Week 8 Flashcards

1
Q

What is the clinical definition of hypertension?

A
  • sustained daytime BP > 135 mmHg and/or > 85 mmHg diastolic
  • sometimes isolated as systolic or diastolic
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2
Q

Primary (essential) hypertension makes up how many cases of hypertension? What is the cause?

A

90%; idiopathic

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3
Q

If cause of hypertension is known, it is considered…

A

secondary hypertension

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4
Q

The risk of cardiovascular disease double with increments of ____ mmHg above _____ mmHg

A

20/10; 115/75

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5
Q

What are the risk factors for hypertension?

A
  • age
  • family history
  • obesity
  • diet e.g. high salt intake
  • low physical activity
  • excess alcohol, smoking, stress
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6
Q

What are the effects of uncontrolled hypertension?

A
  • endothelial cell injury (atherosclerosis)
  • cardiac consequences (CAD, left ventricular hypertrophy (due to higher afterload), heart failure)
  • organ damage (kidneys, brain, eyes)
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7
Q

What is the neural mechanism of blood pressure regulation?

A

baroreceptors in carotid arteries → info to medulla

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8
Q

What is the renal/hormonal mechanism of blood pressure regulation

A
  • ADH leadts to + H2O resporption → increased BV
  • glomaruler filtration rate
  • renin release
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9
Q

What is the vascular mechanism of blood pressure regulation

A

endothelial cells → increase in nitric oxide (→ vasodilation) or increase in endothelin I (→ vasoconstriction)

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10
Q

What is the pathophysiology of primary hypertension?

A
  • elevation in blood volume (due to defect in Na+; increased Na= due to excess Na+ intake and/or resorption) → increased MAP
  • increased peripheral vascular resistance
    → endothelial cell dysfunction → promoted vasocontriction
    → activation of RAAS
    → increased activation of SNS → increased cardiac output and heart rate
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11
Q

What is the treatment for hypertension?

A

pharmaceuticals: vasodilators, diuretics, cardioinhibitory drugs
diet: DASH diet, reduce Na+, reduce caffine intake (positve inotrope)
other lifestyle modifications: increased PA levels, smoking cessation, decrease alcohol intake, decrease stress

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12
Q

What is post exercise hypotension

A
  • lowering physiological response after exercise
  • observed following multiple types of exercise; likely due to vasodilation
  • if done daily, ideal dose as treatment for reducing BP
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13
Q

What is acute hypotension?

A
  • inadequate tissue perfusion → tissue ischemia/hypoxia, cellular damage (we maintain tissue perfusion by maintaining BP)
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14
Q

What are the general signs & symptoms of shock?

A
  • tachycardia
  • decreased urine output
  • dizziness, feeling faint, altered mental status
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15
Q

What are the 5 major classifications of shock?

A
  • hypovolemic
  • cardiogenic
  • anaphylactic
  • septic
  • neurogenic
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16
Q

What are the two types of “cold” shock?

A

hypovolemic & cardiogenic

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17
Q

What is ‘cold’ shock? What is the compensation?

A
  • decreased cardiac output
  • compensation: vasoconstriction → increased resistance → increased MAP (blood flow redirected to vital organs)
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18
Q

What is hypovolemic shock?

A
  • hemorrhagic & non-hemorrhagic (diarrhea, vomiting)
  • decreased blood volume → decreased venous return → decreased CO
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19
Q

What is cardiogenic shock?

A
  • problems with heart function (e.g. heart failure, arrhythmia, myocardial infarction, valve dysfunction) → decreased ability for heart to pump → CO
20
Q

What are the types of “warm” shock?

A

anaphylactic and septic

21
Q

What is ‘warm’ shock? What is the compensation?

A
  • decreased systemic vascular resistance due to peripheral vasodilation
  • compensation: increased HR
22
Q

What is anaphylactic shock?

A

the most extreme reaction to an allergen
- mast cells release histamine & bradykinin → vasodilation, edema, brochoconstriction
- treatment: IM epinephrine → increased CO, smooth muscle relax (airways), vasoconstriction

23
Q

What is septic shock?

A

e.g. due to an infection in bloodstream
- macrophage activation → cytokine release → vasodilation
- treatment: IV fluids & antibiotics

24
Q

What is neurogenic shock?

