Chapter 5 - Cardiovascular System Flashcards
Think of the heart as 2 pumps – The right side is the small pump and it …
Pumps blood to the lungs and back to the heart
The left side of the heart is the larger and stronger pump and it …
Pumps blood throughout the remainder of the body and back to the heart
Veins carry blood ________ the heart
Towards
Arteries carry blood ________ the heart
Away from
The purpose of the valves in the heart …
To allow blood to flow in a SINGLE direction and to prevent blood from flowing backwards
(True/False) Valves pump blood through the heart
FALSE. Valves open and close passively in response to changes in blood pressure on either side of the valve
Vena Cava
Vessels returning blood to the RIGHT side of the heart
Right Atrium
Receives blood from the superior and inferior vena cava and delivers it to the right ventricle
Tricuspid Valve / Right Atrioventricular (AV) Valve
Valve between the right atrium and right ventricle of the heart
Right Ventricle
Lower chamber (right), pumps blood through the pulmonary trunk and arteries to the capillaries of the lungs
Pulmonic Valve
Valve between the right ventricle and the pulmonary arteries
Pulmonary Arteries
Carry blood from the right ventricle to the lungs
Pulmonary Veins
Carry blood from the lungs back to the heart
Left Atrium
Receives blood from the pulmonary veins and delivers it to the left ventricle
Mitral Valve / Left Atrioventricular (AV) Valve
Valve in the heart that controls blood flow from the left atrium into the left ventricle
Left Ventricle
Lower chamber (left), pumps oxygenated blood out through the aorta into systemic arteries
Aortic Valve
Valve in the heart between the left ventricle and the aorta
Aorta
Main trunk from which the systemic arterial system proceeds - Arises from the left ventricle of the heart
Ascending Aorta
Arises from the left ventricle and passes upward
Aortic Arch
Bends over
Descending Aorta
Proceeds downwards (divided into upper/thoracic part and a lower/abdominal part)
When the heart beats the “lubb-dupp” sound you hear is what action?
The sudden closing of the valves in response to the pressure change
Cardiac diseases related to mechanical functions include the following 3 things …
1) Muscular chambers fail to contract with sufficient strength. 2) Valves fail to close or open completely. 3) Unnatural holes connect chambers or major vessels, allowing blood to blow in abnormal directions.
Sinoatrial (SA) Node
** The hearts pacemaker **
Group of specialized conduction cells in the right atrium that depolarize more rapidly than any other cells in the heart.
These cells set the pace of the depolarization of the heart (the subsequent contraction that is felt is the pulse rate)
Depolarization Wave
“Firing” of cells through the heart (electrical conduction)
Contractile Muscle Cells
Actually pump the blood
Conduction Cells
Modified muscle cells that initiate and conduct the depolarization wave along a specific conduction pathway so that the muscle cells contract in the proper order
Automaticity
The ability to depolarize (fire) spontaneously and independently without any external stimulation
SA Node Depolarization
Sends a wave of depolarization outward in all directions through the right atrium and left atrium (as the wave of depolarization passes from one cardiac muscle cell to another, each cell contracts)
P Wave
Atrial depolarization (and contraction of atrial muscle cells) – appears as the small bump or deflection on ECG
PR Interval
Period of conduction delay in the AV Node – appears as a flat line after the P wave
QRS Complex
Represents ventricular depolarization (and contraction)
T Wave
Ventricular repolarization- Ventricle muscle cells relax and repolarize (reset) to prepare electrically for the next depolarization wave
Arrhythmia
Any deviation from the normal pattern of cardiac depolarization or repolarization, can result in tachycardia/bradycardia
(True/False) ECG is not used to diagnose mechanical abnormalities to the heart (poorly functioning valves/weak cardiac muscle)
TRUE. ECG is only useful in identifying electrical abnormalities in the conduction pathway or detecting an increase in the overall mass of the heart
Bundle Branches
Specialized conduction cell pathway that splits into right and left parallel tracts, they rapidly conduct the electrical impulse to the Purkinje Fibers
Purkinje Fibers
Modified cardiac fibers composed of Purkinje cells - interlaced network at the apex of the heart. Receives and distributes electrical impulse rapidly from the ventricular muscle cells, from the apex to the heart valves, and pushes blood through the pulmonic and aortic valves and out to the lungs and body
Ventricular Diastole
Relaxation phase between contractions
End Diastolic Volume
Amount of blood that fills the ventricular chambers after the ventricular diastole
Venous Return
Volume of blood returning to the heart
Venous Return System
Large veins carrying blood back to the heart from the body
Diuresis
Decreased blood volume as the result of water loss through the kidneys
Ascites
Fluid in the abdominal cavity
Systemic Hypertension
Increased blood pressure within the systemic arteries
Aortic Stenosis
Narrowing of the opening around the aortic valve
Mitral Valve insufficiency
Damage to the valve between the left atrium and left ventricle
Depolarization
When a cardiac or specialized conduction cell “fires”
Repolarization
When a cell resets itself in preparation to fire again
Resting State (polarized cell)
The cell is polarized (having two distinct ‘poles’ or segregated areas of electrical charge on either side of the cell membrane)
What are the 3 most prominent ions found in the body?
