Med Surg Cardiovascular
Unoxygenated blood – vena cavas, right atrium, tricuspid valve, right ventricle, pulmonic valve, pulmonic
arteries, to lungs.
Oxygenated blood – lungs, pulmonary veins, left atrium, mitral valve, left ventricle, aortic valve, aorta.
Artery – away from the heart, deoxygenated.
Veins – toward the heart, oxygenated.
Classification of hypertension
Normal 90-119 and 60-79
Prehypertension 120-139 and 80-89
Stage 1 hypertension 140-159 and 90-99
Stage 2 hypertension >160 and >100
Isolated systolic >/=140 and <90
Primary hypertension – essential (majority)
Secondary hypertension – something is causing it (acute)
BP= CO x SVR
CO – affected by heart rate, contractility, and conductivity. Fluid volume controls kidneys (RAAS).
Natriuretic peptides (induces sodium secretion by kidneys)
ANP atrial natriuretic peptide
BNP brain natriuretic peptide (too much blood in heart – release of this gets rid of H2O) it helps
diagnose heart failure
SVR (systemic vascular resistance) -- affected by vessel diameter (if vessel decreases blood pressure
increases)
Sympathetic – vasoconstriction and vasodilation
Neurohormonal vasoconstrictors (angiotensin/ norepinephrine)
Local regulation prostaglandins, nitric oxide (dilator) endothelin (constrictor)
Blood pressure is regulated by: autonomic nervous system, heart, kidneys and hormones.
The fastest mechanism for blood pressure regulation is the sympathetic stimulation of the nervous
system.
Long standing hypertension can reset the baroreceptors
Stats:
More men have BP than women
More common on non- Hispanic black
, BP control is higher in white
Key points:
Weight loss is the most effective lifestyle change to help BP regulation
To diagnose hypertension there needs to be two or more BP readings at 2 or more visits
Hypertension can damage heart, eyes, kidneys, shift of the heart or enlargement. It can also
affect the brain.
Patients should be educated on sodium restriction, weight reduction and smoking cessation
Norepinephrine A1 and B1 receptors – vasoconstrict and increase heart rate.
Hypertensive crisis – life threatening. Diastolic is greater than 120, there is a high risk for target
organ damage. Headache, drowsiness, confusion, dyspnea, tachycardia. Goal for reduction is to
decrease MAP by no more than 25% within 1 hour. Treatment consist on IV anti-hypertensives
(drip) and patient monitoring.
Renin- Angiotensin- aldosterone system
Overactivated in a pt with hypertension and HF
ACE inhibitors work at the lungs – they prevent the conversion of angiotensin 1 to 2
ARBs work and the arterioles and adrenal cortex – angiotensin receptor blockers.
Medications for Hypertension
Diuretics (work by getÝng rid of excess water allowing a decrease in the cardiac output)
- Hydrochlorothiazide 12.5 mg (first line)
- Furosemide (Lasix) strong medication
- Spironolactone (K+ sparing) weakest
Beta 1 blockers (olol) propranolol hydrochloride – decrease heart rate, myocardial contractility
and conduction.
ACE inhibitors (pril) lisonopri, captopril, benazepril. FIRST LINE MEDICATION side effect is
chronic cough. prevents conversion of angiotensin 1 to 2. Less effective in African americans.
ARB’s (angiotensin receptor blockers) sartan losartan, valsartan. Prevents sodium reabsorption
by the kidney and vasodilation of the arterioles.
SIDE EFFECTS OF ACE AND ARB’s:
- Hyperkalemia (especially in patients with renal impairment)
- Angioedema (inflammation of vessels especially in the upper airways)
CV changes with aging
Cardiac valves calcify and degenerate (mitral and aortic due to high pressure)
Conduction system (reduction on the number of pacemaker cells, fewer muscle fibers,
conduction time increases)
Left ventricle (size increases, becomes stiff – prevents blood flow from coming in)
Aorta/ large arteries (thickening, less distensible)
Unoxygenated blood – vena cavas, right atrium, tricuspid valve, right ventricle, pulmonic valve, pulmonic
arteries, to lungs.
