes the effects on prolonging the action
potential. The l-isomer causes significant beta-blocking effects
at doses well below those required for the antiarrhythmic
effects of the d-isomer.
Avoid abrupt cessation, avoid drug combos that enhance effects, (beta-blockade, QT prolongation, AV blockade) |
|
|
Term
|
Definition
(Class III/other) prolongs QT interval, yet its potential to cause proarrhythmias (torsades) is significantly lower than other Class
III agents and it is one of the few antiarrhythmic agents to have consistently decreased mortality in many trials.
• It is approved for use in refractory life-threatening ventricular
arrhythmias, but its therapeutic role has been expanding to include a variety of arrhythmias ranging from supraventricular to ventricular
- average half life 53 days, takes weak to achieve steady state levels.
• *The most common serious adverse effects are pulmonary fibrosis and interstitial pneumonitis (2-15% of patients on chronic amiodarone), which is fatal in 10% of these patients. The pneumonitis is reversible if drug is stopped early on, thus clinical assessment and chest x-rays are required every 3 months.
– *hepatotoxicity (which can be fatal; 30% of patients have elevated serum liver enzymes)
– *hyperthyroidism and hypothyroidism (2-24% incidence;
amiodarone is structurally similar to thyroid hormone and contains large quantities of iodine)
• *Amiodarone can interfere with the clearance of many drugs |
|
|
Term
|
Definition
acts by inhibiting the sodium/potassium ATPase. This ion pump is ubiquitously expressed so digoxin affects a variety of excitable tissues including the heart, CNS and ANS.
• Digoxin is used to control ventricular rate in patients
with atrial tachycardias
• Digoxin increases vagal tone, thus inhibiting AV nodal
conduction
• Dioxin can actually exacerbate atrial arrhythmias
because it can cause calcium overload, but
therapeutic efficacy is measured by the drug's
ability to protect the ventricles by reducing the
number of impulses passing through the AV node
• *Digoxin has a relatively narrow therapeutic index and is known to interact pharmacokinetically with
quinidine and other antiarrhythmic agents |
|
|
Term
|
Definition
agonist for purinergic receptors, given as a rapid IV bolus to acutely treat
paroxysmal supraventricular tachycardia, potently blocks AV nodal conduction within 10-30 seconds. • It has a half-life of elimination of 1.5-10 seconds
• *Common side effects, which are short-lived, including facial flushing, dyspnea, and chest pressure |
|
|
Term
| Three trial-and-error approaches are widely used to determine the appropriate antiarrhythmic drug |
|
Definition
– Empiric. Based upon the clinician's past experience
– Serial drug testing guided by electrophysiological study
(EPS). Requires cardiac catheterization and induction of
arrhythmias by programmed electrical stimulation of the heart,
followed by a delivery of test drugs
– Drug testing guided by electrocardiographic monitoring
(Holter monitoring). Continuous 24-hour recording of a ECG before and during each drug test to predict optimal efficacy |
|
|
Term
| Class I Na channel blockers common toxicities |
|
Definition
| Proarrhythmic effects (IA-Torsades de pointes*) (IC-CAST proarrhythmia**), Negative inotropic effect (IC drugs), Infranodal conduction block |
|
|
Term
| Class II Beta-blockers common toxicities |
|
Definition
| Sinus bradycardia (adrenergic-dependent). AV block (adrenergic dependent). Depression of LV function (adrenergicdependent). |
|
|
Term
| Class III common toxicities |
|
Definition
Prolong repolarization, Sinus bradycardia, Proarrhythmic effects
(Torsades de pointes*) |
|
|
Term
| Class IV common toxicities |
|
Definition
| AV Block, Negative Inotropic effect |
|
|
Term
|
Definition
supplies blood to the anterior and anterolateral left ventricle through its
diagonal branches and to the anterior two thirds of the interventricular septum through its septal branches. |
|
|
Term
| Distribution of the left circumflex artery |
|
Definition
| lateral aspect of the left ventricle through obtuse marginal branches, as well as gives off branches to the left atrium. |
|
|
Term
| Difference between right, left and codominant |
|
Definition
