Cardiovascular Physiology, Pathology, and Weight Control

Comprehensive vocabulary flashcards covering cardiac electrophysiology, cardiovascular disease pathology, and obesity epidemiology and exercise guidelines.

Sinoatrial (SA) Node

The primary physiological pacemaker of the heart, located in the upper right corner of the right atrium, that spontaneously generates electrical action potentials at an intrinsic rate exceeding $100\,\text{bpm}$, regulated down to $60\text{--}100\,\text{bpm}$ at rest by parasympathetic vagal tone.

Atrioventricular (AV) Node

A specialized bundle of nodal tissue situated in the lower left corner of the right atrium that introduces an intrinsic conduction delay of approximately $0.13\,\text{s}$ ($130\,\text{ms}$) to ensure complete ventricular filling before serving as a secondary pacemaker at $40\text{--}60\,\text{bpm}$.

Bundle of His and Purkinje Fibers

Ventricular conduction pathways within the interventricular septum and ventricular walls that conduct action potentials rapidly ($30\,\text{ms}$) and function as the heart's final backup pacemaker with an inherent firing rate of $20\text{--}40\,\text{bpm}$.

Slow Cardiac Action Potential

The spontaneous electrical action potential found in nodal tissue (SA and AV nodes) characterized by Phase 4 diastolic depolarization via leaky funny currents ($\text{Na}^+$ influx), Phase 0 upstroke driven by $\text{Ca}^{2+}$ influx, and Phase 3 repolarization governed by $\text{K}^+$ efflux.

Fast Cardiac Action Potential

The five-phase action potential occurring in atrial myocytes, ventricular myocytes, and Purkinje fibers, featuring Phase 0 rapid depolarization ($\text{Na}^+$ influx), Phase 1 slight repolarization, Phase 2 plateau ($\text{Ca}^{2+}$ influx), Phase 3 rapid repolarization ($\text{K}^+$ efflux), and Phase 4 resting membrane potential.

12-Lead Electrocardiogram (ECG)

A noninvasive recording of the summated electrical activity of the heart collected via 10 surface electrodes: 4 placed on the limbs to derive leads I, II, III, aVR, aVL, and aVF (measuring the frontal plane), and 6 placed across the chest to form precordial leads $\text{V}_1\text{--}\text{V}_6$ (measuring the transverse plane).

P Wave

The initial deflection on an electrocardiogram tracing representing atrial depolarization, normally having a duration of $0.08\text{--}0.10\,\text{s}$ ($\sim 2\text{--}2.5$ small boxes).

PR Interval

The electrocardiographic interval measured from the onset of the P wave to the beginning of the QRS complex, lasting normally between $0.12\,\text{s}$ and $0.20\,\text{s}$ ($3\text{--}5$ small boxes) and reflecting the conduction time from the SA node through the AV node.

QRS Complex

The major waveform representing ventricular depolarization on an ECG, having a normal duration of $0.06\text{--}0.12\,\text{s}$ ($1.5\text{--}3$ small boxes).

ST Segment

The electrocardiographic segment connecting the J point (end of the QRS complex) to the beginning of the T wave, which is normally isoelectric at the level of the T-P segment and serves as a primary marker for myocardial ischemia or acute infarction.

T Wave

The ECG deflection produced by ventricular repolarization, which displays a net positive deflection because repolarization occurs in the opposite anatomical direction of depolarization, generating a double-negative effect.

1500 Method

An ECG calculation method to determine heart rate during regular rhythms by dividing 1500 by the number of small blocks between two consecutive R waves ($\text{HR} = 1500 / \text{small boxes}$).

Sinus Arrhythmia

A rhythm originating from the SA node that meets all normal morphological criteria except that the R-R interval varies irregularly by $\ge 3$ large boxes ($\ge 0.60\,\text{s}$) between beats.

Atrial Fibrillation

The most common clinical cardiac arrhythmia, characterized by quivering atrial myocardium without coordinated pumping due to multiple simultaneous ectopic foci, resulting in an absent P wave, a chaotic baseline, and an increased risk of thromboembolic stroke.

First-Degree AV Block

A benign cardiac conduction delay characterized by a uniform, prolonged PR interval exceeding $0.20\,\text{s}$ ($>5$ small boxes) where every atrial impulse (P wave) successfully conducts to the ventricles (QRS complex).

