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Medical School > MF1 CARDIO > Flashcards

MF1 CARDIO Flashcards

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USMLE® Step 1 flashcards
1
Q

Tachycardia arrhythmogenesis

A
  1. Increased Automaticity: increased sympatheric nervous system tone
    >Hypovolemia
    >Hypoxia
    >Sympathomimetic drugs
    >Pain/anixety
    >Increased metabolic activity of cells
  2. Triggered activity
    >Irritable area starts firing leading to abnormal sequence of conduction
  3. Re-entrant circuit
    >Most common; self-sustaining closed-loop circuit
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2
Q

Arrhythmia Classifications

A

—Tachyarrhythmia—

  • Supraventricular
    >Sinus tachycardia (SA too fast)
    >Paroxysmal supraventricular tachycardia
    –>AVNRT (re-entrant circuit in AV)
    –>AVRT (re-entrant circuit through accessory pathway btw atria/vs)
    >Atrial tachyarythmia (irritable area in atria; AV before SA)
    –>Focal atrial tachycardia (one ectopic focus)
    –>Multifocal atrial tachycardia (multiple ectopic areas firing abnormally)
    –>Atrial Fibrillation (multiple ectopic areas firing fast)
    –>Atrial Flutter (abnormal re-entrant circuit at tricuspid valve)
  • Ventricular
    >Ventricular fibrillation (multiple ectopic foci in ventricle firing)
    >Ventricular tachycardia
    –>Monomorphic (one irritable area)
    –>Polymorphic (multiple irritable areas); torsades depointed

—Bradycardias—
- Sinus bradycardia (SA too slow)
- Sick sinus syndrome (too fast & too slow)
- Heart Block (conduction block in AV)
–>1st degree
–>2nd degree
——> Mobitz I
——> Mobits II
–>3rd degree

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3
Q

Atrial flutter

A
  • Supraventricular tachycardia caused by re-entry circuit in RA
  • Atrial rate is regular bu fast (150-400 bpm); only some reach ventricles and rest blocked by AV node
  • Fixed AV block: ventricular rate constant fraction of atrial (ex. 2:1)
  • Variable AV block: ventricular response irregular, may mimic fibrillation
  • Are in a ring of inlets of SVC, IVC and coronary sinus called CAVO TRICUSPID ISTHMUS propogates signal slowly, allowing closed-loop
  • UNLIKE ATRIAL FIBRILLATION: atria have regular rate, and are contracting

ECG:
- Inverted flutter waves in II, III, aVF (because counter clockwise circuit)
- Positive flutter waves VI (may resemble P waves)
- Sawtooth wave patterns

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4
Q

Carotid sinus massage

A
  • Located at bifurcation of common carotid (at level of thyroid cartilage)
  • Induce stimulation of parasympathetic nerves and inhibition of sympathetic nerves (bc sense arterial BP change through barorecs)
  • Slows impulse formation at SA, delays conduction across AV, decreases vascular tone
    -Transient slowing of ventricular rate may allow for better diagnosis of the type of tachycardia
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5
Q

Coronary circulation

A

Aortic sinus –>
1. Right coronary sinus –>
————————————-a. marginal artery –> small cardiac vein
————————————-b. posterior interventricular artery –> middle
2. Left coronary sinus –>
————————————-a. anterior interventricular artery –> great
————————————-b. circumflex –> posterior vein of LFV

–>Coronary sinus

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6
Q

Arteriosclerosis

A
  • Umbrella term for diseases where wall of artery becomes thicker, harder and less elastic

> Arteriolosclerosis: hardening of small vessels by HTN and diabetes
–>HTN → stiffen → lumen narrower → stiff → hypoxia → often arteriolonephrosclerosis (→ chronic renal failure)
–>Diabetes → damage endothelium

> Atherosclerosis: hardening from plaque
–> LDL, smoking, high BP damage → LDLs enter endothelial → monocytes follow → “foam cells” → releases cytokines → recruit more monocytes → fatty streak→ thrombogenic → platelets gather → release platelet-derived growth factor → smooth muscle infiltration → smooth muscle releases collagen, proteoglycans, elastin fibrous cells → fibrous cap → fatty streak + fibrous cap = plaque → deposit calcium creating crystals → stiffens walls of arteries → inflammation → C-reactive protein release