| Refers to which artery becomes the posterior descending artery. 85% of people are right dominant - RCA becomes PDA and supplies posterior left ventricle (PLV). 10% are left dominant - LCx becomes PDA and supplies PLV. In the remaining individuals, the RCA gives rise to the PDA and the LCx gives rise to the PLV in a so-called co-dominant circulation. |
|
|
Term
|
Definition
| SA nodal artery, which is a branch of the RCA in approximately 70 percent of the population or a branch of the LCx in 25 percent. |
|
|
Term
|
Definition
| AV nodal artery, which is a branch of the RCA in approximately 85 percent of the population or a branch of the LCx in 15 percent. |
|
|
Term
| Blood supply to right bundle branch |
|
Definition
receives most of its blood supply from
septal perforators that branch off of the LAD. There may also be collateral blood supply from the RCA or LCX. |
|
|
Term
| Blood supply to left anterior fascicle |
|
Definition
septal perforators from the LAD and is
particularly susceptible to ischemia and infarction. |
|
|
Term
| The main determinants of Mvo2 in the heart |
|
Definition
| heart rate (HR), contractility, and wall tension |
|
|
Term
|
Definition
| Wall tension = (P x r)/(2 x Th) |
|
|
Term
| Blood flow in the coronary arteries is determined by 3 different resistances |
|
Definition
| 1) viscous resistance, 2) compressive resistance, and 3) vascular resistance (vascular tone). |
|
|
Term
| Relationship of flow, resistance and radius |
|
Definition
| Flow is proportional to r^4, resistance is proportional to 1/r^4 |
|
|
Term
3 groups of individuals in which a classical presentation of angina is not
always the case. |
|
Definition
| Females, Diabetics, Elderly |
|
|
Term
| Typical Angina History: Quality |
|
Definition
Angina, means tightness or constriction. It is not so much as a
pain but rather a discomfort that may be perceived as: crushing or pressurelike,
squeezing or vise-like, strangling or constricting, band-like, heavy or
like a weight on the chest, but only occasionally as burning. Angina is
generally NOT sharp or stabbing. |
|
|
Term
| Typical Angina History: Location |
|
Definition
Most consistently retrosternal, but it can be parasternal, left precordial, or across the anterior chest. At times it occurs only in the
anterior neck, jaw or arm. It is generally diffuse in nature, a highly
localized (finger point) pain is generally not angina. |
|
|
Term
| Typical Angina History: Radiation |
|
Definition
The most characteristic pattern of radiation is to the left arm,
but it may radiate to the right arm or both arms. The shoulders, neck, jaw,
teeth and epigastrium also are sites of radiation. Pain radiating down
beyond the umbilicus is NOT characteristic of angina pectoris. |
|
|
Term
| Typical Angina History: Duration |
|
Definition
Most typically the discomfort last from 2-10 minutes. It is
uncommon for stable angina to last more than 10 minutes or be only
seconds in nature. |
|
|
Term
| Typical Angina History: Precipitating factors |
|
Definition
Exertion, emotional stress, meals, and exposure to
cold or wind are frequent precipitating factors. Due to variations in
coronary vascular tone, the amount of exertion required to bring on angina
may be variable over time, be brought on by less activity, and be more
severe shortly after arising. |
|
|
Term
| Typical Angina History: Relieving factors |
|
Definition
|
|
Term
| Typical Angina History: Other features |
|
Definition
The discomfort is usually steady and is not improved or
worsened by change of position or change in respiratory pattern. At times
dyspnea, nausea, palpitations, shortness of breath, or diaphoresis may
accompany angina. The features that characterize typical angina are the
consistent pattern of pain occurrence with exertion and relief with rest. |
|
|
Term
| Unstable angina is defined as |
|
Definition
| (1) an accelerated pattern of angina (increased angina severity, frequency, duration, or precipitated by less effort); (2) rest angina (greater than 20 minutes duration); or, (3) new onset angina, brought on with mild effort (CCS Class III, of less than 2 months duration). |
|
|
Term
| The diagnosis of CAD is established by |
|
Definition
A. History of typical angina pectoris
B. Acute myocardial infarction
C. Unequivocal evidence of prior MI by ECG, or imaging defect.
D. Positive exercise tests
E. Pharmacologic stress tests
F. Coronary arteriography |
|
|
Term
| Imaging modality should be used during a stress test when... |
|
Definition
There is LBBB, ST segments, V-paced, LVH, or pre-excitation on ECG prior to test.