Sodium (Na+)
Potassium (K+)
Chloride (Cl-)
Sodium-Potassium -ATPase Pump
Sodium-Potassium Adenosine Triphosphatase
Pump (specialized protein) located in the cell membrane that maintains the separation of sodium and potassium by active transport, which gets its energy from the enzyme ATPase (the cells stored energy molecule)
Fast Sodium (Na+) Channels
Channel that when open allows Sodium to rapidly move into the cell driven by its concentration gradient
Potassium (K+) Channels
When the charge within the cell becomes positive (+) enough the Sodium fast channels close and the Potassium channels open, allowing Potassium to be driven out of the cell because of its influx of positively charged Sodium ions
When a rapid influx of Sodium moves INTO the cell (making it positively charged +) this is referred to as …
Depolarization - because the two ion populations are no longer kept separated or polarized across the cellular membrane
When the charge within the cell becomes positive enough, the Na+ fast channels close and the K+ channels open to allow Potassium to leave the cell. This is referred to as …
Repolarization - because the positive charges from the potassium are leaving the cell due the to influx of sodium ions entering the cell, causing the charge inside of the cell to become more negative again
Preload
The pressure exerted on the myocytes within the walls of the ventricles by the “load” or volume of blood in the ventricles just before ventricular contraction
Afterload
The tension or pressure the ventricles must create to eject blood out of the ventricles and into the aorta and pulmonary arteries
How many phases of charge are there inside the cardiac muscle cell with depolarization and repolarization?
5 total
Phase 0-IV
Phase 0
Depolarization
Sodium fast channels open, allowing positive sodium ions to rush into the cell and make it more positive
Phase I
Repolarization
After the Na+ influx, sodium channels close, potassium channels open, K+ leaves the cell causing the charge inside the cell to become less positive
Phase II
depolarization/repolarization curve
Opening of other Na+ and Ca++ channels causes a cause a further influx of positively charged ions that offset the loss of K+ creating a Plateau Phase
Phase III (Repolarization - Baseline charge)
When slow Na+ and Ca++ channels shut, continued outward movement of positive K+ ions now takes the charge inside the cell to a negatively charged baseline
Phase IV
Resting State
Potassium channels close and the Sodium-Potassium ATPase Pump redistributes the Na+ ions from Phase 0 back outside the cell, while moving the K+ from Phase I, II, and III back into the cell.
This causes NO net change in charge inside the cell, so the line remains flat (resting) until the next stimulus opens the fast Na+ channels again (Phase 0)
What are the 4 specialized cells of the hearts electrical cardiac conduction system
SA Node
AV Node
Bundle branches
Purkinje Fibers
Do cardiac conduction cells depolarize and repolarize exactly the same as cardiac muscle cells do?
