Cardiovascular Pathophysiology Practice Questions
72 multiple-choice questions on Cardiovascular pathophysiology for paramedic and EMT students, from Chapter 9 (Pathophysiology). Read each question, pick your answer, then tap Show answer to check it and read the explanation.
72 practice questions
Atherosclerosis is:
- A. Weakening and dilation of a vessel
- B. Spasm of a coronary artery
- C. Inflammation of the heart muscle
- D. Plaque buildup that narrows arteries
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Answer: D. Plaque buildup that narrows arteries
Plaque builds in arterial walls, narrowing the lumen and damaging the endothelium. Plaque rupture triggers the clot that causes most heart attacks.
Myocardial ischemia occurs when:
- A. Oxygen supply does not meet demand
- B. A heart valve becomes incompetent
- C. Coronary flow exceeds demand
- D. Heart rate slows during restful sleep
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Answer: A. Oxygen supply does not meet demand
Ischemia is reversible; infarction is not. A slower heart rate lowers oxygen demand.
An acute myocardial infarction most often results from:
- A. Severe anemia lowering oxygen content
- B. Plaque rupture with occlusive clot
- C. Coronary spasm without any plaque
- D. Sudden failure of the aortic valve
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Answer: B. Plaque rupture with occlusive clot
Rupture of an atherosclerotic plaque triggers clot formation that occludes the artery. This is why time to reperfusion matters so much.
Left-sided heart failure typically produces:
- A. Peripheral edema and JVD
- B. Pulmonary congestion with crackles
- C. Ascites and abdominal distention
- D. Liver enlargement and tenderness
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Answer: B. Pulmonary congestion with crackles
Blood backs up into the lungs, causing dyspnea and crackles.
Right-sided heart failure typically produces:
- A. Wheezing from bronchospasm
- B. Hemoptysis with pink frothy sputum
- C. Pulmonary edema with crackles
- D. JVD and peripheral edema
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Answer: D. JVD and peripheral edema
The most common cause of right heart failure is left heart failure. Liver congestion and ascites may also develop.
Chronic hypertension damages the body by:
- A. Thinning and weakening the ventricular wall
- B. Dilating small arteries throughout
- C. Lowering afterload over time
- D. Injuring vessels and causing hypertrophy
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Answer: D. Injuring vessels and causing hypertrophy
Hypertension injures vessel walls and forces the heart to pump against higher resistance, leading to hypertrophy and organ damage. Stroke, kidney failure, and heart failure follow. The ventricle thickens rather than thins, small arteries narrow and stiffen, and afterload stays high.
Preload is reduced by:
- A. Hemorrhage, dehydration, or venodilation
- B. Leg elevation increasing venous return
- C. Venoconstriction from catecholamines
- D. A rapid IV crystalloid bolus
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Answer: A. Hemorrhage, dehydration, or venodilation
Nitroglycerin reduces preload through venous dilation.
Increased afterload causes:
- A. Reflex bradycardia and low preload
- B. A fall in arterial blood pressure
- C. Easier ejection and higher output
- D. Harder ejection, lowering stroke volume
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Answer: D. Harder ejection, lowering stroke volume
The ventricle must work harder to eject blood against higher resistance, reducing stroke volume. Severe hypertension worsens heart failure this way.
An aortic aneurysm is:
- A. A congenital narrowing of the aorta
- B. Inflammation of the aortic lining
- C. A weakened, dilated aortic wall
- D. A clot lodged in the aorta
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Answer: C. A weakened, dilated aortic wall
An aneurysm is a weakened, dilated section of the aortic wall that may dissect or rupture, causing catastrophic bleeding.
Deep vein thrombosis is significant because the clot may:
- A. Block the carotid artery
- B. Travel to a coronary artery
- C. Lodge in the hepatic portal vein
- D. Embolize to the lungs
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Answer: D. Embolize to the lungs
A DVT may break loose and travel to the pulmonary circulation as a pulmonary embolism. Immobility, surgery, and clotting disorders raise the risk. Clots from the leg veins return through the vena cava to the right heart; they do not enter the portal vein, which drains the gut.
A pulmonary embolism causes hypoxia by:
- A. Triggering diffuse bronchospasm
- B. Lowering hemoglobin concentration
- C. Blocking airflow into the alveoli
- D. Leaving ventilated lung unperfused
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Answer: D. Leaving ventilated lung unperfused
PE obstructs pulmonary blood flow, creating ventilated but unperfused lung (dead space). It also strains the right ventricle.