The patient is taking Digoxin |
|
|
Term
| Most common types of Dyslipidemias |
|
Definition
| IIa (high LDL), IIb (high LDL, VLDL), IV (high VLDL), Low HDL |
|
|
Term
|
Definition
(↑LDL) Bad athero – (premature) – Familial Hypercholesterolemia (tendon xanthomas)
– Other polygenic (more common, no xanthomas)
– Diet (↑sat. fat, ↑chol) |
|
|
Term
|
Definition
(Insulin-resistance, “Atherogenic
Dyslipidemia”)—↑TG from ↑production + ↓clearance:
– VLDL enriched in CE (more atherogenic)
– Small, dense LDL (more atherogenic)
– Small HDL=breaks apart (apo A-I lost, low HDL—no type #, less atheroprotection) |
|
|
Term
|
Definition
| (combination of both ?IIa and IV?)—”mixed dyslipidemia” |
|
|
Term
| What is a low HDL usually related to? |
|
Definition
|
|
Term
| Type I (Minor Dyslipidemia) |
|
Definition
– Severe TG
– Pancreatitis
– Very Rare
- Missing LPL |
|
|
Term
| ↑Lp(a) (no type #)(Minor Dyslipidemia) |
|
Definition
– LDL + apo(a)
– Poorly cleared
– Highly oxidized
– Very atherogenic
– Uncommon |
|
|
Term
| Type III (Minor Dyslipidemia) |
|
Definition
Type III disease
– ↓ Remnant removal (apo E defect + ?)
– Bad (premature) athero
– Orange palmar creases
– Relatively rare |
|
|
Term
| Hypertension treatment with co-existing conditions of Heart failure |
|
Definition
| ACE inhibitors, Diuretics |
|
|
Term
| Hypertension treatment with co-existing conditions of MI |
|
Definition
| β-blockers, ACE inhibitors |
|
|
Term
| Hypertension treatment with co-existing conditions of diabetes |
|
Definition
| ACE Inhibitors, AVOID- β−blockers |
|
|
Term
| Hypertension treatment with co-existing conditions of isolated systolic hypertension (older person) |
|
Definition
| Diuretics preferred, calcium channel antagonist |
|
|
Term
| Hypertension treatment with co-existing conditions of renal insufficiency |
|
Definition
|
|
Term
| Hypertension treatment with co-existing conditions of angina |
|
Definition
| β−blocker, Calcium channel antagonists |
|
|
Term
| Hypertension treatment with co-existing conditions of Asthma |
|
Definition
| Ca++ channel blockers, AVOID- β−blockers |
|
|
Term
| Brain natriuretic peptide |
|
Definition
Mostly produced in the left ventricle in response to pressure & volume expansion. Synthesis & secretion is a protective response that is up regulated in heart failure, causing vasodilation & diuresis/natriuresis. Elevated BNP are seen in hypertension, tachycardia, cardiomyopathy, MI, mitral & aortic stenosis.
Clinical utility
Detect asymptomatic CHF
Objectively assess heart failure severity – correlates with NYHA classification
Used to monitor therapy & disease progression - Predicts 30-day & 10-month mortality after MI
BNP < 100 pg/ml – no heart failure
BNP 100-300 pg/ml – indeterminant (100-500 in some series)
BNP 300-600 pg/ml – mild heart failure
BNP 600-1000 pg/ml – moderate heart failure
BNP >1000 pg/ml – severe heart failure |
|
|
Term
| Mönckeberg’s arteriosclerosis |
|
Definition
Basic lesion - ringlike calcification in the media of medium-sized to small muscular arteries in individuals over 50 years of age. Bone and bone marrow can be seen in the calcified media.
Lesions do not produce narrowing or occlusion of the vascular lumen.
Site of involvement - femoral, tibial, radial and ulnar arteries
Pathogenesis - unknown but related to prolonged vasotonic influence |
|
|
Term
| Hyaline arteriolosclerosis |
|
Definition
| associated with benign hypertension and diabetes mellitus. homogeneous pink, hyaline thickening of the walls of arterioles with loss of underlying structure and narrowing of the lumen. Lesions may reflect leakage of plasma proteins across vascular endothelium. |
|
|
Term
| Hyperplastic arteriolosclerosis |
|
Definition
| associated with malignant or accelerated phase hypertension. concentric, laminated, onionskin thickening of the walls of arterioles with proliferation of smooth muscle cells and layer of collagen narrowing of the lumen frequently accompanied by deposits of fibrin and acute necrosis. |
|
|
Term
|
Definition
right ventricular hypertrophy and dilatation in response to pulmonary hypertension not secondary to left heart failure or congenital heart disease.
