- most common - unknown cause -

- most effective (edema) -- fuorosimide (lasix) - photosensitivity fluid overload, HYPERNATREMIA

- mannitol -- decreased ICP and IOP - blurry vision, fluid imbalance

cardiac Flashcards by Norah St John

isolated systolic hypertension

most common in >65 years old
aorta becomes rigid

How well did you know this?

Not at all

Perfectly

manifestations of hypertension

H: CAD, acute coronary syndrome, HF
brain: stroke
kidneys: chronic kidney disease/failure
eyes: retinopathy/blindness

How well did you know this?

Not at all

Perfectly

preeclampsia

systolic: >/ 140; diastolic: >/ 90 (AND/OR)
- thrombocytopenia: platelets </ 100,000
- renal insufficiency: increased creatinine (1.1)
- decreased liver function: increased liver transaminases
- pulmonary edema
* visual/cerebral disturbances *

How well did you know this?

Not at all

Perfectly

thiazides

** most common for HTN
- promotes Na depletion, dec EC fluid, dec BP
** none with renal insufficiency

How well did you know this?

Not at all

Perfectly

beta blockers

ENDS IN OLOL
** metoprolol
- dec CO by dec SNS response to basal sympathetic tone = dec vascular resistance = dec BP
** Use with caution in DM

How well did you know this?

Not at all

Perfectly

centrally acting alpha

**methyldopa (GOOD FOR PREGNANCY)
— crosses placental barrier
- decreases perph vascular resistance + inc vasodilation = dec BP

NO CLONIDINE IN PREGNANCY

How well did you know this?

Not at all

Perfectly

alpha adrenergic blockers

ENDS IN ZOCIN

** good for pts w/ kidney issues**
- decreases LDL and VDLD; increases HDL

s/x: NASAL CONGESTION, NSAID related GI distress

– no NSAIDS (increases peripheral edema)

How well did you know this?

Not at all

Perfectly

alpha beta blockers

LABETOLOL
(lABetolol = Alpha Beta)
– vasodilation (A), decreased BP (B)

** DO NOT GIVE W ASTHMA**
s/x: paresthesia

How well did you know this?

Not at all

Perfectly

direct acting vasodilators

HYDRALAZINE (FAST)

relaxes muscles, opening blood flow
used w/ beta blockers and diuretics

— reflex tachycardia, palpitations, edema, paresthesia

How well did you know this?

Not at all

Perfectly

ACE inhibitors

ENDS IN PRIL
** lisinopril **
-blocks release of aldosterone, decreases BP
** s/x PRILL COUGH**
- doesn’t work well in AA or geriatrics w/out diuretics

How well did you know this?

Not at all

Perfectly

angiotensin II receptor blockers

ENDS IN SARTAN
** LOSARTAN**
acts on RAAS to vasodilate and reduce perph resistance

s/x hyperkalemia

How well did you know this?

Not at all

Perfectly

calcium channel blockers

cankles from calcium channel blockers

AMLODIPINE
- blocks Ca2 promoting vasodilation, dec perph resistance + dec BP
* highly protein bound, SHORT half life*
** ankle edema

How well did you know this?

Not at all

Perfectly

primary HTN

most common
## unknown cause

How well did you know this?

Not at all

Perfectly

secondary HTN

increase if peripheral vascular resistance/CO

causes: renal disease, drugs, hyperaldosteronism

How well did you know this?

Not at all

Perfectly

loop diuretics

most effective (edema)
– fuorosimide (lasix)
photosensitivity
fluid overload, HYPERNATREMIA

How well did you know this?

Not at all

Perfectly

osmotic diuretics

mannitol
– decreased ICP and IOP
blurry vision, fluid imbalance

How well did you know this?

Not at all

Perfectly

carbonic anhydrase inhibitors

acetazolamide
- decreased IOP in pts w/ glaucoma
– kidney stones and hemolytic anemia

How well did you know this?

Not at all

Perfectly

potassium-sparing diuretics

spironolactone
- hyperkalemia paresthesia
- edema due to CHF, cirrhosis of the liver

How well did you know this?

Not at all

Perfectly

systolic dysfunction

decreased myocardial contractility

How well did you know this?

Not at all

Perfectly

diastolic dysfunction

abnormality in ventricular relaxation and filling

How well did you know this?

Not at all

Perfectly

left-sided heart failure

MORE common than right-sided
- LUNGS

How well did you know this?

Not at all

Perfectly

right-sided heart failure

EDEMA

right ventricular dysfunction

can’t move deo blood into lungs

left ventricular dysfunction

cant move blood from lungs back to heart

frank starling mechanism

> heart stretch = > contraction

inotropic agents

- +: increased availability of Ca = noradrenaline, thyroid hormone - -: decreased availability of Ca = Ca blocker, electrolyte imbalance

afterload

increased resistance = less blood leaving = increased AL = decreased Stroke Volume +AL, - SV = -AL, +SV

chronotropic agents

SNS - increases HR PSNS - decreases HR (bc of vagus nerve)

Labs to check for HF

BNP (increased = HF)

cardiac glycosides (digoxin)

- + inotropic action + SV - - inotropic action - HR - used in C + D HF (second line)

Digoxin toxicity

- dig til you PUKE, dig til you're YELLOW -- treatment digoxin immune Fab IV

PDEs

milrinone - + stroke volume & cardiac output, promotes vasodilation s/x: dysrhythmias

stable angina

predictable stress; goes away with rest

unstable angina

frequent with progressive severity to activity - narrowing of coronary arteryvariant

variant angina

occurs at rest - vessel spasm

nitroglycerine

sublingual (1-3mins) - increased blood flow through coronary arteries

statins

break down cholesterol **** MYOPATHY AND RHABDO -- STOP IMMEDIATELY****

anticoagulants

inhibit clot formation

heparin

prevent clots in veins --- monitor PTT and aPTT - antidote: protamine sulfate \

LMWH (Lovenox)

enoxaparin -- take at home; no monitoring required - contraindicated in: stroke, ulcers

warfarin

monitor PT INR!!!!!!!!! NO NSAIDS prevents clots in veins

antiplatelet drugs

(aspirin) - prevent clots in arteries by decreasing platelet aggregation

thrombolytics

(-telpase) DISSOLVE CLOTS - used for strokes alteplase (Tpa)

arterial flutter

HR 240-450 bpm

AFib

irregular rate and rhythm

shock

cardiovascular system fails to perfuse

cardiogenic shock

decreased cardiac output w/ adequate blood volume

neurogenic shock

PSNS causes massive vasodilation

Sodium channel blockers

- Class IA: slow conduction, prolonged repolarization * Quinidine, procainamide, disopyramide - Class IB: slow conduction, shortened repolarization * Lidocaine, mexiletine HCL - Class IC: prolonged conduction, little/no effect on repolarization * Flecainide

CLASS III=drugs that prolong repolarization

* Emergency treatment of ventricular dysrhythmias when other drugs are ineffective * AMIODARONE=increases refractory period and prolongs action potential duration (cardiac cell activity)

CLASS II=BETA BLOCKERS

* Decrease conduction velocity, automaticity, recovery time * Used more frequently for dysrhythmias than sodium channel blockers * Need to be tapered off when discontinued

Class IA indications

atrial and ventricular dysrhythmias, paroxysmal atrial tachycardia (PAT), supraventricular dysrhythmias

Class IB indications

acute ventricular dysrhythmias

Class IC indication

life threatening ventricular dysrhythmias