Week 2 Flashcards

1
Q

Define sudden cardiac arrest

A

Sudden cardiac arrest is the abrupt loss of heart function, breathing and consciousness. The condition usually results from an electrical disturbance in your heart that disrupts its pumping action, stopping blood flow to your body

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2
Q

advanced cardiac life support protocol for cardiac arrest

A
  • Start CPR, give oxygen and attach AED
  • Assess rhythm
  • if shockable -> shock -> if they do not have a return of spontaneous circulation then start CPR and repeat process again but this time by giving Epi IO-> if they have a shoackble rhythm again and you shock and they do not have a ROSC then begin CPR again and give amiodarone and try to treat reversible causes
  • If unshockable rhythm then re-start CPR give EPI and then re-assess rhythm
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3
Q

normal cardiac cycle

A
  • Diastole represents the period of time when the ventricles are relaxed; blood is passively flowing from the left atrium (LA) and right atrium (RA) into the left ventricle (LV) and right ventricle (RV),
  • Systole represents the time during which the left and right ventricles contract and eject blood into the aorta and pulmonary artery,
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4
Q

mechanism of action of amiodarone and the rationale for its use in dysrhythmias

A
  • inhibits adrenergic stimulation; affects sodium, potassium, and calcium channels; markedly prolongs action potential and repolarization; decreases AV conduction and sinus node function
  • prevents the recurrence of life-threatening ventricular arrhythmias
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5
Q

risk factors for HCM

- specifically

A
  • genetic

- gene for cardiac myosin binding protein C (MYBPC3) or beta-myosin heavy chain (MYH7)

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6
Q

structural changes that occur with HCM

A
  • Hypertrophy
  • Interstitial fibrosis
  • Myocyte disarray that is disorganized
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7
Q

how diastolic dysfunction occurs with HCM

A
  • HCM causes the myocytes to not work so in order for them to still pump blood they end up hypertrophing, this causes a decrease in size of cavity so there is not as much fillinf during diastole
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8
Q

Explain how cardiac conduction would be altered in cardiac hypertrophy and indicate how it would be depicted on an ECG

A
  • A-fib in more severe cases
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9
Q

Describe how ICD is used as a secondary precaution for sudden cardiac arrest

A
  • help prevent sudden cardiac arrest by shocking heart when it analyzes a potentially dangerous cardiac impulse (V-tach)
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10
Q

Role of beta blocker in HCM

A

help with negative inotropy

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11
Q

signs and symptoms associated with dilated cardiomyopathies

A
  • Fatigue, dyspnea;
  • Lateral displaced point of maximum impulse (PMI) –> can indicate that the heart is enlarged;
  • chest pain on exertion
  • Holosystolic murmur (mitral valve regurgitation during systole)
  • S3 sound (blood rushing into and slamming into a dilated left ventricular wall during diastole)
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12
Q

effects of chronic alcohol use on the heart

A

Acetaldehyde is a metabolite of alcohol and is thought to produce toxic effects through myocardial depression through a process that most likely involves mitochondrial dysfunction, oxidative damage, and impaired calcium ion homeostasis;

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13
Q

Describe how ventricular preload and contractility are altered in DCM and their effects on
cardiac output

A
  • diameter of the chamber increases -> increased preload-> overtime there is a decrease in contractility because the ventricle becomes too compliant
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14
Q

risk factors of DCM

- ID BIG MAPS

A
  • Idiopathic,
  • Drugs (Doxorubisin and cocaine),
  • Beriberi (wet: affects heart; decrease thiamine levels impair myocardium energy production),
  • Infection (Coxsackie virus),
  • Genetic (Duchenne muscular dystrophy, hemochromatosis),
  • Myocarditis,
  • Alcoholism,
  • Peripartum cardiomyopathy
  • Sarcoidosis
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15
Q

Describe how heart conduction is altered in DCM

A
  • involves dilation of all 4 chambers of the heart; Dilation of the atria can lead to altered heart conduction such that multiple ectopic foci are sending AP to the AV node resulting in A-fib
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16
Q

Explain why BNP is a marker for heart failure

A
  • Ventricular cells are recruited to secrete both ANP and BNP in response to the high ventricular filling pressures
17
Q

Relate left-sided heart failure to elevated JVP and weakened pulses in lower extremities

A
  • Left sided HF –> LV is usually hypertrophied (often dilated) –> build up of fluid in the LA (dilated LA) –> blood backs up into the pulmonary circuit (pulmonary hypertension) –> blood can further back up into the RV and RA –> causes right sided HF –> causes back up of blood into the venous system –> (no valves in SVC?) increase blood flow through Jugular vein;
  • Left sided HF –> failure to pump out enough oxygenated blood to systemic circulation –> decreased/weakened pulses in lower extremities;
18
Q

inotropic qualities of digoxin for the treatment of heart failure with reduced ejection fraction

A
  • Blocks Na/K pump → ↑ intracellular Na → ↓ Ca exiting the cell via Na/Ca exchanger ∴ more Ca is pumped into SR -> When subsequent APs excite the cell ↑Ca than normal is released to myofilaments → ↑ force of contraction
19
Q

role of diuretics (furosemide, spironolactone) in CHF

A

relieve signs & symptoms of volume overload

20
Q

role of ACE-inhibitors in CHF

A
  • Ace-inhibitors → ↑ bradykinin → ↓ remodeling?
21
Q

Describe how alcoholism can lead to thiamine deficiency and exacerbate DCM

A
  • Interferes w/conversion of thiamine → TPP (active form of thiamine)
  • Interferes w/transport & absorption of thiamine at intestinal level
  • Depletes amount of stored thiamine
  • Thiamine is needed in ETC and so w/o it the ETC does not work properly