Second-Degree AV Block Mobitz Type I (Wenckebach)

An AV nodal conduction impairment characterized by progressive lengthening of the PR interval on successive beats until a QRS complex is completely dropped.

Second-Degree AV Block Mobitz Type II

An infranodal conduction block where the PR interval remains strictly constant across all conducted beats, but occasional P waves fail to conduct to the ventricles, resulting in intermittently dropped QRS complexes.

Third-Degree AV Block

Complete heart block where no electrical action potentials conduct from the atria to the ventricles, causing the atria and ventricles to beat completely independent of each other via separate pacing sites.

Right Bundle Branch Block (RBBB)

An intraventricular conduction delay in the right bundle branch resulting in a prolonged QRS complex ($>0.12\,\text{s}$ or $>3$ small boxes) with a characteristic 'rabbit ears' or M-shaped configuration in leads $\text{V}_1$ and $\text{V}_2$.

Premature Ventricular Complex (PVC)

The most common ventricular dysrhythmia, characterized by an ectopic ventricular focus firing prematurely to produce a wide, bizarre QRS complex without a preceding P wave, interrupting the underlying rhythm.

Ventricular Bigeminy

A dysrhythmia pattern where every normal sinus beat is immediately followed by a premature ventricular complex (PVC), which can reduce cardiac output and lead to weakness, dizziness, or syncope.

Ventricular Tachycardia (VT)

A rapid, dangerous ventricular rhythm characterized by $100\text{--}250\,\text{bpm}$, wide and bizarre QRS complexes, absent PR intervals, and T waves deflected opposite to the R wave, which can deteriorate into ventricular fibrillation.

Ventricular Fibrillation (VF)

A fatal cardiac dysrhythmia characterized by chaotic, uncoordinated quivering of the ventricular muscle driven by multiple ectopic foci firing out of sync, yielding zero cardiac output and death without immediate defibrillation.

Commotio Cordis

Sudden cardiac arrest triggered by a blunt, non-penetrating mechanical impact to the precordium during the electrically vulnerable repolarization window corresponding to the upslope of the T wave.

Cardiac Output ($Q$)

The total volume of blood pumped out of each ventricle per minute, mathematically defined as the product of heart rate and stroke volume ($Q = \text{HR} \times \text{SV}$).

Stroke Volume (SV)

The volume of blood ejected by a ventricle during a single mechanical contraction, averaging approximately $70\,\text{ml/beat}$ at rest and calculated as end-diastolic volume minus end-systolic volume ($\text{SV} = \text{EDV} - \text{ESV}$).

Ejection Fraction (EF)

The percentage of end-diastolic volume pumped out of the ventricle with each beat ($\text{EF} = (\text{SV} / \text{EDV}) \times 100\%$), providing a clinical index of pump function that averages $55\%\text{--}60\%$ at rest.

Preload

The degree of ventricular stretch at the conclusion of diastole, directly determined by end-diastolic volume (EDV) and venous return.

Afterload

The arterial pressure and vascular resistance that the ventricles must produce sufficient force to overcome in order to open the semilunar valves and eject stroke volume.

Mean Arterial Pressure (MAP)

The average arterial driving pressure across the systemic circulation, calculated as cardiac output multiplied by total peripheral resistance ($\text{MAP} = \text{CO} \times \text{TPR}$).

Exercise Blood Pressure Response

The physiological hemodynamic adjustment to exercise where systolic blood pressure increases linearly by approximately $10\,\text{mm\,Hg}$ per MET of increased workload while diastolic blood pressure remains constant or slightly decreases ($\le 10\,\text{mm\,Hg}$ increase).

Atherosclerosis

A chronic inflammatory vascular condition characterized by the formation of fibrofatty plaques in arterial walls in response to hypertension, smoking, high LDL cholesterol, hyperglycemia, and endothelial injury.

Right Coronary Artery (RCA)

The coronary vessel delivering arterial blood to the right atrium, right ventricle, posterior interventricular septum, inferior wall of the left ventricle, the AV node, bundle branches, and the SA node in approximately $60\%$ of individuals.

Left Anterior Descending (LAD) Artery

A principal branch of the left coronary artery supplying oxygenated blood to the anterior and apical myocardium of the left ventricle and the anterior two-thirds of the interventricular septum.

