WEEK 8 - BLOOD CLOTS - EFFECT ON HEART AND CIRCULATION Flashcards

1
Q

Coronary arteries function

A

supply the myocardium with blood
- split into left and right coronary arteries

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2
Q

nodes contraction rate

A

SA node - 70-100bpm
AV node - 40 -60bpm

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3
Q

SNS influence on HR

A
  • begins in medulla, cardioacceleratory centre
  • travels down spine to T1 - T4, transfers across to paravertebral ganglia
  • sympathetic nerve innervates SA, AV nodes and myocardium
  • the innervation of nodal cells allows an influx of Ca and Na, releasing noradrenaline and innervating B1 receptors, creating contraction and allowing further influx of Ca and Na into the cell
  • STRENGTH OF INNERVATION EFFECTS FORCE OF CONTRACTION
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4
Q

PNS effect on HR

A
  • dorsal aspect of the medulla, cardioinhibitory centre
  • interacts with neurons of the vagus nerve (cranial nerve)
  • innervates SA and AV node
    • releases acetylcholine, forcing K+ out of nodal cells
    • creates a larger gap between voltage and threshold, slowing the rate of contraction.
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5
Q

RAAs system

A
  • angiotensinogen secreted by the liver
  • renin interacts with angiotensinogen, producing angiotensin I
  • angiotensin I travels through the blood, and interacts with angiotensin converting enzyme (ACE) in the lungs, producing angiotensin II
  • angiotensin II innervates aldosterone secretion in the adrenal cortex, along with the stimulation of the pituitary gland, increasing the release of ADH, these factors lead to sodium/water retention, increasing BP
  • angiotensin II also promotes systemic vasoconstriction along with adjusting the hypothalamus to increase thirst.
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6
Q

what is a myocardial infarction
How?

A
  • caused by a blockage in the coronary arteries, leading to the death of myocardiocytes leading to reduced heart function.
  • can be caused by the rupture of plaque following athlereosclerosis, allowing a thrombus to form and cause blockage
  • Due to poor blood flow, sympathetic reactions occur and spark an increase in adrenaline release throughout the body. This causes the heart to race, all whilst the thrombus continues to block the coronary artery.
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7
Q

types of MI

A

stemi - full thickness infarct (large artery blocked)
n-stemi - partial thickness infarct (smaller artery blocked)

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8
Q

symptoms of MI

A
  • pain in chest
  • referred pain in arms + upper abdomen
  • dyspnoea
  • tachycardia
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9
Q

antihypertensive medication

A

Diuretics
- increase the release of sodium and water from body, decreasing BV

Sympathetic inhibitors
- a and b blockers - decreases CO, SVR and venous return

renin-angiotensin blockers

vasodilators

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10
Q

Cardiac arrhythmia

A

An irregular heartbeat, either too fast, slow, or inconsistently. Occurs when the electrical signals that tell the heart to beat don’t work properly.

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11
Q

cardiacc arryhtm. types

A
  • sinus bradycardia (>60bpm)
  • sinus tachycardia (<100bpm)
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12
Q

Pulmonary embolism - mechanics

A
  • ventilation/perfusion mismatch
  • blood channeled to other parts of lungs
  • shunting
  • pulmonary ischemia
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13
Q

causes/risk factors of PE
signs and symptoms of PE

A
  • blood stasis
    • immobilisation; post surgery, varicose veins, atrial fibrilation
  • hypercoagulability
    • pregnancy
    • cancer
    • eostrogen
  • vascular injury
    • smoking
    • procedures
    • obesity
  • atherlosclerosis
    • plaque break off

symptoms
- dyspnea
- tachypnea
- chest pain
- haemoptysis (coughing blood)
- sudden cardiac death

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