Topic 5.3 - Cardiovascular Disorders III Flashcards
Which fetal structure permits blood flow between the aorta and pulmonary arteries?
Ductus arteriosis
Which fetal structure permits blood flow between the atria?
Foramen ovale
What are some causes of congenital heart malformations?
Both genetic and environmental influences are probable.
Studies show that teratogens may play a bigger role than genetics.
What is a right to left shunt? How else can this be described/classified.
A congenital heart malformation that allows unoxygenated blood to enter systemic circulation and bypass lungs.
aka cyanotic
What is a left to right shunt? How else is this classified/described?
A congenital heart malformation that allows oxygenated blood to flow back into pulmonary circulation. Creates extra work for right side of the heart.
aka acyanotic
How do congenital obstructions in the heart affect the infant? How are they classified?
They are classified as acyanotic and lead to increased workload for the side of the heart affected. Can lead to heart failure.
What is atrial septal defect? How is is classified?
Acyanotic (L-R shunt)
–>Abnormal opening between atria
(Failure of foramen ovale to close)
What kind of effects are seen on the rest of the heart due to an atrial septal defect?
Right side enlargement due to left to right shunting
What is ventricular septal defect? How is it classified?
Acyanotic (L - R shunt)
–> Abnormal communication between ventricles
How does a ventricular septal defect affect the rest of the circulatory system?
Increase in pulmonary flow leads to pulmonary HNT
Where does VSD usually occur?
Near the bundle of His
What is the most common congenital heart anomaly?
VSD
What is PDA? How is it classified?
Acyanotic (L - R defect)
–>Patent ductus arteriosus allows blood from aorta to enter pulmonary arteries
What are some effects of a patent ductus arteriosus?
Increased pulmonary bloodflow leads to increase venous return, which increases workload on the left side of the heart.
Increased pulmonary HNT can also lead to right-sided HF
What is coarctation of the aorta? How is it classified?
Acyanotic
–> Narrowing of aorta, usually just after the ductus arteriosus
What are some effects of coarctation of the aorta?
Low pressure in legs
Can lead to LV HNT + hypertrophy
What is tetralogy of Fallot? How is it classified?
Cyanotic (R - L Shunt)
1. Large VSD
2. Pulmonary stenosis
3. Overriding of aorta that straddles VSD
4. RV hypertrophy
What is transposition of the great arteries? How is it classified?
Cyanotic
–> When two separate, noncommunicating systems are established
–> Usually, the pulmonary arteries attach to the left ventricle, and the aorta attaches to the right
–> Incompatible with life, unless mixing occurs through other defects
What is Truncus arteriosus? How is it classified?
Cyanotic (R - L Shunt)
–> When the aorta and PA establish as one vessel that splits into three arms. All receive blood from both sides of heart and share a single valve due to a VSD
What are some effects of truncus arteriosus?
Increases pulmonary blood flow leads to pulmonary HNT and RV hypertrophy
Increases pulmonary resistance leads to increased cyanosis, because it forces more venous blood back into systemic circulation
What are the most important predisposing risk factors leading to CHF?
ischemic heart disease, HNT, and diabetes
What side of heart failure is most common?
Left-sided, but it will affect both sides over time
What is the commonly used criteria of diagnosis for heart failure? (7)
–> Dyspnea
–> Pulmonary rales
–> Cardiomegaly
–> Pulmonary edema
–> S3 gallop
–> Tachycardia
–> Neck vein distention
What is normal ejection fraction?
60-80%
What is reduced ejection fraction heart failure? What is its etiology?
Systolic heart failure with an EF < 40%
Characterized by reduced contractility, often onset by MI
What is preserved ejection fraction heart failure? What is its etiology?
Inability of LV to fill during diastole with EF > 50%
Often caused by coronary artery disease, HNT, other anomalies that prevent cardiac filling.
how does Left-failure affect pulmonary + systemic circulation?
Backward effects:
Increased pulmonary pressure leads to right ventricular hypertrophy (due to afterload) and pulmonary congestion
Forward effects:
Decreased cardiac output leads to decreased tissue perfusion and RAAS activation –> Fluid retention
Whatare the backward and forward effects of right-side HF?
Backward effects:
Decreased ejection fraction and increased right ventricular preload leads to increased right atrial pressure and systemic congestion
Forward effects:
Decreased output by left ventricle leads to RAAS activation and decreased tissue perfusion.