Cardiac tamponade impairs the heart by:
- A. Compressing the heart so it can't fill
- B. Directly weakening contractility
- C. Blocking flow in coronary arteries
- D. Causing acute valve regurgitation
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Answer: A. Compressing the heart so it can't fill
Fluid in the pericardial sac compresses the heart so the ventricles cannot fill. Narrow pulse pressure and muffled heart sounds are classic signs.
Dysrhythmias impair perfusion when they:
- A. Arise from the atria rather than ventricles
- B. Produce occasional isolated PVCs
- C. Change rate within normal limits
- D. Are too fast to fill or too slow
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Answer: D. Are too fast to fill or too slow
Rhythms so fast that filling time is lost, or so slow that output falls, impair perfusion. Rate and rhythm both affect cardiac output. Atrial rhythms can impair perfusion when the rate is extreme, and occasional isolated PVCs rarely affect output.
Compensatory tachycardia in heart failure eventually becomes harmful because it:
- A. Lengthens diastolic filling time
- B. Shortens diastole and raises O2 demand
- C. Lowers systemic afterload
- D. Improves long-term contractility
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Answer: B. Shortens diastole and raises O2 demand
Tachycardia shortens diastolic filling and coronary perfusion time while raising myocardial oxygen demand. The compensation itself begins to cause harm.
Atherosclerosis begins with:
- A. Dilation of the vessel wall
- B. Endothelial injury and lipid entry
- C. Clot forming in the lumen
- D. Rupture of a mature plaque
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Answer: B. Endothelial injury and lipid entry
Hypertension, smoking, and lipids injure the endothelium.
A fatty streak is:
- A. A mature plaque with a fibrous cap
- B. The earliest atherosclerotic lesion
- C. A small saccular arterial aneurysm
- D. A platelet clot on the vessel wall
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Answer: B. The earliest atherosclerotic lesion
Present in young adults.
A fibrous plaque contains:
- A. Calcium deposits without lipid
- B. Lipid alone, without any cap
- C. Fibrous tissue with no lipid
- D. A lipid core under a fibrous cap
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Answer: D. A lipid core under a fibrous cap
Cap thickness determines stability.
A vulnerable plaque has:
- A. Fibrous tissue with no lipid
- B. Dense, heavy calcification
- C. A thick fibrous cap and small core
- D. A thin cap over a large lipid core
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Answer: D. A thin cap over a large lipid core
A thin cap over a large lipid core is prone to rupture. Size does not predict rupture.
Why is aspirin given early in suspected acute coronary syndrome?
- A. It dissolves the existing clot in the artery
- B. It dilates the coronary arteries to improve flow
- C. It lowers the heart rate and oxygen demand
- D. It inhibits platelet aggregation at the plaque
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Answer: D. It inhibits platelet aggregation at the plaque
ACS usually starts with plaque rupture, which exposes material that makes platelets aggregate and form a thrombus. Aspirin blocks platelet thromboxane and limits clot growth. It does not dissolve existing clot (fibrinolytics do), dilate the coronary arteries (nitrates do), or slow the heart.
Stable angina occurs when:
- A. A plaque suddenly ruptures
- B. The left ventricle begins to fail
- C. Fixed stenosis limits flow on exertion
- D. A coronary artery goes into spasm
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Answer: C. Fixed stenosis limits flow on exertion
A fixed stenosis limits flow during increased demand, so pain is predictable with exertion.
Unstable angina occurs when:
- A. Complete occlusion causes infarction
- B. Plaque disruption causes partial occlusion
- C. Demand rises on a fixed stenosis
- D. A coronary artery spasms at rest
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Answer: B. Plaque disruption causes partial occlusion
Rest pain or new pattern.
Prinzmetal angina results from:
- A. Left ventricular failure
- B. Plaque rupture with thrombus
- C. Fixed coronary stenosis
- D. Coronary artery spasm
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Answer: D. Coronary artery spasm
Often at rest, especially early morning.
NSTEMI differs from STEMI in that NSTEMI:
- A. Is always more severe than STEMI
- B. Usually involves partial occlusion
- C. Involves complete transmural occlusion
- D. Causes no myocardial cell death
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Answer: B. Usually involves partial occlusion
NSTEMI usually involves partial occlusion with subendocardial injury: troponin is elevated without ST elevation.
