Unit 3 : Cardiovascular 1 - Blood Pressure Flashcards

1
Q

What are the 3 elements determining Blood Pressure (BP)?

A
  1. Heart Rate (HR)
  2. Stroke Volume (SV)
  3. Total Peripheral Resistance
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2
Q

Describe the BP categories used to rate the severity of Hypertension (HTN) in an adult.

A

Normal: <120/<80
Pre-HTN: 120-139/80-89
St1 HTN: 140-159/90-99
St2 HTN: ≥160/≥100

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3
Q

When can hypotensive states occur?

A
  • When the heart muscle is damaged & unable to pump effectively
  • Severe blood loss → volume ↓ dramatically
  • Extreme stress when body’s levels of norepinephrine are depleted
    ↳ Body is unable to respond to stimuli to ↑ BP
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4
Q

4 Step care approach for HTN.

A

Step 1: Lifestyle modifications
Step 2: If not sufficient, drug therapy is added
Step 3: If not sufficient, drug dose or class may be changed or + another drug
Step 4: Includes all of the above + more antihypertensive agents until BP is controlled

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5
Q

Coronary Artery Disease (CAD) risks related to HTN.

A
  • Thickening of heart muscle
  • ↑ pressure generated by muscle on contraction
  • ↑ workload on the heart
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6
Q

What conditions can develop if HTN is left untreated?

A
  • CAD and Cardiac death
  • Stroke
  • Renal failure
  • Loss of vision
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7
Q

What are 5 types of drugs used to control BP?

Think:
A(x2),B,C,D

A
  1. Diuretic: ↓ serum sodium and blood volume
  2. Beta-Blocker: Leads to a ↓ in HR and strength of contraction, vasodilation
  3. ACE Inhibitor: Blocks conversion of angiotensin 1 to angiotensin 2 (powerful vasoconstrictor)
  4. Angiotensin 2 Receptor Blocker: Blocks effects of angiotensin on blood vessels
  5. Calcium Channel Blockers: Relaxes muscle contraction or other autonomic blockers → vasodilation
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8
Q

What are 5 Sympathetic Nervous System (SNS) blockers?

A
  1. Beta-Blockers
  2. Alpha-Blockers
  3. Alpha1-Blockers
  4. Alpha2-Blockers
  5. Alpha-Adrenergic Blockers
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9
Q

ACE INHIBITOR

What are the Actions?

A
  • Block ACE from converting angiotensin1 to angiotensin2 → a ↓ in BP, ↓ in aldosterone production & a small ↑ in serum K+ levels with sodium & fluid loss
  • ↓ cardiac workload
  • ↓ peripheral resistance & blood volume
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10
Q

ACE INHIBITOR

What are the Indications?

A

Treatment of HTN, CHF, diabetic nephropathy, L ventricular dysfunction after a Myocardial Infarction (MI)

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11
Q

ACE INHIBITOR

What are the Pharmacokinetics?

A
  • Well absorbed, widely distributed
  • Metabolized in the liver
  • Excreted in urine & feces
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12
Q

ACE INHIBITOR

What are the Contraindications?

A

Allergies, impaired renal function, pregnancy, and lactation

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13
Q

ACE INHIBITOR

What is a huge CAUTION when using this drug?

A

CHF - Change in hemodynamics can be very harmful

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14
Q

ACE INHIBITOR

What are some adverse effects?

A
  • Related to effects of vasodilation and alterations in blood flow – reflect tachycardia
  • GI irritation
  • Renal insufficiency
  • Cough
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15
Q

ACE INHIBITOR

What are the drug-to-drug interactions?

A

If taken with…

  • Allopurinol. This ↑ risk in hypersensitivity
  • NSAID’s. Will have a ↓ anti-hypertensive effect.
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16
Q

ACE INHIBITOR
Prototype?

“Ace” showers bring “-pril” flowers
Give ‘em an ace, they’ll cough in your face

A

-PRIL

CAPTOPRIL

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17
Q

ANGIOTENSIN 2
RECEPTOR BLOCKERS

What are the actions & indications?

A

They selectively bind with angiotensin 2 receptors in vascular smooth muscle & adrenal cortex to
↳Block vasoconstriction and aldosterone release.
↳Blocks BP ↑ effects of renin-angiotensin system
This lowers BP.
- Can be used alone or in combination
- Found to sllloooww progression of renal disease in persons with HTN and type 2 diabetes

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18
Q

ANGIOTENSIN 2
RECEPTOR BLOCKERS

What are the Contraindications?