A
  • loss of sympathetic tone
    → autonomic balance tips towards PNS leading to vasodilation & bradycardia
25
What are the causes of neurogenic shock?
→ spinal cord injury → traumatic brain injury → vasovagal reflex (overreaction of vagus nerve → an abnormal response to pain, fear, emotion, sight of blood etc.)
26
What is orthostatic hypotension?
sudden, sustained drop in BP by standing up from a sitting or laying position → SBP decreases by at least 20 mmHg or DBP decreases by at least 10 mmHg for the first 3 mins in upright position
27
What are the causes of orthostatic hypotension?
→ impaired baroreceptor reflex function, hypovalemia, blood pooling in legs → most commonly due to medication (anti-hypertensives, diuretics, vasodilators) → increased risk in older adults
28
What are the signs and symptoms of orthostatic hypotension?
pallor, vertigo, blurred vision, feeling faint, dizziness, nausea
29
What is the treatment for orthostatic hypotension?
- water & salt intake, compression stalkings, sleeping in a slight incline - leg resistance exercise
30
What are cardiac arrhythmias? What are the consequences?
abnormalities in either rate (automaticity) or in path of electrical conduction - consequences: can lead to disorganized contractions → impaired cardiac output
31
What are the two heart arrythmia abnormalities in rate? They are due to an issue with...
- sinus bradycardia and sinus tachycardia - due to an issue with automaticity
32
What is sinus tachycardia?
HR is faster than normal (> 100 bpm)
33
What is sinus bradycardia?
HR is slower than normal (<60 bpm)
34
How is the automacity of the heart normally modulated?
SA node automatically sets pace of the heart (no NS input required) - SNS: epinepherine & norepinepherine released onto SA node cells & bind to beta-adrenergic receptors → increased phase 4 slope → increased SA node AP frequency - PNS: acetylcholine released onto SA node cells & bind to 'muscarinic' receptors → decreased phase 4 slope → decreased SA node AP frequency
35
Increase automaticity is due to...
increased sympathetic nervous system activity
36
What are the 5 reasons for increased automaticity?
1. hypovolemia → decreased MAP → + baroreceptors → + SNS 2. hypercapnia (high blood CO2) of hypoxia (low blood CO2) → + chemoreceptors → + SNS 3. Pain or anxiety → fight or flight → + SNS 4. increased metabolic activity of pacemaker cells → increased body temo, hyperthyroidism 5. Drugs that act like NE or Epinepherine → cocaine or meth
37
What are the 4 reasons for decreased automaticity?
1. increased parasympathetic NS activity → vasovagal reflex 2. decreased metabolic activity of pacemaker cells → decreased body temperature, hypokalemia 3. electrolyte imbalance → decreased excitability of SA node 4. heart damage or disease → leading to slowed electrical conduction
38
Arrhythmias due to altered electrical conduction can happen as a result of triggered activity. What does this mean?
irritable area somewhere in the atria or ventricles that trigger 'ecotopic' firing (spontaneous action potentials fired outside of normal stimulus from conduction system)
39
Arrhythmias due to altered electrical conduction can happen as a result of re-entry circuits. What does this mean?
abnormal conduction pathway is formed either due to an additional 'accessory' path or a block in normal path
40
What are the 3 common arrhythmias to know?
- premature ventricular contractions, paroxysmal supraventricular tachycardia, fibrillation
41
What causes premature ventricular contractions?
- triggered activity: an eletrical signal is initiated by the Purkinji fibers instead of the SA → ventricles contract 'prematurely' → a brief pause follows before normal rhythm returns
42
What causes paryoxysmal supraventricular tachycardia?
- next conduction pathway that begins somewhere in the atria (outside of normal conduction) → new signal travels down to the ventricles → ventricular tachycardia - begins and ends suddenly
43
What is fibrillation?
electrical activity independent of SA node → chaotic contractions
44
What is atrial fibrillation? What are the symptoms?
heart still functions as a pump symptoms: palpitations, chest discomfort, shortness of breath, dizziness
45
What is ventricular fibrillation?
heart does not function as an effective pump - collapse (electrical shock required to reset normal sinus rhythm)
46
What is the treatment for arrythmias?
- drugs that control HR & rhythm: beta blockers or Na+, K+, or Ca2+ channel blockers - ablation therapy: map out the electrical activity of heart → destroy specific region of heart tissue causing issue - pacemaker implantation: regulated rhythm through low energy electrical pulses → implantable cardio defibrillator: senses a stopped heart & delivers a strong electrical shock to restart the heart