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Cardiovascular Disease: Epidemiology, 2018
Cardiovascular Disease: Epidemiology, 2018
EPIDEMIOLOGY, 2018
Source:
https://www.statista.com/statistics/1120528/philippi
nes-leading-causes-mortality-by-disease/
HYPERTENSION
o Hypertension, also known as HIGH BLOOD PRESSURE, is a condition in which the blood vessels have persistently
raised pressure (WHO).
o Most common cardiovascular disease.
o Untreated high blood pressure damages blood vessels, accelerates atherosclerosis, and produces left ventricular
hypertrophy. These abnormalities contribute to the development of IHD, stroke, heart failure, renal failure, which
are among the most common causes of death worldwide.
DIASTOLE
Indicates how
DETERMINANTS:
much pressure the
• Cardiac Output blood is exerting
• Peripheral Vascular Resistance against the artery
• Elasticity of vessel walls walls while the heart
is resting between
beats.
HYPERTENSION
JNC 8 CLASSIFICATION
SYSTOLIC BP DIASTOLIC BP
CATEGORY
(mmHg) (mmHg)
Normal 120 80
GESTATIONAL HYPERTENSION
Feature Gestational HTN Pre-Eclampsia Eclampsia
→ Pre-Eclampsia + Tonic-clonic Seizures
HTN + ++
Management: IV Epsom Salt
Proteinuria Negative Positive
BP = CO x PVR
CARDIAC OUTPUT Determinants of Stroke Volume
→ volume of blood pumped out by the ventricle per minute (mL/ minute) A. HEART RATE
→ Positive and Negative Chromotropic agents
STROKE VOLUME
CO = HR x SV → Volume of blood pumped out by the
ventricles per contraction/ beat
→ Volume (mL)/ beat
HEART RATE B. INOTROPY
→ heart conductivity → defined as the strength or force of contraction
→ beats/minute
HTN Blood Pressure Control and Regulation
C. PRELOAD/ End Diastolic Volume
→ defined as the volume of blood in the ventricles prior to contraction (heart
is relaxed; ventricles are being filled with blood)
VENODILATION
BP = CO x PVR
PERIPHERAL VASCULAR
VENOCONSTRICTION
RESISTANCE
Aka: Total Vascular Resistance (TVR), Systemic
__ Afterload → ___ BP
Vascular Resistance (SVR), AFTERLOAD
Afferent Afferent
Nerve IX Nerve X
Efferent Pre-ganglionic
Nerve X sympathetic fibers
Parasympathetic Sympathetic
Action Action
HTN Mechanisms of BP Regulation
RENIN-ANGIOTENSIN ALDOSTERONE SYSTEM (RAAS)
ACE
RENIN (Angiotensin Converting Enzyme)
ANGIOTENSINOGEN ANGIOTENSIN I ANGIOTENSIN II
AG II binds to AG IA receptors
Kininase II
Effects:
Peptidyl Dipeptidase
1. Stimulation of autonomic ganglia.
Triggers of Renin Release 2. Triggers the release and synthesis
1. Beta-1 stimulation ACE degrades Bradykinin
and Substance P in the lungs of Aldosterone.
2. Renal Hypoperfusion 3. Release of Vasopressin.
3. Renal Hypotension