Hypertrophy, Hypertensive Heart Disease & Heart Failure Flashcards
(35 cards)
How much blood does a normal heart pump daily?
- pumps about 6000 L of blood daily
- perfuses tissues with nutrients
- facilitates the removal of waste products
Normal weight:
250-300g adult female
300-350g adult male
** Left Ventricle is thicker (1.3-1.5cm) instead of Right Ventricle (0.3-0.5cm)
What is Cardiomegaly?
Cardiomegaly means an enlarged heart.
🫀 What does that mean?
* It’s not a disease itself — it’s a sign seen on imaging (like a chest X-ray or echocardiogram).
* It means the heart is larger than normal, often because it’s overworked, damaged, or trying to compensate for a problem.
(hypertrophy of the myocardium and dilation of the chambers)
What are some normal histological characteristics of the heart muscle?
- centrally located nucleas helps the heart muscle function as a coordinated unit
- intercelated discs allow impulses to pass quickly between cells and facilitates synchronized contractions
How does a normal heart muscle function?
🫀 How the Heart Increases Output (Cardiac Reserve)
The heart can pump more blood when the body needs it (e.g., during exercise, stress, illness). It does this through two main mechanisms:
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- Ventricular Dilatation
(The heart stretches to pump harder)
* The ventricles fill with more blood, causing them to stretch.
* This stretch increases the force of contraction, based on the:
⚖️ Frank-Starling Law
“The more the heart fills (stretches), the harder it contracts.”
* Think of it like stretching a rubber band: the more you stretch, the more snap-back force you get — up to a point.
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- Ventricular Hypertrophy
(The heart muscle thickens to pump stronger)
* The muscle fibers get thicker (myofiber hypertrophy).
* A thicker wall means more contractile force to pump blood.
* This happens in response to chronic stress like high blood pressure or valve disease.
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❌ When Compensation Fails → Heart Failure
If these adaptations go too far or last too long, they backfire:
* Overstretched heart → can’t snap back → weak contractions
* Excessively thick muscle → less space for blood → poor filling
* Eventually leads to heart failure (heart can’t meet the body’s needs)
What is Preload and Afterload?
🫀 Preload vs. Afterload
🔄 1. Preload
“How much the heart fills before it contracts.”
* ✅ Definition:
The volume of blood in the ventricles at the end of diastole (just before contraction).
* ✅ What it depends on:
* Venous return — how much blood is coming back to the heart (mainly to the right side).
* ✅ Effect on heart:
* More preload → more stretch of cardiac muscle
* Stretch increases force of contraction
* Follows the Frank-Starling law
* 💥 Result: Increased stroke volume
* ✅ Example:
Giving IV fluids increases preload → increases cardiac output.
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🚧 2. Afterload
“How hard the heart has to push to get blood out.”
* ✅ Definition:
The resistance the left ventricle must overcome to eject blood during systole.
* ✅ What it depends on:
* Blood pressure (systemic vascular resistance)
* Aortic valve resistance
* ✅ Effect on heart:
* Higher afterload = heart works harder
* If too high, the heart can’t eject as much blood
* 💥 Result: Decreased stroke volume
* ✅ Example:
In hypertension, afterload is high → heart has to pump harder → can lead to hypertrophy or failure.
What is Ventricular Hypertrophy and when does it happen?
🫀 What is Ventricular Hypertrophy?
Ventricular hypertrophy is a compensatory change where the heart muscle thickens to deal with increased workload.
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⚙️ Why does it happen?
The heart works harder in conditions like:
1. Systemic hypertension (high blood pressure)
2. Valvular stenosis (narrowed valve = harder to pump through)
3. Valvular insufficiency (leaky valve = extra volume to handle)
To keep up, myocytes (heart muscle cells) enlarge and contract more forcefully.
What is Concentric and Eccentric hypertophy of the Left Ventricle?
❤️🔥 Left Ventricular Hypertrophy (LVH)
Commonly due to high systemic blood pressure or aortic valve disease (stenosis)
Concentric LVH:
- Pressure overload (e.g., hypertension, aortic stenosis)
- Walls thicken inward; chamber size stays the same or shrinks
Eccentric LVH
- Volume overload (e.g., aortic or mitral regurgitation)
- Walls stretch outward with chamber dilation
What is Concentric and Eccentric hypertophy of the Right Ventricle?
