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How can having congestive heart failure affect the heart?
weak cardic muscles
What do arrythmias do to the heart?
disrupt normal electrical activity
What are two things that can cause increase work load on the heart?
-vasoconstriction
-heartworms
True or False: Decrased heart function can impact every other organ system
True
What are 3 things that cardio drugs can focus on?
-pumping function
-electrical coordination
-vasculature diameter
Blood returns from the body through what chamber?
right atrium
What chamber pumps blood TO the lungs?
right ventricle
What chamber returns blood FROM the lungs?
Left atrium
What chamber pumps blood TO the body (oxygenated)?
Left ventricle
The left ventricle pumps blood out to the body through what valve?
pulmonic valve
The right ventricle pumps blood out to the lungs through what valve?
Aortic valve
What is the pacemaker of the heart?
SA node
What is the structure that slows the depolarization wave going from the atria to the ventricles?
AV node
What carries the impulse to the apex of the ventricles?
Bundles of His and the right and left Bundle Branches
What does the P wave represent?
depolarization (contraction) of the atria
What does the QRS complex represent?
depolarization of ventricle, repolarization of atria
What does the T wave represent?
repolarization of the ventricles
What part of the ECG represents the depolarization wave as it passes through the AV node
PR segment (this is where the ventricles fill)
Why is there no wave representing atrial repolarization?
It happens at the same time as ventricle repolarization
Why is the SA node the pacemaker of the heart?
It depolarizes spontaneously (has automaticity) more frequently than any other spontaneously depolarizing cell in the heart
Why does the whole heart not contract at once?
The AV node delays depolarization wave long enough for blood to be physically moved from the atria (by atrial contraction) into the ventricles (PR segment)
What is a wave of depolarization?
The influx of sodium causing adjacent sodium channels to also open up causing a depolarization wave along the cell
(separatre "poles" of sodium and potassium no longer exist)
What is repolarization?
The poles are re-established
What is the term for the time during which the cardiac cell cannot depolarize REGARDLESS of the strength of the stimulus?
Absolute Refractory Period (ARP)
What is the term for the time during which the cardiac cell may depolarize IF a sufficient stimulus is provided?
Relative Refractory Period
What is fibrillation?
where the heart is not contracting in a coordinated manner
What cardiac changes do you see when the sympathetic nervous system is engaged?
-Increased HR
-Quicker conduction of depolarization wave from atria to ventricles
-Greater force of contraction
-Vasoconstriction
Vasoconstriction makes it harder or easier for heart to eject blood into the arterial system?
harder
What cardiac changes do you see when the parasympathetic nervous system is engaged?
-Slow HR
-Slows conduction of depolarization wave from atria to ventricles
-NO effect on cardiac muscle or vasculature
What 2 beta receptors do norepinephrine and epinephrine act on?
adrenergic receptors
1. Beta 1 receptors
2. Beta 2 receptors
What to Beta 1 receptors do and where are the located?
-located on SA node, AV node and cardiac muscle
-increase HR and force of contraction
What to Beta 2 receptors do and where are the located?
-located on bronchioles and skeletal muscle vessels
-dilates bronchioles by relaxing smooth muscle, vasodilation
Where are alpha 1 receptors located and what do they do?
-located on peripheral vasculature (skin, SQ tissues and mucous membranes), GI, kidneys
-arterial vasoconstriction --> increases work load on the heart
Where are alpha 2 receptors located and what do they do?
-located on the presynaptic terminal of the neuron that releases norepinephrine
-will shut down further release of norepi
What do antagonist drugs do to receptors?
blocks the receptor attaching site
Do beta blockers (that block B1 receptors) increase or decrease HR?
decrease
Do cholinergic blockers (that block acetylcholine receptors) increase or decrease HR?
increase
Do drugs that mimic acetylcholine increase or decrease HR?
decrease
Do drugs that can stimulate B1 receptors increase or decrease HR?
Increase
What is an arrhythmia?
any abnormal pattern of electrical activity of the heart
What is ectopic focus?
can be damaged myocardial cells that become leaky to sodium and fires on its own before the normal depolarization waves arrives
Can an ectopic focus cause arrhythmias?
yes
What are premature ventricular contractions (PVCs)?
a SINGULAR ectopic focus beat that can cause ventricles to contract prematurely
What is a short series of PVCs called?
paroxysm
What is a longer series of PVCs called?
flutter
When the organization of the contractions completely breaks down so that no recognizable pattern can be recognized on ECG, this is called what?
fibrillation
What is it called when there is a short burst of PVCs with rapid HR?
Paroxysmal ventricular tachycardia
What is it called when there is a prolonged series of PVCs but stil some organization to it?
Ventricular flutter
What is it called when there is no organization on the ECG, heart is not effectively pumping?
Ventricular fibrillation
What does supraventricular mean?
That the problem orginated in the SA node "above" the ventricles
What are all the sodium channel blocker antiarrhythmic drugs?
-lidocaine
-mexiletine
-procainamide
-quinidine
How do sodium channel blocker antiarrhythmic drugs work?
-reverse arrhythmias by blocking the fast sodium channels that allow Na+ influx into the cell (depolarization)
What is the drug of choice for control of PVCs and ventricular arrhythmias?
lidocaine
What drug has little efficacy against atrial fibrillation or flutter?
lidocaine
What route is lidocaine usually administered and why?
