Term
| Blood returns to the heart from the: |
|
Definition
|
|
Term
| Blood flows from the vena cava to the: |
|
Definition
|
|
Term
| Blood flows from the right atrium to the right ventricle via this valve: |
|
Definition
|
|
Term
| Blood blows from the right ventricle: |
|
Definition
| Through the pulmonary valve to the lungs |
|
|
Term
| Blood returns to the heart from the lungs via: |
|
Definition
|
|
Term
| Oxygenated blood from the lungs re-enter the heart in this structure: |
|
Definition
|
|
Term
| Blood flows from the left atrium to the left ventricle via this valve: |
|
Definition
|
|
Term
| Blood flows from the left ventricle to the systemic circulation via this valve: |
|
Definition
|
|
Term
| In what order does electrical conduction flow in the heart (i.e. put the following in order: Bundle of His, Right & Left bundle branches, SA node, AV node) |
|
Definition
| SA node --> AV node --> Bundle of His --> Right and left bundle branches |
|
|
Term
| The longest delay in electric conduction of the impulse through the heart occurs at: |
|
Definition
|
|
Term
| The round rise of the SA node conduction is caused by: |
|
Definition
|
|
Term
| The down shape of the SA node conduction is caused by: |
|
Definition
|
|
Term
| The SA node is composed primarily of these voltage gated channels: |
|
Definition
|
|
Term
| The fast rise of atrial conduction is due to: |
|
Definition
|
|
Term
| The downward shape of atrial conduction is caused by: |
|
Definition
|
|
Term
| The round rise of AV node conduction is caused by: |
|
Definition
|
|
Term
| The downward shape of AV node conduction is caused by: |
|
Definition
|
|
Term
| The sharp rise in the Purkinje fibers and ventricles conduction is caused by: |
|
Definition
|
|
Term
| Cardiac cells have greater _______ Ca++ and Na+. |
|
Definition
|
|
Term
| Cardiac cells have greater _____ K+. |
|
Definition
|
|
Term
| For cardiac myocyte depolarization, there must be: |
|
Definition
| Ca++ and/or Na+ influx; K+ efflux |
|
|
Term
| EKG P waves are associated with: |
|
Definition
|
|
Term
| EKG QRS waves are associated with: |
|
Definition
|
|
Term
| EKG T waves are associated with: |
|
Definition
| Ventricular repolarization |
|
|
Term
| There is a pause between beats to ensure: |
|
Definition
| That blood is pumped out of the ventricles into the systemic circulation |
|
|
Term
| The pacemaker cells of the heart are found primarily in the: |
|
Definition
|
|
Term
| Describe Phase 0 of cardiac action potential: |
|
Definition
| Rapid depolarization; Na+ influx |
|
|
Term
| Describe Phase 1 of cardiac action potential: |
|
Definition
| Partial repolarization; Na+ channels close; K+ channels open --> K+ efflux |
|
|
Term
| Describe Phase 2 of cardiac action potential: |
|
Definition
| K+ efflux; Ca++ influx; These cancel each other --> plateau |
|
|
Term
| Describe Phase 3 of cardiac action potential: |
|
Definition
| Repolarization; Ca++ channels close; K+ efflux |
|
|
Term
| Describe Phase 4 of cardiac action potential: |
|
Definition
| Pacemaker depolarization; some pacemaker channels are open; Na+ efflux; Ca++ efflux; Na+/K+ ATPase active |
|
|
Term
| Why is the T wave larger than the P wave in an EKG? |
|
Definition
| The T wave reflects ventricular repolarization. The P wave reflects atrial contraction. The mass of the ventricles is much greater than that of the atria. |
|
|
Term
| Cardiac contraction depends on the intrinsic levels of: |
|
Definition
|
|
Term
| The "pre-load" is described as: |
|
Definition
| Intraventricular blood volume (i.e., the volume when the left ventricle is filled with blood) |
|
|
Term
| The "after-load" is described as: |
|
Definition
| The resistance against which the left ventricle ejects (i.e., the resistance felt at the aorta) |
|
|
Term
| The Frank-Starling Law states that: |
|
Definition
| End diastolic pressure is proportional to the stroke volume |
|
|
Term
| As end diastolic pressure increases, these also increase: |
|
Definition
| Contractile force, cardiac output |
|
|
Term
| Cardiac output is equal to: |
|
Definition
| Heart rate times contractility (stroke volume) i.e., CO = HR X SV |
|
|
Term
| Epinephrine and norepinephrine have this effect on the heart: |
|
Definition
| Increase HR and contractility |
|
|
Term
| Epi/NE increase cardiac automaticity, which means: |
|
Definition
|
|
Term
|
Definition
|
|
Term
| The parasympathetic system has this effect on the heart: |
|
Definition
| Cardiac slowing, reduced automaticity, inhibition of AV conduction |
|
|
Term
| ACh binds these receptors in the heart: |
|
Definition
|
|
Term
| ACh binds M2 receptors in the heart which causes: |
|
Definition
| Binding to Gi --> inhibition of cAMP --> K+ efflux --> Hyperpolarization |
|
|
Term
