Final_Week 3 Flashcards
Primary HTN
“essential HTN”
95% of all HTN
pathogenic factors: familial/inherited biochemical abnormalities
Secondary HTN
- renovascular dx
- cushings syndrome
- hyperaldosteronism
- aortic coarctation
- pregnancy induced HTN
- pheochromocytoma
- renal parynchymal dz
Primary HTN: pathophysiology
- specific etiology is unclear
- contributing factors: sympathetic nervous system activity, dysregulation of RAAS, deficient production of endogenous vasodilators
PAH
Mean PAP > 25
PAH crisis - Tx
- Oxygen, anticoagulation, diuretics
- CCBs
- Phosphodiesterase inhibitors (Viagra)
- Inhaled NO
- Prostacyclins (Flolan, Remodulin, Ventavis)
- Endothelin receptor agonists (Tracleer)
- Surgical tx (Balloon atrial septostomy, Lung TX)
Frank-Starling relationship
- Increased filling pressure stretches the heart and increases the force of contraction
- Increasing the force of contraction expels more blood from the LV, so that CO increases when preload increases
- SV increases as LVEDV increases
- SV increases as tension on the cardiac muscle increases
- Magnitude of SV increase depends on myocardial contractility
Stages of HF
I (Mild): asymptomatic
II (Mild): s/s w/ ordinary exertion
III (Moderate): s/s with less than ordinary exertion
IV (severe): s/s at rest
Tx - severe HF
-ACEI + BB
-Na+ restriction, diuretics, digoxin
-if BBB present: cardiovert
-revascularization/mitral valve surgery
-aldosterone antagonist, nesiritide
Special intvn: isotopes, VAD, transplant, hospice
HTN emergency S/S
*evidence of target organ damage •Angina Pectoris •LVH •CHF •Cerebrovascular disease •Stroke •PVD •Renal Insufficiency
HTN Urgency S/S
S/s: H/A, epistaxis, anxiety
HTN Crisis: Tx
•Lower BP 20% in 1st hour
•More gradually over 2 – 6 hrs
-SNP, Nicardipine, fenoldopam, esmolol, labetolol
HTN Crisis: DOC
-Sodium nitroprusside: 0.5-10 mcg/kg/min
HTN Crisis: Rx for any type
Labetolol
PAH anesthesia
- avoid hypoxia, hypercarbia, acidosis
- have NO available
- opioids + prop ok
- avoid ketamine/etomidate