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7
Q

Dx of atherosclerosis

A

> Physical exam (weakened pulse over blockage,
Bruits (whooshing sound due to turbulent flow and vibration)
Angiogram (dye in vessel) shows narrowing

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8
Q

Types of Angina

A
  • Decreased blood flow to the heart
    1. Stable angina: subendocardium ischemia (70% block); on exertion
    >Release of adenosine, bradykinin → pain
    >ST depression on ECG
    >Can be due to atherosclerosis (less supply), thickened heart walls (more demand)
  1. Unstable angina: subendocardium ischemia; at rest
    >Can lead to MI
    >ST depression on ECG
  2. Vasospastic angina (prinzmetal): transmural ischemia; episodes do not correlate with exertion
    >Often involves vasoconstrictors like thromboxane A2
    >ST elevation on ECG
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9
Q

Emergencies with chest pain

A
  • Pulmonary embolism: pleuritic chest pain, tachycardia, increased HR, SOB, DVT, immobilization
  • Esophageal rupture: vomiting, chest/epigastric pain, anxiety, recent instrumentation
  • Tension pneumothorax: tracheal deviation, sudden SOB, pleuritic chest pain, recent instrumentation
  • Myocardial infarction: retrosternal chest pain worse on exertion, radiating to arm/jaw, diaphoresis (excess sweating), decreased BP, hypotension, relieved by nitroglycerin
  • Aortic dissection/rupture: tearing, upper back pain, increased blood pressure, change in blood pressure by 20mmHg
  • Cardiac tamponade: SOB, Beck’s triad (hypotension, JVD, muffled heart sounds)
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10
Q

Medication for atherosclerosis

A
  • Aspirin: anti-platelet to reduce clotting (COX-1 inhibitor)
  • Beta blockers: block effects of epinephrine; slow HR, vasodilate
    >Labetalol, metoprolol
  • Statins: cholesterol medication; HMG-CoA reductase inhibitor
    >Atorvastatin, rosuvastatin
  • Nitroglycerine: vasodilator
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11
Q

Funny channels

A
  • Funny current refers to a specific current in the heart
  • Has effects opposite to those of most other heart currents
  • Properties suitable for generating repetitive activity and for modulating spontaneous rate
  • Degree of activation of the funny current determines steepness of phase 4 depolarization (frequency)
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12
Q

Systole and diastole

A

Systole:
>End-diastolic: mitral valve closes, blood in left ventricle
>Aortic valve opens
>Ejection into aorta

Diastole:
>End-systolic: aortic valve closes, blood fills atrium
>Mitral valve opens: blood fills the ventricle

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13
Q

Systolic heart failure

A
  • Ventricles can’t pump hard enough (flabby)
  • Decreased contractility: MI, dilated cardiomyopathy
  • Increased preload: mitral/aortic regurgitation
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14
Q

Diastolic heart failure

A
  • Not enough blood fills the ventricles
  • Normal ejection fraction, low total volume
  • Heart is stiff, fibrotic, noncompliant
  • Reduced preload: MI, restrictive cardiomyopathy, constrictive pericarditis, tamponade, tachyarrhythmia,
  • Increased afterload: HTN, aortic stenosis, coarctation
  • Can progress to systolic
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15
Q

Left sided heart failure

A
  • Usually occurs with underlying CVD; increased CO needed to meet higher demand
    COMPENSATION: low CO = HoTN → activate sympathetic → increase HR and contractility (B1 rec on myocardium), universal vasoconstriction → JG renin release → AII → overwork of heart
  • Left sided HF usually systolic, often due to damage to the myocardium
    >Ischemic heart disease
    >Long-standing HTN (TPR increase, hypertrophy)
    >Dilated cardiomyopathy (dilated to fill more blood)
  • Left sided diastolic:
    >Long-standing HTN (hypertrophy, aortic stenosis)
    >Restrictive cardiomyopathy (stiff muscles)
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16
Q

Targets of angiotensin II

A
  • Stimulate pituitary release of ADH → fluid retension
  • Vasocontriction of arterioles → increased TPR
  • Stimulate adrenal aldosterone → Na and H20
17
Q

