Cardiovascular diseases Flashcards

1
Q

What is heart failure, and what are its causes?

A

Heart failure is a condition where the heart is unable to pump blood efficiently, leading to reduced cardiac output and congestion. Common causes include hypertension, coronary artery disease, ischemic heart disease, dilated cardiomyopathy, and valvular heart disease.

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2
Q

What is “Heart Failure with reduced ejection fraction” ?

A

It is heart failure with reduced left ventricular pump function. Heart failure is not a disease but a syndrome – a combination of signs and symptoms – caused by the failure of the heart to pump blood to support the circulatory system at rest or during activity.

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3
Q

What is the pathophysiology of heart failure?

A

The heart struggles to pump blood, leading to neurohormonal activation (e.g., RAAS, sympathetic nervous system). This causes fluid retention, cardiac remodeling, and reduced cardiac output. The heart may enlarge or thicken, and fluid accumulates in the lungs or systemic circulation, causing edema.

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4
Q

What are the clinical manifestations of heart failure?

A

Symptoms include fatigue, difficulty exercising, pulmonary congestion (dyspnea, orthopnea), systemic edema (swelling, weight gain), tachycardia, and reduced cardiac reserve.

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5
Q

What is the pathophysiology of chronic (not acute) heart failure with reduced ejection fraction

A

Heart failure is caused by any condition that reduces the efficiency of the heart muscle, through damage or overloading. Over time, these increases in workload, which are mediated by long-term activation of neurohormonal systems such as the renin–angiotensin system and the sympathoadrenal system, lead to fibrosis, dilation, and structural changes in the heart

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6
Q

Explain the hemodynamics and the occurrence of “shortness of breath” in a patient with heart failure with reduced pump function of the left ventricle

A

The left side of the heart receives oxygen-rich blood from the lungs and pumps it to the rest of the circulatory system in the body. Failure of the left side of the heart causes blood to back up into the lungs (congestion).

Exertion-induced shortness-of-breath (when walking or active, as activity of large muscle groups require a larger cardiac output, which the failing heart cannot match).Cyanosis.

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7
Q

What are the typical signs of a patient with heart failure with backward failure of the right ventricle.

A
  • pitting peripheral edema or anasarca
  • ascites
  • liver enlargement
  • spleen enlargement
  • Elevated central venous pressure/ dilated jugular veins
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8
Q

What is ischemic heart disease, and what causes it?

A

Ischemic heart disease occurs when the heart’s oxygen supply is insufficient due to obstruction (usually from atherosclerosis). It results in chest pain (angina pectoris) and, if severe, myocardial infarction.

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9
Q

What is the pathophysiology of ischemic heart disease?

A

Atherosclerosis causes plaque buildup, narrowing coronary arteries, reducing blood flow, and leading to ischemia. Plaque rupture can form a clot, further obstructing blood flow and triggering myocardial infarction.

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10
Q

What are the clinical manifestations of ischemic heart disease?

A

Clinical signs include chest pain (angina), shortness of breath, nausea, and sweating. Severe cases may result in acute coronary syndrome or myocardial infarction

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11
Q

What is atherosclerosis?

A

Atherosclerosis is a chronic inflammatory condition where plaque (comprised of fat, cholesterol, and other substances) builds up inside the arterial walls, leading to thickening and narrowing of arteries. This restricts blood flow and can cause ischemia, leading to complications like heart attack and stroke.

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12
Q

What causes atherosclerosis?

A

The primary cause is endothelial dysfunction, often triggered by factors like:

High LDL cholesterol
Hypertension
Smoking
Diabetes
Obesity
Chronic inflammation
Non-modifiable risk factors include age, sex, and family history.

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13
Q

How does Atherosclerosic develop lesions as a progressive process involving four steps

A

The development of atherosclerotic lesions is a (progressive) process involving (a) endothelial cell injury, (b) migration of inflammatory cells, (c) (SMC proliferation and) lipid deposition, and (d) (gradual) development of the atheromatous plaque (with a lipid core).

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14
Q

What is the pathophysiology of atherosclerosis?

A

Endothelial injury: Damaged endothelial cells allow lipids (especially LDL cholesterol) to penetrate the arterial wall.

Inflammatory response: Monocytes are attracted to the site of injury and transform into macrophages, which ingest lipids and become foam cells.

Plaque formation: Foam cells release cytokines and growth factors that lead to smooth muscle cell migration and collagen deposition, forming a fibrous plaque.

Plaque rupture: If the fibrous cap is weakened, the plaque may rupture, exposing its contents to the bloodstream, which triggers thrombosis (blood clot formation).

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15
Q

What is a vulnerable plaque in atherosclerosis?

A

A vulnerable plaque is a type of atherosclerotic plaque that has a large lipid core and a thin fibrous cap. These plaques are more likely to rupture, leading to the formation of a blood clot and obstructing blood flow, which can result in acute cardiovascular events like heart attacks or strokes.

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16
Q

What are the clinical manifestations of atherosclerosis?

A

Atherosclerosis is often asymptomatic until a significant event occurs. Manifestations may include:

Angina pectoris (chest pain due to ischemic heart disease)
Myocardial infarction (heart attack)
Stroke (due to cerebral artery obstruction)
Peripheral artery disease (leg pain or claudication)
Aneurysms (e.g., abdominal aortic aneurysm)

17
Q

When (time course) do the clinical manifestations typically occur for a patient?

A

Clinical manifestations of atherosclerosis typically do not become evident for (20) years (or longer).

18
Q

What is hypertension, and what are its types?

