Ch. 10 & 11 Cardiomyopathies & Mechanisms of Cardiac Arrhythmias Flashcards

1
Q

What are cardiomyopathies?

A

Heart disorders that have abnormalities of the myocardium.

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2
Q
  1. What are three different types of cardiomyopathy?
A

Dilated cardiomyopathy, Hypertrophic Cardiomyopathy,

Restrictive Cardiomyopathy

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3
Q

Explain Dilated Cardiomyopathy etiology, pathology/pathophysiology, clinical findings & treatment/prognosis.

A

(1) Dilated Cardiomyopathy: an enlarged ventricle that has impaired contraction functions. It can happen from a variety of issues and includes acute viral myocarditis, alcoholic cardiomyopathy, idiopathy cardiomyopathy, and peripartum cardiomyopathy. Ultimately cardiac output decreases due to the decreases contractile function. This can lead to volume overload which can cause pulmonary and systemic congestion. A patient will typically present with cool extremities, low arterial pressure, and tachycardia. Relief of symptoms and preventing complications such as arrhythmias and thromboembolic events are the goal of treatment. Heart transplant can help, although this is not an easy-to-come-by solution. Some patients (~1/2) spontaneously improve.

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4
Q

Explain Hypertrophic Cardiomyopathy etiology, pathology/pathophysiology, clinical findings & treatment/prognosis.

A

. (2) Hypertrophic Cardiomyopathy: The ventricle wall is thickened, therefore there isn’t much room in the ventricular chamber and there are diastolic issues. This often is a genetically inherited disorder and can be seen in young athletes. It poses a high risk because it can cause sudden cardiac death. HCM has characteristics of short, wide, hypertrophied fibers in chaotic directions, often in the ventricular septum. Unfortunately, the first symptom can be v-fib and sudden death. Other symptoms can be dyspnea, angina, and syncope, but many patients can be asymptomatic. Upon physical examination, S4 can be heard, a quick decline in carotid pulse during diastole, and during Valsalva maneuver the murmur intensifies. Beta-blockers are commonly prescribed for HCM, and antiarrhythmics can be too. Myomectomy or percutaneous septal ablation are more invasive methods to try to treat HCM.

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5
Q

Explain Restrictive Cardiomyopathy etiology, pathology/pathophysiology, clinical findings & treatment/prognosis.

A

(3) Restrictive Cardiomyopathy: the myocardium is abnormally stiff and diastole is impaired. The most common cause is amyloidosis. There is high diastolic pressure due to reduced compliance of the ventricles. This causes elevated systemic and pulmonic pressure and decreases stroke volume & cardiac output. Right and left sided HF are consequences. During a physical examination pulmonary rales, distended neck veins, ascites, and peripheral edema can be seen. The prognosis is poor, but treatment can try to treat the underlying causes. Salt restriction, maintenance of sinus rhythm, and anticoagulant therapy may be used for treatment efforts.

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6
Q
  1. What is automaticity?
A

A cardiac cell’s unique ability to depolarize itself and generate a spontaneous action potential. It is important to note the cardiac cells are the only ones in the body with this capacity. Arrhythmias occur when normal cardiac cells convert and obtain automaticity. No point deduction.

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7
Q
  1. How is pacemaker current important in automaticity? What currents lead to gradual depolarization?
A

The pacemaker sets the current and pace to depolarize the rest of the cardiac cells. The ionic currents contribute to gradual depolarization. These currents are a slow inward calcium current, decline of an outward potassium current, and additional inward sodium current.

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8
Q
  1. Explain AP upstroke & its significance.
A

The Action Potential upstroke is caused by the slow inward current of calcium ions. Natural pacemaker cells have a lower membrane potential than other cells. The action potential relies on Ca++ current and a slower rise-rate. Because of this, they can fire first, setting the rate for the heart.

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9
Q
  1. What are the three variables that determine intrinsic rates of firing?
A

(1) The rate of spontaneous depolarization of phase 4. (2) The maximum negative diastolic potential. (3) Threshold potential.

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10
Q
  1. What role to gap junctions play in automaticity?
A

They allow the spread of action potential from cell to cell so that the neighboring cell can come to a threshold level and depolarize.