Right-sided heart failure

A
  • Blood backed up to body so congestion of veins in systemic circulation (JVP, hepatosplemomegaly, ascites, edema)
  • Increased afterload: pulmonic stenosis, pulmonary HTN (PE, COPD, bronchiectasis, cor pulmonale)
  • Increased preload: tricuspid/pulmonary regurgitation
  • Decreased contractility: inferior MI, myocarditis
  • Most often caused by left sided heart failure
18
Q

Framingham Diagnostic criteria

A
  • For heart failure; 2 major or 1 major and 2 minor
    MAJOR:
    > Acute pulmonary edema
    > Cardiomegaly
    > Hepatojugular reflex
    > Neck vein distention
    > PND/orthopnea
    > S3 heart sound
    MINOR:
    > Ankle edema
    > Dyspnea on exertino
    > Hepatomegaly
    > Nocturnal cough
    > Pleural effusion
    > Tachycardia
19
Q

Diagnostic tools for CHF

A
  • CXR
  • BNP (brain natriuretic peptide; protein by heart in stress)
  • Echocardiogram (ventricles dilated, stiff, etc)
  • Ventriculography (cardiac catheterization)
20
Q

CHF treatment

A
  • ACEi: ramipril
  • ARBs: AII rec blocker
  • Beta blocker: decrease HR, contractility, afterload (**never use in decompensated HF!!)
  • Diuretics: furosemide (lasix), HCTZ (thiazide)
  • Aldosterone antagonists (spirinolactone)
  • Digoxin: increase contractility
21
Q

The layers of the heart

A

EPICARDIUM: single sheet of squamous epithelial cells overlying delicate connective tissue; in older patients, often infiltrated with fat
MYOCARDIUM: thick contractile middle layer of uniquely constructed and arranged muscle cells (bulk of the heart)
ENDOCARDIUM: white sheet of squamous epithelium that rests on a thin connective tissue layer; lines the chambers, continuous with great vessels`

22
Q

Pericardium

A

FIBROUS PERICARDIUM: outer wall; tough, dense, connective tissue that protects, anchors, and prevents overfilling
SEROUS PERICARDIUM: is thin serous membrane
> Parietal layer: lines internal surface of the fibrous pericardium
> Visceral layer/epicardium: outermost layer of the heart
> Parietal space

23
Q

Dilated cardiomyopathy (path, causes, treatment)

A
  • Dysfunction of myocardium due to dilated heart chambers; ventricular dilation and thin walls (eccentric hypertrophy; added in series); S3
  • CAUSES: most common idiopathic, alcohol, Beriberi (thiamine deficiency), Coxackie B myocarditis, cocaine, Chagas, Doxorubicin toxicity, , 3rd trimester pregnancy
  • TREATMENT:
    > Decrease preload: diuretics, fluid restriciton
    > Decrease afterload: ACEi/ARBs, hydralazine (vasodilator)
    > Increase contractility: digoxin
    > Increase EF: pacemaker
    > Decrease remodelling: BB, ACEi, aldosteron antagonist
    > Anticoagulation: warfarin, DOACs
24
Q

Hypertrophic cardiomyopathy

A
  • Asymmetric hypertrophy of interventricular septum; S4 (atrial kicks)
  • CAUSES: genetic (mutation in HCM protein in sarcomeres; Freidreich ataxia), HTN
  • Small ventricular diameter and thick walls (concentric hypertrophy; parallel)
  • Decreased coronary perfusion (angina, SOBOE, vtach/vfib), decreased systemic perfusion (syncope)
  • Venturi effect can lead to mitral regurgitation
  • TREATMENT:
    >Increase preload: no diuretics
    >Increase afterload: avoid ACEi/ARBs
    >Decrease contractility: BBs, CCB; avoid digoxin
25
Q

Restrictive cardiomyopathy

A
  • Myocardial dysfunction due to fibrosis/infiltration of cardiac tissue
  • CAUSES: most common idiopathic, radiation, amyloidosis, sarcoidosis, hemochromatosis
  • S3 heart sounds because rapid ventricular filling; bilateral atrial enlargement so mitral and tricuspid regurg
  • TREATMENT:
    > Gently decrease preload: diuretics
    > Gently decrease afterload: ACEi, hydralazine
    > Anticoagulation: warfarin, DOACs
26
Q