STEMI involves:
- A. Partial occlusion with no ST change
- B. Complete occlusion, transmural injury
- C. Coronary spasm only, no clot
- D. Ischemia without any infarction
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Answer: B. Complete occlusion, transmural injury
Time to reperfusion determines salvage.
Myocardial cells begin to die after approximately:
- A. About 5 minutes of occlusion
- B. About 2 hours of occlusion
- C. 20 to 40 minutes of occlusion
- D. About 24 hours of occlusion
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Answer: C. 20 to 40 minutes of occlusion
Cell death begins after roughly 20 to 40 minutes of complete occlusion. Time is muscle.
Infarct size depends on:
- A. Vessel, duration, and collateral flow
- B. Only the duration of occlusion
- C. Only which vessel is occluded
- D. Only the amount of collateral flow
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Answer: A. Vessel, duration, and collateral flow
Infarct size depends on the vessel occluded, duration, collateral circulation, and oxygen demand. Collaterals develop with chronic disease.
Inferior MI commonly involves the:
- A. Right coronary artery
- B. Left main coronary
- C. Circumflex artery
- D. Left anterior descending
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Answer: A. Right coronary artery
Leads II, III, aVF.
Anterior MI commonly involves the:
- A. Right coronary artery
- B. Circumflex artery
- C. Right marginal branch
- D. Left anterior descending
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Answer: D. Left anterior descending
Leads V1 through V4.
Lateral MI commonly involves the:
- A. Posterior descending artery
- B. Circumflex artery
- C. Right coronary artery
- D. Left anterior descending
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Answer: B. Circumflex artery
Leads I, aVL, V5, V6.
Right ventricular infarction complicates:
- A. Lateral MI
- B. Septal MI
- C. Inferior MI
- D. Anterior MI
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Answer: C. Inferior MI
Preload dependent; nitroglycerin can cause profound hypotension.
Complications of MI include:
- A. None if reperfusion occurs
- B. Heart failure only, weeks later
- C. Dysrhythmias, heart failure, and shock
- D. Dysrhythmias only, within the first hour
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Answer: C. Dysrhythmias, heart failure, and shock
Dysrhythmias, heart failure, cardiogenic shock, and rupture can follow; dysrhythmia is the early killer.
Papillary muscle rupture after MI causes:
- A. Acute pericarditis
- B. Pericardial tamponade
- C. Acute mitral regurgitation
- D. Sudden complete heart block
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Answer: C. Acute mitral regurgitation
Acute mitral regurgitation causes pulmonary edema and a new murmur.
Ventricular free wall rupture after MI causes:
- A. Tamponade and sudden death
- B. Isolated ventricular ectopy
- C. Embolic stroke from a mural clot
- D. Gradual heart failure
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Answer: A. Tamponade and sudden death
Free wall rupture causes cardiac tamponade and sudden death, typically days after the MI.
Dressler syndrome is:
- A. Heart failure months after MI
- B. Rupture within hours of MI
- C. Pericarditis weeks after MI
- D. VF in the first hour after MI
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Answer: C. Pericarditis weeks after MI
Dressler syndrome is an autoimmune pericarditis occurring weeks after MI.
Heart failure with reduced ejection fraction involves:
- A. A primary valve failure
- B. A stiff ventricle that fills poorly
- C. Weakened contraction
- D. Normal or strong contraction
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Answer: C. Weakened contraction
Systolic dysfunction.
Heart failure with preserved ejection fraction involves:
- A. Stiff ventricle that fills poorly
- B. Weakened contraction with dilation
- C. An ejection fraction below 40%
- D. Primary valve regurgitation
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Answer: A. Stiff ventricle that fills poorly
Diastolic dysfunction.
Compensatory mechanisms in heart failure include:
- A. Reduced circulating volume
- B. Slowing of the heart rate
- C. Systemic vasodilation and diuresis
- D. Sympathetic and RAAS activation
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Answer: D. Sympathetic and RAAS activation
Sympathetic activation, RAAS activation, and ventricular remodeling help initially but are harmful long term.
Ventricular remodeling refers to:
- A. Steady improvement after injury
- B. Normal growth during childhood
- C. Ventricular change in size and shape
- D. Repair that restores normal function
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Answer: C. Ventricular change in size and shape
Remodeling is change in ventricular size, shape, and function in response to injury, often dilation and thinning.