💙 Right Ventricular Hypertrophy (RVH)
Caused by pulmonary hypertension, lung disease, or pulmonary valve problems
Concentric RVH:
- Pressure overload (e.g., pulmonary hypertension)
- Thick walls without much dilation
Eccentric RVH
- Volume overload (e.g., tricuspid/pulmonary regurgitation)
- Dilated chamber with thicker walls
Hypertrophy helps at first, but prolonged stress leads to:
* Less flexibility
* Poor oxygen delivery to thickened walls
* Eventual heart failure
What is difference between Concentric and Eccentric Hypertrophy?
🫀 What is Hypertrophy?
Hypertrophy is when the heart muscle gets thicker to handle extra stress.
There are two main types depending on what kind of stress the heart is under:
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1️⃣ Concentric Hypertrophy
🧱 Thick walls, small space
📌 Cause:
→ Pressure overload
Examples:
* Systemic hypertension
* Aortic stenosis
* Pulmonary hypertension (in right ventricle)
🧬 What happens:
* Heart must push harder against high pressure.
* Muscle fibers grow inward (parallel growth).
* Wall thickness increases, but chamber size shrinks or stays the same.
📉 Result:
* Initially stronger contractions, but over time, stiff ventricle → poor filling → diastolic heart failure
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2️⃣ Eccentric Hypertrophy
📦 Dilated chamber, thinner or stretched wall
📌 Cause:
→ Volume overload
Examples:
* Mitral or aortic regurgitation
* Dilated cardiomyopathy
* High endurance training (physiological)
🧬 What happens:
* Heart must handle extra volume of blood.
* Muscle fibers stretch out (in series).
* Chamber dilates, and wall may thin or mildly thicken.
📉 Result:
* Initially increases stroke volume, but over time can lead to systolic heart failure (weaker pump)
What histological sign do we see in a Hypertrophic Myocardium?
- enlarged myocytes
** Enlarged Box Car Nuclei
What are consequences of Ventricular Hypertrophy?
💔 Consequences of LVH (Left Ventricular Hypertrophy)
When the left ventricle becomes thickened (usually due to long-term pressure overload), several problems can follow:
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1️⃣ Heart Failure (Left or Right-sided)
* Thickened ventricle becomes stiff → doesn’t relax properly → poor filling
→ Diastolic heart failure (heart pumps fine but fills poorly)
* Over time, backup of blood into the lungs → pulmonary hypertension
→ Right-sided heart failure can also develop
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2️⃣ Angina (Chest Pain)
* Thicker heart muscle needs more oxygen, but:
* Capillary supply doesn’t increase enough to match the growth (coronary vessels aren’t able to supply the new size of the growing heart)
* Blood supply can’t meet the demand → ischemia
* Even with normal coronary arteries, patients may feel angina
(especially during exertion)
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3️⃣ S4 Heart Sound
Also called the “atrial gallop”
* Happens in late diastole when the atria contract * Blood hits a stiff, noncompliant ventricle (because of hypertrophy) * Best heard with the bell of the stethoscope at the apex, in left lateral decubitus position
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⚠️ Other Possible Consequences:
* Arrhythmias: especially atrial fibrillation due to high left atrial pressure
* Sudden cardiac death: especially in athletes with undiagnosed hypertrophic cardiomyopathy
* Impaired exercise tolerance
What are the different types of Hypertrophy that can develop?
🫀 Types of Cardiac Hypertrophy & Remodeling
The heart adapts differently depending on the type of stress:
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✅ 1. Physiologic Hypertrophy
➡️ Good stress (reversible, adaptive)
Examples:
* Exercise (athletes)
* Pregnancy
What happens:
* Cardiomyocytes increase in both length and width
* Balanced eccentric hypertrophy:
* Chambers enlarge slightly
* Walls and septum thicken proportionally
Key feature:
✅ Healthy adaptation — the heart becomes stronger without dysfunction
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❌ 2. Pathologic Hypertrophy
➡️ Harmful stress (can lead to failure)
Triggers:
* Hypertension
* Aortic stenosis
* Hypertrophic cardiomyopathy (HCM)
🟥 Early Phase: Concentric Hypertrophy
* Cardiomyocytes increase mostly in width (not length)
* Wall and septum thicken
* Chamber size decreases or stays the same
Consequence:
* Stiff ventricle → diastolic dysfunction
* Can lead to S4 heart sound, angina, arrhythmias
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🟧 Late Phase: Eccentric (Dilated) Hypertrophy
* If stress continues or worsens:
* Cardiomyocytes become overstretched
* Length increases, but width decreases
* Result:
* Large, dilated chambers
* Thin walls, high wall tension
* Systolic dysfunction → poor contraction
Seen in:
* Dilated cardiomyopathy
* Chronic volume overload
* Advanced stages of previously concentric hypertrophy
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🧬 Key Point:
Some diseases (like viral myocarditis, alcohol abuse, or genetic DCM) can directly cause dilated cardiomyopathy without going through a concentric phase.
