Cardiovascular Post MidTerm Flashcards
What is endocarditis?
Inflm of of the endocardium and valves. Normally caused by bacterial infection
What are the 3 challenges facing bacteria trying to infect the heart?
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)
`What might allow bacteria to adhere in the heart. Where are they likely to grow?
Sutures/ trauma/ defective valves
Likely to colonize amongst platelets and fibrin
What are the mnfts of endocarditis?
- Those of infection (local and systemic)
- Impaired heart fx
- Valvular dysfunction
- Murmur (whooshing sound)
- Potential Distal embolization
How might you Dx and Tx endocarditis?
Dx • C&S to identify microbe (blood) • Echocardiogram Tx • Eradicate microbe (Antibiotics) • Deal with complication associate with heart dysfunction
What causes Rheumatic heart disease?
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.
What is rheumatic fever?
Mediator? What is effected?
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
What is RHD?
difference between acute and chronic RHD?
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.
What is the Tx for RHD?
- Penicillin or erythromycin (no infection in heart- autoimmunity and inflm)
- Decrease cardiac work load (bed rest)
- Symptomatic management (pain, swelling)
- Monitor for cardiac failure
What is Congestive Heart failure?
Is it a Disease?
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
Common Etiology of CHF
- MI
- Cardiomyopathy
- Persistent or Excessive cardiac workload
- Valvular disease
- Hypervolemia
- Uncontrolled HTN
Risk factors for developing Heart Failure?
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
What is Cardiac reserve?
Refers to the difference between the rate at which the heart pumps blood and its maximum capacity for pumping blood at any given time
What is the difference between cardiac reserve in healthy heart or weak/compromised heart?
Healthy= heart can inc cardiac output 5x resting level, Weak/compromised heart= very limited cardiac reserve
How does Left sided heart failure commonly manifest?
Pulmonary congestion and Pulmanary edema
Text:
Decreased cardiac output (activity intolerance + signs of decreased tissue perfusion), impaired gas exchange, orthopnea, cough and sputum
Common Mnfst of Right side heart failure?
Systemic congestion, Peripheral edema, Abd organ distention
Text:
Specifically liver congestion, ascites/edema, GI tract congestion, GI distress (weight loss, anorexia)
Pathology of Left Ventricle Failure
- 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
Why might someone be asymptomatic with CHF?
Due to compensatory factors limiting manifestations until disease is well progressed
Name 6 compensatory mechanisms in response to CHF
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
Describe Ventricle dilation (Frank-Sterling law) as compensatory mechanism
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
Describe SNS (Sympathetic Nervous System) as a compensatory mechanism?
Hormones invovlved
Activated by dec CO Causes: (Baroreceptors?)
1) vasoconstriction
2) tachycardia
3) inc contractility All lead to inc CO
Catecholamines- epinephrine and norepinephrine
Describe Renin-Angiotension Loop as a compensatory mechanism for CHF?

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)
Describe the Natriuretic Peptides (ANP & BNP) as a compensatory mechanism?
Where do they come from?
When do they “kick IN”?
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
Describe Endothelia’s as a compensatory mechanism in CHF
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)