NO. With cardiac conduction cells there is no plateau phase, and in Phase IV the conduction cell moves gradually upward immediately after completion of repolarization
Threshold
Once the phase IV slope attains a certain level of positive charge, the conducting cell depolarizes (fires) allowing Na+ and Ca++ ions to flow into the cell via their channels
Refractory Period
The time in the depolarization/repolarization cycle when the cardiac cell cannot depolarize again until it has completed the repolarization phase of the cycle
Absolute Refractory Period
A cardiac cell (or nerve) is absolutely refractory to depolarization stimulus during Phase 0, no matter how strongly the cell is stimulated to depolarize again they will not
Relative Refractory Period
Only a stronger than normal stimulus may be able to cause the sodium channels to open again, evoking a depolarization response
(Atria/Ventricle) Flutter or Fibrillation
A continuous series of rapid, uncoordinated contractions
Arterioles
Small artery blood vessels
List 3 Catecholamines
Epinephrine
Norepinephrine
Dopamine
What response do Catecholamines produce when they bind to Adrenergic (Catecholamine) receptors?
The combination of Catecholamines and Adrenergic receptors found on tissues and organs produces the physiologic changes observed as the “Fight or Flight” response
Adrenergic Agonists
Sympathomimetic Drugs
Any drugs that have intrinsic activity on these adrenergic receptors can mimic the effects of Epinephrine and Norepinephrine
Adrenergic Antagonists
Drugs that are able to bind to these adrenergic receptors but have NO intrinsic activity. They block catecholamine molecules from combining with receptors, which blocks their sympathetic effect
List the 4 Adrenergic Receptors (Fight or Flight/Sympathetic) having the greatest role in adrenergic drug actions
Alpha-1 (α1)
Alpha-2 (α2)
Beta-1 (β1)
Beta-2 (β2)
Stimulation of the Alpha-1 (α1) adrenergic receptors causes …
- Vasoconstriction of precapillary arterioles in the skin, abdominal organs including the GI tract and kidney (shunts blood away from these organs and towards the heart and skeletal muscles)
- Mydriasis (dilation of pupil)
Stimulation of the Alpha-2 (α2) adrenergic receptors (located on the ends of adrenergic neurons) causes …
- Inhibition of release of further norepinephrine from nerve terminal (regulates the release or norepinephrine)
Stimulation of the Beta-1 (β1) adrenergic receptors (located primarily in the heart) causes …
- Increased heart rate and force of contraction (Beta for beat!)
Stimulation of the Beta-2 (β2) adrenergic receptors (found on smooth muscle cells surrounding arterioles that supply the heart and skeletal muscles and surrounding bronchioles) causes …
- Increased bronchiole (bronchodilation) diameter by relaxing smooth muscle
- Dilation of blood vessels in skeletal muscles (for fleeing or fighting)
List the 2 Cholinergic Receptors (Rest and Digest/Parasympathetic) having the greatest role in cholinergic drug actions
Muscarinic Cholinergic Receptors
Nicotinic Cholinergic Receptors
Stimulation of the Muscarinic cholinergic receptors cause …
- Increased secretion and motility of GI tract
- Slows heart rate (but has no effect on force of contraction)
- Urination
- Bronchoconstriction
Stimulation of the Nicotinic cholinergic receptors cause …
- Voluntary skeletal muscle contraction
Tachycardia
Faster than normal heart rate
Bradycardia
Slower than normal heart rate
Ectopic Focus
Abnormal site or initial depolarization, often caused by damaged myocardial or conducing cells with membranes that leak Na+ into the cell more rapidly than normal (which is what produces spontaneous depolarization)
(True/False) Similar to diagnosing mechanical abnormalities, ECG cannot be used to detect arrhythmia’s cause by ectopic foci
FALSE.