Does Concentric hypertrophy always lead to Eccentric hypertrophy?
No, concentric hypertrophy does not always lead to eccentric hypertrophy, but it can — especially if the underlying stress (like high blood pressure or aortic stenosis) is severe or prolonged and not treated.
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🔁 When Concentric Can Lead to Eccentric:
* In chronic pressure overload, the heart initially adapts by thickening the walls (concentric hypertrophy).
* Over time, this thickened muscle becomes stiff and less efficient.
* Eventually, the heart decompensates:
* It can’t keep up with demand
* The walls begin to stretch
* The chamber dilates
* This leads to eccentric (dilated) hypertrophy and eventually systolic heart failure
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⛔️ When It May Not Lead to Eccentric:
* If the underlying cause is treated early (e.g., controlling hypertension, replacing a stenotic valve), the heart can maintain concentric remodeling or even partially reverse it.
* In some hypertrophic cardiomyopathies, the heart stays in a concentric state for years or decades without dilating.
What is Dilated Cardiomyopathy?
💔 Dilated Cardiomyopathy (DCM)
Dilated cardiomyopathy is a disease of the heart muscle where the ventricles become enlarged (dilated) and the walls become thin and weak, leading to impaired systolic function (the heart can’t pump blood effectively).
🩺 Symptoms
These are due to heart failure and poor cardiac output:
* Fatigue
* Dyspnea (shortness of breath)
* Orthopnea (can’t breathe lying down)
* Paroxysmal nocturnal dyspnea (PND)
* Edema (swelling in legs)
* Palpitations or arrhythmias
* S3 heart sound (due to volume overload)
🧠 Summary:
Dilated cardiomyopathy is a condition where the heart is big, weak, and can’t pump well, usually leading to systolic heart failure.
In DCM, does Eccentric hypertrophy happen before Concentric Hypertrophy?
✅ Yes — in many cases, Dilated Cardiomyopathy (DCM) is a form of eccentric hypertrophy without a preceding concentric phase.
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🧬 Let’s break it down:
🟣 Eccentric Hypertrophy in DCM
* In DCM, the ventricles dilate (especially the left ventricle).
* Cardiomyocytes grow in length (not width).
* Wall thickness stays the same or decreases → thin, floppy walls.
* Chamber size increases a lot.
This matches the definition of eccentric hypertrophy, where the heart dilates under volume overload or injury.
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❌ No Prior Concentric Hypertrophy? Often True
Unlike conditions like hypertension or aortic stenosis, where the heart first goes through concentric hypertrophy (thick walls from pressure overload), in DCM:
* The primary problem is myocyte injury, dysfunction, or stretch, not pressure.
* There’s no need for concentric adaptation first.
* Many DCM cases are due to:
* Genetic mutations
* Viral myocarditis
* Toxins (like alcohol or chemo)
* Idiopathic causes
These causes directly lead to dilation → DCM as a primary eccentric process.
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⚠️ Note:
That said, in some chronic heart diseases, concentric hypertrophy can eventually decompensate into dilation — leading to eccentric hypertrophy secondarily.
But in primary DCM, the heart often:
Starts and stays in an eccentric state, without ever being concentric first.
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🔑 Bottom Line:
Yes — DCM is typically a primary eccentric cardiomyopathy, without a prior concentric phase.
What is Hypertrophic Cardiomyopathy (HCM)?
- Hypertrophic cardiomyopathy is a genetic heart disease characterized by thickening (hypertrophy) of the heart muscle, especially the left ventricle and interventricular septum, without an obvious cause like high blood pressure or valve disease.
🩺 Symptoms:
* Often asymptomatic initially
* Exertional dyspnea (shortness of breath)
* Chest pain (angina)
* Syncope (fainting), especially during exercise
* Palpitations or arrhythmias (can cause sudden cardiac death)
* S4 heart sound (due to stiff ventricle)
🫀 Heart muscle: Marked hypertrophy, especially of the septum (asymmetric)
🧬 Cause: Usually autosomal dominant mutations in genes encoding sarcomere proteins (e.g., beta-myosin heavy chain)
💔 Chamber size: Usually normal or decreased (due to thick walls)
⚙️ Function: Often impaired relaxation (diastolic dysfunction)
What is Congestive Heart Failure?