ACE inhibitors help heart failure by:
- A. Blocking RAAS to cut afterload
- B. Speeding the heart to boost output
- C. Increasing preload with fluid retention
- D. Raising afterload to boost pressure
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Answer: A. Blocking RAAS to cut afterload
Blocking RAAS reduces afterload and remodeling. Cornerstone therapy.
Beta blockers help heart failure by:
- A. Blunting chronic sympathetic drive
- B. Acutely increasing contractility
- C. Increasing the heart rate and output
- D. Increasing systemic afterload
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Answer: A. Blunting chronic sympathetic drive
Beta blockers reduce harmful sympathetic stimulation over time. Counterintuitive but proven.
Acute decompensated heart failure presents with:
- A. Bradycardia and warm, dry skin
- B. Pulmonary edema, often with hypertension
- C. Clear lungs with signs of dehydration
- D. Hypotension in nearly all presenting cases
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Answer: B. Pulmonary edema, often with hypertension
Severe dyspnea and pulmonary edema are typical, often with hypertension from a sympathetic surge.
Flash pulmonary edema results from:
- A. Sudden LV failure, as from ischemia
- B. An allergic airway reaction
- C. Slow fluid buildup over weeks
- D. Bacterial pneumonia filling alveoli
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Answer: A. Sudden LV failure, as from ischemia
Sudden left ventricular failure, often from ischemia or hypertensive crisis, causes rapid onset.
Cor pulmonale is:
- A. Pericarditis after viral illness
- B. Left heart failure from ischemia
- C. Right heart failure from lung disease
- D. Valve disease from rheumatic fever
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Answer: C. Right heart failure from lung disease
COPD and pulmonary hypertension.
Hypertension damages:
- A. The brain alone, through stroke
- B. Only the heart muscle itself
- C. The kidneys alone, sparing the heart
- D. Heart, brain, kidneys, eyes, vessels
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Answer: D. Heart, brain, kidneys, eyes, vessels
Target organ damage.
Hypertensive emergency involves:
- A. Severe HTN with acute organ damage
- B. Mild elevation from anxiety
- C. Long-standing chronic hypertension
- D. Any reading above 180/120
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Answer: A. Severe HTN with acute organ damage
Hypertensive emergency is severe hypertension with acute target organ damage: stroke, MI, aortic dissection, encephalopathy. A high reading alone is not an emergency.
Hypertensive encephalopathy results from:
- A. An ischemic stroke from a clot
- B. Failed autoregulation causing edema
- C. Cerebral hypoperfusion from low BP
- D. Rupture of a cerebral aneurysm
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Answer: B. Failed autoregulation causing edema
Failure of cerebral autoregulation causes cerebral edema: headache, confusion, seizures.
Aortic dissection involves:
- A. Rupture of an aneurysm into the abdomen
- B. A clot occluding the aortic lumen
- C. Spasm of the aortic smooth muscle
- D. An intimal tear splitting the wall
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Answer: D. An intimal tear splitting the wall
A tear in the intima allows blood to split the vessel wall layers; tearing pain radiates to the back.
Aortic dissection risk factors include:
- A. Asthma and chronic bronchitis
- B. Varicose veins and prior venous clots
- C. Hypertension, Marfan, cocaine use
- D. Chronic low blood pressure
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Answer: C. Hypertension, Marfan, cocaine use
Hypertension, Marfan syndrome, and cocaine use are risk factors. Look for a blood pressure differential between arms. Lung disease and venous disease do not weaken the aortic wall.
Abdominal aortic aneurysm rupture presents with:
- A. Back pain, pulsatile mass, and shock
- B. Flank pain with fever and painful urination
- C. Crushing chest pain and diaphoresis
- D. Isolated leg pain with cool foot
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Answer: A. Back pain, pulsatile mass, and shock
Abdominal or back pain, a pulsatile mass, and shock. Most patients die before reaching surgery. Flank pain with fever and painful urination suggests pyelonephritis.
Peripheral arterial disease causes:
- A. Varicose superficial veins
- B. Claudication and cool limbs
- C. Clots in the deep veins
- D. Pitting edema of both legs
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Answer: B. Claudication and cool limbs
Atherosclerosis in the legs causes claudication, cool limbs, and poor wound healing.
Acute arterial occlusion presents with:
- A. Pain, pallor, and pulselessness
- B. Edema and bronze discoloration
- C. Redness with a tender cord
- D. Warm, swollen, red limb
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Answer: A. Pain, pallor, and pulselessness
The six Ps: pain, pallor, pulselessness, paresthesia, paralysis, and poikilothermia. Limb-threatening emergency.
