Heart Failure Flashcards

1
Q

What is Congestive Heart Failure?

A

Congestive Heart Failure (CHF), is a common usually progressive condition with poor prognosis. It occurs when the heart is unable to pump blood at a rate sufficient to meet metabolic demands of the tissue. It can develop insidiously from the cumulative effects of a series of problems like valve disease, hypertension, ischemic heart disease etc. It can also be acute such as an abrupt valvular failure or MI.

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2
Q

What is cardiac hypertrophy and why is it important?

A

Sustained increase in mechanical work due to pressure or volume overload cause myocytes to increase in size cumulatively, this induces increase in size and weight of the heart.

In pressure-overload hypertrophy due to hypertension or aortic stenosis, new sarcomeres are predominantly assembled in parallel to the long axes of cells, expanding the cross-sectional area of myocytes in ventricles and causing a concentric increase in wall thickness.

In contrast, volume-overload hypertrophy is characterized by new sarcomeres being assembled in series within existing sarcomeres, leading primarily to ventricular dilation.

Hypertrophy is not accompanied by proportional increase of capillaries, therefore blood supply and nutrients. An hypertrophied heart has higher metabolic demands and thus is at a higher risk of ischemic related issues that could lead to death.

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3
Q

Why is hypertrophy dangerous for the cardiac tissue?

A

A hypertrophied heart demands a high quantity of oxygen and nutrients due to its increase in mass, HR and contractility. As a result it is more vulnerable to ischemia related issues which in turn can lead to CHF. This happens also because there is not a proportional increase of capillaries feeding the cardiac tissue. In addition hypertrophy is often accompanied by interstitial fibrosis.

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4
Q

Left Sided Heart Failure?

A

It is most often caused by ischemic heart disease, hypertension, aortic an mitral valve disease and cardiomyopathies. Clinically it is due to passive congestion in the pulmonary circulation, stasis of left sided chambers and inadequate perfusion downstream. Macroscopically the left ventricle is often hypertrophied and dilated. Histologically there is alveolar edema and hemosiderin contains cells in the alveoli.

Early symptoms include cough and dyspnea. As it progresses atrial fibrillation, diminished renal perfusion and later on also cerebral hypoperfusion.

Left sided heart failure can be divided into systolic and diastolic.

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5
Q

What is systolic failure?

A

Defined as a decrease in the amount of blood ejected from the ventricle during systole. Ejection fraction can decrease because of ischemic injury, valvular disease or ventricular dilation.

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6
Q

What is Diastolic Failure?

A

The ventricle is abnormally stiff and cannot relax during diastole. Since the ventricle is not able to expand it cannot fill adequately so pressure is transferred back into the pulmonary circulation causing pulmonary edema.

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7
Q

Right Sided Heart failure?

A

It is most commonly caused by left sided heart failure. Isolated right sided heart failure is a possibility but very infrequent and occurs in patients that have disorder affecting the lungs such as obstructive sleep apnea, emphysema. The common feature is pulmonary hypertension. The major morphological clinical effects that differ from left sided heart failure are that pulmonary congestion is minimal while engorgement of systemic and portal venous system is pronounced. Standard therapy is diuretics, ACEi and beta blockers.

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8
Q

What is the definition of Ischemic Heart Disease?

A

IHD defines a group of pathophysiologically related syndromes resulting in myocardial ischemia. Ischemia limits tissue oxygenation, availability of nutrients and removal of metabolic waste. It is mostly a consequence of reduced coronary blood flow due to obstructive artherosclerotic vascular disease, thus in most cases there is a long buildup period. IHD is still the leading cause of death in developed countries, although it has decrease over the years. Prevention like modifying important risk factors like smoking, blood LDL, and hypertension, exercise etc. has helped.
Manifestations of IHD are :
• Angina Pectoris : Pain and can be stable or unstable which means even at rest.
• MI: the severity and duration can cause cell death.
• Chronic IHD with CHF : progressive cardiac decompensation after MI, heart eventually fails.
• Sudden Cardiac Death : Consequence of tissue damage from MI.

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9
Q

What is Angina Pectoris and what are the different types?

A

Sudden and recurrent attacks of substernal or precordial chest discomfort caused by transient myocardial ischemia that is insufficient to cause myocyte death.

• Stable Angina : pressure, burning sensation that is relieved at rest or by administering vasodilators like nitroglycerin.
• Prinzmetal Angina : Caused by coronary artery spasm. It responds well to vasodilators.
• Unstable Angina : ACS, characterized by long episodes even at rest, acute MI may be imminent.

