HSCI 382 Exam 2 Study Guide Flashcards: Cardiovascular and Respiratory Topics (Vocabulary)

A comprehensive set of vocabulary-style flashcards covering hypertension, atherosclerosis, coronary artery disease, heart failure, cerebrovascular disease, stroke, and respiratory system physiology and control. Useful for quick recall of definitions, mechanisms, diagnostic considerations, and treatments relevant to the lecture notes.

Primary (essential) hypertension

Chronic elevation of blood pressure with no identifiable secondary disease causing it.

Secondary hypertension

High blood pressure due to an underlying disorder (renal disease, endocrine disorders, vascular lesions, medications).

Pulmonary hypertension

High blood pressure localized to the pulmonary circulation.

Nonmodifiable risk factors for primary hypertension

Family history/genetics; sex; advanced age; race; inherited insulin resistance with compensatory hyperinsulinemia.

Modifiable risk factors for primary hypertension

High salt intake; obesity; low dietary potassium; excess alcohol; obesity/acquired insulin resistance.

Mechanisms linking high salt to hypertension

Increased extracellular volume leading to higher stroke volume and cardiac output, elevating blood pressure.

Mechanisms linking obesity/insulin resistance to hypertension

Increased sympathetic tone and renal sodium retention; vascular remodeling increasing systemic vascular resistance.

Mechanisms linking low potassium to hypertension

Impaired renal sodium excretion and promotion of vasoconstriction.

Mechanisms linking excess alcohol to hypertension

Increased sympathetic activity and catecholamines.

Genetics/race/age effects on hypertension

Alterations in RAAS, endothelial function, arterial stiffness, and renal sodium handling.

Brain effects of primary hypertension

Increased risk of transient ischemic attack (TIA), stroke, and cognitive changes from cerebrovascular damage.

Vascular effects of hypertension

Endothelial injury leading to atherosclerosis and arterial stiffening.

Cardiac effects of hypertension

Left ventricular hypertrophy, ischemia, arrhythmias, heart failure.

Hypertensive eye changes

Hypertensive retinopathy with arteriolar narrowing, hemorrhages, exudates.

Kidney effects of hypertension

Nephrosclerosis with chronic kidney disease and proteinuria.

Secondary hypertension etiologies

Renal hypertension (renal/hepatic artery disease); adrenocortical disorders (↑aldosterone; Cushing’s); pheochromocytoma; coarctation of the aorta; oral contraceptive–associated hypertension.

Renal/renal artery hypertension mechanism

↓ renal perfusion → ↑ RAAS and sympathetic activity → sodium/water retention and vasoconstriction.

Adrenocortical disorders mechanism in HTN

↑ aldosterone/cortisol → sodium and water retention; ↑ systemic vascular resistance.

Pheochromocytoma mechanism in HTN

Tumor secretes catecholamines → marked vasoconstriction and tachycardia.

Coarctation of the aorta mechanism in HTN

↑ proximal arterial pressure with reduced distal flow → compensatory ↑ stroke volume and BP.

Oral contraceptives effect on HTN

Hormonal effects on RAAS/endothelium with increased thrombosis risk.

Clinical manifestations of hypertension

Often asymptomatic; when present: headaches, dizziness, vision changes, epistaxis, chest pain, dyspnea; target-organ signs.

Hypertension pharmacologic therapy classes

Diuretics; ACE inhibitors; ARBs; calcium channel blockers; β-blockers; α1-blockers; direct vasodilators.

Goal of hypertension treatment

Reduce blood pressure and limit target-organ damage.

Lifestyle changes for hypertension

Healthy diet (low sodium, heart-healthy), regular exercise, weight reduction, limit alcohol, smoking cessation, stress management.

Diuretic mechanism in HTN

↑ Na+ and water excretion → ↓ plasma volume and cardiac output; long-term ↓ SVR.

ACE inhibitor mechanism

↓ Ang II and ↑ bradykinin → vasodilation; ↓ aldosterone → natriuresis.

ARB mechanism

Block AT1 receptors → vasodilation and ↓ aldosterone without bradykinin effects.

Calcium channel blocker mechanism (vascular/non-DHP)

↓ Ca2+ entry in vascular smooth muscle; vasodilation; ↓ heart contractility/rate (non-DHPs).

β-blocker mechanism

↓ heart rate and contractility; ↓ renin release from juxtaglomerular cells.

α1-blocker mechanism

Inhibit peripheral vasoconstriction → ↓ systemic vascular resistance.

