Cardiovascular System

• Components:

  • Heart

  • Veins

  • Arteries

  • Capillary beds

• Valves:

  • Atrioventricular Valves: Mitral, Tricuspid

  • Semilunar Valves: Aortic, Pulmonic

  • Valves in large veins

  • Function: Keep blood flowing in one direction

• Regulation:

  • Nervous System:

    • Autonomic Nervous System (Sympathetic and Parasympathetic)

    • Sympathetic Stimulation: Norepinephrine/Epinephrine binds beta1-adrenoreceptors -> Increases SA node discharge rate (Cardioacceleration/Positive chronotropic effect). Can be blocked by beta-adrenergic blocking agents (eg, propranolol, atenolol, metoprolol, esmolol, carvedilol).

    • Parasympathetic Stimulation: Acetylcholine binds cholinergic receptors -> Decreases SA node discharge rate (Cardiodeceleration/Negative chronotropic effect). Can be blocked by a parasympatholytic (vagolytic) compound (eg, atropine, glycopyrrolate).

  • Hormones:

    • Produced by heart/blood vessels (paracrine or autocrine).

    • Produced at a distance (endocrine).

    • Examples influencing tone of vascular smooth muscle: constricting (adrenergic agonists, angiotensin II, vasopressin, endothelin), relaxing (norepinephrine, atriopeptin, bradykinin, adenosine, nitric oxide).

    • Natriuretic peptides (BNP from ventricles, ANP from atria) released by stretching of receptors in atria/ventricles. BNP/NT-proBNP levels correlate with degree of heart stretch in dogs.

• Cardiovascular Disease:

  • Prevalence: Slightly >10% of domestic animals examined have some form (clinically significant or insignificant). True prevalence likely underestimated.

  • Varying prevalences based on species, breed, and etiology (congenital vs acquired).

  • Nature: Similar to other chronic diseases, may not resolve but progress and become more limiting over time, potentially leading to death.

  • Heart Failure (CHF):

    • Usually abolishes or diminishes RSA. (May persist with comorbid conditions increasing vagal activity, like respiratory or neurologic disease).

    • Baroreceptors become fatigued, reducing afferent signals to medulla.

    • Results in less vagal efferent signaling.

    • Dogs in CHF have a decrease in heart rate variability.

    • Frequently present with an underlying sinus tachycardia.

    • Afterload is often increased.

    • Characterized by an increase in sympathetic tone and relative increases in heart rate.

    • Ultimate impact is an inefficient myocardium that can result in deleterious remodeling.

    • Inappropriate handling of calcium may result in arrhythmogenesis.

    • Inappropriate handling of calcium may be the most important factor leading to reduced force of contraction (systolic dysfunction) and reduced rate of relaxation (diastolic function).

    • Increased resistance of arterial, arteriolar, and venous smooth muscle due to increased angiotensin II, vasopressin, and endothelin.

    • If the left ventricle is unable to eject normal stroke volume/cardiac output, ventricular function might be improved by decreasing vascular resistance. Decreasing afterload (arterial vasodilation) is one therapeutic goal in heart failure therapy.

• Evaluation of the Heart:

  • Physical Assessment: Assessment of heart sounds and murmurs, arterial pulses, degree of jugular vein distention, strength and location of the apex beat.

  • Diagnostic Imaging/Tests: Electrocardiography (ECG), Radiography, Cardiac biomarkers, Echocardiography, other advanced imaging techniques (angiography, fluoroscopy, CT scan with angiography, cardiac MRI).

• Heart Rate & Electrocardiogram (ECG):

  • Pacemaker: The sinoatrial (SA) node is the pacemaker of the heart.

  • Origin of Heartbeat: Wave of depolarization begins in the SA node at the juncture of the cranial vena cava and the right atrium.

  • SA Node Discharge Rate (Resting): Species dependent.

    • Horses: ~30 times/min.

    • Cats: >120 times/min (typically 180–220 times/min in a hospital setting).