Acute - right ventricular dilatation following massive pulmonary embolism.
Chronic form can be due to diseases of the lungs, pulmonary vessels, disorders affecting chest movement, metabolic acidosis or hypoxemia. |
|
|
Term
| Nonbacterial verrucous endocarditis |
|
Definition
(Libman-Sacks disease)
Mitral & tricuspid valvulitis with active systemic lupus erythematosus with mucoid pooling, fibrinoid necrosis, & fibrosis in valvular connective tissue. |
|
|
Term
| most common type of aneurysm |
|
Definition
|
|
Term
| Important risk factors for AAA |
|
Definition
|
|
Term
| common complication of AAA |
|
Definition
|
|
Term
| What determines the risk of rupture of an AAA |
|
Definition
Risk of rupture correlates with aneurysm
diameter |
|
|
Term
| Size threshold for elective repair of AAA |
|
Definition
|
|
Term
| When should a AAA be repaired? |
|
Definition
|
|
Term
| Classic triad of ruptured AAA |
|
Definition
Back pain, hypotension, pulsatile
abdominal mass. Present in less then 50% of ruptures. |
|
|
Term
Symptoms NOT (typically) due to
carotid atherosclerosis |
|
Definition
• Posterior circulation
– Dizziness
– Ataxia
– Light-headedness
• Syncope (implies global cerebral
hypoperfusion)
• Binocular visual disturbances |
|
|
Term
| Symptoms of Carotid Atherosclerosis |
|
Definition
• Stroke
• Transient Ischemic Attack (TIA)
– Ipsilateral ophthalmologic
(amaurosis fugax)
– Contralateral somatic
• Aphasia |
|
|
Term
|
Definition
combines real-time gray scale imaging
with pulsed doppler
– Best screening tool for PAD
– Can be definitive diagnostic test |
|
|
Term
| When to due a Carotid Endarterectomy |
|
Definition
• Symptomatic
– >70% >> CEA
– 50-70% >> probable CEA
– <50% >> medical therapy (antiplatelet)
• Asymptomatic
– Depends on surgeon/center perioperative stroke rate
– ≥60% stenosis– modest but significant reduction in stroke risk with CEA
– Patient preference |
|
|
Term
|
Definition
Characterized by rest pain and tissue loss.
• Rest pain
– Blood supply inadequate to meet resting metabolic needs
– Affects tissue furthest from the heart
– May be relieved by dependency
• Tissue loss
– Non-healing traumatic ulcer
– Spontaneous gangrene |
|
|
Term
| Indications for surgery in chronic, nonischemic MR |
|
Definition
– Acute symptomatic MR in which repair is
likely
– NYHA Class II-IV symptoms with normal LV
function (EF > 60%) and LVESD < 45 mm
– Symptomatic or asymptomatic with mild LV
dysfunction (EF 50-60%) and/or LVESD 50-55
mm
– Symptomatic or asymptomatic with moderate
LV dysfunction (EF 30-50%) and/or LVESD
50-55 mm |
|
|
Term
| Dilated cardiomyopathy (DCM)causes |
|
Definition
Systolic dysfunction. Can be genetic. Other common causese include:
• Myocarditis – viral, non-viral infectious, idiopathic (immune)
• Toxins – alcohol, drugs (anthracylines)
• Pregnancy (peripartum cardiomyopathy)
• Nutritional deficiencies - thiamine (beriberi), vitamin C (scurvy), selenium
• Endocrine - DM, hyper/hypothyroidism,
hyperparathyroidism,
pheochromocytoma, acromegaly
• Autoimmune diseases - RA, SLE, dermatomyositis
• Tachycardia-induced |
|
|
Term
| Hypertrophic cardiomyopathy (HCM) |
|
Definition
| Mutation in Beta myosin or troponin. Asymmetric hypertrophy, esp. septem which leads to outflow obstruction and mitral regurge. Obstruction is worsened by decreased preload or increased contractility. Conduction disturbances are cause of sudden death. The most frequent symptom is dyspnea on exertion, which causes marked elevation of left ventricular filling pressures and pulmonary venous pressures, pulmonary congestion and limitation in cardiac output. |
|
|
Term
| Restrictive cardiomyopathy (RCM) |
|
Definition
Decreased ventricular compliance. Diastolic Dysfunction of LHF.