A

Allergies, pregnancy, and lactation.

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19
Q

ANGIOTENSIN 2
RECEPTOR BLOCKERS

What are huge CAUTIONS when using this drug?

A

Be wary of hepatic or renal dysfunction, and hypovolemia (↓ blood volume)

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20
Q

ANGIOTENSIN 2
RECEPTOR BLOCKERS

What are some adverse effects?

A
  • Headache, dizziness, syncope, weakness
  • GI complaints
  • Skin rash or dry skin
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21
Q

ANGIOTENSIN 2
RECEPTOR BLOCKERS

What are the drug-to-drug interactions?

A

Phenobarbital

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22
Q

ANGIOTENSIN 2
RECEPTOR BLOCKERS

Prototype?

The SARTAN (sultan) ARBitrarialy (ARB- Angiiotensin II Receptor Blocker) beats his camel

A

-SARTAN

LOSARTAN

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23
Q

CALCIUM CHANNEL BLOCKERS

What are the Actions?

A
  • Inhibits movement of CA+ ions across the membranes of cardiac and arterial muscle cells
  • Depressing the impulse and leads to slowed conduction
  • ↓ myocardial contractility, ↑ dilation of arterioles
    ↳this ↓ BP & ↓ myocardial oxygen consumption
24
Q

CALCIUM CHANNEL BLOCKERS

What is the Indication?

A

Treatment of essential HTN

25
Q

CALCIUM CHANNEL BLOCKERS

What are the Pharmacokinetics?

A

Well absorbed, metabolized in liver, & excreted in the urine.

26
Q

CALCIUM CHANNEL BLOCKERS

What are the Contraindications?

A

Allergy, heart block / sick sinus syndrome, renal / hepatic dysfunction, pregnancy, and lactation

-If PT has damage to ECS, CA+ blockers can exacerbate the issue.
↳ Can use an ECG to find out if damage is present

27
Q

CALCIUM CHANNEL BLOCKERS

What are some adverse effects?

A
  • Related to effects on cardiac output
  • GI symptoms i.e. nausea
  • CV Symptoms: hypotension, bradycardia, peripheral edema
28
Q

CALCIUM CHANNEL BLOCKERS

What are the drug-to-drug interactions?

A

Cyclosporine (used to prevent tissue rejection) toxicity possible when taken with Diltiazem

29
Q

CALCIUM CHANNEL BLOCKERS

Prototype?

A

DILTIAZEM

30
Q

VASODILATORS

Are used to __ __.

A

↓ BP. (They are very potent & immediate)

31
Q

VASODILATORS

How is this done?

A

Vasodilators act directly on vascular smooth muscle, leading to vasodilation & ↓ BP

32
Q

VASODILATORS

What is the indication?

A

Severe HTN

33
Q

VASODILATORS

What are the pharmacokinetics?

A
  • Rapidly absorbed & widely distributed.

- Metabolized in the liver, excreted in the urine

34
Q

VASODILATORS

What are the contraindications?

A
  • Allergy, pregnancy, lactation, cerebral insufficiency
35
Q

VASODILATORS

What are huge CAUTIONS when using this drug?

A

Peripheral vascular disease, CAD, CHF, or tachycardia

36
Q

VASODILATORS

What are some adverse effects?

A
  • Related to changes in BP
  • GI upset
  • Cyanide toxicity
37
Q

VASODILATORS

What are some drug-to-drug interaction?

A

Based on the individual drug

38
Q

VASIDILATORS

Prototype?

A

NITROPRUSSIDE

39
Q

CARDIOTONIC AGENTS

What dangerous drug do we need to wash out for?

A

DIGOXIN - It ↑ the tone is heart muscle, assists in contraction

40
Q

Congestive Heart Failure (CHF)

A

Condition in which the heart fails to effectively pump blood throughout the body.
It is from a variety of heart problems and cannot be cured. We can only slow down the effects as much as possible.

41
Q

What are some underlying muscle function problems in HF

A
  • Muscle damage
    ↳ CAD (atherosclerosis) or cardiomyopathy
  • ↑ workload required to maintain efficient output
    ↳ may be caused from HTN or valvular disease
  • Structural Abnormality
    ↳ Congenital cardiac defects leading to ↑ pressure within the heart
42
Q

What are some causes of CHF?