ECG can be used to detect these arrhythmia’s
Premature Ventricular Contraction (PVC)
Ectopic focus located in the ventricles, which generates a single, large, bizarre wave on the ECG in place of the normal QRS complex
Paroxysm
Multiple PVCs occurring one after the other in a short series of waves
Ventricular Flutter
A longer series of PVCs
Ventricular Fibrillation
Rapidly Fatal
Conduction disturbance is severe and depolarization wave is so totally disrupted it is not identifiable on ECG (ventricles are quivering and unable to produce a coordinated contraction to eject blood)
Ventricular Tachycardia
Abnormal cell in the ventricles rapidly depolarizing and causing a rapid heartbeat
Atrial Flutter
Premature electrical impulse that arises in the atria, resulting in a faster than normal heart rate
(Rhythm may be regular or irregular in frequency)
Atrial Fibrillation
Very rapid contractions or twitching of the heart muscle in the atria. Ventricles will then contract more rapidly than normal
(Rhythm may be regular or irregular in frequency)
Sinus Rhythm
Normal rhythm controlled by the SA node
Tachyarrhythmia
Fast abnormal heart rhythm
can produce a faster ventricular heart rate or tachycardia
Bradyarrhythmia
Slow abnormal heart rhythm
can produce slower than normal heart rate or bradycardia
Supraventricular Rhythm
Indicates that the source or the arrhythmia is “above” the ventricles, meaning it originates in the Atria, SA Node, or AV Node
Ventricular Arrhythmia
Indicates that the problem originates somewhere in the ventricles or conduction pathways to the ventricles
Tolerance
Becoming resistant to the effects of a drug, occurs from upregulation (is not caused by induction of drug metabolism in cases of B1 blockers)
Upregulation
Occurs after a B1-adrenergic receptor has been blocked by B1-Blocker drugs for a long period of time. This causes the cell to begin to produce more B1-Receptors on the cell surface.
Negative Inotropic Effect
Causes a decreased force of contraction
Automaticity
Capacity of a cell to initiate an impulse, such as depolarization, without an external stimulus
Downregulation
Cells remove some of the B1-Receptors from the cells surface, reducing the number of receptors available, reducing the cells ability to respond to adrenergic drug stimulation
(also decreases the positive inotropic effect)
Positive Inotropic Effect
Increases the strength of contraction in a weakened heart
Class I
Antiarrhythmic Drugs
Sodium Influx Inhibitors - Work primarily by decreasing the rate of Na+ movement into the cell through the sodium fast channels
List 2-4
(Class I) Antiarrhythmic Drugs
- Lidocaine
- Mexiletine
- Procainamide
Class II
Antiarrhythmic Drugs
B-Blockers (antagonists) Work by blocking the B1-Sympathetic nervous system receptors on the heart
List 2-5
(Class II) Antiarrhythmic Drugs
- Propanolol (non selective antagonists (can combine with B1 and B2 receptors)) older drug
- Atenolol (Newer, selective B1 Blocker)
- Esmolol (Newer, Selective B1 Blocker) Very short acting
- Metoprolol (Newer, selective B1 Blocker)
- Carvedilol (Newer, Selective B1 Blocker)
Class III
Antiarrhythmic Drugs
Other antiarrhythmic Drugs - Work by inhibiting the potassium channels, making them slower to open and prolonging the repolarization period and extending the refractory period
List 1-2
(Class III) Antiarrhythmic Drugs
- Sotalol
- Amiodarone
Class IV
Antiarrhythmic Drugs
Calcium channel blockers - Block the slow calcium channels in conduction system cells, decreasing automaticity
List 1-3
(Class IV) Antiarrhythmic Drugs
- Diltiazem
- Verapamil
- Digoxin
Positive Inotropic Drugs
Drugs that increase the strength of contraction of a weakened heart, most work by making Ca++ more available to contractile proteins
Inodilator Drugs
Drugs that have both a positive inotropic effect and a vasodilation effect
Catecholamines
Increase the force on contraction through the B1-Receptors by causing a greater release of Ca++ from intracellular storage sites within the cardiac muscle
What are the body’s 3 natural positive inotropic agents (catecholamines) ?
- Epinephrine
- Norepinephrine
- Dopamine
Dobutamine
Adrenergic drug that produces a positive inotropic effect by stimulating B1-Receptors in the cardiac muscle and the conduction system cells - strong positive inotropes, but only improve cardiac contractility for a relatively short period of time
Pimobendan (Vetmedin)
Inodilator - Does not increase release of Ca++ from storage cell sites. Instead increases the Ca++ binding with the contractile elements, resulting in a more effective contraction of the cardiac muscle cell. Approved for Veterinary use in 2007.