Caused by a number of things including tropical endomyocardial fibrosis, amyloidosis, sarcoidosis, pompes disease, hemochromatosis, scleroderma etc... anything that causes stiffening of ventricular wall. |
|
|
Term
| Arrhythmogenic right ventricular cardiomyopathy or dysplasia (ARVC, ARVD) |
|
Definition
| autosomal dominant disease with male predominance characterized by progressive replacement of right ventricular myocardium by fibrous and adipose tissue. presenting symptom is usually arrhythmia – palpitations, syncope, or sudden cardiac death. |
|
|
Term
| Altered Adrenergic Signal Transduction in the Failing Human Heart |
|
Definition
| Usually 80% B1 and 20% B2. During heart failure B1 are downregulated to levels equal to B2. Neuronal norepinephrine is also markedly depleted in the failing human hearts making indirect beta agonists less effective. |
|
|
Term
| Risks of Positive Inotropes in heart failure |
|
Definition
•Proarrhythmia
•Adverse effects on myocardial energetics (potential for ischemia)
•Potential to impair cardiac relaxation
•With long term use may accelerate the progression of disease |
|
|
Term
| HFSA 2006 Practice Guidelines for Acute Heart Failure: Intravenous Inotropes |
|
Definition
(milrinone or dobutamine) may be considered to relieve symptoms
and improve end-organ function in patients with advanced heart failure characterized by:
–Left ventricular dilitation,
–Reduced left ventricular ejection fraction,
–And diminished peripheral perfusion or end-organ dysfunction (low output
syndrome).
Particularly if these patients:
–Have marginal systolic blood pressure (< 90 mm Hg),
–Have symptomatic hypotension despite adequate filling pressure,
–Or are unresponsive to, or intolerant of , intravenous vasodilators.
-not recommended unless left heart filling pressures are known
to be elevated based on direct measurement or clear clinical signs. |
|
|
Term
| HFSA 2006 Practice Guidelines for Acute Heart Failure: Intravenous Inotropes |
|
Definition
(milrinone or dobutamine) may be considered to relieve symptoms
and improve end-organ function in patients with advanced heart failure characterized by:
–Left ventricular dilitation,
–Reduced left ventricular ejection fraction,
–And diminished peripheral perfusion or end-organ dysfunction (low output
syndrome).
Particularly if these patients:
–Have marginal systolic blood pressure (< 90 mm Hg),
–Have symptomatic hypotension despite adequate filling pressure,
–Or are unresponsive to, or intolerant of , intravenous vasodilators.
-not recommended unless left heart filling pressures are known
to be elevated based on direct measurement or clear clinical signs. |
|
|
Term
|
Definition
•Dose dependent actions:
0.5 to 2.0 μg/kg/min: dopaminergic agonist
2.0 to 10 μg/kg/min: β-agonist
> 10 μg/kg/min: α-agonist
Tolerance develops due to neuronal norepinephrine depletion
Danger with extravasation
Contraindicated in pheochromacytoma |
|
|
Term
|
Definition
| predominantly a direct β1-adrenergic agonist, with weak β2 activity, and α1 selective activity. Not associated with tolerance. Do not add to sodium bicarbonate or other strongly alkaline solution. |
|
|
Term
|
Definition
phosphodiesterase inhibitor.It has positive inotropic, vasodilating and minimal chronotropic effects. Can cause fatal arrythmias. Direct vasodilatory action via increase in cGMP in vascular smooth muscle cells
Not associated with tolerance |
|
|
Term
| Surviving Sepsis Campaign Guidelines:Vasopressors in Septic Shock |
|
Definition
Vasopressors are indicated when an appropriate fluid challenge fails to restore adequate
blood pressure and organ perfusion.