    • Dogs: 60–120 times/min (range of 40–260 bpm, with average daily rate of 80 bpm for an adult dog based on 24-hour Holter monitoring).

    • In general, the larger the species, the slower the rate of SA node discharge and the slower the heart rate.

    • Birds: ~115–130 beats/min resting. Active heart rates up to 670 beats/min. Hummingbirds active rate >1,200 beats/min.

  • Factors Affecting SA Node Rate: Sympathetic stimulation (increases), Parasympathetic stimulation (decreases).

  • Conduction Pathway: SA node -> Preferential pathways (interatrial, internodal, atrionodal) -> Atrioventricular (AV) node -> Specialized conduction system (bundle of His, right and left bundles branches, Purkinje network) -> Subendocardium of ventricles/ventricular septum -> Ventricular myocardium.

  • AV Node: Speed of conduction is slowed through the nodal tissue, giving atria time to contract and eject more blood into ventricles, allowing for atrioventricular synchrony.

  • Ventricular Activation:

    • Differs between domestic mammals based on 3 fronts (waves) of depolarization.

    • Category A (dog, human, monkey, cat, rat): Depolarization travels slowly through myocardium (subendocardial to epicardial).

    • Category B (goat, horse, cow, pig, sheep): More extensive Purkinje fiber networks throughout the ventricular myocardium into the epicardium. Wave front does not spread from endocardium to epicardium as in category A.

  • ECG Waveforms and Intervals:

    • P wave: Produced as wave of depolarization traverses the atria. Represents atrial depolarization (atriogram). Followed by atrial contraction (atrial kick).

    • PR/PQ Interval: Interval on ECG between onset of P wave and onset of QRS complex. Measures time for electrical wave to begin at SA node, traverse AV node, and reach ventricles. As heart rate increases, PR interval shortens; when heart rate slows, PR interval lengthens. Factors speeding/slowing SA node rate (chronotropy) also speed/slow conduction through AV node (dromotropy).

    • QRS Complex: Produced as depolarization travels through ventricular myocardium. Represents ventricular depolarization. Followed by mechanical ventricular contraction.

    • T wave: Represents repolarization of the ventricles. Affected by electrolyte imbalance (eg, hypo-/hyperkalemia, hypo-/hypercalcemia), myocardial injury, or ventricular enlargement.

    • Ta wave (Atrial repolarization): Rarely seen in small animals due to low voltage deflection, occurs during the larger QRS complex. Occasionally seen with AV nodal disease or slow heart rates (e.g., horses), appearing as a “hammock” after the P wave.

  • ECG Lead Systems:

    • Can be studied in three anatomic planes (frontal/X-axis, sagittal/Y-axis, horizontal/Z-axis).

    • For Category A mammals: Bailey's hexaxial system (frontal plane), precordial or chest lead system (horizontal plane), bipolar orthogonal system (all three planes).

    • For Category B mammals: Base-apex lead configuration is used. Cannot determine chamber enlargement from this lead; ECG is only used to assess cardiac rhythm.

  • ECG Interpretation: Should be performed systematically. Includes assessment of heart rate and rhythm, evaluating waveforms (P, QRS, T) and segments (PR/PR, ST, QT), and assessing for presence of a P wave for every QRS wave and vice versa. In-depth review is beyond the scope.

  • Electromechanical Dissociation: Rare condition where there is depolarization without contraction.

• Heart Rate Variability:

  • Respiratory Sinus Arrhythmia (RSA): Cyclic variation of heart rate with respiration in quiet, healthy animals. Results from decreased vagal activity during inspiration (increase in SA node discharge rate, increased HR) and increased vagal activity during expiration (decrease in SA node discharge rate, decreased HR). Other mechanisms contribute (cardiopulmonary/baroreceptors, Frank-Starling, Bainbridge reflex). RSA is a good indicator of cardiac health. Uncommonly documented in cats in the hospital setting due to their higher sympathetic tone.