Direct vasodilator mechanism

Relax arteriolar smooth muscle → ↓ SVR.

Arteriosclerosis vs atherosclerosis

Arteriosclerosis: general arterial hardening; atherosclerosis: lipid-rich plaques narrowing arteries.

Nonmodifiable atherosclerosis risk factors

Advanced age; male sex; family history; genetics.

Modifiable atherosclerosis risk factors

High LDL; low HDL; hypertension; diabetes; smoking; obesity; elevated CRP.

Endothelial injury in atherosclerosis

Initiates inflammation, LDL infiltration, foam cell formation, and plaque development.

Plaque types in atherosclerosis

Stable plaque: thick fibrous cap, small lipid core; Vulnerable/unstable plaque: thin cap, large lipid core; Calcified/fibrotic plaque: rigid and calcified.

Foam cells and fatty streaks

Macrophages ingest oxidized LDL leading to lipid-rich lesions in early atherosclerosis.

Common sites of atherosclerosis

Abdominal aorta; coronary arteries; peripheral arteries (legs); cerebral arteries.

Ischemic effects of abdominal aorta atherosclerosis

Abdominal pain; aneurysm risk.

Tests to diagnose atherosclerosis

Risk assessment, lipid/glucose/CRP tests; ECG; chest X-ray; ABI; echocardiography; stress testing; CT; angiography.

Atherosclerosis treatment goals

Reduce thrombosis risk, prevent progression, relieve symptoms, improve perfusion.

Atherosclerosis lifestyle changes

Heart-healthy diet, exercise, weight management, smoking cessation, stress control.

Atherosclerosis lipid-lowering therapy

Statins reduce LDL and stabilize plaques.

Atherosclerosis antihypertensive therapy

ACE inhibitors/ARBs/CCBs/β-blockers reduce BP and shear stress.

Atherosclerosis antiplatelet/anticoagulant therapy

Aspirin, warfarin, heparin used as indicated to reduce thrombosis.

Percutaneous interventions for atherosclerosis

Angioplasty ± stent; atherectomy/thrombectomy; bypass grafting; endarterectomy; thrombolysis.

Ischemic heart disease (CAD) definition

Atherosclerosis of epicardial coronaries, microcirculatory abnormalities, or intracoronary thrombus causing insufficient blood supply.

CAD risk factors

Cigarette smoking; hypertension; high LDL; low HDL; diabetes; age; abdominal obesity; physical inactivity.

Pathophysiology of CAD

Atherosclerosis and thrombosis narrowing coronary arteries, causing supply-demand mismatch.

Noninvasive tests for CAD

ECG; exercise/pharmacologic stress testing; echocardiography; nuclear imaging; cardiac CT/MRI.

Invasive CAD tests

Cardiac catheterization with coronary arteriography; may proceed to PCI.

Chronic ischemic heart disease subtypes

Chronic stable angina; vasospastic (Prinzmetal) angina; silent ischemia; cardiac syndrome X; ischemic cardiomyopathy.

Chronic stable angina mechanism

Fixed atherosclerotic narrowing causing demand-induced ischemia.

Variant angina mechanism

Transient coronary vasospasm causing transient ischemia, often at rest.

Silent ischemia

Objective ischemia without angina, occurring in various CAD contexts.

Cardiac syndrome X

Microvascular dysfunction with anginal symptoms but normal epicardial coronaries.

Ischemic cardiomyopathy

Chronic ischemia leading to LV dysfunction and heart failure.

ACS subtypes

Unstable angina (UA); non-ST-elevation MI (NSTEMI); ST-elevation MI (STEMI).

ACS plaque disruption

Atherothrombotic plaque rupture/erosion with platelet aggregation and fibrin-rich thrombus.

ECG findings in UA/NSTEMI vs STEMI

UA/NSTEMI: ST depression and/or T wave inversion; STEMI: ST elevation with evolving Q waves.

Cardiac markers in ACS

UA: no elevation; NSTEMI/STEMI: troponin rises (~3 hours) and remains elevated for days; CK-MB rises earlier.

MONA in ACS

Morphine, Oxygen, Nitrates, Aspirin/anticoagulants as initial management.

PCI in ACS

Percutaneous coronary intervention with angioplasty ± stent; preferred for STEMI if feasible.

CABG in CAD

Coronary artery bypass grafting for multivessel or left main disease.

Heart failure definition

Clinical syndrome of low cardiac output unable to meet metabolic needs.