A
  • CAD
  • Cardiomyopathy
  • HTN
  • Valvular Heart Disease
43
Q

What are some signs and symptoms of R-Sided HF?

A
  • ↑ jugular venous pressure
  • Enlargement of the spleen and liver (splenomegaly & hepatomegaly)
  • ↓ in renal perfusion when standing, ↑ in renal perfusion when flat (supine) → nocturia
  • Extremity edema
44
Q

What are some signs and symptoms of L-Sided HF?

A
  • Anxiety
  • Lungs: tachypnea, dyspnea, orthopnea
  • Heart: cardiomegaly, ↑ HR
  • GI: GI upset, nausea, abdominal pain
  • ↓ peripheral pulses, hypoxia
45
Q

Compensatory Mechanisms

*Unfortunately, the comp. mechanisms WORSEN HF

A
  • ↓ Cardiac output
    ↳ SNS stimulation (HR ↑)
    ↳ Release of renin (Blood volume ↑)
  • Cellular changes
46
Q

What are 3 treatments for CHF?

A
  1. Vasodilators (ACE Inhibitors & Nitrates)
    ↳ ↓ workload of overworked cardiac muscle
  2. Diuretics
    ↳ ↓ blood volume, which ↓ venous return & BP
  3. Beta-Andrenergic Agonists
    ↳ Stimulate the beta-receptors in SNS, ↑ CA+ flow into myocardial cells, & causing ↑ contraction
47
Q

CARDIAC GLOYCOSIDES

What are the Actions?

A

↑ intracellular CA+ & allows more CA+ to enter the myocardial cell during depolarization.
↳ + inotropic effect, ↑ renal perfusion with a diuretic effect & ↓ in renin release & ssllloowwwed conduction through the AV node

48
Q

CARDIAC GLOYCOSIDES

What are the Effects?

  • Chronotrope: -, ↓ frequency of beats
  • Inotrope: +, ↑ contractility
A
  • ↑ force of myocardial contraction
  • ↑ cardiac output & renal perfusion
  • ↑ urine output & ↓ blood volume
  • Slloowwed HR
  • ↓ conduction velocity through the AV node
49
Q

CARDIAC GLOYCOSIDES

What are the Indications?

A
  • Treatment of HF
  • Atrial fibrillation
    ↳ An issue b/c cardiac output is affected. SV ↓ at least 25%
    ↳ PT @ risk of CVA. A thrombus tends to form in the blood which pools in atrium & can become mobile → embolus can travel to the brain
50
Q

Describe atrial fibrillation

A

Every heart cell have the ability to originate a beat but the SA node controls these to synchronize. A.Fib is when this fails and the cells in L. & R. atrium compete to initiate a beat.

51
Q

CARDIAC GLOYCOSIDES

What are the Contraindications?

A
  • Allergy
  • Ventricular tachycardia or fibrillation, heart block, or sick sinus syndrome
  • Idiopathic hypertrophic sub aortic stenosis (disease characterized by marked hypertrophy of the left ventricle)
  • Acute MI, renal insufficiency, & electrolyte abnormalities
52
Q

What is the normal serum level of K+?

A

3.5-5

53
Q

CARDIAC GLOYCOSIDES

What are huge CAUTIONS when using this drug?

A
  • Do not use if pregnant or breastfeeding

- Not advised for paediatric and geriatric PT

54
Q

CARDIAC GLOYCOSIDES

What are the pharmacokinetics?

A
  • Rapidly absorbed and widely distributed in body

- Primarily excreted unchanged in urine

55
Q

CARDIAC GLOYCOSIDES

What are the adverse effects?

A
  • Headaches, weakness, drowsiness, and vision changes (commonly “halos around lights”)
  • GI upset and anorexia
  • Arrhythmia development
56
Q

CARDIAC GLOYCOSIDES

What are some drug-to-drug interactions?

A
  • Verapamil, amiodarone, quinidine, quinine, erythromycin, tetracycline, or cyclosporine (↑ effects of and risk for toxicity)
  • K+ losing diuretics (risk of hypokalemia & arrhythmias)
  • Cholestyramine, charcoal, colestipol, bleomycin, cyclophosphamide, or methotrexate (↓ absorption of cardiac glycoside)
57
Q

CARDIAC GLOYCOSIDES

PROTOTYPE?

A

DIGOXIN