300: HTN & HF

The "silent killer

-Hypertension
-Many pt. are asymptomatic

Main worry with HTN

-Not so much #'s, but their effect on target organs like brain, heart, kidneys, etc.

HTN Emergency

BP >220/40
-develops over hours to days
-EVIDENT acute target organ damage

HTN Urgency

-develops over days or weeks
-BP severely high, but no evidence of target organ damage yet.

Misc. causes of HTN crisis

-noncompliance
-crack cocaine use
-tumor of adrenal medulla, etc.

HTN is significant risk factor for:

1. CVA
2. MI (major)
3. Renal Failure

BP

force exerted by blood against walls of blood vessels

BP=

CO x SVR (systemic vascular resistance)

CO

amount of blood pumped out of heart each minute

SVR

arteries' resistance to blood flow
-Think of aferload

C
hr
onotropic

heart rate

Inotropic

contactility

Sympathetic N.S. effect on BP

-Increases HR & cardiac contractility
-net effect is increase in arterial pressure by increasing CO & SVR
-Epi & norepi

Arterial Baroreceptors

-Found in carotid, aorta, & walls of Left Ventricle
-monitors level of arterial pressure

Renal System's Effect on BP

-Control sodium excretion & ECV
-RAAS

Endocrine System's Effect on BP

-Release of epi & norepi
-Release of aldosterone
-Release of ADH

Primary HTN

-most common
-Essential/Idiopathic
-Examine contributing factors

Secondary HTN

-non-essential
-elevated BP w/specific cause that can be corrected
-EX. pheochromocytoma (tumor of adrenal medulla)

Hypertensive Patient Presentation

-Asymptomatic in itself but presents effects on target organs:
-CAD
-CVA
-PVD
-Retinal damage
-Renal Failure

Diagnostic Studies

-check BP both arms (use higher reading)
-Follow-up is to take it twice (5 min apart)
-Metabolic panel w/creatinine
-CBC
-Cardiac work-up
-U/A or urine test to assess 2ndary causes

Cardiac Work-Up

-EKG
-Echo
-Stress test

First Line HTN Drugs

-Thaizide diuretics
-Ca Channel Blockers
-ACE Inhibitors
-ARBs (angiotensin Receptor Antagonists)

HTN Drugs Side Effect Management

-gum/hard candy for dry mouth
-slow position chgs for orthostatic hypotension
-discuss sex dysfunction
-schedule diuretics to avoid nocturia

Heart Failure

-impaired cardiac pumping and/or filling which leads to lowered cardiac output
-CO = HR x SV

Systolic HF

-Inability to pump effectively
HALLMARK
: decrease in LV ejection

Diastolic HF

-inability of ventricles to relax and fill during diastole (stiff ventricles)
-normal ejection fraction though

Compensations to improve CO when heart fails....

-Sympathetic N.S.
-Dilation
-Hypertrophy
-Neuro-hormonal response (RAAS)
**All increase O2 demand of heart which is already struggling, so a little is good, but too much is a bad thing

HF Clinical Manifestations

-dominant feature: increased intravascular volume
-depend on extent of failure & which ventricle is affected though

Left & Right Sided Failure

-Can fail separately
-Left usual precedes Right

Acute Decompensated HF (ADHF)

-Manifest as acute pulm. edema
-pulm venous pressure increases R/T decreased efficiency of LV

Left Sided HF S/S

-All have to do w/ lack of blood flow to system & backing up into lungs

PND (Paroxysmal nocturnal dyspnea)

-Seen in L. Failure
-fluid accumulating around heart and pulm. circulaton when pt. lying down
-pt will feel suffocated and want to sit up.

Nocturia in L-sided HF

-caused by fluid sitting still in areas and getting absorbed into vascular compartment and kidneys are stimulated to excrete it

R-sided HF S/S

all R/T systemic fluid back-up
-Edema
-Hepatomegaly
-JVD
-Ascites
-Anorexia & nausea
-Weakness

Medications used for HF

-Diuretics (watch K+)
-ACE/ARBs (interfere w/ RAAS)
-Inotropic Drugs (increase contractility and CO)
-Beta blockers (reduce workload of heart/HR)
-EX: DIGOXIN (lowers HR but increases contractility)

Digoxin Toxicity

FIRST SIGN
=N/V
-be careful when giving Digoxin & Lasix (which causes you to lose K+)

3 meds used for HF

1. Diuretics: decrease preload & circulating B.V.
2. Beta Blockers: decrease HR & force of contraction (so lower cardiac O2 demand)
3. ACE-I: vasodilation decreases afterload, increases preload, prevents ventricular remodeling

Why would someone be taken off Ace-I's?

Angioedema & cough (caused by bradykinin)