💔 Congestive Heart Failure (CHF)
CHF is a clinical syndrome where the heart cannot pump blood effectively to meet the body’s needs, leading to fluid buildup (congestion) in the lungs and/or peripheral tissues (unable to effectively eject blood)
- MC hospital admission diagnosis in elderly patients
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🧠 What happens in CHF?
* The heart’s pumping ability is reduced (either because it can’t contract well or it can’t fill properly).
* Blood backs up behind the failing side of the heart.
* This causes fluid to leak out into lungs (pulmonary edema) or body tissues (peripheral edema).
- Can be Left or Right side
What are causes of Left sided Heart Failure?
🚩 Causes of Left-Sided Heart Failure
1. Ischemic Heart Disease
* Reduced blood flow to the heart muscle → weakens the left ventricle
* Example: Coronary artery disease, leading to chronic ischemia or infarction
2. Hypertension (High Blood Pressure)
* Increases pressure the left ventricle must pump against (afterload)
* Leads to concentric hypertrophy and eventually heart failure (harder for coronaries to oxygenate new size of heart = ischemia and angina)
3. Dilated Cardiomyopathy (DCM)
* Enlarged and thickened, weakened left ventricle → poor systolic function
4. Myocardial Infarction (Heart Attack)
* Sudden death of heart muscle → scar formation → loss of contractile function
5. Restrictive Cardiomyopathy
* Stiff ventricles (impaired filling, diastolic dysfunction) → inadequate cardiac output
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🧠 How these cause Left-Sided Heart Failure:
* Impaired contractility (ischemia, MI, DCM) → decreased pumping
* Increased afterload (hypertension) → hypertrophy → eventual failure
* Impaired filling (restrictive cardiomyopathy) → reduced stroke volume
Which “direction” is Left sided Heart Failure classified as?
** FORWARD FAILURE (left side cannot eject blood into the Aorta)
🔄 Forward Perfusion
* Forward perfusion means the amount of blood the left ventricle pumps out into the aorta and systemic circulation to supply the body’s organs and tissues.
🫀 In Left-Sided Heart Failure:
* Because the left ventricle is weak or stiff, it cannot pump enough blood forward into the body.
* This leads to reduced cardiac output — meaning less oxygen and nutrients reach organs like the brain, kidneys, muscles.
* The body senses this poor forward perfusion as a problem.
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⚠️ Consequences of Poor Forward Perfusion
* Symptoms of low blood flow: fatigue, weakness, dizziness, poor kidney function (less urine output)
* The body tries to compensate by:
* Activating the sympathetic nervous system (increases heart rate & contractility)
* Activating the renin-angiotensin-aldosterone system (RAAS) → fluid retention to increase preload
* But these compensations can make heart failure worse by increasing workload on the heart.
- Pulmonary Edema results
What are mechanisms leading to mechanisms leading to Left-Sided Heart Failure (LSHF)?
⚙️ Mechanisms of Left-Sided Heart Failure
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- Decreased Ventricular Contraction (Systolic Dysfunction)
The heart muscle’s ability to contract and pump blood is reduced due to:
* Myocardial infarction (MI): Dead heart muscle replaced by scar tissue → weaker contraction
* Myocardial fibrosis: Scarring from various causes → stiff, weak muscle
* Myocarditis: Inflammation damaging heart muscle
* Cardiomyopathy: Diseases weakening heart muscle (e.g., dilated cardiomyopathy)
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- Noncompliant Ventricle (Diastolic Dysfunction)
The ventricle becomes stiff and can’t fill properly during relaxation (diastole) because of:
* Concentric Left Ventricular Hypertrophy (LVH): Thickened walls reduce chamber size and compliance
* Infiltrative diseases: Deposition of abnormal substances in muscle
* Amyloidosis (amyloid deposits)
* Hemochromatosis (iron overload)
* Glycogen storage diseases (e.g., Pompe’s disease)
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- Increased Workload on the Heart
The heart faces extra strain from either pressure or volume overload:
* Increased Afterload (Pressure Overload):
* Systemic hypertension → heart pumps against higher resistance
* Increased Preload (Volume Overload):
* Mitral regurgitation → excess blood volume returning to the left ventricle
What are Clinical signs of Pulmonary Congestion (Pulm. Edema) caused by LSHF?