Digoxin
Positive Inotrope - Causes more Ca++ to be released from the intracellular storage sites, making more Ca++ available for the contractile elements, enhancing strength of contraction
Vasodilator Drugs
Increase the diameter of blood vessels and are very important in treating CHF
Arterial Vasodilators
Directly reduces the resistance the heart must overcome to successfully eject the blood from the ventricles
Reducing the amount of blood left in the ventricles after contraction
Reducing backup of blood in the atria and vessels returning blood to the heart
Reducing backup and lowered pressure decreases pressure in the capillaries
Reducing forces pushing water into tissues and ultimately decreasing edema formation
Amlodipine
Arterial Vasodilator - Calcium channel blocker, can be used in dogs but used primarily in cats with hypertension secondary to kidney, hyperthyroid, or diabetes and not typically used to treat cardiac disease
Hydralazine
Arterial Vasodilator - Directly causes arteriolar smooth muscle to relax, the mechanism by which this occurs is not yet completely understood, but thought to inhibit some Ca++ movement into smooth muscle cells. Used to relieve some signs of CHF caused by severe mitral valve insufficiency
Nitroglycerine
Venous Vasodilator - Primarily relaxes blood vessels on the venous side of circulation, resulting in blood ‘pooling’ in the expanding venous blood vessels, reducing the volume of blood in the arterial side of circulation and decreasing arterial blood pressure
Mixed “Balanced” Vasodilators
Theoretically combines the benefits of arterial vasodilation (lowered arterial BP, ease of ventricular ejection of blood) and Venodilation (lowered pulmonary circulation BP, decreased edema formation)
Nitroprusside
Potent Mixed Vasodilator - used short term to help stabilize dogs/cats with severe dyspnea cause by pulmonary edema secondary to heart failure. Cannot be administered to patients that are hypotensive
ACE Inhibitors
Mixed or balanced vasodilators that relax smooth muscle of both arterioles and veins.
Produce vasodilation by blocking/inhibiting Angiotensin Converting Enzyme (ACE) preventing formation of Angiotensin II (potent vasoconstrictor) and Aldosterone (hormone that increases blood volume by causing Na+ retention)
** Must be used with caution in animals with pre-existing kidney disease
List 2-4
ACE Inhibitor Drugs
- Enalapril
- Benazepril
- Lisinopril
- Captopril
Hypertension
Increased blood pressure
Hyoptension
Decreased blood pressure
Congestive heart Failure (CHF)
The heart muscle is too weak to eject sufficient blood to maintain normal tissue functions. Decreased cardiac output results in decreased arterial blood pressure
Baroreceptors
Special pressure receptors located in the walls of large arterial blood vessels (primarily in carotid artery and aortic arch) detect change in blood pressure.
When BP is normal: receptors send a constant low-level signal to inhibit activation of the SNS.
When Arterial BP decreases: Stop sending the inhibitory signal, the SNS becomes activated (releasing epinephrine and norepinephrine to stimulate B1 and A1 receptors) which increases arterial BP
Renin
A compound that is released into the blood when the specialized cells in the renal tubules detect decreased blood flow
Angiotensinogen
A compound produce by the liver, product of Renin conversion
Angiotensin I
Product of Angiotensinogen which is quickly converted by the Angiotensin-Converting-Enzyme (ACE) to Angiotensin II
Angiotensin II
Product of Angiotensin I, one of the body’s most potent vasoconstrictors. Its release is designed to increase arterial BP and theoretically restore renal blood flow and urine formation
(but increased arterial pressure also causes increase to the hearts workload by increasing the volume of circulating blood)
Aldosterone
Hormone released from the adrenal cortex when stimulated by Angiotensin II.
