Cardiovascular Drugs, Heart Physiology

• Cardiovascular drugs act on the heart or blood vessels.

Function & Physiology

• The heart functions as a distribution system, pumping oxygenated blood, nutrients, and hormones to tissues.
• It also removes waste from tissues.
• SA node initiates the heart's electrical impulses
• Conduction of electrical impulses normally originates in the SA node.

Conduction system

• Proper heart contractions should be rhythmic at regular intervals.

Rate of Conduction System (heart rate)

• Primarily controlled by the nervous system.
• Nerve endings are located close to the SA node.
• Parasympathetic release of neurotransmitters (NT) can increase or decrease heart rate (HR) by inhibiting impulse formation or electrical conduction.
• Sympathetic release of NTs can increase or decrease HR by promoting impulse formation/electrical conduction and decreasing time between contractions.

Contractility, Preload, Afterload

• Contractility is the force of ventricular contraction.
• Preload is the pressure within the ventricle before contraction.
• Afterload is the force needed for the ventricle to push blood out of the ventricles.
• Stroke volume is the volume of blood ejected from the left ventricle with each contraction.
• Cardiac output is the volume of blood expelled from the heart in one minute which is heart rate x stroke volume or contractions / min

Blood Pressure

• Systemic vascular resistance (SVR) is resistance in arterioles due to smooth muscle
• Blood pressure (BP) is influenced by the autonomic nervous system (ANS) and hormones and is calculated as Cardiac Output x Systemic Vascular Resistance
• Cardiac output(CO) is heart rate (HR) x Stroke volume

Sick Heart conditions

• CHF (Congestive Heart Failure)
• Arrythmias
• Cardiomyopathy which is a chronic disease of the heart muscle
• Valve disease

Congestive Heart Failure

• End stage of any cardiac muscle disease.
• Can be caused by cardiomyopathy, hypertension, or valvular disease.
• Fluid builds up in the lungs (pulmonary edema), around the lungs (effusion), or in the abdomen.

Arrhythmias

• Occur when the SA node is not conducting properly.
• Other areas of the conduction system take over to initiate a beat.
• Treatment depends on the type of arrhythmia.

Cardiomyopathy

• Causes: genetics, infection, degeneration
• DCM (Dilated Cardiomyopathy): More common in dogs, heart muscle weakens, reducing its ability to pump; the atria and ventricles are enlarged
• HCM (Hypertrophic Cardiomyopathy): More common in cats, thickened heart muscle makes it harder to pump blood, but the heart muscle develops hypertrophy

Valve Disease

• "Leaking" or backflow of valves exists
• Associated sounds may be present.
• Can lead to CHF.
• Mitral valve issues cause pulmonary edema.
• Tricuspid valve issues can cause ascites.

Compensatory Mechanisms

• Increase in heart rate leads to an increase in cardiac output, but chambers don't have time to fill.
• Increase in contractility improves ventricular emptying, increasing stroke volume.
• Decrease in arteriole vascular tone reduces the work the heart has to do.
• Cardiac remodeling enlarges the heart to attempt to pump more blood.
• Dilation of heart chambers increases the amount of blood it can hold, increasing stroke volume
• Thickening the myocardium increases the force of contraction.

Clinical Signs

• Coughing, difficulty breathing, exercise intolerance, murmurs(valves) arrythmias etc
• Blood electrolyte changes (Na+ & K+)
• Ultrasound and x-ray images, blood flow and ECG anomalies
• Alterations to heart rate, rhythm or pulse quality

Cardiovascular Drugs: Actions

• Dromotropy = Conduction of myocardial electrical impulses -↑ conduction = positive dromotropic drugs -↓ conduction = negative dromotropic drugs
• Chronotropy affects heart rate -↑ heart rate = positive chronotropic drugs -↓ heart rate = negative chronotropic drugs
• Inotropy is the force of myocardial contractions -Strengthen contractions = positive inotropic drugs
• A drug can have multiple functions.

Alpha and Beta Receptors

• Alpha (α) 1 Receptors in arteriole blood vessels (smooth muscle):
  • Stimulation causes VASOCONSTRICTION
  • Blocking causes VASODILATION
• Beta (β) Receptors in heart & lungs Beta 1:
  • Stimulation causes ↑ chronotropy + inotropic effects
  • Blocking causes ↓ chronotropy + negative inotropic effects
  • Beta 2 Receptors in bronchioles (smooth muscle)
    • Stimulation causes BRONCHODILATION
    • Blocking causes BRONCHOCONSTRICTION

Cardiovascular Drug Categories

• Drugs acting on the heart
• Drugs acting on blood vessels.

Drugs Acting on the Heart

• Cardiac stimulants
• Drugs used to treat Congestive Heart Failure (CHF)
• Antiarrhythmic drugs

Cardiac Stimulants (Catecholamines)

• SYMPATHOMIMETIC action
• Epinephrine
• Dopamine
• Dobutamine

Epinephrine (α₁ & β)

• Effects:
  • Increases force and rate of contraction, increasing cardiac output (CO) via Beta 1 receptor activity.
  • Vasoconstriction increases blood pressure (BP) via Alpha 1 receptor activity.
• Use: To treat cardiac arrest and anaphylactic shock.
• Routes: IV, IC, IT, IM, or SC
• Side Effects: Potential arrhythmia and hypertension.

Dopamine (α₁ & β₁)

• Effects: Dose-dependent increases in blood pressure (BP), heart rate (HR), & contractility.
• Use: To treat acute heart failure, severe shock, and during general anesthesia(GA)
• Routes: CRI
• Side Effects: Tachycardia, dyspnea, vomiting.

Dobutamine (β₁)

• Effects: Increases contractility.
• Use: To treat cardiac depression with hypotension, shock where patients are unresponsive to fluid therapy alone.
• Routes: CRI
• Side Effects: Tachycardia, ventricular arrhythmias.

Drugs used to treat Congestive Heart Failure (CHF)

• Act on the RAAS system