Vasopressor therapy may also be required transiently to sustain life and maintain
perfusion in the face of life-threatening hypotension, even when a fluid challenge is in
progress and hypovolemia has not yet been corrected.
Either norepinephrine or dopamine is the first-choice vasopressor agent (through a central
catheter as soon as available).
All patients requiring vasopressors should have an arterial catheter placed as soon as
practical if resources are available.
Vasopressin use may be considered in patients with refractory shock despite adequate
fluid resuscitation and high dose conventional vasopressors. |
|
|
Term
|
Definition
Relative adrenergic receptor potency: α1 > β1 >> β2.
Potent vasopressor.
Dose range: 2 to 15 μg/min.
Should be used with caution with monoamine oxidase inhibitors because severe, prolonged hypertension may result. Risk from extravasation. |
|
|
Term
|
Definition
Also know as:
–Arginine vasopressin (AVP)
–Antidiuretic hormone (ADH).
Effects mediated by multiple receptors:
–Vasocontriction via vasopressin1A receptor
–Neural effects via vasopressin1B receptor
–Antidiuretic effects via vasopressin 2 receptor.
Dose range: 0.01 to 0.03 U/min.
May be used with catecholamines. |
|
|
Term
|
Definition
most common form of cyanotic heart disease in infancy and childhood• Anterior deviation of the outlet ventricular septum is the cause of all four abnormalities seen in tetralogy of Fallot. “boot-shaped” heart secondary to RVH and small main pulmonary artery segment
1. Pulmonary stenosis
2. Large VSD
3. Overriding aorta
4. Right ventricular hypertrophy
Severity of cyanosis proportional
to severity of RVOT obstruction |
|
|
Term
|
Definition
| (acrocyanosis) is associated with normal cardiac and pulmonary function and is related to sluggish blood flow through the capillary bed. It typically involves the extremities and usually spares the trunk and mucous membranes. Exposure to cold is the most frequent cause of acrocyanosis |
|
|
Term
|
Definition
| classic chest x-ray seen in tetralogy of Fallot |
|
|
Term
|
Definition
| classic chest x-ray in transposition |
|
|
Term
| “snowman appearance” heart |
|
Definition
| classic chest x-ray appearance of supracardiac TAPVR |
|
|
Term
| The chest x-ray in infracardiac TAPVR |
|
Definition
shows significant pulmonary edema due to the significant obstruction to
pulmonary venous flow. This form of TAPVR is associated with severe and lifethreatening cyanosis. |
|
|
Term
| largest cardiac silhouettes on a newborn chest x-ray are usually due to |
|
Definition
Ebstein’s malformation of the tricuspid
valve. |
|
|
Term
| hypercyanotic or “tet” spell |
|
Definition
Seen in Children with Tetrology of fallot, due to an acute change
in the balance between the pulmonary vascular resistance (PVR) and the systemic vascular resistance (SVR), which
causes an increase in right-to-left shunting and profound cyanosis. |
|
|
Term
| Treatment of a “tet” spell |
|
Definition
directed at maneuvers that increase SVR and decrease PVR.
1. The knee chest position increases SVR.
2. Supplemental oxygen.
3. An IV fluid bolus increases SVR.
4. IV morphine is administered to decrease agitation and decrease overall oxygen consumption. In addition, morphine may have an effect on decreasing the
dynamic RVOT obstruction.
5. Sodium bicarb is administered to correct metabolic acidosis and reduce PVR.
6. Phenylephrine is a peripheral vasoconstrictor which is administered to increase SVR.
7. Beta-blockers (such as propranolol) are administered to decrease dynamic right ventricular outflow tract obstruction. |
|
|
Term
| D-transposition of the Great Arteries (d-TGA) |
|
Definition
Defect in spiraling septum. It is the
most common cause of cyanosis in the newborn period. classic chest x-ray in transposition is described as an “egg on a string”. |
|
|
Term
| initial management of D-TGA |
|
Definition
1. PGE1 is used to maintain ductal patency.
2. The atrial septum is enlarged to improve mixing at the atrial level. The Rashkind
procedure involves placement of a balloon tipped catheter within the left atrium.
The balloon is inflated and pulled back across the atrial septum, tearing the atrial
septum and allowing mixing to occur at the atrial level.