  • Marey's Law: Heart rate is inversely related to systemic arterial blood pressure. When blood pressure increases, heart rate decreases; when blood pressure decreases, heart rate increases. Occurs via high-pressure arterial baroreceptors signaling the medulla oblongata, affecting vagal efferents to the SA node.

• Force of Ventricular Contraction:

  • Determined by: End-diastolic volume (preload) and Myocardial contractility (inotropy).

  • Preload: The volume of blood within the ventricles just before they begin to contract (end-diastolic volume). Determined by difference in end-diastolic pressure (ventricle vs pleural space) divided by ventricular myocardial stiffness. End-diastolic pressure determined by ratio of blood volume and myocardial compliance. Regulated predominantly by low-pressure volume receptors in the heart and large veins. Stimulation by increased blood volume/distention -> body makes more urine and dilates veins to decrease blood volume/pressure. Increase in end-diastolic volume (preload) stretches the ventricular wall, resulting in a more forceful contraction as per the Frank-Starling mechanism, or Starling's law of the heart. Stretching receptors in atria/ventricles causes release of natriuretic proteins (BNP, ANP).

  • Myocardial Contractility (Inotropy): Rate of cycling of the microscopic contractile units. Determined by availability of ATP and calcium for myosin-actin cross-bridging. Rate of ATP energy liberation partly determined by norepinephrine binding beta1-adrenergic receptors. Down-regulation of myocardial beta1-receptors is one of the most important factors in heart failure.

• Oxygen and the Myocardium:

  • Oxygen is essential for ATP production, which fuels contraction and relaxation.

  • Myocardial Oxygen Content: Balance between how much oxygen is delivered to the heart vs consumed.

  • Oxygen Delivery: Depends on lung function, Hgb present, and how much blood flows through coronary arteries. If lungs/Hgb are normal, coronary blood flow determines delivery. Coronary blood flow determined by pressure difference (aorta - right atrium). Coronary flow is greatest during diastole. Slower heart rates (preferentially increase diastolic interval) are associated with improved myocardial oxygen delivery.

  • Myocardial Oxygen Consumption: Determined principally by wall tension and heart rate.

  • Wall Tension: Expressed by the law of LaPlace. Tension increases with increases in pressure or diameter of the ventricle. Tension decreases with increases in wall thickness. Tension increases with conditions that increase afterload (stenosis, hypertension) or preload (valve insufficiency, shunts, dilated cardiomyopathy).

  • Heart Rate: Increases in heart rate result in increasing myocardial oxygen consumption while decreasing time for diastole (when coronary flow is greatest). This combination can set the stage for an imbalance in myocardial oxygen demand and supply, leading to myocardial ischemia.

• Hindrance to Blood Flow:

  • Cardiac Output: Blood flow from the heart via left and right ventricles. Determined by heart rate and ventricular stroke volume. Critical to satisfactory function of the heart and consequent perfusion of organs.

  • Normal Cardiac Output: Dogs 100–200 mL/kg/min, Cats 120 mL/kg/min.

  • Most Hindrance: Degree of constriction of the arterioles, termed vascular resistance (>90%).

  • Some Interference: Stiffness of great arteries closest to ventricles, termed impedance. Impedance is the sum of external factors opposing left ventricular ejection, closely related to afterload. Great arteries expand to accommodate stroke volume, then recoil during ventricular relaxation to keep blood moving. Aortic and pulmonic valves close to prevent stroke volume return to ventricle.

  • Systemic Vascular Resistance (SVR): Opposing blood flow that must be overcome to push blood through peripheral circulation. Calculated by: (mean arterial pressure – central venous pressure)/cardiac output. (Right atrial pressure can substitute CVP). Increased in heart failure.

  • Pulmonary Vascular Resistance: Calculated: (mean pulmonary artery pressure - pulmonary arterial wedge pressure)/cardiac output. (Left atrial pressure can substitute PAWP). Increased in pulmonary vascular obstruction or pulmonary hypertension.