Peripheral Artery Disease (PAD)

Atherosclerotic occlusion of lower-extremity peripheral arteries that restricts perfusion beyond the lesion, resulting in intermittent claudication, weak or absent distal pulses, impaired wound healing, and risk of gangrene.

Stable Angina

Exertional chest discomfort lasting $5\text{--}10\,\text{min}$ that maintains a constant frequency and severity pattern for $6\,\text{weeks}$ or more, brought on by increased physical work or stress and readily relieved by rest or sublingual nitrates.

Unstable Angina

Prolonged ($15\text{--}20+\,\text{min}$), unpredictable chest pain occurring at rest or escalating in frequency, intensity, or duration, caused by acute thrombus formation over an unstable plaque tear and indicating high risk of myocardial infarction.

Prinzmetal (Variant) Angina

An atypical form of angina occurring in approximately $4\%$ of angina patients, caused by transient vasospasm of coronary arteries typically occurring at rest between midnight and early morning.

Silent Ischemia

Myocardial perfusion insufficiency causing objective ECG changes without provoking subjective chest pain or symptoms, observed frequently in diabetic patients due to autonomic neuropathy.

ST-Elevation Myocardial Infarction (STEMI)

Acute transmural myocardial necrosis caused by abrupt, complete coronary occlusion, manifesting on an ECG as ST-segment elevation of $\ge 1\,\text{mm}$ in limb leads or $\ge 2\,\text{mm}$ in precordial chest leads.

Congestive Heart Failure (CHF)

The inability of the heart to pump sufficient volumes of blood to meet systemic metabolic demands, divided into systolic dysfunction (impaired contraction) and diastolic dysfunction (impaired filling), resulting in fatigue, dyspnea, and peripheral or pulmonary congestion.

Percutaneous Coronary Intervention (PCI)

A catheter-based revascularization procedure in which a flexible balloon-tipped catheter is introduced through the femoral or radial artery to mechanically compress atherosclerotic plaque and deploy an endovascular stent.

Leptin

A peptide satiety hormone encoded by the ob gene and secreted by adipocytes that crosses the blood-brain barrier to bind hypothalamic receptors, suppressing appetite when body fat reaches its homeostatic setpoint.

Ghrelin

A hunger-stimulating peptide hormone synthesized and stored primarily within the stomach mucosa and pancreas that surges prior to meals to trigger food-seeking behavior.

Adipocyte Hypertrophy vs. Hyperplasia

The two cellular mechanisms of adipose expansion: hypertrophy refers to the enlargement of existing fat cells due to lipid accumulation (typical of adult weight gain), whereas hyperplasia denotes an increase in the total number of adipocytes.

Waist Circumference Risk Criteria

Anthropometric clinical thresholds categorizing very high cardiometabolic risk as a waist circumference exceeding $120\,\text{cm}$ ($>47.0\,\text{in}$) in men and exceeding $110\,\text{cm}$ ($>43.5\,\text{in}$) in women.

Metabolic Syndrome

A clinical cluster of cardiometabolic risk factors diagnosed when an individual presents with at least 3 of 5 criteria: abdominal adiposity, elevated triglycerides ($\ge 150\,\text{mg}\cdot\text{dL}^{-1}$), reduced HDL cholesterol, elevated blood pressure ($\ge 130/85\,\text{mm\,Hg}$), and elevated fasting glucose ($\ge 100\,\text{mg}\cdot\text{dL}^{-1}$).

Ketogenic Diet

A nutritional regimen mandating severe carbohydrate restriction to $20\,\text{g/day}$ or less for the initial 2 weeks to induce hepatic ketosis, posing risks such as elevated uric acid, kidney stones, glycogen depletion, dehydration, and acidosis.

FITT Recommendations for Obesity

Clinical exercise guidelines specifying aerobic activity on $\ge 5\,\text{days}\cdot\text{wk}^{-1}$, moderate intensity ($40\%\text{--}59\%\,\text{VO}_2\text{R}$ or HRR) progressing to vigorous ($\ge 60\%$), and duration increasing from $30\,\text{min}\cdot\text{d}^{-1}$ ($150\,\text{min}\cdot\text{wk}^{-1}$) to $60\,\text{min}\cdot\text{d}^{-1}$ ($250\text{--}300\,\text{min}\cdot\text{wk}^{-1}$).