3. Surgical management of D-TGA involves the arterial switch procedure. In this
procedure, the aorta, coronary arteries and pulmonary arteries are transected just
above the semilunar valves and re-anastomosed in their correct anatomical
position. The normal circulation is therefore restored. |
|
|
Term
|
Definition
| aorta, pulmonary arteries and coronary arteries arise from a single truncal vessel. The truncal vessel overrides a large ventricular septal defect. The etiology of this disorder is failure of septation of the embryonic truncus arteriosus. This is an uncommon form of congenital heart disease. Associated with DiGeorge syndrome (22q11 deletion) |
|
|
Term
| Total Anomalous Pulmonary Venous Return (TAPVR) |
|
Definition
| occurs as a result of failure of the pulmonary veins to fuse with the developing left atrium. |
|
|
Term
|
Definition
most common form of TAPVR. In this case,
the pulmonary venous confluence connects to an ascending vertical vein which connects
to the innominate vein and the superior vena cava. |
|
|
Term
|
Definition
| the pulmonary venous connection is either directly to the right atrium or through the coronary sinus and into the right atrium. |
|
|
Term
|
Definition
| pulmonary venous confluence connects to a descending vein which passes through the portal system and into the inferior vena cava. |
|
|
Term
|
Definition
| failure of formation of the tricuspid valve. There is an obligate right-to-left shunt at the atrial level. The great arteries are normally related 70% of the time and transposed 30% of the time.nearly always a ventricular septal defect and a small hypoplastic right ventricle. The pulmonary valve may be normal, stenotic, or atretic. The degree of cyanosis in this disorder is proportional to the degree of pulmonary stenosis. The necessity for PGE1 is therefore related to the degree of pulmonary stenosis. |
|
|
Term
|
Definition
| result of abnormal formation of the pulmonary valve. The pulmonary arteries are often normal in size, however, the right ventricle is usually significantly hypoplastic and hypertrophied. The tricuspid valve is also hypoplastic. Pulmonary atresia is a ductal dependent lesion and presents with significant cyanosis at birth. PGE1 is required to maintain oxygenation. |
|
|
Term
| Ebstein’s Malformation of the Tricuspid Valve |
|
Definition
tricuspid valve leaflets attach to the right ventricular wall rather than the tricuspid valve annulus. right-to-left shunting at the atrial level. Massive right atrial dilatation due to severe tricuspid regurgitation. The degree of
cyanosis is related to the size and compliance of the functional portion of the right ventricle. Cyanosis usually improves as pulmonary vascular resistance falls within the first weeks of life |
|
|
Term
|
Definition
Basically the opposite of digoxin. inhibitor of late sodium current (late INa), the first new drug for angina in >20 years. Decreases Ca overload.
– Calcium overload increases myocardial oxygen consumption, and prevents full myocardial relaxation which impairs myocardial perfusion
– No hemodynamic effects (heart rate, contractility, blood pressure, venous return are essentially unchanged)
– Causes QT prolongation, but there is no evidence that this leads to torsades de pointes
– Possible testicular toxicity |
|
|
Term
| Organic Nitrates / Nitrovasodilators |
|
Definition
nitroglycerin, isosorbide dinitrate, isosorbide mononitrate, amyl nitrite.
• NO activates a cytosolic form of guanylate cyclase in smooth muscle
– Activated guanylate cyclase catalyzes the formation of cGMP which activates cGMP-dependent
protein kinase
– Activation of this protein kinase results in phosphorylation of several proteins that reduce
intracellular calcium and hyperpolarize the plasma membrane causing relaxation.
– Dilation of veins predominates over that of arterioles.
