Pathophysiology of Hypertension
Classification of blood pressure
Category Systolic blood pressure (mmHg) Diastolic blood pressure
>140/90
Optimal blood pressure Normal blood pressure High-normal blood pressure Grade 1 Hypertension (mild)
180 140-159 >160
110 <90 <90
Grade 2 Hypertension (moderate) Grade 3 Hypertension (severe) Isolated Systolic Hypertension (Grade 1) Isolated Systolic Hypertension (Grade 2)
BHS classification
Types of Hypertension
Essential (primary): 90-95% of cases. (cause
unknown) Secondary: 5-10%
Renal disorders Endocrine disorders Pregnancy induced Vascular Medicines: steroids, OCPs
Risk factors for primary HBP
Genetic- familial: heritability Obesity Smoking Males Alcohol High Na++ Low K+ Ca++ Mg ++
Pathophysiology of HBP
BP = CO X (SV x HR) X PVR PVR
Pathophysiology: A. Volume overload B. Increase in PVR
A. Volume overload: i. salt water retention (renin-angiotensinaldosterone system) ii. Changes in ANP activity/production iii. Change on adrenomedullin activity iv. Disorder in endothelial function v. Insulin resistance
B. Increase PVR i. increase sympathetic tone ii. Remodeling of peripheral vessels.
Investigations
Urine dipstick Chest x ray ECG, Echo Blood tests: sugar, electrolytes, kidney function, lipids, thyroid function. Specific tests for secondary causes.
Principles of treatment
Reduce volume overload: Salt restriction, diuretics Reduce peripheral resistance: Vasodilators Prevent angio II induced remodeling of vessels and heart: ACEI, Angio II blockers Reduce heart rate: Beta-blockers Central acting drugs: Methyldopa.
End (target) organ damage in HBP
Hypertension
Heart Brain Kidneys Arteries
LVH
Ischemia
Proteinuria Retinopathy PVD
CAD
CHF
Stroke
Kidney failure
Pathophysiology of Congestive heart failure
Poor pumping by the heart: inadequate cardiac output Cardiac output depends upon 1. initial stretch (Starlings law); myocardial contractility 2. preload (venous return) 3. after load (resistance) 4. heart rate Positive and negative inotropism
Factors affecting: * O2 * nerve supply: symphathetic +ve; parasymph: -ve * hormones: catechols; thyroxine * drugs: digoxin; dobutamine for +ve inotropism
Common causes of CHF
1. IHD (most common and important)
2. Hypertension
3. Valvular heart disease
Increased pre-load or after load Dilatation/hypertrophy
myocardial ischemia
Ventricular remodeling
Poor contractile function Decreased CO
poor kidney perfusion
RAAS activation
Increase ED volume
Fluid retention by kidneys
Catecholamines, angio II, aldo, ADH, TNF alpha, endothelin play part in the above.
Role of sympathetic activity in CCF
CHF Myocardial contractility
Baroreceptors
Contractility & HR
Reflex symphathetic activation
disadvantage
advantage
Peripheral resistance
O2 consumption In already damaged heart
Helps maintain CO for some time
Work load of heart
Overall situation worsens
CHF
Kidney helps to retain fluid & electrolytes
Sympathetic excitation
Both together initially help to maintain CO
But later worsens failure Because O2 consumption increases further
Symptoms and signs
• • • • • • • • Breathlessness (dyspnoea) Cough Fatigue Edema Cyanosis in severe cases Raised JVP. Fast low volume pulse Low BP.
Investigations
ECG, CXR, electrolytes
Echo.
Principles of treatment
Reduce preload: Reduce blood volume; salt restriction, Diuretics Reduce after load: Angio II blockers Improve symptoms: O2 when required, B-blockers Increase contractility: inotropic drugs; digoxin
Principles of nursing Help to relief symptoms Maintain urine output chart Diet; Low salt/ salt free
Pulmonary edema
Acute left ventricular failure after: i. a myocardial infarction ii. left ventricular hypertrophy hypoxia of myocardium
Inability of LV to pump
blood-accumulates in lungs
Severe breathlessness
(air hunger or paroxsymal nocturnal dyspnea)
moist lung sounds (rales)
Other causes: valvular heart disease, cardiomyopathies
Right Heart (ventricular) failure. Causes: Secondary to Left heart failure. Lung disease: chronic bronchitis/ emphysema Pathophysiology:
inflow of blood into lungs is blocked back pressure on the venous circulation accumulation of fluid. Symptoms: Pitting Edema, Raised JVP, Ascites, liver enlargement
HIGH out put failure: CO increases
Causes - severe anemia - hyperthyroidism - septicemia
Valvular Heart Disease
Normal structure and function of heart valves i. separate atria and ventricles ii separate the great arteries from the ventricles iii. ensure one way flow between atria and ventricles
iv. prevent backflow into atria during ventricular contraction
v. generation of heart sounds vi. help generate required pressures
Alteration in valve function 1) Stenosis (narrowing)
hypertrophy and dilatation of chamber behind the stenosed valve
i) Aortic stenosis:
Left ventricular hypertrophy
Left ventricular failure
Pulmonary congestion, back pressure
Backpressure on left atrium - Stagnation of blood
Right side chambers Raised JVP, enlarged liver, peripheral pitting edema ; Cyanosis
ii) Mitral stenosis.
Common variety of stenosis Common cause is Rheumatic heart disease.
Backpressure on left atrium - Stagnation of blood
Pulmonary congestion, back pressure
Right side chambers Raised JVP, enlarged liver, peripheral pitting edema ; Cyanosis
2) Regurgitation (incompetence, insufficiency)
Continuous leak back into ventricles Leading to hypertrophy and failure Effect of back pressure
Heart sound
Murmurs are abnormal heart sounds. Could be systolic or Diastolic.
S1
S1
S2