Deep vein thrombosis risk factors are summarized by:
- A. Cushing triad: HTN, bradycardia, irregular breathing
- B. Beck triad: JVD, muffled tones, hypotension
- C. Virchow triad: stasis, injury, hypercoagulability
- D. Trauma triad: hypothermia, acidosis, coagulopathy
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Answer: C. Virchow triad: stasis, injury, hypercoagulability
Virchow triad is stasis, endothelial injury, and hypercoagulability: immobility, surgery, cancer, pregnancy.
Pulmonary embolism pathophysiology involves:
- A. Bronchospasm from airway inflammation
- B. Vessel obstruction and right heart strain
- C. Bacterial infection of lung tissue
- D. Left heart failure with pulmonary edema
Show answer
Answer: B. Vessel obstruction and right heart strain
Obstruction of pulmonary vessels causes V/Q mismatch and right heart strain; massive PE causes obstructive shock.
A stab-wound patient has hypotension, distended neck veins, and muffled heart sounds. A fluid bolus helps only briefly. Why?
- A. The heart is pumping too forcefully against the sac
- B. Pericardial pressure keeps the ventricles from filling
- C. The lungs are filling with fluid from the stab wound
- D. The blood vessels are dilated from blood loss
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Answer: B. Pericardial pressure keeps the ventricles from filling
In tamponade, blood in the pericardium compresses the heart, so the ventricles cannot fill. Fluids raise venous pressure briefly but cannot overcome the compression, so pericardial decompression is needed. The heart is not hyperdynamic. Pulmonary edema and vasodilation are not the mechanism.
Pulsus paradoxus is:
- A. A rapid, irregularly irregular radial pulse
- B. A normal rise in pressure on inspiration
- C. Alternating strong and weak beats
- D. Exaggerated inspiratory drop in systolic BP
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Answer: D. Exaggerated inspiratory drop in systolic BP
Pulsus paradoxus is a drop of more than 10 mmHg in systolic pressure during inspiration, seen in tamponade and severe asthma.
Pericarditis pathophysiology involves:
- A. Infarction of the heart muscle
- B. Infection of the heart valves
- C. Fluid compressing the ventricles
- D. Inflamed pericardial sac
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Answer: D. Inflamed pericardial sac
Pericardial inflammation causes sharp pain and a friction rub; ECG shows diffuse ST elevation.
Myocarditis is often caused by:
- A. Viral infection
- B. Fungal infection
- C. Blunt chest trauma
- D. Bacterial infection
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Answer: A. Viral infection
Can cause sudden death in young patients. Coxsackievirus and other viruses are the classic causes.
Aortic stenosis causes:
- A. Right ventricular pressure overload
- B. Left ventricular volume overload
- C. Right ventricular volume overload
- D. Left ventricular pressure overload
Show answer
Answer: D. Left ventricular pressure overload
Classic symptoms are syncope, angina, and heart failure. The patient is preload-dependent, so nitroglycerin can cause collapse.
Mitral regurgitation causes:
- A. Pressure overload of the left atrium only
- B. Volume overload of the right atrium and ventricle
- C. Pressure overload of the left ventricle and aorta
- D. Volume overload of the left atrium and ventricle
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Answer: D. Volume overload of the left atrium and ventricle
Acute cases from papillary muscle rupture.
Mitral stenosis causes:
- A. Aortic root dilation and wide pulse pressure
- B. Left atrial enlargement and pulmonary congestion
- C. Left ventricular dilation and volume overload
- D. Left ventricular hypertrophy and aortic dilation
Show answer
Answer: B. Left atrial enlargement and pulmonary congestion
The enlarged left atrium predisposes to atrial fibrillation and pulmonary congestion. Rheumatic heart disease is the classic cause.
Rheumatic heart disease results from:
- A. Immune reaction to untreated strep infection
- B. Direct viral invasion of the heart valves
- C. Congenital malformation of the valve leaflets
- D. Bacterial vegetations growing on the valves
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Answer: A. Immune reaction to untreated strep infection
Rare now in developed countries. Antibodies against group A streptococcus cross-react with valve tissue.
Congenital heart defects may present in:
- A. Only during the first year of life
- B. Infancy or later, depending on severity
- C. Only during fetal life, before birth
- D. Only in adulthood, once symptoms accumulate
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Answer: B. Infancy or later, depending on severity
Some are found in adults.