Four pathological changes causing heart failure

Volume overload; impaired ventricular filling; degeneration of ventricular muscle; decreased contractile function.

Heart failure etiologies/risk factors

Ischemic cardiomyopathy, chronic hypertension, valvular disease, dysrhythmias, infections, COPD, pulmonary hypertension, age, diabetes, obesity, lifestyle.

Heart failure classifications

Acute vs chronic; systolic vs diastolic; high vs low output; right vs left; forward vs backward.

Forward vs backward failure (left/right)

Forward: reduced systemic perfusion; backward: congestion in respective circuits (lungs for LV, systemic for RV).

Left-sided forward symptoms

Fatigue, weakness, cold/clammy skin, confusion; low LVEF on echo.

Left-sided backward symptoms

Pulmonary congestion: dyspnea, orthopnea, crackles, cyanosis; cardiomegaly on imaging.

Right-sided backward symptoms

JVD, hepatomegaly, ascites, peripheral edema; possible hyponatremia.

Heart failure compensation mechanisms

RAAS and SNS activation → vasoconstriction and Na+/water retention; ventricular remodeling with hypertrophy and fibrosis.

Consequences of chronic RAAS/SNS activation in HF

Increased afterload/preload, further contractile dysfunction, adverse remodeling, and progression.

HF diagnostics

Echocardiography (EF, structure); chest X-ray (congestion, cardiomegaly); BNP/ANP; hemodynamics (PCWP, CVP).

HF treatment principles

Lifestyle modifications; diuretics; RAAS blockade (ACEi/ARB); beta-blockers; nitrates; inotropes; consider CRT/heart transplant in advanced disease.

Cardiac resynchronization therapy (CRT)

Device therapy to improve ventricular synchrony and pump efficiency in select HF patients.

Heart transplant indication

End-stage heart failure refractory to medical/device therapy.

Cerebrovascular disease arteries

Internal carotid arteries (anterior circulation ~80%) and vertebral arteries (posterior ~20%), contributing to the Circle of Willis.

Cerebral autoregulation factors

Metabolic factors: CO2, pH, and oxygen levels adjust cerebral blood flow; increased CO2 or H+ dilates vessels; severe hypoxia dilates as well.

TIA definition

Transient, reversible neurological deficit without infarction; warns of impending stroke.

Stroke definitions

Ischemic stroke: sustained ischemia with infarction; hemorrhagic stroke: bleeding into brain tissue.

Ischemic stroke subtypes

Large-artery thrombosis; small penetrating (lacunar) disease; cardiogenic embolism; cryptogenic/other.

Ischemic stroke signs

Location-dependent deficits: aphasia, hemiparesis, hemianopia, neglect.

Hemorrhagic stroke subtypes

Intracerebral hemorrhage; subarachnoid hemorrhage (often aneurysmal) and AVM-related bleeds.

TIA clinical significance

Major warning sign for imminent stroke risk; indicates transient cerebral ischemia.

Ischemic stroke treatment

Rapid reperfusion: IV tPA within window if no bleed; mechanical thrombectomy; manage edema.

Hemorrhagic stroke treatment

Secure bleeding source (clip or coil), blood pressure control, manage complications (hydrocephalus, seizures, vasospasm).

Aphasia types in stroke

Broca (expressive) aphasia: nonfluent, good comprehension; Wernicke (receptive) aphasia: fluent but nonsensical speech, poor comprehension.

Cerebrovascular diagnostic imaging

CT/CTA; cerebral angiography for aneurysm/AVM; MRI as indicated.

Aneurysm treatment options

Surgical clipping or endovascular coiling to prevent rupture.

Respiratory system: four processes of respiration

Ventilation; external gas exchange; gas transport in blood; tissue gas exchange.

Pressure gradients in respiration

Air flows from high to low pressure; inspiration lowers intrapulmonary pressure; expiration raises it.

Pulmonary pressures involved in ventilation

Patm (atmospheric), Palv (intrapulmonary/alveolar), Pip (intrapleural); Pip is normally negative to Palv.

Inspiration mechanism

Thoracic expansion → Pip becomes more negative → Palv < Patm → air flows in.

Expiration mechanism

Thoracic recoil → Palv > Patm → air flows out.

Lung volumes: tidal volume

Air moved in a normal breath.

Lung volumes: inspiratory reserve volume

Extra air inhaled beyond tidal volume.

Lung volumes: expiratory reserve volume

Extra air exhaled beyond tidal volume.