Action Potential
An electrical impulse consisting of a self-propagating serioes of polarizations and depolarizations transmitted across the plasma membranes of a muscle cell during contraction
Automacity
the ability of cardiac tissue to initiate its own action potentials
Depolarization
Discharge of the electrical impulse generated by the influx of cations (Na, Ca, K) through ion channels in the membrane
Repolarization
The process by which the membrane potential of a muscle cell is restored to the cell's resting potential
Refractory Period
The time between repolarization and depolarization
What are absolute and relative refractory periods?
Absolute= part of the refractory period when a response cannot be generated by an outside stimulus.
Relative= part of the refractory period when a depressed response is possible w/ a strong stimulus
Cardiac output
The amount of blood ejected by the ventricles each minute. HR X SV
Stroke Volume
Volume of blood ejected w/ each contraction (~2-3 oz)
Preload
The degree of myocardial fiber stretch at the end of diastole. Determined by venous return.
What increases and decreases preload?
Increased by fluid volume & Na excess.
Decreased by hemorrhage, dehydration
Afterload
resistance of impedence the ventricle must overcome in systole in order to eject its volume.
What determines afterload?
Blood viscosity, aortic impedance, peripheral resistance
What is peripheral resistance (or peripheral vascular resistance, PVR)?
resistance to the flow of blood determined by the tone of vascular musculature and the blood vessel diameter
Contractility
The strength of force when the heart contracts.
What increases contractility? Decreases?
Increases: SNS stimulation (drug or natural)
Decreases: Heart failure, Beta/Ca channel blockade.
Ejection Fraction
% of blood present in ventricle before systole that is ejected w/ the ventricular contractio (~65%)
What is inotropic? What does a positive and negative inotrope do?
Contractility. Positive= increases contractility. Negative= decreases contractivty
What is chronotropic? What does a positive and negative chronotrope do?
Heart rate. Positive= increase HR. Negative= decrease HR
What is dromotropic? What does a positive and negative dromotrope do?
Conduction of AP through the heart. Positive= enhane conduction. Negative= decrease/slow conduction.
How does blood flow through the body?
Inf/Sup Vena Cava>>R. Atrium>>Tricuspid>>R. Ventricle>>Pulmonic valve>>Pulmonary Artery>>lungs>>Pulmonary veins>>L. Atrium>>mitral valve>>L. ventricle>>aortic valve>>aorta>>arteries>>arterioles>>capillaries>>venules>>veins
What helps carry blood back to the heart?
Valces, muscle contractions, and slight negative pressure in the R. atrium draw blood back to the heart.
What is the difference between arteries and veins?
Arteries= away from heart. Thick muscular walls, high pressure.
Veins= to heart. Thinner, distensible walls, low pressure. Reservoir for blood.
What system controls arterioles?
Sympathetic
Describe the physiology of the Heart.
Sinoatrial (SA) node initiates the impulse (automaticity).
Atrioventricular (AV) node slows conduction. Impulse travels down bundle of His, splits and travels down right/left bundle branches, and is distributed by Purkinje fibers. Also controlled by sympa
What is the total blood volume of an average adult?
5 liters.
What is the average stroke volume?What does it equal in a healthy heart?
70 ml/beat. It should be equal to venous return. Each ventrile should push forward an equal amount.
What factors contribute to cardiac output?
Heart rate (influenced by ANS), Stroke volume (myocardial contractility, cardiac preload, afterload).
What system of the ANS controls arterial pressure?
Sympathetic Nervous System
What does the SNS do r/t arterial pressure?
Maintains vasoconstriction to maintain a steady state of arterial pressure.
What do baroreceptors do r/t arterial pressure (AP)?
@ aortic arch and carotid sinuses, maintain AP at a predetermined 'set' point. Info is sent to the medulla to cause vasoconstriction (arteries and veins) and to ? HR.
What role does the Renin-Angiotension-Adolsterone System (RAAS) have in maintaining AP?
Kidneys respond to ? blood volume by producing renin. Renin converts angiotension 1 to angiotension 2, which causes vasoconstriction. A2 also stimulates the adrenal medulla to make adolsterone, which causes Na & H20 retention.
What role does the Kidney have in maintaining AP?
Low AP causes kidneys to retain water (? renal blood flow and ?urine production).
What role to Natriurietic peptides have in maintaining AP?
Produced in response to ? blood volume. Shift volume in blood vessels to tissues (vascular permability), cause kidney to lose H20 and Na, and dilate arteries/veins by supressing SNS outflow from the CNS.
What are the three types of positive inotropic agents?