Oxygenated blood – lungs, pulmonary veins, left atrium, mitral valve, left ventricle, aortic valve, aorta.
Artery – away from the heart, deoxygenated.
Veins – toward the heart, oxygenated.
Classification of hypertension
Normal 90-119 and 60-79
Prehypertension 120-139 and 80-89
Stage 1 hypertension 140-159 and 90-99
Stage 2 hypertension >160 and >100
Isolated systolic >/=140 and <90
Primary hypertension – essential (majority)
Secondary hypertension – something is causing it (acute)
BP= CO x SVR
CO – affected by heart rate, contractility, and conductivity. Fluid volume controls kidneys (RAAS).
Natriuretic peptides (induces sodium secretion by kidneys)
ANP atrial natriuretic peptide
BNP brain natriuretic peptide (too much blood in heart – release of this gets rid of H2O) it helps
diagnose heart failure
SVR (systemic vascular resistance) -- affected by vessel diameter (if vessel decreases blood pressure
increases)
Sympathetic – vasoconstriction and vasodilation
Neurohormonal vasoconstrictors (angiotensin/ norepinephrine)
Local regulation prostaglandins, nitric oxide (dilator) endothelin (constrictor)
Blood pressure is regulated by: autonomic nervous system, heart, kidneys and hormones.
The fastest mechanism for blood pressure regulation is the sympathetic stimulation of the nervous
system.
Long standing hypertension can reset the baroreceptors
Stats:
More men have BP than women
More common on non- Hispanic black
, BP control is higher in white
Key points:
Weight loss is the most effective lifestyle change to help BP regulation
To diagnose hypertension there needs to be two or more BP readings at 2 or more visits
Hypertension can damage heart, eyes, kidneys, shift of the heart or enlargement. It can also
affect the brain.
Patients should be educated on sodium restriction, weight reduction and smoking cessation
Norepinephrine A1 and B1 receptors – vasoconstrict and increase heart rate.
Hypertensive crisis – life threatening. Diastolic is greater than 120, there is a high risk for target
organ damage. Headache, drowsiness, confusion, dyspnea, tachycardia. Goal for reduction is to
decrease MAP by no more than 25% within 1 hour. Treatment consist on IV anti-hypertensives
(drip) and patient monitoring.
Renin- Angiotensin- aldosterone system
Overactivated in a pt with hypertension and HF
ACE inhibitors work at the lungs – they prevent the conversion of angiotensin 1 to 2
ARBs work and the arterioles and adrenal cortex – angiotensin receptor blockers.
Medications for Hypertension
Diuretics (work by getÝng rid of excess water allowing a decrease in the cardiac output)
- Hydrochlorothiazide 12.5 mg (first line)
- Furosemide (Lasix) strong medication
- Spironolactone (K+ sparing) weakest
Beta 1 blockers (olol) propranolol hydrochloride – decrease heart rate, myocardial contractility
and conduction.
ACE inhibitors (pril) lisonopri, captopril, benazepril. FIRST LINE MEDICATION side effect is
chronic cough. prevents conversion of angiotensin 1 to 2. Less effective in African americans.
ARB’s (angiotensin receptor blockers) sartan losartan, valsartan. Prevents sodium reabsorption
by the kidney and vasodilation of the arterioles.
SIDE EFFECTS OF ACE AND ARB’s:
- Hyperkalemia (especially in patients with renal impairment)
- Angioedema (inflammation of vessels especially in the upper airways)
CV changes with aging
Cardiac valves calcify and degenerate (mitral and aortic due to high pressure)
Conduction system (reduction on the number of pacemaker cells, fewer muscle fibers,
conduction time increases)
Left ventricle (size increases, becomes stiff – prevents blood flow from coming in)
Aorta/ large arteries (thickening, less distensible)