| Atrial cells have a specialized endocrine function; the atria store and release: |
|
Definition
| Atrial natriuretic peptide |
|
|
Term
| Stretching of the atria causes release of: |
|
Definition
| Atrial natriuretic peptide |
|
|
Term
| Atrial natriuretic peptide binds to the kidney causing: |
|
Definition
|
|
Term
| Atrial natriuretic peptide increases cGMP via: |
|
Definition
|
|
Term
| Blood is supplied to cardiac tissue via these three structures: |
|
Definition
|
|
Term
| Coronary blood flow occurs during: |
|
Definition
| Diastole (heart is relaxed) |
|
|
Term
| This shortened the most during tachycardia: |
|
Definition
|
|
Term
| During diastole, ________ is the difference between the aortic and ventricular pressures. |
|
Definition
| Effective perfusion pressure |
|
|
Term
| Stenosis of the aortic valve causes: |
|
Definition
|
|
Term
| This is an abnormality with the pacemaker causing a faster intrinsic rate of firing than the normal SA nodal rate: |
|
Definition
|
|
Term
| This is caused by a slow SA node; a latent pacemaker initiates an impulse. |
|
Definition
|
|
Term
| Ischemia, electrolyte abnormalities, and heightened sympathetic tone are common causes of: |
|
Definition
|
|
Term
| Arrhythmia may be caused by these four occurences: |
|
Definition
| Early afterdepolarization, delayed afterdepolarization, re-entry, conduction block (heart block) |
|
|
Term
| Early afterdepolarization is caused by: |
|
Definition
| A condition the prolong the action potential |
|
|
Term
| Delayed afterdepolarization occurs when: |
|
Definition
| Intracelluar Ca++ accumulation activates the Na/Ca exchanger |
|
|
Term
| _____ influx may cause early afterdepolarization leading to arrhythmias. |
|
Definition
|
|
Term
| These two conditions are required for re-entry: |
|
Definition
| Unidirectional block; slowed retrograde conduction velocity |
|
|
Term
| Re-entry can result in a sustained pattern of: |
|
Definition
| Rapid depolarizations that trigger tachyarrhythmias |
|
|
Term
| Conduction block occurs when: |
|
Definition
| An impulse slows down substantially or fails to propagate because of the presence of an area of inexcitable cardiac tissue |
|
|
Term
| Re-entry describes the situation in which the impulse re-excites regions of the myocardium after the refractory period has subsided, causing: |
|
Definition
| Continuous circulation of action potential |
|
|
Term
| In complete heart block, the atria and ventricles beat: |
|
Definition
| Independently of one another; the ventricles beating at a slow rate determined by whatever pacemaker picks up distal to the blocks |
|
|
Term
| Ectopic pacemaker activity is encouraged by: |
|
Definition
|
|
Term
| Conduction block results from disease in the conducting system, especially the: |
|
Definition
|
|
Term
| Symptoms of conduction block include: |
|
Definition
| Lightheadedness, syncope, palpitation |
|
|
Term
| First degree AV block causes: |
|
Definition
|
|
Term
| 2nd degree AV block causes: |
|
Definition
| Skipped beats, missing QRS |
|
|
Term
| 3rd degree AV block causes: |
|
Definition
| Random repeating; the P and QRS waves are independent; (requires a pacemaker) |
|
|
Term
| Bradycardia is classifed as less than ____ beats per minute. |
|
Definition
|
|
Term
| Tachycardia is classified as more than _____ beats per minute. |
|
Definition
|
|
Term
| This condition causes irregular beat intervals, but normal waves: |
|
Definition
|
|
Term
| This abnormal rhythm is caused by very fast beats, and is characterized by missing P waves: |
|
Definition
|
|
Term
| Atrial flutter may be caused by: |
|
Definition
|
|
Term
| This condition is characterized by random atrial beats and random, chaotic QRS: |
|
Definition
|
|
Term
| This condition may cause huge QRS waves, and may be due to re-entry related to trauma: |
|
Definition
|
|
Term
| This condition is characterized by no clear QRS wave and heart failure: |
|
Definition
|
|
Term
| Class I antiarrhythmic agents block these channels: |
|
Definition
|
|
Term
| Class II antiarrhythmic drugs act through: |
|
Definition
| Beta-adrenoceptor antagonism |
|
|
Term
| Class III antiarrhythmic drugs act by blocking: |
|
Definition
|
|
Term
| Class IV antiarrhythmic drugs act by blocking: |
|
Definition
|
|
Term
| Beta blockers and Ca++ channel blockers block conduction through the: |
|
Definition
|
|
Term
| Beta blockers and Ca++ channel blockers can be used to treat these arrhythmias: |
|
Definition
| Atrial flutter/fibrillation |
|
|
Term
| K+ channel blockers have these effects: |
|
Definition
| Prolong action potential, blocks re-entry, increase refractory period of Na+ channels |
|
|
Term
| Disopyramide is this class of antiarrhythmic drug: |
|
Definition
|
|
Term