🫁 Clinical Signs of Pulmonary Congestion / Pulmonary Edema
- Symptoms
- Dyspnea (shortness of breath), especially on exertion
- Orthopnea: Difficulty breathing when lying flat (due to increased venous return worsening lung congestion)
- Paroxysmal Nocturnal Dyspnea (PND): Sudden nighttime episodes of severe breathlessness that wake the patient up
- Physical Examination Findings
- Crackles (rales): Fine, moist sounds heard on lung auscultation, especially at lung bases
- Tachypnea: Rapid breathing due to low oxygen levels
- Cough: Often with frothy sputum, sometimes pink-tinged (if severe edema causes capillary rupture)
- Laboratory / Microscopic Findings
- ‘Heart failure cells’: Macrophages in the lungs containing hemosiderin (brown pigment) due to breakdown of red blood cells from capillary leakage — a sign of chronic pulmonary congestion
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🔑 Why These Signs Occur:
* Left heart failure → increased left atrial pressure → pulmonary venous congestion → fluid leaks into alveoli → impaired gas exchange → symptoms/signs above.
Does LSHF lead to decreased blood flow (perfusion) to the kidneys?
Yes, in left-sided heart failure, there is often decreased blood flow (perfusion) to the kidneys. Here’s why and what happens:
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🩸 Decreased Kidney Perfusion in Left-Sided Heart Failure
* When the left ventricle fails to pump effectively, less blood is delivered to the systemic circulation, including the kidneys.
* This results in reduced renal blood flow.
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🔄 Consequences
1. Activation of RAAS (Renin-Angiotensin-Aldosterone System):
* Kidneys sense low perfusion → release renin
* Leads to formation of angiotensin II → vasoconstriction + aldosterone release → salt and water retention
* This increases blood volume, which initially helps maintain cardiac output but later worsens heart failure by increasing preload and congestion.
2. Decreased urine output (oliguria):
* Kidneys try to conserve fluid due to perceived low blood volume.
3. Worsening edema and congestion:
* Fluid retention leads to swelling in legs, lungs, and abdomen.
What are key signs and symptoms in Left-Sided Heart Failure (LSHF)?
💓 Heart Sounds and Murmurs in LSHF
- Left-Sided S3 Heart Sound
- What: Extra heart sound heard early in diastole (right after S2)
- Cause: Blood rushing into a volume-overloaded and dilated left ventricle
- Significance: Often the first cardiac sign of left heart failure
- Note: Intensity increases with expiration (because expiration increases venous return to the left heart)
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- Mitral Valve Regurgitation Murmur
- Cause: Stretching of the mitral valve annulus due to left ventricular dilation → valve leaflets don’t close properly
- Sound: Pansystolic (holosystolic) murmur best heard at the apex of the heart
- Changes with respiration: Murmur gets louder during expiration
- Reason: Expiration increases venous return from pulmonary veins to the left heart → more volume leaks back through the incompetent valve
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🌙 Symptoms Related to Venous Return and Pulmonary Congestion
- Paroxysmal Nocturnal Dyspnea (PND)
- What: Sudden episodes of severe breathlessness and choking sensation at night
- Cause: Lying down increases venous return to the failing left ventricle → heart can’t handle the volume → blood backs up into lungs → pulmonary edema
- Relief:
- Sitting up or standing reduces venous return via gravity
- Using pillows to prop up the head (orthopnea) helps ease breathing by reducing blood volume returning to the heart
What is difference between S2/S3/S4 sounds?
S2 = “Dub” sound (normal)
* Happens when the aortic and pulmonary valves close after the heart pumps blood out.
* It’s the normal “dub” you hear in “lub-dub.”
* Usually not a problem—just tells you the heart finished pushing blood out.
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S3 = Extra sound after “dub” (lub-dub-S3)
* Happens right after S2, early when blood rushes into the heart.
* Means the heart’s left ventricle is stretched out or overloaded with blood — like a balloon getting too full.
* Happens in:
* Heart failure (especially left-sided, where the heart can’t pump well)
* Dilated cardiomyopathy (heart muscle is weak and big)
* Mitral valve regurgitation (valve leaks, causing more blood to flow back and overload the heart)
* You can think of it as a “sloshing-in” sound because the ventricle is too full.
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S4 = Extra sound before “lub” (*S4-lub-dub)
* Happens just before the normal first heart sound (S1, the “lub”), when the atrium squeezes to push blood into the ventricle.
* Means the ventricle is stiff or thick and doesn’t relax well, so the atrium has to push harder.
* Happens in:
* Hypertrophic cardiomyopathy (heart muscle is thick)
* Hypertension causing thick heart muscle (concentric hypertrophy)
* Restrictive cardiomyopathy (heart muscle stiff and hard to fill)
* Think of it like the atrium struggling to push blood into a tight ventricle.
Why it matters for you
* If you hear S3 → heart is struggling with too much blood volume (failing heart or valve leak)
* If you hear S4 → heart muscle is stiff or thick, making it hard to fill
* S2 is normal but can change if valves or pressures are off