Sympathomimetics, cardiac glycosides, and phosphodiesterase inhibitors.
What are the two sympathomimetics? When are they used?
Dopamine and Dobutamine. In critical situations
What does Dopamine do to the heart? Kidneys?
Activates B1 to increase contractility/HR. Increase renal blood flow and urine output.
At high doses, dopamine can trigger alpha 1 receptors in blood vessels to cause what?
Vasoconstriction, causing vascular resistance (afterload) and reducing CO.
What does dobutamine do?
Activates B1 receptors to increase contractility.
What are the adverse effects of dopamine and dobutamine?
Tachycardia, which causes decreased CO.
What do we use cardiac glycosides to treat?
Heart Failure.
How to cardiac gycosides work?
They increase CO through positive inotropic, negative chronotropic, and negative dromotropic effects.
What are the consequences of increase CO?
Reduced HR, Reduces AV conduction, Increased SV, Diuresis (improved renal circulation), and improvement of cough, cyanosis, shortness of breath
What are contraindications to cardiac glycosides?
drug allergy, heart block, atrial fibrillation, diastolic heart failure.
What are the adverse effects of cardiac glycosides?
Narrow therapeutic range, dysrythmias (bradycardia or tachycardia) with hypokalemia, fatigue, N/V, diarrhea, vision defects (@ toxic levels)
How do we treat an overdose of cardiac glycosides?
Digoxin Immune FABG (Digibind)
Why do cardiac glycosides interact with many different drugs?
Reacts with any that can alter heart rhythm (beta blockers), or those that deplete potassium (diruretics).
What do phosphodiesterase inhibitors do?
Increase the force of contraction and dilate blood vessels.
How do phosophodiesterase inhibitors work?
Make more calcium available to increase heart contraction force, and dilates blood vessels to reduce workload of the heart.
When are phosophodiesterase inhibitors contraindicated?
Drug allergy, severe valvular (aortic/pulmonic) disease, Heart Failure related to diastolic dysfunction
What is a dysrythmia?
Any deviation form the normal rhythm of the heart due to abnormally functioning cardiac cells.
What do class 1 antidysrythmics do?
Stabilize the membrane by blocking Na channels.
What do class 2 antidysrythmics do?
Beta Blockers to block sympathetic stimulation of the hrt and slow depolarization.
What do class 3 antidysrythmics do?
Block potassium channels to increase action potential duration and prolong repolarization.
What do class 4 antidysrythmics do?
Block Ca channels to slow depolarization
What are contraindications to antidysrythmics?
Drug allergies, A/V block, bundle branch block
WHat are side effects of antidysrythmics?
Allergic rxn, N/V, dizziness, HA, blurred vision, dysrythmias.
What can cause an interaction with antidysrythmics?
Drugs that cause dysrythmias, hypotension/hypertension, respiratory distress. Drugs that compete for binding sitesP
What causes angina?
Poor O2 supply>>ischemia>>angina>>necrosis and scarification
What do antianginal drugs do?
Increase blood flow and decrease demand
What do nitrates/nitrites do?
Dilate all blood vessels, particularly coronary arteries and venous vascular beds.
What are contraindications to nitrates?
Drug allergy, hypotension
What are adverse effects of nitrates/nitrites?
Headache, tachyphylaxis tolerance
What drugs would nitrates interact with?
Drugs that produce vasodilation to cause an additive effect
What do Beta Blockers do?
Block sympathetic increase in HR (slow heart rt)
What are beta blockers used for?
To treat exertional angina, by blunting HR and BP so myocardial O2 demains remains stable.
How to beta blockers work?
Slow conduction thru AV node, and suppresses RAAS
When are beta blockers indicated?
Angina, post MI (to prevent more MIs), hypertensio
What are contraindications to beta blockers?
Asthma (spillage to b2 receptors possible). Conduction disturbances
What are some adverse effects of beta blockers?
Fatigue, lethargy, bradycardia, hypotension
What drugs can beta blockers interact with?
Those that cause hypotension>> additive effect
How do Calcium Channel BLockers work?
Block Ca needed for excitation/contraction in cardiac/vascular smooth msucle cells. Reduces contractility and decreases HR. Vasodilation to decrease afterload.
What are indications for Calcium Channel BLockers?
Angina, hypertension, tachycardia, migraine Raynaud's disease
What are contraindications for calcium channel blockers?
Drug allergy, hypotension, heart block
What are adverse effects of Calcium channel blockers?
Overexpression of benefits (bradycardia, hypotension)
What drugs can calcium channel blockers interact with?
Antihypertensives (additive effect)