Cardiovascular and Coagulation Systems Review

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Comprehensive vocabulary flashcards generated from cardiovascular and coagulation lecture notes, covering AV blocks, arrhythmias, heart failure, hypertension, shock, valvular diseases, and coagulation disorders.

Last updated 2:21 PM on 9/29/26
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46 Terms

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First Degree AV Block

A cardiac conduction abnormality where atrial impulses are conducted through the AV node to the ventricles at a rate slower than normal, characterized by normal P and QRS waves and a PR interval of >.20 seconds>.20\,\text{seconds}.

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Second Degree AV Block Type 1 (Wenckebach)

A conduction block where atrial impulses in a group of beats are conducted at a lengthened interval until one fails to conduct, characterized by a shortening PR interval with each beat, progressive P wave separation, and dropped QRS complexes.

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Second Degree AV Block Type 2 (Mobitz II)

A conduction block where some atrial impulses are unpredictably conducted through the AV node, with the block occurring below the AV node in the bundle of His, bundle branches, or Purkinje fibers, characterized by dropped QRS complexes and a PR interval that remains the same.

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Third Degree AV Block

A complete heart block characterized by more P waves than QRS complexes with no clear relationship between them.

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Right Bundle Branch Block (RBBB)

A conduction block in the right bundle branch carrying impulses from the Bundle of His to the right ventricle, causing impulses to travel through the left ventricle first, presenting in lead V1 with a normal P wave and a widened, notched QRS (RSR pattern resembling the letter M or bunny ears).

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Left Bundle Branch Block (LBBB)

A conduction delay between the left atrium and left ventricle characterized by normal or inverted P waves, and a widened QRS with a deep S wave and an interval of >0.12 seconds>0.12\,\text{seconds} in V1 resembling a "W".

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Endocarditis

Infection of the lining of the heart that covers the heart valves, resulting in deformed valves, diagnosed via blood cultures, Echo, and ECG, and treated with antimicrobials for 4–6 weeks4\text{--}6\,\text{weeks} or surgical valve placement.

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Myocarditis

Inflammation of the cardiac myocardium usually triggered by viral infection, bacteria, fungi, or parasites, causing heart dilation, thrombi development, infiltration of blood cells around coronary arteries, and an enlarged, weak heart.

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Pericarditis

Inflammation of the pericardial sac with or without increased pericardial fluid, characterized by elevated WBC, ESR, CRP, and cardiac enzymes, treated with NSAIDs, Colchicine 0.5 mg0.5\,\text{mg} BID for 6 months6\,\text{months}, or pericardiectomy in extreme cases.

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Gallop (S3)

A heart sound coming after S2 in children and young adults that can indicate heart failure and left ventricular failure.

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S4 Heart Sound

A heart sound occurring before S1 during atrial contraction that can indicate CAD, HTN, and aortic valve stenosis.

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Opening Snap

A high-pitched heart sound occurring after S2 that can indicate stenosis of the mitral valve from rheumatic heart disease.

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Friction Rub

A harsh, grating heart sound indicative of pericarditis.

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Mean Arterial Pressure (MAP)

A measurement evaluating organ perfusion throughout the cardiac cycle, where systole makes up 1/31/3 and diastole makes up 2/32/3 of the cycle; normal range is 70–100 mmHg70\text{--}100\,\text{mmHg}, with >60 mmHg>60\,\text{mmHg} needed for perfusion of vital organs.

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Preload

The amount of elasticity in the myocardium at the end of diastole when the ventricles are filled to maximum volume and muscle fiber stretch is greatest.

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Afterload

The amount of systemic vascular resistance to left ventricular ejection and pulmonary vascular resistance to right ventricular ejection.

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Troponin I

A cardiac protein (0.05 ng/ml0.05\,\text{ng/ml} threshold) released into the bloodstream upon tissue injury that appears 2–6 hours2\text{--}6\,\text{hours} after injury and peaks at 15–20 hours15\text{--}20\,\text{hours}.

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Troponin T

A cardiac protein (0.2 ng/ml0.2\,\text{ng/ml} threshold) that increases 2–6 hours2\text{--}6\,\text{hours} after myocardial infarction and stays elevated.

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AHA/ACC Hypertension Classification (2017)

Defines normal blood pressure as <120/<80 mmHg<120/<80\,\text{mmHg}, elevated as 120–129/<80 mmHg120\text{--}129/<80\,\text{mmHg}, Stage 1 HTN as 130–139/80–89 mmHg130\text{--}139/80\text{--}89\,\text{mmHg}, and Stage 2 HTN as >140/>90 mmHg>140/>90\,\text{mmHg}.

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Hypertensive Emergency

Acute hypertension, usually >220 mmHg>220\,\text{mmHg} systolic and 120 mmHg120\,\text{mmHg} diastolic, that must be treated immediately to lower blood pressure and prevent vital organ damage.

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Hypertensive Urgency

Acute hypertension that must be treated within a few hours, but where vital organs are not in immediate danger.

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STEMI

A severe type of myocardial infarction involving complete blockage of one or more coronary arteries with myocardial damage, resulting in ST elevation and often developing Q waves indicating irreversible damage.

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NSTEMI

A type of myocardial infarction presenting without ST elevation, treated with nitroglycerin, beta-blockers, aspirin, statins, ACE inhibitors, ARBs, and clopidogrel.

