Please enable JavaScript.
Coggle requires JavaScript to display documents.
Heart Failure, hypertension
myocardial infraction
CAD
metabolic…
-
- hypertension
- myocardial infraction
- CAD
- metabolic syndrome
- diabetes mellitus
- amount of blood pumped by LV per minute
- cardiac output = HR x SV (stroke volume)
-- approx. 5L/min at rest
- cardiac index = cardiac output/body surface area
- Preload
- amount heart is filled per beat (EDV: end-diastolic volume)
- incr. EDV leads to incr. SV (to a point)
- Afterload
- resistance that heart pumps against
- incr. afterload reduces cardiac output
- Contractility
- force of contraction
- incr. preload incr. contractility (to a point)
- SNS activation incr. contractility
- High afterload reduces contractility
- aortic pressure against the left ventricle
- the amount of force in the wall of the ventricle necessary to overcome the pressure against it = afterload
- Incr. preload fills the heart
- weakened heart can not adequately pump excess fluid
- excessive filling overtaxes ventricular fibers leading to decr. contractility
- SV (stroke volume) and cardiac output decr.
- Renin-angiotensin-aldosterone system (RAAS)
- Renin
- from JG (juxtaglomerular) cells of kidneys in response to low pressure or perfusion
- converts angiotensinogen (from liver) to angiotensin I
- Angiotensin I converted to angiotensin II
- ACE (angiotensin-converting enzyme) in the lung
- ACE inhibitors (anti-hypertensive medications) block
- Angiotensin II
- potent vasoconstrictor
- stimulates cardiac remodeling (hypertrophy, apoptosis, fibrosis)
- activates aldosterone from adrenal cortex
- Aldosterone stimulates sodium and water retention by kidneys to incr. blood volume and pressure
- Compensatory mechanisms: detrimental effects over time, as failing heart is overloaded with fluid leading to edema
- Incr. fluid volume or volume overload
- impaired ventricular filling
- degeneration of ventricular muscle
- decr. ventricular contractile function
- Ischemic heart disease
- heart tissue compromised, unable to generate adequate pressure
- Hypertension leading to LVH
- coronary circulation unable to meet demand
- restrictive cardiomyopathy: less filling space due to enlarged LV
- Cor pulmonale
- right side heart failure due to pulmonary issue
- COPD- hypoxia-pulmonary vasoconstriction- increased workload on R-side of heart
- Cardiomyopathies
- ischemic
-- myocardial fibrosis and scarring of heart
- dilated
-- enlargement of ventricles
- restrictive
-- can not fill
- hypertrophic
-- usually LV muscle enlarged, encroaches on ejection of blood into aorta
-- primary: genetic
-- secondary: due to HTN
- Dysrhythmia
- irregular heart rhythm may precipitate failure
- both tachyarrhythmias and bradyarrhythmias
- Cardiac infection
- endocarditis, myocarditis
- Pulmonary embolism
- acute RV failure due to increased pulmonary artery pressure
- Heart valve abnormalities
- mitral regurgitation (insufficiency)
- may occur after transmural LV MI
- valve does not close properly, backward flow into right atrium (decr. blood ejected from LV)
- aortic stenosis
- LV must generate more pressure to eject blood
- LVH develops
Step 1: Chronic hypoxia develops due to lung disease
Step 2: Chronic hypoxia causes pulmonary arterial vasoconstriction (called pulmonary hypertension)
Step 3: Pulmonary hypertension causes high resistance against the right ventricular failure occurs.
- age
- ethnicity
- family history
- diabetes
- obesity
- sleep apnea
- congenital heart defects
- smoking
- sedentary
- mediations
- anabolic steroids
- viral myocarditis
- alcohol abuse
- kidney conditions
- Acute vs chronic
- systolic vs diastolic
- high output or low output
- right side or left side
-- failure of one side leads to failure of other side
-- most common way to classify heart failure
-- forward effects: decr. pressure and perfusion
-- backward effects: backup of hydrostatic pressure due to hearts failure to eject blood
- Systolic
- difficulty ejecting blood (HFrEF)
- decr. SV and cardiac output
- activation of RAAS, SNS, vasoconstriction place more stress on heart
- backup of fluid from failed ventricle
- Diastolic
- difficulty relaxing/filling (HFpEF)
- stiff or enlarged ventricles can not easily fill
- EF may be normal (due to reduced EDV)
High:
- heart can not meet high circulatory needs
- relatively uncommon
- thyrotoxicosis, severe anemia
Low:
- impaired venous return
- eg. severe leg trauma preventing blood return
- can occur with both diastolic (can't fill) and systolic (can't eject) forms
- diastolic
-- LVH due to HTN
- systolic
-- damage to heart (ie. MI) prevents adequate pressure generation
- Forward effects
- decr. perfusion
- activate SNS, RAAS
- backward effects
- hydrostatic pressure backup into pulmonary circulation
- crackles, orthopnea, paroxysmal nocturnal dyspnea (PND)
- Backward effect most significant
- JVD: jugular vein distention
- incr. central venous pressure (CVP)
- hepatojugular reflex may be present
- venous congestion of GI tract causing anorexia, nausea
- hypoxia and cyanosis may develop
- peripheral edema
- Lifestyle modifications
- exercise, low sodium diet, smoking cessation
- medications
- diuretics
-- reduce fluid volume (some can lead to hypokalemia)
- aldosterone antagonist
- ACE inhibitors
-- block angiotensin-converting enzyme (ACE)
-- cornerstone of heart failure treatment
- Left ventricular assist device (LVAD)
- pump that enhances LV ejection
- helps pump blood into aorta
- Cardiac transplantation
- based on age and presence or absence of comorbidities
- compatibility of donor and recipient