Dysrhythmia pathophysiology involves:
- A. Valve stenosis, chamber dilation, or septal defect
- B. Abnormal automaticity, reentry, or conduction block
- C. Vasodilation, hypovolemia, or low afterload
- D. Coronary spasm, plaque rupture, or thrombosis
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Answer: B. Abnormal automaticity, reentry, or conduction block
Reentry is the most common tachycardia mechanism.
Atrial fibrillation increases stroke risk because:
- A. The fast rate raises pressure in cerebral vessels
- B. Ventricular failure throws clots into the lungs
- C. Low cardiac output starves the brain of flow
- D. Blood stagnates in the atria and forms clots
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Answer: D. Blood stagnates in the atria and forms clots
Anticoagulation reduces it. These clots can embolize to the brain.
Sick sinus syndrome involves:
- A. SA node dysfunction causing bradycardia and pauses
- B. Ventricular irritability causing frequent PVCs
- C. An accessory pathway causing reentrant tachycardia
- D. AV node block causing dropped QRS complexes
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Answer: A. SA node dysfunction causing bradycardia and pauses
Often requires a pacemaker. It can also cause alternating fast and slow rhythms (tachy-brady syndrome).
Third-degree heart block involves:
- A. No conduction between atria and ventricles
- B. Progressively longer PR until a beat drops
- C. A fixed, prolonged PR interval on every beat
- D. Intermittent dropped QRS with a constant PR
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Answer: A. No conduction between atria and ventricles
Ventricular escape rhythm. Complete AV dissociation leaves the ventricles driven by an escape rhythm.
Ventricular fibrillation results in:
- A. Reduced but adequate cardiac output
- B. No effective cardiac output
- C. Low output with a palpable pulse
- D. Output maintained by atrial kick
Show answer
Answer: B. No effective cardiac output
Immediate defibrillation.
Sudden cardiac death most commonly results from:
- A. Ventricular dysrhythmia, often from ischemia
- B. Pump failure from chronic heart failure
- C. Massive hemorrhagic stroke in the brainstem
- D. Pericardial tamponade from a ruptured wall
Show answer
Answer: A. Ventricular dysrhythmia, often from ischemia
The first symptom of coronary disease in many.
Cardiac arrest pathophysiology involves:
- A. Ischemia of the brain while other organs are spared
- B. Isolated ischemia limited to the myocardium
- C. Hypoxia limited to the lungs and pulmonary vessels
- D. Global ischemia of all organs, especially the brain
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Answer: D. Global ischemia of all organs, especially the brain
Neurologic outcome is the goal.
Post-cardiac arrest syndrome includes:
- A. Isolated brain injury with a normal heart and organs
- B. Isolated myocardial stunning that resolves in minutes
- C. Brain injury, myocardial dysfunction, and reperfusion injury
- D. Rapid full recovery of all organs once a pulse returns
Show answer
Answer: C. Brain injury, myocardial dysfunction, and reperfusion injury
Targeted temperature management addresses it. The reperfusion injury is a systemic ischemia-reperfusion response.
Syncope pathophysiology involves:
- A. Transient global cerebral hypoperfusion
- B. Abnormal electrical discharge in the cortex
- C. Focal cerebral ischemia from a blocked artery
- D. Low brain glucose from excess insulin
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Answer: A. Transient global cerebral hypoperfusion
Cardiac causes are the dangerous ones.
Cardiac syncope red flags include:
- A. Fainting triggered by pain or emotional upset
- B. Exertional onset, no prodrome, or abnormal ECG
- C. Fainting on standing after prolonged sitting
- D. Warm, nauseated prodrome before fainting
Show answer
Answer: B. Exertional onset, no prodrome, or abnormal ECG
These patients need admission. A family history of sudden death is another red flag.
More Pathophysiology practice questions
- Cellular injury and adaptation (64)
- Fluids, electrolytes, and acid-base balance (95)
- Genetics and risk factors (60)
- Perfusion and shock (68)
- Immunity and inflammation (71)
- Infectious disease processes (63)
- Cardiovascular pathophysiology
- Respiratory pathophysiology (62)
- Neurologic, endocrine, and other systems (79)
Want the whole chapter mixed together? The Chapter 9: Pathophysiology practice test gives you a 10 Question Blitz or a full 100-question exam simulation with a section-by-section score. This topic is part of the Cardiology and Resuscitation practice questions exam area. Browse every paramedic topic or try the NREMT paramedic practice test.
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