– Large epicardial coronary arteries are dilated without impairing autoregulation in small coronary
vessels
– Collateral flow may be increased
– Decreased preload improves subendocardial perfusion
– Although organic nitrates can relax vasospastic coronary arteries, they have little or no effect on
total coronary blood flow in patients with typical angina due to atherosclerosis
– Dilation of coronary arteries can paradoxically result in aggravation of angina - a phenomenon known as “coronary steal” |
|
|
Term
|
Definition
not subject to first-pass metabolism and is 100% available after oral
administration |
|
|
Term
|
Definition
gas at room temperatures and can be administered by inhalation
– Rapid onset, short duration (3-5 min) |
|
|
Term
|
Definition
rapid onset of action (1-3 min) when administered sublingually, but the short
duration of action (20-30 min) is not suitable for maintenance therapy |
|
|
Term
| Adverse Effects of Nitrovasodilators |
|
Definition
| *Orthostatic hypotension, *Severe throbbing headache, contraindicated in patients with elevated intracranial pressure |
|
|
Term
| Effects of Calcium Channel Blockers on Vascular Smooth Muscle |
|
Definition
• Ca++ channel blockers inhibit L-type and/or T-type voltage-dependent Ca++ channels
• Have little or no effect on receptor-operated channels or on release of Ca++ from SR
• “Vascular selectivity” is seen with the Ca++ channel blockers
– Decreased intracellular Ca++ in arterial smooth muscle results in relaxation (vasodilatation) ->
decreased cardiac afterload (aortic pressure)
– Little or no effect of Ca++-channel blockers on venous beds -> no effect on cardiac preload
(ventricular filling pressure)
– Specific dihydropyridines may exhibit greater potencies in some vascular beds (e.g.- nimodipine
more selective for cerebral blood vessels, nicardipine for coronary vessels)
– Little or no effect on nonvascular smooth muscle |
|
|
Term
| Desired Therapeutic Effects of Calcium Channel Blockers for Angina |
|
Definition
• Improved oxygen delivery to ischemic myocardium
– Vasodilate coronary arteries
– Particularly useful in treating vasospastic angina
– May inhibit platelet aggregation
• Reduced myocardial oxygen consumption
– Decrease in afterload by dilating arterioles (no effect on preload)
– Non-dihydropyridines also lower heart rate and decrease contractility
(*Note: Dihydropyridines may aggravate angina in some patients due to reflex increases in heart rate and contractility; these sympathetic effects can be prevented by co-administration of β-adrenergic
blockers) |
|
|
Term
| Ca++ Channel Blockers: Toxicities |
|
Definition
– Adverse effects are typically direct extensions of their therapeutic effects and are relatively rare
– Major adverse effects:
– *Depression of contractility and exacerbation of heart failure
– *AV block, bradycardia, and cardiac arrest |
|
|
Term
| Ca++ Channel Blockers: Drug Interactions |
|
Definition
• *β-blockers in combination with verapamil or diltiazem due to additive effects on heart.
• *Some calcium channel blockers (verapamil, diltiazem) can cause an increase in plasma digoxin |
|
|
Term
| Which Beta blocker can also cause vasodilation due to alpha block |
|
Definition
|
|
Term
| Adverse Effects, Contraindications and Drug Interactions of β-Blockers |
|
Definition
• *May exacerbate symptoms in patients with moderate to severe heart failure
• *Contraindicated in patients with asthma
• *Should be used with caution in patients with diabetes since hypoglycemia-induced tachycardia can
be blunted or blocked
• *May depress contractility and heart rate and produce AV block in patients receiving nondihydropyridine
calcium channel blockers (i.e., verapamil, diltiazem), and other drugs that inhibit the
SA and AV nodes (e.g., many antiarrhythmic drugs and digoxin) |
|
|
Term
| EKG findings in pericarditis |
|
Definition
| ST elevation and "knuckle sign" = PR elevation in lead aVR |
|
|
Term
|
Definition
| Dressler's syndrome is a secondary form of pericarditis that occurs in the setting of injury to the heart or the pericardium, typically treated with NSAIDs |
|
|
Term
| According to Fick equation Cardiac output = |
|
Definition
| VO2/(Ca-Cv) Where VO2 is total oxygen consumption, Ca = Oxygen content of arterial blood and Cv = Oxygen content of mixed venous blood |
|
|
Term
| Which leads localize to inferior portion of heart |
|
Definition
|
|
Term
| LAD infarctions show ST changes in what leads |
|
Definition
|
|
Term
| Histology of Aschoff bodies |
|
Definition
| Noncaseating granulomas with multinucleated giant cells |
|
|
Term
| Which two leads measure pretty much left to right |
|
Definition
|
|
Term
| QT interval is measured from where to where |
|
Definition
| Beginning of Q to end of T |
|
|
Term
| PR interval is measured from where to where? |
|
Definition
| Beginning of P to Beginning of QRS |
|
|
Term
|
Definition
| Pseudo R’ in V1 during tachycardia |
|
|
