Cardiovascular Flashcards
(40 cards)
define action potential
conductivity
excitability
automaticity
deoplarization
action potential: electrical impulses of the heart muscle cells.
conductivity: cells ability to transmit electrical impulses
excitability: cells ability to respond to electrical impulses
automaticity: cardiac cells own ability to contract with no external nerve stimuli. (most pacemaking capacity is in the SA node; high in the RA)
depolarization: contraction of heart cells
Class I (Sodium Channel Blockers)
target?
effect?
sodium enters cell rapidly, calcium enters slowly
target: Na+ channels
effect: slows depolarization
Speed bump slows down impulses
Class II (Beta Blockers)
target?
effect?
Target: Beta-adrenergic receptors
Effect: Slows heart rate & AV node conduction
Example: Metoprolol, propranolol
Analogy: Calms a nervous driver (reduces adrenaline effects)
Class III (Potassium Channel Blockers)
target?
effect?
potassium rapidly out of cell, calcium channel closes
Target: K⁺ channels
Effect: Prolongs repolarization (Phase 3), increases refractory period
Example: Amiodarone, sotalol
Analogy: Longer red light delays next heartbeat
Class IV (Calcium Channel Blockers)
target?
effect?
Target: Ca²⁺ channels
Effect: Slows pacemaker activity and AV node conduction
Example: Verapamil, diltiazem
Analogy: Quieter starter gun delays the race (heartbeat)
define ejection fraction (EF)?
pre-load?
after load?
EF - amount of blood pumped out in each cycle compared to how much is left over at the end of diastole (recovery, refilling, ventricle relaxed)
preload - pressure created in left ventricle by the amount of blood at the end of diastole
afterload - the pressure that the left ventricle must overcome to push blood out. Affected by systemic vascular resistance i.e. HTN
explain the renin-angiotensin-aldosterone system (RAAS)
low BP or low sodium -> release of renin -? activates angiotensin I -> turns into angiotensin II by enzyme called ACE-> vasoconstriction = increase in BP
low sodium = aldosterone secretion = reabsorption of sodium and chloride in kidneys which attracts water and increases blood volume.
what is pericarditis?
pathology pathway
causes? most common?
The pericardial layers become inflamed, and may rub against each other, causing chest pain.
Sometimes extra fluid builds up between the layers — this is called a pericardial effusion.
In severe cases, too much fluid can cause cardiac tamponade (pressure on the heart that limits its ability to pump).
most common cause is viral infections; other are autoimmune, surgery/procedure, trauma
clinical manifestations of pericarditis?
dyspnea, chest pain, usually in anterior chest; sharp
pain increases with deep breaths or when lying flat. flue like symptoms.
PERICARDIAL FRICTION RUB; grating sound heard in the apex auscultation area
What is infective endocarditis?
cause?
clinical manifestations?
bacterial infection of endocardium (inner lining of the chambers of the heart)
cause: bacteria entering the blood stream and adhering to inner lining of the heart.
endothelial damage -? attracts platelets and creates thrombus. The bacteria adhering to the inner lining goes INTO the thrombus, protected by the fibrin and thrombus picks up more “vegetation” then with each contraction the bits of vegetation gets dislodged, microthrombi throughout the body. emboli
CM: heart murmur, heart failure, arterial amboli.
what is myocarditis?
common cause?
clinical manifestations?
dx?
inflammation of myocardium (MIDDLE layer of heart)
commonly caused by viruses, sometimes allergic reactions, chemical exposure.
CM: fluelike symptoms, chest pain, palpitations, pericardial rub, tachyarrhythmias
dx: EKG, blood cultures, troponin is MORE commonly elevated than creatinine kinase.
Valvular disorders
define stenosis
regurgitation?
stenosis - is the narrowing of the heart valves. less blood flows through the narrowed openings, but there is NO backflow of blood
regurgitation - blood flows freely forward but goes backwards through the valve because they do not completely close. (increase cardiac workload, causing chambers to dilate to make up for extra blood volume in heart)
Clinical manifestations of aortic stenosis
cardiovascular effects?
symptoms
respiratory
heart sounds?
cause?
less blood going throughout the body
left ventricular hypertrophy; angina; Bradycardia
fatigue
dyspnea on exertion
systolic murmur
cause - rheumatic fever, degenerative calcification (stiffening). Congenital calcification of bicuspid valve
Clinical manifestations of aortic regugitation
cardiovascular effects?
symptoms
respiratory
heart sounds?
cause?
blood going back into the heart, less going out , leaky valve
left HEART hypertrophy, angina; palpitation. Water hammer pulse (BOUDNING pulse but collapses quickly)
dyspnea exertion
DIASTOLIC murmur
cause - infection endocarditis, aortic root diseases (age, degeneration, bicuspid aortic valve)
Clinical manifestations of Mitral stenosis
cardiovascular effects?
symptoms
respiratory
heart sounds?
cause?
mitral valve is on the left side, restricted blood flow to the left ventricle. pressure backs into atrium -> pressure backs up in lungs causing pulmonary HTN. which means the right side of the heart has to work harder to make up for it.
dypsnea on exertion, orthopnea, pulmonary htn
DIASTOLIC murmur, opening snap, prolonged first heart sound (cuz right side has to work harder)
cause: rheumatic fever
Clinical manifestations of mitral regurgitation
cardiovascular effects?
symptoms
respiratory
heart sounds?
cause?
*blood flowing back to left atrium *
left heart hypertrophy, angina
murmur without systole
what is cardiomyopathy? 3 main types?
heart disease, affected structure or function of the heart muscle
dilated
hypertrophic
restrictive
explain dilated cardiomyopathy?
ventricles becomes enlarged/dilated but normal wall thickness. heart chambers get weaker because of dilation. affects systolic function
usually starts in the left ventricle that eventually affects right vent.
HEART FAILURE, a fib
explain hypertrophic cardiomyopathy?
mainly affects diastolic function; ventricles hypertrophied. sometimes tissue gets scarred or fibrotic.
it cant relax to refill so there is an increase in diastolic pressure.
the septum of the ventricles is the most common place of hypertrophy.
explain restrictive cardiomyopathy?
rigid myocardium and diastolic dysfunction. Cant refill ventricles because of rigidness, pressure inside vent. increases. STIFF but not thickened.
define heart failure?
heart is unable to pump enough blood for the body’s needs. sometimes its because of MI or HTN.
cardiac capacity is intact but the demands is too high = high out put failure. Increased metabolic demand like hyperthyroidism
what are the two broad categories of heart failure?
HFrEF - heart failure with reduced EF; EF of less than 40% = SYSTOLIC dysfunction
HFpEF - heart failure with preserved EF; EF of more than 50%= DIASTOLIC dysfucntion
explain the difference of left sided heart failure and right sided heart failure
LEFT- left ventricle cannot pump blood into body, so it backs up into left atrium -> then pulmonary circulation = pulmonary congestion.
dypsnea on exertion, fatigue, Orthopnea (when laying flat dyspnea)
Paroxysmal nocturnal dyspnea (waking up gasping for air); fluid shift when laying flat increases pulmonary pressure
RIGHT - right ventricle cannot pump blood towards the lungs well -> fluid backs up into the body = leg swelling, edema, weight gain. JVD
cause by left sided HF, OR cor pulmonae (lung diseases)
what are septal defects?
congenital heart defects; holds in the wall that separates the atria or the ventricles.
