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Green Patho > Cardiovascular Post MidTerm > Flashcards

Cardiovascular Post MidTerm Flashcards

1
Q

What is endocarditis?

A

Inflm of of the endocardium and valves. Normally caused by bacterial infection

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2
Q

What are the 3 challenges facing bacteria trying to infect the heart?

A

1) bacteria must enter into the circulation CVS (Cardio Vascular system)
2) and must survive immunity (your defenses must be compermised)
3) must have an adherence/adhesion surface (because the heart is smooth muscle)

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3
Q

`What might allow bacteria to adhere in the heart. Where are they likely to grow?

A

Sutures/ trauma/ defective valves

Likely to colonize amongst platelets and fibrin

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4
Q

What are the mnfts of endocarditis?

A
  • Those of infection (local and systemic)
  • Impaired heart fx
  • Valvular dysfunction
  • Murmur (whooshing sound)
  • Potential Distal embolization
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5
Q

How might you Dx and Tx endocarditis?

A 
Dx
• C&S to identify microbe (blood)
• Echocardiogram
Tx
• Eradicate microbe (Antibiotics)
• Deal with complication associate with heart dysfunction
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6
Q

What causes Rheumatic heart disease?

A

Rheumatic Fever

Permanent damage to the heart valves, known as rheumatic heart disease (RHD), usually only occurs after multiple attacks but may occasionally occur after a single case of Acute rheumatic fever.

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7
Q

What is rheumatic fever?

Mediator? What is effected?

A

Generally-> Rheumatic fever, also known as acute rheumatic fever (ARF), is an inflammatory disease that can involve the heart (RHD), joints, skin, and brain. The disease typically develops two to four weeks after a throat infection

1) acute immune-mediated, multi system inflm disease
2) ∼ 3% incidences (5-15 year olds mostly)
3) preceded (1-4 wks) by strep infection (pharynx)
4) Abs and T cells attack strep
5) Also attack antigens in heart and joints (molecular mimicry Auto Immune Attack)
6) Also affects joints, CNS, and integument

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8
Q

What is RHD?

difference between acute and chronic RHD?

A

inflm of valves, myocardium, pericardium The acute form is self-limiting but you must closely monitor and treat the infection otherwise death

NOTE-
The majority of morbidity and mortality associated with rheumatic fever is caused by its destructive effects on cardiac valve tissue.` The pathogenesis of RHD is complex and not fully understood, but it is known to involve molecular mimicry and genetic predisposition that lead to autoimmune reactions.

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9
Q

What is the Tx for RHD?

A
  • Penicillin or erythromycin (no infection in heart- autoimmunity and inflm)
  • Decrease cardiac work load (bed rest)
  • Symptomatic management (pain, swelling)
  • Monitor for cardiac failure
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10
Q

What is Congestive Heart failure?

Is it a Disease?

A

Congestive = pooling of blood from ineffective pumping action (pools in chambers, systemic circuit, pulmonary circuit)

Not in itself a disease, however is the endpoint of serious heart disease

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11
Q

Common Etiology of CHF

A
  • MI
  • Cardiomyopathy
  • Persistent or Excessive cardiac workload
  • Valvular disease
  • Hypervolemia
  • Uncontrolled HTN
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12
Q

Risk factors for developing Heart Failure?

A 
HTN*
Ischemic Heart Disease*
Diabetes Type 1 & 2
Hyperlipidemia
smoking
obesity
older age
sex ethnicity
Alcohol abuse
Excessive salt intake
Cardiotoxic agents
Family history
Low ejection fraction*
impaired diastolic fx
left ventricle hypertrophy
Elevated neurohormonal biomarkers
Abnormal electrocardiogram
Increased cardiothoracic ratio
Microabluminouria
Elevated resting heart rate
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13
Q

What is Cardiac reserve?

A

Refers to the difference between the rate at which the heart pumps blood and its maximum capacity for pumping blood at any given time

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14
Q

What is the difference between cardiac reserve in healthy heart or weak/compromised heart?

A

Healthy= heart can inc cardiac output 5x resting level, Weak/compromised heart= very limited cardiac reserve

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15
Q

How does Left sided heart failure commonly manifest?

A

Pulmonary congestion and Pulmanary edema

Text:
Decreased cardiac output (activity intolerance + signs of decreased tissue perfusion), impaired gas exchange, orthopnea, cough and sputum

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16
Q

Common Mnfst of Right side heart failure?

A

Systemic congestion, Peripheral edema, Abd organ distention

Text:
Specifically liver congestion, ascites/edema, GI tract congestion, GI distress (weight loss, anorexia)

17
Q

Pathology of Left Ventricle Failure

A
  • LV does not eject sufficient volume -> residual volume in Left ventricle -> LA pumps harder to empty blood in LV -> fails to empty fully -> LA unable to receive full pulmonary return -> pulmonary congestion and edema -> RV workload increases -> RV hypertrophy
  • RV failure usually follows LV failure
18
Q

Why might someone be asymptomatic with CHF?