IV, when given orally it has a strong first pass effect (a lot of the drug is metabolized and removed before reaching systemic circulation)
What species is more sensitive to lidocaine and require a lower dose?
cats, they are more sensitive to side effects
Why must lidocaine be given as a CRI?
rapid metabolism of the drug
What can you see with CNS toxicity from lidocaine?
-low dose tox: sedation, ataxia, drowsiness
-high dose tox: excitement and seizures
Lidocaine WITH epinephrine is ONLY used for what? why?
local anesthesia, if epi is given to patients with arrhythmias, the effects could make the arrhythmias worse because epi causes vasoconstriction
What drug is an orally-adminstered drug in the same class as lidocaine
Mexiletine
Why is Mexiletine used over Lidocaine if the patient needs to be maintained long-term on it?
It has minimal first pass effect so more of it will reach systemic circulation, also has a longer half life
What 2 drugs are in the same class as lidocaine, but can control ventricular foci and atrial fibrillation/flutter?
Procainamide and Quinidine
What species is procainamide used for?
small animals
What species is quinidine used for and why is it used?
horses for atrial fibrillation and flutter
After giving a horse quinidine, a horses HR should decrease because the AV node is being bombarded by atrial depolarization less, why doesn't the HR decrease?
it has an anti-vagal effect = it blocks acetylcholine at the AV node so it blocks the slowing effect of parasympathetic system --> increasing HR
What are the 4 beta blocker antiarrhythmic drugs?
-propanolol
-atenolol
-esmolol
-metoprolol
How do beta blockers work?
-block B1 receptors
-prevent norepi from reaching site and increasing HR and force
-also makes heart electrically unstable
-allow parasympathetic to dominate (poss. AV block)
What drug is an older type of beta blocker drug that blocks B1 AND B2, has bronchdilation effects
propanolol
What is upregulation?
the cell creates more receptors in responses to the increased dose
What do positive inotropic agents do? What is the older antiarrhythmic drug in this class?
increase the cardiac muscle force of contraction; digoxin
What is one side effect of digoxin?
increased parasympathetic effect on AV node (AV block)
What do inodilators do?
incrase the strength of contraction AND dilate the arterioles which reduce resistance to blood flow and work load on the heart
-increase calcium available to contractile elements
What are catecholamines? Give 2 drugs in this group?
-description used on drugs that are similar in chemical nature to epinephrine and norepinephrine
-dobutamine and dopamine
Why can't you use catecholamines chronically?
cells downregulate from the overstimulation and retract B1 receptors from the muscle surface --> less responsive to the drug
What is pimobendan also known as?
Vetmedin
What is the most commonly used inodilator (largely replaced digoxin for most commonly used positive inotropoic drug)?
Pimobendan
What does phosphodiesterase (PDE) do?
an enzyme that causes relaxation of smooth muscles surrounding arterioles (vasodilation)
When do we use pimobendan?
-advanced heart failure (showing signs) associated with dilated cardiomyopathy or severe valvular disease in dogs or cats
Why should pimobendan not be used in hypertrophic cardiomyopathy?
thickened ventricles obstruct outflow tracts and that contraction prevents the ejection of blood by ventricles
What is the site of action for digoxin?
sodium-potassium-ATPase pump on cell membrane
Which drug is a cardiac glycoside and natural poison found in foxglove plants?
digoxin
What are side effects of digoxin?
-vomiting and anorexia (stimulates CRTZ)
-bradycardia and AV block
-excreted in kidneys so caution in patients with kidney disease
_________ is a protective mechanism by which the body keeps arterial blood pressure elevated in the normal range
vasoconstriction
Name the arterial vasodilators.
-amlodipine
-hydralazine
Name the venous vasodilators.
-nitroglycerin
Name the mixed vasodilators.
-nitroprusside
-ACE inhibitors-enalapril
Explain how vasoconstriction can affect heart disease.
-it creates resistance to blood flow which = increase BP, but the heart has to work so hard to increase it so eventually muscle failure worsens = decompensated congestive heart failure
What do the kidneys release when decreased BP in the kidneys is detected?
renin
What does renin do?
Converts liver from angiotensinogen to angiotensin 1
What is angiotensin 1 converted to and by what?
angiotensin 2 by angiotensin-converting enzyme (ACE)
What is the body's most potent vasoconstrictor?
angiotensin 2
What does angiotensin 2 stimulate the release of and from what?
aldosterone from the adrenal gland
What does aldosterone do?
increases sodium reabsorption from the urine back into the body which pulls water and increases fluid volume --> increased BP
(also increases workload on the heart)
What is the main goal of using vasodilators?
-used to attempt to reduce resistance and blood ejection from heart which ultimately reduces work load on the heart
How do vasodilators reverse vasoconstriction?
-block alpha 1 receptors
-block the renin-angiotensin-aldosterone system (RAAS)
-direct relaxation of arteriole smooth muscles
Why can't we use vasodilators on animals on beta blockers?
the beta blockers prevent norepi from correctine hypotension through b1 --> increases hypotension
aterial vasodilation does what?
directly lowers resistance the heart must overcome to successfully eject blood
What drug is used in cats more with hypertension secondary to CKD, hyperthyroidism or diabetes (can be used in dogs too)?
amlodipine
What drug is also a calcium channel blocker as well as an arterial vasodilator? what does it do?
amlodipine; reduces amount of calcium available for contraction --> vasodilation
What drug is an arterial vasodilator that is a direct arteriolar smooth muscle relaxant?
hydralazine