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Undersensing (Pacemaker)

A pacemaker problem where sensitivity is too low to detect spontaneous cardiac depolarization, causing unneeded electrical contractions.

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Oversensing (Pacemaker)

A pacemaker problem where sensitivity is too high and misinterprets artifact or non-depolarization events as contractions, failing to trigger pacing and decreasing cardiac output.

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Noncapture (Pacemaker)

A pacemaker problem where the pacemaker pulse generator fires but fails to trigger cardiac contractions.

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Cardioversion

A procedure sending timed electrical stimulation to the heart to convert a tachydysrhythmia to normal sinus rhythm, requiring anticoagulation therapy for 3 weeks3\,\text{weeks} before elective procedure and stopping digoxin for 48 hours48\,\text{hours}.

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Emergency Defibrillation

A non-synchronized electrical shock given to treat acute ventricular fibrillation, pulseless ventricular tachycardia, or polymorphic ventricular tachycardia, using monophasic (200–360 J200\text{--}360\,\text{J}) or biphasic (100–200 J100\text{--}200\,\text{J}) energy.

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Cardiogenic Shock

A state where the heart fails to pump enough blood to provide adequate circulation and oxygen, commonly caused by acute MI, presenting with hypotension, altered mental status, oliguria, tachypnea/tachycardia, cool extremities, JVD, and pulmonary edema.

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Obstructive Shock

Shock occurring when right ventricular diastolic filling (preload) is obstructed, caused by great vessel obstruction (PE), excessive afterload, direct compression (tamponade or tension pneumothorax), or aortic dissection.

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Mitral Stenosis

Narrowing of the mitral valve that obstructs blood flow from the left atrium to the left ventricle, enlarging the left atrium, increasing pulmonary capillary pressure, and causing exertional dyspnea, right-sided heart failure, loud S1/S2, and a mid-diastolic murmur.

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Mitral Valve Insufficiency (Regurgitation)

Incomplete closure of the mitral valve leading to backflow of blood into the left atrium from the left ventricle during systole, decreasing cardiac output.

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Aortic Stenosis

Stricture or narrowing of the aortic valve controlling blood flow from the left ventricle, leading to left ventricular wall thickening.

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Pulmonic Stenosis

Stricture of the pulmonary blood vessel controlling blood flow from the right ventricle to the lungs, resulting in right ventricular hypertrophy and decreased pulmonary blood flow.

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Acute Venous Thromboembolism

A condition including deep vein thrombosis and pulmonary emboli, driven by Virchow's triad (stasis, endothelial injury, hypercoagulability) and presenting with aching pain, positive Homan sign, unilateral erythema/edema, dilated vessels, and cyanosis.

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Primary Hemostasis

The initial hemostatic response occurring within seconds that results in platelet plug formation at the site of vascular injury.

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Secondary Hemostasis

The plasma coagulation process taking minutes that generates fibrin to strengthen the primary platelet plug.

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<p>Cell-based Model of Coagulation</p>

Cell-based Model of Coagulation

A model describing coagulation through initiation, amplification, and propagation phases on cell surfaces, where tissue factor release and activated platelets enhance tenase and prothrombinase activity.

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Coagulation of Liver Disease

Impaired synthesis of clotting factors (II, V, VII, IX, and fibrinogen) with increased factor VIII, characterized by prolonged PT that corrects on mixing study, prolonged thrombin time, and treated with liver transplant or cryoprecipitate.

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Disseminated Intravascular Coagulation (DIC)

A secondary disorder involving pathologic formation of microvascular thrombi and paradoxical bleeding due to factor depletion; lab findings include decreased fibrinogen, prolonged PT, elevated D-dimer, and thrombocytopenia (cardinal finding).

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Hemophilia A and B

X-linked recessive genetic deficiencies of Factor VIII (Hemophilia A, 80%80\% of cases) or Factor IX (Hemophilia B), presenting with joint bleeding, intracranial bleeding, hematuria, and prolonged aPTT that corrects on mixing study.

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Acquired Antibodies of Factor 8

An acquired autoimmune condition occurring in adults without hemophilia history, presenting with soft tissue bruising, hematomas, decreased Factor VIII activity, and prolonged aPTT that does NOT correct on mixing study.

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Antiphospholipid Syndrome

An acquired cause of thrombophilia caused by antibodies to phospholipid-binding proteins (Lupus anticoagulant, anticardiolipin, beta 2 macroglobulin), presenting with arterial/venous thrombi, recurrent fetal loss, thrombocytopenia, and elevated aPTT.

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Prothrombin Time (PT)

A test measuring the integrity of the extrinsic and common pathways (normal range 11–13.2 seconds11\text{--}13.2\,\text{seconds}), used to screen for bleeding disorders and monitor warfarin therapy via INR.

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Activated Partial Thromboplastin Time (aPTT)

A test evaluating the intrinsic and common coagulation pathways (normal range 30–40 seconds30\text{--}40\,\text{seconds}, critical $>70\,\text{seconds}$$), commonly used to monitor heparin therapy.

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Mixing Study

A follow-up test for abnormal PT/INR or aPTT where patient blood is mixed with normal blood; clotting indicates a factor deficiency (treat with vitamin K), while failure to clot indicates a factor inhibitor or lupus anticoagulant.