Troponin

A
  • Substance released into bloodstream upon death of cardiomyocytes
  • Elevated early in disease process
27
Q

Medications for MI

A
  • Aspirin: anti-platelet
  • Ticagrelor: antiplatelet medicine
  • Enoxaparin: anticoagulant (Xa)
28
Q

post-MI complications

A
  • Decreased contractility → HoTN → less to coronary arteries → cardiogenic shock
  • Electrical instability → arrhythmias
  • Tissue necrosis → pericarditis, ventricular septal defect, ventricular rupture (→ tamponade), chordae tendinae (→ valve regurgitation)
29
Q

Pericarditis (acute v chronic)

A
  • Acute: less than 3months
    > CAUSES:
    –> Infectious: mostly viral, S. aureus, TB
    –> Autoimmune: Ab-mediated agitation (RA, SLE)
    –> Uremia: end stage renal disease, AKI
    –> Neoplasia: primary cancer can seed (most likely lung cancer > non-hodgkins > leukemia > renal cell carcinoma > breast
    –> Radiation: destruction of pericardial tissue
    –> Post-MI: ischemia → dead myocardium → immune cell cleanup → cytokines → inflammation → leaky vessels → fluid buildup
  • Chronic: more than 3 months
  • Can lead to pericardial effusion → squeeze heart → reduce ventricular filling → cardiac tamponade
30
Q

Electrical alternans

A
  • Electrical alternans: alternating QRS amplitudes in any or all leads on an electrocardiogram (ECG) with no additional evident changes in conduction pathways of the heart
  • This rhythm is typically associated with pericardial effusion from fluid surrounding the heart (fluid sloshing, messing up vectors)
31
Q

Pericardial effusion treatment

A
  • NSAIDS (7-10 days)
  • Colchicine: inhibit neutrophils (recurrence)
  • Steroids: reduce inflammatory process in TB patients and autoimmune
  • Pericardiocentesis
32
Q

MI Bloodwork

A
  • Troponins: certain subtypes only found in heart muscle cells; most specific marker for heart damage
  • Myoglobin: found elsewhere in body and heart cells
  • Creatine kinase mB: more specific, sometimes looked for
33
Q

Endocarditis (causes, Dx)

A
  • Most cases are due to microbial infection of endocardium, often around valves because tiny vessels supply them
    > Gram (+) bacteria (Viridans streptococcu, S. aurea [IV drugs], S. epidermidis [mech valves]
  • Mitral and aortic valve most often affected; prosthetic valves, congenital defects, damage to valves (rheumatic heart disease), IV drug use all risks
  • Non-bacterial thrombotic endocarditis → bacteremia → infective endocarditis → bacteria bind NBTE → vegetation → immune system involvement → proteases → valve destruction → regurgitation
  • Septic emboli and immune complexes (osler nodes, roth spots, glomerulus) deposit around body and cause problems/symptoms
  • Mitral valve regurgitation → increased preload → eccentric hypertrophy → left sided HF
34
Q

Aortic valve

A
  • Three leaflets, opens in systole
  • STENOSIS: doesn’t open all the way, hard to pump
    > Chronic rheumatic fever: repeated inflammation and repair → fibrosis → leaflets fuse (commissural fusion)
    >Bicuspid aortic valve: <70 y/o; congenital, 2 leafs
    >Calcified aortic valve: >70 y/o; calcium deposition (HTN, hyperlipidemia, smoking, DM)
    > High pressure on stiff valves → ejection click; turbulence (small opening) murmur (crescendo-decrescendo)
    > Left ventricle hypertrophies
    > Risk of heart failure because reduction in blood flow out of the heart to aorta (syncope and angina in exercise) → S4
  • REGURGITATION: leak back to atria
    > 50% cases due to aortic root dilation (root gets wider, leaflets pulled apart; mostly idiopathic, aneurysms and syphilis)
    >Valvular damage such as endocarditis or chronic rheumatic fever
    >Early decrescendo diastolic murmur because blood flowing back to the valve
    >Ventricular blood volume increases, increasing stroke volume → more pressure to pump out, but less blood in the atrium → bigger gap between systole and diastole → increased pulse pressure (difference) = hyperdynamic circulation where pulses are very violent, can cause head bobbing and capillary beds in fingers to pulsate (Quincke’s sign)
    >Increase in blood volume leads to left ventricle hypertrophies
35
Q