A

Hypertension is high blood pressure, often above 140/90 mmHg.

It can be primary (no underlying cause) or

secondary (caused by other conditions like kidney disease or hormonal disorders).

19
Q

What are the risk factors for hypertension?

A

Non-modifiable risks include age (risk increases with age), sex (higher prevalence in men), and family history (seen more with family members also having it).

Modifiable risks include diet (high sodium and fat), smoking, alcohol consumption, obesity, and physical inactivity.

20
Q

What are the clinical manifestations of primary hypertension?

A

Often asymptomatic,

High blood pressure can damage organs and blood vessels, raising the risk of atherosclerosis and further reducing blood flow, especially to organs needing good circulation.

21
Q

What are the clinical manifestations of secondary hypertension?

A

chronic hypertension can lead to organ damage, causing angina, heart failure, stroke, kidney disease, and retinopathy.

22
Q

What is circulatory shock?

A

Circulatory shock is an acute failure of the circulatory system to supply the peripheral tissues and organs of the body with an adequate blood supply, resulting in cellular hypoxia.

23
Q

What are the four causes of circulatory shock

A

It can be caused by
1. hypovolemia (a decrease in blood volume )
2. cardiogenic failure (an alteration in cardiac function)
3. distributive shock (excessive vasodilation with maldistribution of blood flow)
4. obstruction of blood flow through the circulatory system (obstructive shock)

24
Q

What is the pathophysiology of circulatory shock?

A

Shock leads to anaerobic metabolism (lactate production) and ATP depletion, disrupting fluid balance and causing cellular swelling. Blood flow to vital organs (heart, brain) is initially preserved but eventually fails, leading to organ damage.

25
Q

What are the stages of circulatory shock?

A
  1. Non-progressive state (compensated): Vital organs are maintained, though non-vital organs may show signs of ischemia.
  2. Progressive state (uncompensated): Organ perfusion decreases, leading to tissue breakdown and hypotension.
  3. Irreversible stage: Organ failure becomes severe, and death is imminent.
26
Q

What is the pathophysiology Hypovolemic shock:

A

Hypovolemic shock is caused by a loss of blood, plasma, or extracellular fluid (e.g., hemorrhage, burns, or dehydration). This leads to reduced blood volume, decreased venous return, and inadequate filling of the heart, resulting in low cardiac output and poor tissue perfusion.

27
Q

What is the pathophysiology Cardiogenic shock:

A

Cardiogenic shock occurs due to the heart’s inability to pump blood effectively, leading to decreased cardiac output (CO) and tissue hypoxia despite adequate blood volume. Causes include myocardial infarction (MI), arrhythmias, and cardiac surgery. It results in poor myocardial contractility, increased preload and afterload, and impaired coronary perfusion, worsening cardiac function.

28
Q

What is the pathophysiology of Distributive shock?

A

In distributive shock (e.g., septic, anaphylactic, neurogenic), blood vessels lose tone, causing vasodilation and expansion of the vascular compartment. This redistributes blood away from the central circulation, resulting in inadequate tissue perfusion despite normal or increased blood volume.

29
Q

What is the pathology of Obstructive shock?

A

Obstructive shock occurs when mechanical obstruction (e.g., pulmonary embolism, cardiac tamponade, or pneumothorax) blocks blood flow through the heart or lungs. This causes increased right heart pressure, reduced venous return, and signs of right-sided heart failure, such as jugular vein distention.

30
Q

What does a normal ECG show?

A

A normal ECG includes:

P wave: Atrial contraction
PR interval: Time for impulse travel from atria to ventricles (0.12–0.20 s)
QRS complex: Ventricular contraction (less than 0.12 s)
ST segment: Flat
T wave: Ventricular recovery
QT interval: Time from ventricular contraction to recovery (0.35–0.45 s)
Normal heart rate: 60–100 bpm with regular rhythm.

31
Q

What is atrial fibrillation (AFib)?

A

AFib is an irregularly irregular rhythm with no distinct P waves. It leads to ineffective atrial contraction, increasing the risk of clot formation and stroke.

32
Q

What is atrial flutter?

A

Atrial flutter is characterized by rapid, regular atrial contractions (250-350 bpm), seen as “sawtooth” P waves. The ventricular rate is typically slower than the atrial rate, often 2:1 block.

33
Q

What is ventricular tachycardia (VT)?

A

VT is a fast rhythm originating from the ventricles, characterized by wide QRS complexes (>0.12 s). It can lead to hypotension, syncope, and cardiac arrest.

34
Q

What is ventricular fibrillation (VF)?

A

VF is a chaotic, erratic rhythm with no identifiable QRS complexes, P waves, or T waves. It leads to cardiac arrest and requires immediate defibrillation.

35
Q

What is the pathway of blood through the heart and lungs?

A

Deoxygenated blood enters the right atrium from the body (via the superior and inferior vena cava).
Blood passes through the tricuspid valve into the right ventricle.
The right ventricle pumps blood through the pulmonary valve into the pulmonary arteries.
Blood travels to the lungs for oxygenation.
Oxygenated blood returns to the heart through the pulmonary veins into the left atrium.
Blood passes through the mitral valve into the left ventricle.
The left ventricle pumps blood through the aortic valve into the aorta and then to the rest of the body.

36
Q

How does increased resistance in the lungs affect the right ventricle?

A

Increased resistance in the lungs (e.g., due to pulmonary hypertension) makes it harder for the right ventricle to pump blood into the pulmonary arteries, potentially leading to right heart failure. If the left ventricle is impaired (heart failure), fluid may accumulate in the lungs, causing pulmonary congestion.