| Lidocaine is this class of antiarrhythmic drug: |
|
Definition
|
|
Term
| Flecainide is this class of antiarrhythmic drug: |
|
Definition
|
|
Term
| Propranolol and metoprolol are this class of antiarrhythmic drug: |
|
Definition
|
|
Term
| Amiodarone is this class of antiarrhythmic drug: |
|
Definition
|
|
Term
| Verapamil is this class of antiarrhythmic drug: |
|
Definition
|
|
Term
|
Definition
| Myocardial conduction velocity, excitability, and contractility |
|
|
Term
|
Definition
|
|
Term
| The overall effect of class 1a drugs is increasing the duration of: |
|
Definition
|
|
Term
| Class 1a drugs are used to suppress: |
|
Definition
| Atrial flutter and fibrillation |
|
|
Term
| This drug could be used to treat atrial flutter or fibrillation: |
|
Definition
|
|
Term
| Class 1a drugs prolong these intervals on ECGs: |
|
Definition
|
|
Term
| Class 1b drugs have ___ onset and offset kinetics. |
|
Definition
|
|
Term
| Class 1b drugs decrease ____ in partially depolarized cells. |
|
Definition
|
|
Term
| Class 1a drugs prolong the duration of action of the action potential by blocking: |
|
Definition
|
|
Term
| Class 1b drugs block these channels only: |
|
Definition
|
|
Term
| Class 1b drugs have higher affinity for damaged tissues, so they may be used to treat arrhythmia caused by: |
|
Definition
|
|
Term
| Class 1b drugs are indicated to treat: |
|
Definition
| Ventricular tachycardia, premature ventricular beats, prevention of ventricular fibrillation |
|
|
Term
| This class of drugs have the most potent sodium channel blocking effects: |
|
Definition
|
|
Term
| This class of drugs decrease conductivity, but do not change the action potential duration: |
|
Definition
|
|
Term
| Class 1c drugs are indicated for: |
|
Definition
| Life-threatening ventricular tachycardia or ventricular fibrillation |
|
|
Term
| Beta blockers decrease conduction through: |
|
Definition
|
|
Term
| Beta blockers are indicated for this type of disrhythmia: |
|
Definition
| Supraventricular tachycardia |
|
|
Term
| K+ channel blockers prolong: |
|
Definition
|
|
Term
| K+ channel blockers do not decrease: |
|
Definition
|
|
Term
|
Definition
| Action potential duration and refractory period |
|
|
Term
| Amiodarone is a _______ channel blocker. |
|
Definition
|
|
Term
| Ca++ channel blockers are this class of antidysrhythmic drug: |
|
Definition
|
|
Term
| Ca++ channel blockers slow conduction in: |
|
Definition
|
|
Term
| Ca++ channel blockers shorten this part of the action potential: |
|
Definition
|
|
Term
| Ca++ channel blockers are used to reduce the force of: |
|
Definition
|
|
Term
| Ca++ channel blockers are used mainly to slow conduction: |
|
Definition
|
|
Term
| Angina is caused by an insufficient quantity of this element to the cardiac tissues: |
|
Definition
|
|
Term
| Chronic coronary artery disease is a common cause of this type of angina: |
|
Definition
|
|
Term
| Acute coronary syndromes may cause this type of angina: |
|
Definition
|
|
Term
| Chest pain on exertion is a characteristic of: |
|
Definition
|
|
Term
| Chest pain that occurs with little exertion is a characteristic of: |
|
Definition
|
|
Term
| This type of angina occurs because of vasospasms: |
|
Definition
| Variant (Prinzmetal's) angina |
|
|
Term
| Angina pectoris is the principal clinical manifestation of: |
|
Definition
|
|
Term
| Intense vasospasm is a common cause of this type of angina: |
|
Definition
| Variant (Printzmetal's) angina |
|
|
Term
| Chest pain due to ruptured plaque, platelet aggregation, thrombus formation, and/or unopposed vasoconstriction best describes: |
|
Definition
|
|
Term
| Chest pain due to vascular luman narrowing by plaque best describes: |
|
Definition
|
|
Term
| Nitroglycerin ________ oxygen consumption. |
|
Definition
|
|
Term
| Nitroglycerin releases this substance when it is metabolized: |
|
Definition
|
|
Term
| Nitric oxide released from nitroglycerin causes: |
|
Definition
|
|
Term
| Nitroglycerin is used to treat: |
|
Definition
|
|
Term
| Atenolol and metoprolol (B-blockers) are used as ________ of angina. |
|
Definition
|
|
Term
| Beta blockers act as prophylaxis of stable angina by: |
|
Definition
| Decreasing heart rate and contractility --> decrease cardiac oxygen consumption |
|
|
Term
| Diltiazem (CCBs) block Ca++ entry through these channels: |
|
Definition
|
|
Term
| Calcium channel blockers have this effect on the vasculature: |
|
Definition
| Vasodilators --> decrease after-load |
|
|
Term
| Calcium channel blockers have this effect on heart rate: |
|
Definition
| Negative chronotropic effect (decrease HR) |
|
|
Term
| Calcium channel blockers reduce myocardial oxygen demand by: |
|
Definition
| Decreasing after-load --> reduce contractility, reducing heart rate, |
|
|
