Midterm #1 (1/27-2/1) Flashcards
CHF Compensatory mechanisms for decreased cardiac output
- Increased sympathetic discharge to increase force, rate, preload and afterload
- Increased RAAS activity: increase angiotensin II to increase preload, afterload and causes remodeling
- Increase plasma volume, HR, BP and cardiovascular remodeling
Frank-Starling curve in CHF
depressed down: heart cannot adequately remove blood from heart causing edema, and blood pools before it reaches the heart.
Spiraling of CHF
With time, lower cardiac output causes release of NE, AGII and ET which all act to increase afterload, through vasoconstriction. This causes decreased EF also lowering cardiac output. This process repeats over time to keep decreasing EF and CO.
CHF Symptoms
SOB, coughing/wheezing (pulmonary edema), edema, fatigue, lack of appetite, nausea, confusion, tachycardia/arrhythmia
CHF Patient Classification
Class I: no symptoms.
Class II: mild symptoms, comfortable at rest
Class III: marked limitation in activity
Class IV: severe activity limitations, problems lying down and sleeping
Acute Decompensated Heart Failure
Common causes are CHF, pneumonia, MI, arrhythmia, hypertension
Goals: increase cardiac output and increase oxygen delivery
Treatment: Nitroprusside, PDE-3 Inhibitors (Amridone), dobutamine,
Diuretic Resistance in CHF Patients
Causes: noncompliance, decreased GFR, NSAID use (decreases renin), renal disease, and decreased diuretic absorption (gut wall edema or decreased splanchnic blood flow)
Treatment options:
- Increase dosage
- Combine thiazide and loop diuretic. Benefits are synergistic diuresis, but risk is that it is unpredictable and may result in excessive diuresis
- Combine with a K+ sparing diuretic like spironolactone
Types of hypertension
Primary (Essential) Hypertension: 90-95% cause unknown. due to multiple genetic/environmental factors including nutrition, SNPs, age, obesity, renin levels, substance abuse
Secondary hypertension: 5% of all cases. Due to identifiable secondary conditions including renal disease (nephritis), anatomical CVS defects, CAD, adrenal disorders, tumors.
MAP =
CO X TPR
Goals in Hypertension
- Decrease cardiac output: beta-adrenergic receptor antagonists, cardiac Ca 2+ channel blockers, alpha-2 adrenergic receptor agonists
- Decrease plasma volume: thiazides, loop diuretics, ACE/ARB
- Decrease TPR: alpha-2 adrenergic receptor agonists, ACE/ARB, vasodilators, alpha-2 adrenergic receptor antagonists, endothelium receptor antagonists, vascular smooth muscle Ca 2+ channel blockers
Pregnancy Induced Hypertension
> 140/90 mm Hg, increased protein in urine, edema in hands/face
Occurs week 20 –> 6 weeks post-party’s
Leads to organ damage to mother and child
No known cause or cure
Treatment: Labetalol (mixed beta-blocker)
Pulmonary Hypertension
Increased blood pressure in pulmonary artery/vein, lung vascular urge
Symptoms: SOB, dizziness, fainting, cough, angina
Decrease exercise tolerance and heart failure
Risk factors: family history, stimulant/alcohol abuse, tobacco
Survival: 2-3 years post diagnosis
Treatment: Endothelin receptor antagonists
RAAS System Regulation of renin release
Macula densa is located at beginning of DCT. Release prostaglandin that act on juxtaglomerular cells which store renin.
Low blood pressure: lower GFR which increases PGE and stimulates renin release through EP2/EP4 receptors
High blood pressure: high GFR which increases Na in distal tubule causing an increase in ATP/adenosine stimulating A1 receptors to decrease renin release
Renin in hypertension
levels very in hypertensive patients
High renin levels: young, Caucasian males, increased SNS activity and stress. Treated with ACE
Low renin levels: older, African-American females, increased Na + retention. Treat with diuretics
Hypertensive Crisis
SBP > 180 or DBP > 110
Drug of choice: vasodilator, K+ channel openers (Hydralazine) which cause massive hyperpolarization and dilation.
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