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11
Q
  1. How does decoupling affect automaticity?
A

Decoupling of normally suppressed cells may reduce the inhibitory electronic influence and enhance automaticity. This may produce ectopic rhythms.

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12
Q
  1. What three abnormalities of impulse often lead to arrhythmias?
A

(1) Altered automaticity. (2) Abnormal automaticity. (3) Triggered activity.

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13
Q
  1. What controls rate of impulse?
A

Neurohumoral factors such as sympathetic and parasympathetic nervous system.

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14
Q
  1. Explain & give examples of increased/decreased sinus node automaticity.
A

Increases sinus node automaticity is stimulated by the sympathetic nervous system through beta1-adrenergic receptors, causing the SA node to reach threshold and fire earlier than normal. This increased heart rate can happen if you are scared, causing the fight or flight response = increases heart rate to increase cardiac output to run fast or fight hard. Decreases sinus node automaticity is an increase in the parasympathetic nervous system, rest and digest, where cholinergic stimulation reduces the SA node firing. This can happen when you do something such as meditation for stress, the benefit is the slowing of the heart rate through the parasympathetic system.

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15
Q
  1. What are escape rhythms?
A

An escape beat is a protective mechanism of a cardiac cell other than the SA pacemaker firing in place of the SA. This can be the AV node taking over when the SA node is impaired for some reason

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16
Q
  1. What are causes of abnormal automaticity?
A

Abnormal automaticity can be caused by cardiac tissue injury.

17
Q
  1. What is triggered activity? Explain early & delayed afterdepolarizations.
A

Triggered activity are abnormal depolarizations that can cause an extra heart beat or rapid arrhythmias. An early afterdepolarization occurs during the repolarization phase and a delayed afterdepolarization occurs after repolarization is completed.

18
Q
  1. Explain conduction blocks.
A

This happens when the impulse reaches an area of the heart that is electrically unexcitable so the impulse stops there. AV block is common. add why they are unexcitable (prof rob): They are unexcitable due to inflammation, ischemia, scarring, and fibrosis.

19
Q
  1. What is reentry? What are conditions that propagate impulses in this way?
A

Reentry is a circuit where the impulse travels around a pathway causing tachyarrhythmias. Conduction block can cause reentry, unidirectional block and slowed conduction through the reentry path.

20
Q
  1. Define accessory pathway & how it contributes to WPW.
A

An accessory pathway, or bypass tract, can allow the impulse to conduct between the atria and ventricles while bypassing the AV node. WPW is an accessory pathway syndrome that can lead to deadly tachyarrhythmias. It utilizes a bypass tract called the bundle of Kent and the impulse traveling down this will shorten the PR time, which shows as a delta wave on an EKG.

21
Q
  1. What three factors influence treatment of rhythm disorders?
A

(1) Severity (2) mechanism (3) etiology of the rhythm.

22
Q
  1. Describe the benefits vs. risk of pharmacological treatment vs. electronic devices.
A

The benefit of pharmacological treatment is the ease of access and they are non-invasive. The risk is that antiarrhythmic drugs and produce proarrhythmias, they can have contraindications with some patients, and some are not good to use long term with persistent bradycardia. Electronic devices pro is that pacing of the immediate cardiac tissue can happen without the injection/consumption of pharmaceuticals. They can be permanent treatment and can record useful data. The con is that it is a surgical procedure, so it includes risks such a perforation, infection, stroke, pneumothorax, etc.

23
Q
  1. What specific treatments are used for bradyarrhythmias vs. tachyarrhythmias?
A

Bradyarrhythmia treatment options: Pharmaceuticals with anticholinergic drugs or beta1-receptor agonists to increase heart rate. Electronic pacemakers can be placed to pace the heart at a desired rate (faster than the bradycardia). Tachyarrhythmia treatment options: Pharmacological therapies: antiarrhythmic drugs to reduce increased automaticity, interrupt reentrant circuits, or eliminate triggered activity, but they can produce deadly proarrhythmias. Vagus maneuvers such as carotid massage can be performed, cardioversion or defibrillation can be used to bring someone out of a tachyarrhythmia. An ICD can be placed to pace if needed, but primarily watch the heart rhythm and defibrillate if a tachyarrhythmia happens.