How does the body compensate for heart failure?
Baroreceptors trigger SNS –> Increased HR and contractility
RAAS activation –> Fluid retention and increased preload
Increased ventricular wall tension leads to myocyte growth and hypertrophy + Remodeling
What might cause dysrhythmia? (both pathological and mechanisms)
Hypoxia, inflammation, electrolyte imbalance, drugs
Caused either by abnormal automaticity or triggered activity
What causes disorders of impulse formation?
Dysfunction of the SA node, can lead to bradycardia or tachycardia
What is sinus tachycardia?
A heart rate >100bpm
Often a compensatory response to increase demand or decreased stroke volume.
What is sinus bradycardia? What causes it?
Heart rate <60 bpm
Causes by PSNS due to sleep, drugs, increased stroke volume or acute HTN.
What is first degree heart block?
A prolonged PR interval
What might cause disorders of impulse conduction?
Ischemia, infection, medication, inherited abnormalities.
What is second degree heart block?
Some p-waves not conducted to ventricles
What is third degree heart block?
No impulses conducted from atria to ventricle, ventricular escape rhythm present.
How is third degree heart block treated?
With a pacemaker
What is atrial flutter? Hows does it appear on an ECG?
Rapid atrial rate of 240-350 bpm
Sawtooth pattern of atrial depolarization present, with slow ventricular rate (VER)
How is atrial fib/flutter treated?
With anticoagulants to prevent the formation of thrombi within atria due to stagnant blood
What might cause v-fib?
MI/ischemia, myocardium damage, high catecholamine levels, abnormal electrolyte balance.
What is shock?
An acute failure of the circulatory system to supply peripheral tissues and organs of the body with adequate blood supply resulting in hypoxia.
What is cardiogenic shock?
Inadequate cardiac output despite sufficient vascular volume - hypotension and tissue hypoperfusion
What causes cardiogenic shock?
Short term consequences of an MI or severe ischemia
What are the clinical manifestations of cardiogenic shock?
Similar to end-stage heart failure
Decreased MAP + SV
Oliguria
Neurological changes
What is obstructive shock? What causes it?
Mechanical obstruction prevents effective cardiac filling and stroke volume, manifests as right side heart failure
Commonly caused by pulmonary embolism, cardiac tamponade, or pneumothorax
What is hypovolemic shock?
Shock caused by loss of blood, plasma, or interstitial fluid in large amounts - heart still functional
What are the clinical manifestation of hypovolemic shock?
Thirst, tachycardia, cool & clammy skin, decreased arterial BP, oliguria, confusion
What percent of intravascular volume can be lost before a person begins experiencing hypovolemic shock?
15%
What is distributive shock?
Shock characterized by excessive vasodilation and peripheral pooling of blood
What are the kinds of distributive shock?
Anaphylactic, neurogenic, and septic
What causes anaphylactic shock?
Excessive mast cell degranulation mediated by IgE in response to hypersensitivity.
What causes neurogenic shock?
Loss of SNS activation of arteriolar SM.
Might be caused by medullary depression due to injury or OD, or lesions in SNS fibers due to injury.
What causes septic shock?
A severe systematic inflammatory response to a bacterial or fungal infection.
What are the three stages of shock?
- Compensatory
- Progressive
- Refractory
What occurs during the compensatory stage of shock?
Body can maintain adequate tissue perfusion despite CO reduction
SNS activation attempts to maintain BP even though cardiac output has fallen –> Increased CO + vascular resistance
What occurs during the progressive stage of shock?
Hypotension and tissue hypoxia present
Lactate production increases with anaerobic metabolism, but eventual lack of ATP leads to cellular swelling, dysfunction, and death
Presence of free radicals, inflammatory cytokines, and activation of clotting cascade
What occurs during refractory shock?
Constriction of splanchnic vessels, release of aldosterone + cortisol, cool & clammy skin with pallor/cyanosis due to reduces capillary refill. Eventual organ failure.
This kind of shock is lethal.
How is shock treated?
Ventilation Support
—> O2 support prevents pulmonary HTN
Fluid Resuscitation
–> Improve microvascular flow
Vasopressors if hypotension persists despite fluid administration
Vasodilators reduce afterload and increase cardiac output without increasing myocardial demand for O2.
Inotropic agents increase CO.
Which vasopressor is chosen to treat shock?
Adrenergic Agonists
–> First line vasopressors due to their rapid onset, high potency, and short-half life.
