Right and left ventricular hypertrophy

25,840 views 22 slides Jan 16, 2014
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About This Presentation

Rawalpindi Medical college


Slide Content

BY DR.UZMA TALIB

Defination:
Left ventricular hypertrophy is defined as an increase in the
mass of the left ventricle, which can be secondary to an
increase in wall thickness, an increase in cavity size, or both
Causes:
Hypertension
Hypertrophic cardiomyopathy
Aortic stenosis
Athelitic training

Risk factors for left ventricular hypertrophy include the
following:
Age
Gender
High blood pressure, a blood pressure reading greater than
140/90 mm Hg, is the greatest risk factor.
Aortic stenosis, narrowing of the main valve through which
blood leaves the heart, may increase the left ventricle's
workload.
Obesity can cause high blood pressure and increase your
body's demand for oxygen, factors that may lead to left
ventricular hypertrophy.
Genetic factor

 The development of LVH is a relatively early response to
hypertension,
 Ambulatory BP monitoring has suggested that there may be two additional
risk factors for LVH:
The daily BP load (the percentage of pressures above 135/85 during the day
and 120/80 mmHg at night
Nocturnal hypertension (in which the expected nighttime reduction in BP is
not seen)
 maximal daytime blood pressure or peak exercise blood
pressure are most predictive of the level of hypertrophy .
There is also evidence that left ventricular mass may be
increased prior to the development of overt hypertension.

High BP ® ­ LV wall stress
Wall stress µ 1/ wall thickness
LV wall thickening ® ¯ wall stress
Myocyte hypertrophy and ­ collagen matrix
.The same factors, such as angiotensin II, norepinephrine,
epinephrine, increased peripheral and cardiac sympathetic
drive and endothelin, promote both hypertension and LVH.
The tendency to LVH may be an inherited trait that
predisposes to the development of hypertension

›To diagnose LVH you can use the following criteria*:
 R in V5 (or V6) + S in V1 (or V2) > 35 mm, or
avL R > 13 mm

Symptoms:
Shortness of breath
Chest pain
palpitations
Dizziness
Fainting
Rapid exhaustion with physical activity
Fatigue
Syncope
Some time patient shows no symptoms

Signs:
systolic murmur best heard between the apex and
left sternal border
 - increases in intensity with maneuvers that
 decrease preload (Valsalva, squatting to
 standing position).
 - does not radiate to the carotid arteries
• sustained apical impulse
• S4
• bisferiens pulse (carotids, femoral arteries)

Complications that can occur as a result of these problems
include:
Inability of your heart to pump enough blood to your body
(heart failure)
Abnormal heart rhythm (arrhythmia)
Insufficient supply of oxygen to the heart (ischemic heart
disease)
Interruption of blood supply to the heart (heart attack)
Sudden, unexpected loss of heart function, breathing and
consciousness (sudden cardiac arrest)

Defination:
right ventricular hypertrophy is the enlargement of heart’s
right ventricle
Right ventricular hypertrophy, or simply RVH, is considered to
be one of the rare diseases of the heart. Unlike the left
ventricle, which tends to overwork itself when it detects
abnormalities, the right ventricle dilutes itself. This is the
reason why left ventricular hypertrophy is way more common
than right ventricular hypertrophy.

Pulmonary hypertension
Fallot tetralogy
Pulmonary valve stenosis
Ventricular septal defect (VSD)
High altitude
Cardiac fibrosis
Chronic obstructive pulmonary disease (COPD)

Chest pain and tightness
Palpitation
Dizziness
Loss of consciousness
Light headedness
Edema of feet,leg,ankle

To diagnose RVH you can use the following criteria:
 Right axis deviation, and
V1 R wave > 7mm tall

POTASSIUM
MAGNESIUM
CALCIUM

Hyperkalemia
Hypokalemia
Hyperkalemia: affects Na channels and causes
depolarizaion .
Na channels inactivate and refractory.
Ventricular fibrillation and asystole.
At the same time increases activity of potassium
channels and increases memb. repolarization.
Causes:
Renal insufficiency
Medication
Blood transfusion, Massive hemolysis
Addison's disease
congenital adrenal hyperplasia
Burns,necrosis,tumor lysis syndrome
Potassium containg dietary supplements

Hyperkalemia:causes hyperpolarization of RMP.
Greater than normal stimulus is required to generate A.P.
 Opposite in case of heart and it become hyperexcitable. Lower A.P in
atria may cause arrhythmias.
Causes:
Inadequate intake
Postemetic,Diarrhea
Diuretic
Alkalosis
Renal artery stenosis
Tumors of adrenal gland

Hypermagnesemia
Hypomagnesemia
Hypomagnesemia
required for Na/K ATPase. Normal Mg inhibits
release of K . In hypo more K is released so cells depolarize
causing tachyarrhythmias
Causes:
Alcohol abuse
Delirium tremens
Ch.Diarhea
Thiamine deficiency
Diuretics
Aminoglycoside
Gentamycin,tobramycin
Cisplatin,cyclosporin

Hypermagnesemia: Acts as physiological Ca channel
blocker. Causes arrhythmias such as A/F, interventricular
conduction delay.
Causes:
Antacids
Vitamins
Acute renal failure
Maternal eclampsia
Tumor hypoparathyoidism
Iatrogenic
Sis syndrome
Milk alkali syndrome
Hypothyroidism

Hypercalsemia
Hypocalsemia
Hypercalsemia:
rarely too high to effect heart but may cause heart to fail to
relax during diastole and eventually stops in systole(Ca rigor).
Causes:
Hyperparathyroidism
Sarcoidosis
Iatrogenic
Breast cancer
Phaeochromocytoma
Hyperthyroidism
Post renal transplant
Adrenal insufficiency

Hypocalsemia:
 exact mech. nt known but ECG changes are seen.
Cause :
Hypoparathyroidism
Sepsis
Alcoholism
Renal failure
Pacreatitis
Hyperphosphatemia
Phosphate enemas
Malnutrition

THANK YOU