It increases Na+ reabsorption from the urine and pulls it back into the blood, causing a greater retention of Na+. This osmotically attracts and holds water in the blood, increasing the blood volume. This restores/maintains arterial BP but also creates a larger volume of blood for the heart to pump and increasing the workload
Compensated Heart Failure
A patient whose body has successfully initiated the autonomic compensatory response to the weakened heart and falling arterial blood pressure
Diuretics
Increase urine formation and promote water loss (diuresis). Diuretics work by either:
1) preventing reabsorption of Na+ or K+ from the renal tubules
2) They enhance Na+ and K+’s secretion into the tubules
List 2-4 reasons Diuretics may be used
1) Reducing inappropriate accumulation of tissue fluid (pulmonary or cerebral edema)
2) Reducing blood volume
3) Reducing arterial pressure
4) Decreasing the workload on a failing heart in CHF
Loop Diuretics
Referring to the ‘Loop of Henle” located within the renal tubule, which is where these drugs produce diuresis by inhibiting reabsorption of Na+ from the urine at the thick ascending segment of the Loop. Retained Na+ in the urine osmotically retains water in the urine and results in water loss via urine
Furosemide (Lasix)
Loop Diuretic that inhibits reabsorption of Na+, storing Na+ in the urine and osmotically retaining water, resulting in water loss via urine. Helpful in increasing diuresis in early stages or renal damage/disease
Ototoxicity
Toxicity associated with hearing or the inner ear. Furosemide and other Loop diuretics have been implicated in causing ion imbalances, changing the electrolyte balance in the inner ear, resulting in loss of hearing
Thiazide Diuretics
After administration, Thiazides are secreted into the forming urine by the proximal convoluted tubule, pass the loop of henle without causing any effect, and then flow downstream to the initial segment of the distal convoluted tubule where they act to decrease resorption of Na+ and Cl-
(True/False)
Thiazide diuretics have more of a diuretic effect than Furosemide
FALSE.
They are less potent than loop diuretics because of their site of action (distal convoluted tubule). Also typically used in conjunction with Furosemide when kidneys become less responsive to Furosemide alone.
List 1-2
Thiazide Diuretics
- Chlorothiazide
- Hydrochlorothiazide
Potassium-Sparing Diuretics
Diuretics that do not secrete K+ ions, and actually increase Na+ ion excretion and retains K+ in the body instead
Spironolactone
Potassium sparing diuretic. Competitive antagonist of Aldosterone. Useful for animals with excessive fluid retention from CHF that is unresponsive to Furosemide or Thiazide alone
Osmotic Diuretics
Retains water in the renal tubules by its physical presence within the lumen of the renal tubule.
Mannitol
Carbohydrate (sugar) that retains water in the renal tubules by its physical presence. Primarily used to reduce cerebral edema associated with head trauma, reduce damage to the kidneys when they are first injured by a poison or drug, and increase excretion of renally eliminated toxins
Carbonic Anhydrase Inhibitors
May be used to decrease production of aqueous humor in the eye and reduce intraocular pressure in animals with glaucoma
Acetazolamide
Carbonic Anhydrase Inhibitor - relatively weak diuretic effect - Not used to treat cardiac problems in Veterinary patients
Aspirin (Acetylsalicylic Acid)
Inhibits platelet formation of prostaglandins and thromboxanes. This reduces aggregation (clumping) of platelets and reduces the chances for spontaneous platelet plug formation and subsequent larger fibrin clot formation
(True/False)
Use of Aspirin in cats can reduce the risk of spontaneous platelet adhesion and thrombus formation. But it must be given in a 48 hour dose interval.
TRUE
Aspirin can be used in cats to help prevent thrombus formation associated with hypertrophic or congestive cardiomyopathy. 48 hour dosing is required because cats do not metabolize and eliminate the drug as readily as other species do
Sedatives/Tranquilizers
Sometimes use of these drugs by merely calming the animal which reduces the heart rate and reduces the risk of fatal arrhythmia’s. They can also reduce the heart muscles oxygen consumption and improve the heart muscles effectiveness. As always sedatives effects need to be weighed against any possible adverse effects in these situations
Aerophagia
A condition in which the animal is gasping for breath
Hyperkalemia
High concentrations of potassium (K+) in the blood
Hyponatremia
Low sodium (Na+) levels in the blood and body
Hypovolemia
Low blood volume
Edema
Fluid retention in tissues
Syncope
Fainting
Ataxia
Weakness
Ascites
Accumulation of fluid within the abdominal cavity
Is ascites associated/seen with left or right sided heart failure?
Left
Pulmonary Edema
Accumulation of fluid within the tissue of the lungs
Is pulmonary edema associated/seen with left or right sided heart failure?
Right
Thrombus
Large fibrin clot
Thromboxanes
Released by traumatized tissue and make platelets sticky so that they will adhere to each other at small breaks in blood vessels to form a platelet plug that stops the bleeding