Mitral valve

A
  • Two leaflets (anterior and posterior); separate LA and LV
  • STENOSIS:
    > Rheumatic fever: commissural fusion makes opening smaller; higher pressure makes snap sound then diastolic rumble when blood forced to squeeze through (antibodies attacking mitral valve) → back up in left atrium → pulmonary congestion and edema → pulmonary hypertension → right ventricle hypertrophy and failure → RHF
  • REGURGITATION:
    > Primary: involving the leaflets, chordae tendineae, or papillary muscles
    > Secondary: stretch annulus; CHF, dilated cardiomyopathy
    >Leading cause is mitral valve prolapse → weakened connective tissue lead to prolapse
    –>Often associated with marfan syndrome and ehlers-danlos syndrome (connective tissue disorders); infective endocarditis; MI (death of chordae tendineae or papillary muscles)
    –>Usually asymptomatic, heart murmur with midsystolic click (leaflet folding into atrium and suddenly stopped by chordae tendinae), sometimes followed by systolic murmur (if regurgitation)
    >Left sided heart failure leading to ventricular dilation, bigger opening
    >Rheumatic fever → chronic rheumatic heart disease → leaflet fibrosis → holo-systolic murmur (lasts for duration of systole)
36
Q

Tricuspid valve

A
  • Three leaflets, separate RA and RV
  • STENOSIS:
    >Rheumatic fever: if tricuspid effected, mitral and aortic almost always also affected; commissural fusion → snapping sound when opening → RA dilation → blood back up in veins & irritation of pacemaker cells → arrhythmias
  • REGURGITATION:
    >Heard as holosystolic murmur (duration of systole), and sometimes also Carvallo’s Sign, where murmur gets louder on inspiration because more blood to the heart
    >Extra blood leaking increases right ventricular preload → eccentric right ventricular hypertrophy → stretches the annulus (ring of valve, more leakage!) → eventually RV can’t keep up → right HF → JVP, peripheral edema, hepatosplenomegaly
    –>Pulmonary hypertension, increasing RV pressure
    –>Rheumatic heart disease → fibrosis
    –>Damage to papillary muscles from heart attack
    –>Congenital defects
37
Q

Pulmonary valve

A
  • 3 leaflets

-STENOSIS:
> Carcinoid syndrome: diarrhea, rash, wheezing → neuroendocrine tumor cells in heart, secretes serotonin precursor, making valve very stenotic
> Tetralogy of fallot: congenital; VSD, right ventricular hypertrophy, high riding aorta

-REGURGITATION:
>After balloon in repaired tetralogy of fallot

38
Q

Acyanotic congenital heart defects

A
  • Left to right shunts (increase pulmonary blood flow)
  • ATRIAL SEPTAL DEFECT: LA → RA
  • VENTRICULAR SEPTAL DEFECT: LV → RV
  • PATENT DUCTUS ARTERIOSUS: aorta → pulm artery
  • ENDOCARDIAL CUSHION DEFECT: combo ASD and VSD; only 1 leaflet for mitral and tricuspid valves
  • CONSTRICTION OF AORTA: stenotic ring, restrict bloodflow to lower extremities
39
Q

Cyanotic congenital heart defects

A
  • TETRALOGY OF FALLOT: ventricular septal defect, right ventricular hypertrophy, pulm stenosis, overriding aorta
    > Prostaglandin E1: keep ductus arteriosus patent
  • TRANSPOSITION OF GREAT ARTERIES: failed spiraling so RV empties into aorta and LV into pulm arteries (DiGeorge Syndrome, maternal DM)
  • TRUNCUS ARTERIOSUS: VSD and single trunk from RV and LV, bifurcates; total mixing → LHF
  • TOTAL ANOMALOUS PULMONARY VENOUS RETURN: pulmonary veins don’t empty into LA, pulmonary veins empty into RA via connecting veins; no O2 blood to LA, resp distress, pulm edema
  • TRICUSPID ATRESIA: tricuspid valve fails to develop normally with a hypoplastic right heart and VSD

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