A

Due to compensatory factors limiting manifestations until disease is well progressed

19
Q

Name 6 compensatory mechanisms in response to CHF

A

Compensator mechanisms:

1) Ventricle dilation (Frank-Starling Law)
2) SNS (Sympathetic Nervous System)
3) Renin-Angiotension Loop
4) Natriuretic Peptides (ANP & BNP)
5) Endothelins
6) Hypertrophy & remodeling

20
Q

Describe Ventricle dilation (Frank-Sterling law) as compensatory mechanism

A

Inc End-Diastolic Volume (due to pooling)→muscle stretch→inc preload→inc CO
If long term:
1) overstretch of chamber wall
2) inc 02 req for the heart, d/t inc muscle from inc use

Compensation will only last so long before other issues reduce efficacy

21
Q

Describe SNS (Sympathetic Nervous System) as a compensatory mechanism?

Hormones invovlved

A

Activated by dec CO Causes: (Baroreceptors?)

1) vasoconstriction
2) tachycardia
3) inc contractility All lead to inc CO

Catecholamines- epinephrine and norepinephrine

22
Q

Describe Renin-Angiotension Loop as a compensatory mechanism for CHF?


A

Cardiac failure→dec renal perfusion→R-A loop triggered→angiotension 2→aldosterone (retains Na+)
→ hypervolemia (water follows) →inc preload (inc bp) → inc CO
(∼25% of CO goes through kidney, if heart fails only 10% goest to kidneys causing renin angiotesion loop)

23
Q

Describe the Natriuretic Peptides (ANP & BNP) as a compensatory mechanism?

Where do they come from?
When do they “kick IN”?

A

ANP from atrial wall, BNP from ventricular wall, both released in the heart.
(When volume of blood gets too high from R-A loop, this natriuretic peptide kicks in)

  • Potent diuresis (removal of fluid from blood/circulation) & natriuresis (excretion of Na+ in the urine)
  • Affect on smooth muscle in the walls of the vessel

Effect is to inhibit RAAS and Sympathic response

24
Q

Describe Endothelia’s as a compensatory mechanism in CHF

A

Released by endothelial cells, line blood vessels and cardiac muscle cells release as well

  • vasoconstriction (inc bp)
  • growth factors that→hypertrophy and proliferation of smooth muscles (helps with contraction, but needs more space∴fluid to move out to the lungs)
25
Q

Describe Hypertrophy and Remodelling

A
  • inc demand/workload→hypertrophy, but you can’t keep up with the inc demand∴ eventually dec contractility
  • inc O2 req for heart
  • myocardial dysfuction

LONG TERM

26
Q

Do compensatory factors always work to the advantage of patient with CHF?

A

No

Many quickly become maladaptive and contribute to deterioration of heart fx.

27
Q

Mnfts of uncompensated Heart Failure?

A

• Various (as with MI, shock, decreased CO, increased HR)
- Effects of impaired pumping
- kidneys deprived of enough blood to filter, dec.
kidney perfusion→build up of waste and possible
kidney failure
- SNS responses (eg/ tachycardia, vasoconstriciton)
- Risk factors, Hx, Px (physical exam)

TEXT:
Cheyne stokes Resp, Acute Pulmonary Edema, Fatigue, Weakness, Fluid retention, Arrhythmias and sudden Cardiac death

28
Q

Potential Dx tests for uncompensated Heart failure?

A
  • Lab tests (renal fx, WBC, electrolytes)

- ECG, ecocardiogram

29
Q

Tx for Hear Failure?

A
  • Acute: stabilize and correct cause→prevent death
  • Chronic: relieve mnfts, dec risks, inc fx
  • Sx (repairable defect?)
  • Drugs (drugs that enhance the pump performance of
    the heart eg/ digitalis, drugs that dec workload of heart by giving diuretics→dec bp, eg/ duretics, ace inhibitors)

-> • If Ejection Fraction > 40%
o Tx of cause
o Angiotensin receptor blocker (if symptomatic with activity)
o Increase dose or add diuretic if sympt at rest

Systolic Heart failure (ejection fraction EF

30
Q

What is Pericarditis?

A

inflammation of the pericardial membrane

NOTE:
The pericardium is a double-walled sac containing the heart and the roots of the great vessels. The pericardial sac has two layers, a serous layer and a fibrous layer. It encloses the pericardial cavity which contains pericardial fluid.

31
Q

ET and Pathology of Pericarditis

A

ET - d/t infect, injury

- inflm→inc capillary permeability→exudate into
pericardial space (space between the heart wall and the pericardium)→heart can’t fill adequately→dec Cardiac Output
32
Q

What is constrictictive pericarditits?

A

fibrinious scar tissue that restricts cardiac fx

33
Q

3 MNFTS (Triad) of pericarditis

A

1) Chest Pain (worsened by respiration, as lungs expand for the breath they take up space & movement)
2) Friction (pericardial) Rub (you can hear this, its audible)
3) ECG changes

34
Q

Tx for Pericarditis?

A
  • based on cause
  • antibiotics if infection
  • anti-inflammatory drugs
  • note: pericarditis can lead to cardiac tamponade
35
Q

What is the Cardiac Tamponade?

A

external compression on the heart
- d/t accumulation of fluid, pus, air in pericardial
space
- restricts inflow and outflow of blood

Can be life threatening

36
Q

MNFTS of Cardiac Tamponade

A
  • Dec cardiac output
  • Dec arterial pressure
  • Temporary Tachycardia
37
Q

Tx of Cardiac Tamponade?

A

Must remove fluid quickly→pericardiocentesis (removal of fluid via large needle through the chest)

Green Patho (18 decks)

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