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10
Q

What is the definition of Myocardial Infarction?

A

It is defined as the event in which prolonged ischemia causes myocyte necrosis. The major cause is artherosclerosis. Clinically it is recognizable by severe crushing sub sterna chest pain or pressure that can radiate to the neck, jaw and left arm. Unlike angina pectoris the pain is prolonged, more than 30 min. The pulse is weak and rapid, patients have nausea and vomiting, also dyspnea.

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11
Q

What is the pathogenesis of MI?

A

90% of the cases it is caused by coronary artery occlusion. In about 10% of the cases it may occur in absence of coronary artherothrombosis as be caused by vasospasm, emboli or small disorders of coronary vessels such as vasculitis.

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12
Q

What is the flow of events after an MI?

A

The cessation of aerobic metabolism and ATP depletion within seconds, loss of contractility in about 2 minutes, glycogen depletion and mitochondrial swelling and after 20/40 min we have irreversible cell injury. Necrosis involves half of the thickness of the myocardium in 2 to 3 hours and full transmural thickness in 6 hours.

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13
Q

What are the most common Coronary arteries involved in MI and what do they affect?

A

Occlusion of the LAD artery is the cause of 40/50% of all MIs and results in infarction of anterior wall of LV, anterior 2/3 of ventricular septum and most of apex.

Occlusion of LCX artery is the cause of 10/15% of all MIs results in necrosis of the lateral LV.

Occlusion of RCA is the cause of 30/40% of all MI2 and affects the RV.

Occlusion of left main CA, aka widow maker, so much myocardial territory is supplied that an obstruction is typically fatal.

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14
Q

What is a Transmural Infarction?

A

Caused by occlusion of epicardial vessels and necrosis involves the full thickness of the ventricular wall.

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15
Q

What is Subendocardial Infarction?

A

Typically involves inner third of the ventricular wall, area poorly perfused so it is vulnerable to any reduction in blood flow.

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16
Q

What is a Multifocal Microinfarction?

A

Involves smaller intramural vessels. It may occur because of microemboli, vasculitis or vascular spasm.

17
Q

Morphological changes after MI?

A

Macroscopically :

Less that 12 hours it is not grossly apparent however you can stain for lactate dehydrogenase. After 12 to 24 hours it can be identified by a red blue discoloration caused by trapped blood. By the 10th-14th day infarcts are rimmed by highly vascularized granulation tissue which over the few weeks evolves to fibrous scar.

Microscopically :

Within 4 to 12 hours wavy fibers are observable at the edges of infarct and reflect the dead fibers. After a few days macrophages and neutrophils are observable due to acute inflammation. Finally after a few weeks the tissue is replaced by collagenous scars.

Once it has healed it is impossible to distinguish its age.

18
Q

What is reperfusion?

A

Consists in the restoration on blood flow to a ischemic myocardium threatened by infarction. Intervening asap improves short and long term survival and also myocyte function. It can be accomplished by thrombolysis, angioplasty, stent placement, and coronary artery bypass graft surgery (CABG).

Of course reperfusion can cause injury. It has been estimated that up to 50% of the ultimate infarct size can be attributed to its effects. Reperfusion injury may be mediated by oxidative stress, calcium overload and recruitment of inflammatory cells after reperfusion.

19
Q

Markers used to identify MI?

A

Lab Tests : Molecules taken into account include myoglobin, cardiac troponins T and I, creatine kinase and lactate dehydrogenase. Diagnosis is established only when these markers are elevated over the reference limit.

CK-MB rises after 2 to 4 hours within MI, peaks at 24 to 48 and returns normal after 72. While cardiac troponins are normally not found in circulation, are detectable after 2 to 4 hours and remain elevated for 7 to 10 days.

20
Q

STEMI vs NSTEMI?

A

A transmural infarct is sometimes referred to an ST Elevation Myocardial Infarct (STEMI) and a subendocardial infarct is aka Non-ST Elevation Infarct (NSTEMI).

ECG findings in NSTEMI : Does not show ST segment elevation and does not progress to Q wave.

ECG findings in STEMI : Shows ST segment elevation and progresses to Q wave.

21
Q

What are some common complications after MIs? What are some post MI therapies?

A

75% of patients experience one or more of the following :

• Contractile dysfunction
• Papillary muscle dysfunction
• Myocardial rupture
• Arrhythmias
• Pericarditis

The risk of developing further complications depends on the infarct size, site and type.
Therapy : Interventions include morphine and prompt reperfusion, anti platelet agents (aspirin), anti coagulant agents (heparin), anti arrhythmics like beta blockers.