• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/45

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

45 Cards in this Set

  • Front
  • Back
What is congestive heart failure?
Name derives from congestion/backup of blood in the lungs due to left cardiac failure
Why do left heart failure cause right heart failure?
The increased pulmonary venous pressure due to left cardiac failure causes increased afterload on the right ventricle, which eventually cannot work against the increased pressure and failure bocomes present
Clinical symptoms of right heart failure?
Increased jugular venous pressure (JVP)
Accumulation of fluid in abdomen (Ascites)
Hepatic congestion (Portal hypertension and liver failure)
Peripheral lower limb edema
What are the symptoms of forward failure in left cardiac failure?
Weakness
Fatigue
Dyspnea (decreased O2 to respiratory muscles)
Dizziness/drowsyness (decreased O2 to brain)
Pathophysiology of orthopnea in heart failure
In standing position gravity keeps blood pooled in veins of lower legs and abdominal cavity. When patient lies down this blood will be shifted towards to lungs, increasing the pulmonary pressure, and increasing the pulmonary edema
What is paroxysmal nocturnal dyspnea?
When lying down, blood shifts from peripheral venous pool and abdomen to lungs, increasing the pulmonary pressure and edema.
Also the decreased sympathetic stimulation of the heart causes bradycardia and the heart is not able to pump the blood out of the lungs, further increasing pulmonary edema
What is the treatment to increase the forward flow in heart failure?
Increase ventricular contraction by Inotropes (digoxin, dopamine)
Decrease rate of contraction to increase the diastolic filling time by beta-blockers (propranolol)
What is the treatment to decrease the backup of blood in heart failure?
Dilation of veins (nitrates)
Reduce extracellular volume (diuretics, ACE inhibitors)
Dilate the arteries to decrease afterload (ACE inhibitors, hydralazine)
Explain the term "diastolic dysfunction" and under which conditions dous it occur?
The heart is unable to relax, reducing the diastolic filling and cardiac output.
Occurs in cardiac hypertrophy and restrictive cardiomyopathy
Causes of left ventricular hypertrophy?
Genetic hypertrophic cardiomyopathy
Increased afterload (hypertension)
Aortic stenosis (pressure overload)
Causes of right ventricular hypertrophy?
Pulmonary hypertension (left heart failure)
Pulmonary valve stenosis
Pulmonary embolus
Pulmonary fibrosis
Chronic obstructive pulmonary disease
Treatment of cardiac hypertrophy
Treating the diastolic dysfunction by increasing diastolic filling
Beta-blockers reduce the heart rate, increasing diastolic filling time
Calcium-channel blockers (Causes heart muscle to relax, allowing for more filling time)
Causes of restrictive cardiomyopathy
Infiltration of substances into heart muscle (amyloidosis, sarcoidosis, haemochromatosis, Pompe's disease)
Pericardial effusion
Pericardial tamponade
Causes of cardiac dilatation
Genetic
Drugs, alchohol
Viral myocarditis
Valve regurgitation (volume overload)
When can you hear S3 and S4 sounds in heart?
S3 is typical for dilated heart, but can also be physiological in young patients
S4 is typical for hypertrophic heart
Causes of aortic stenosis
Aging (senile calcification)
Congenital bicuspid aortic valve
Rheumatic heart disease
Manifestations of aortic stenosis
On physical examination:
Carotid upstroke
Pulsus parvus et tardus (weak and delayed pulse in carotids)

Left heart hypertrophy
Dizziness, syncope
Dyspnea
Angina, ischemia of left ventricle
Causes of aortic regurgitation
Ehler Danlos syndrome
Marfan's syndrome
Syphilis
Manifestations of aortic regurgitation
On physical examination:
Widened pulse pressure (reduced diastolic pressure)
Corrigans pulse (throbbing carotid artery pulse)
DeMussets sign (head bobbing with pulse)

Heart failure synptoms
Causes of mitral stenosis
Most often rheumatic fever
Less common due to congenital or endocarditis
Manifestations of mitral stenosis
Left atrium dilatation
Atrial fibrilation due to streching of the wall
Pulmonary hypertension (dyspnea)
Opening snap on auscultation
Causes of mitral regurgitation
Ventricular dilatation
Drugs, alchohol
Mitral valve prolapse
Endocarditis
Rheumatic fever
Ischemic heart disease

Acute regurgitation: pappillary muscle rupture
Manifestations of mitral regurgitation
Left ventricular dilatation
Pulmonary hypertension
Dyspnea

In acute regurgitation: Uncompensated
In chronic regurgitation:
Dilatation and forward flow problems (fatigue, dizziness)
How do you treat bradycardia?
Beta-receptor antagonists (isoproterenol)
Pacemaker
Anticholinergic drugs (atropine)
Why is myocardial infarction associated with ventricular tachycardia?
Necrotic tissue has abnormal electrical properties, thus creating an reentrant circuit within the ventricals, which can result in an extremly fast ventricular heart rate (300bpm+)
Types and characteristics of anginas
Stable angina: pain only on exertion
Unstable angina: pain at rest. Highly associated with myocardial infarction
Prinzmetals angina: Not due to occlusion of arteries, but due to vasospasm
What are the symptoms of acute myocardial infarction?
Chest pain (unrelieved by rest)
Pain that radiate down left arm or to jaw
Dyspnea
Nausea/vomiting
Fever
Distress
Treatment of myocardial infarction
Thrombolytis drugs (streptokinase, urokinase, tissue plasminogen activating factor)
Surgery (angioplasty with coronary stenting)
Various (nitrates, statins, beta-blockers)
Etiology of infective and non-infective endocarditis
Infective:
Streptococcus viridans
Staphylococcus aureus
Non.infective:
hypercoagulability
Systemic inflammatory diseases (lupus)
IV drugs
Etiology and manifestations of fheumatic fever
Etilogy
Group A streptococcus infection of upper respiratory tract
Manifestations
affects CNS, skin, joints and heart
Etiology of myocarditis
Coxsackie B virus
Lupus, dermatomyositosis
Drugs, radiation
Etiology of pericarditis
Coxsackie B virus, TB, streptococci, staphylococci
Lupus, rheumatoid arthritis
Radiation, malignancy
Signs and symptoms of constrictive pericarditis
Kussmauls sign (rise in JVP during inspiration)
Pericardial effusion (hypotension, muffled heart sound, elevated JVP)
The 4 abnormalities in Tetralogy of Fallot
Pulmonary valve stenosis, right ventricular hypertrophy, ventricular septal defect, biventricular aorta
Apart from Tetralogy of Fallot, what cyanotic heart diseases exist?
Transposition of the great arteries
Formation of two paralell circulations, instead of one continous
What is Eisenmenger syndrome
The flow through a VSD causes increased pressure in the pulmonary circulation. Because the right ventricle have to pump both the blood from the right atrium as well as from the left ventricle, this will cause right ventricular hypertrophy. This will over time lead to such an increase in the right heart that blood starts flowing over to the left heart, causing cyanosis
What electrolytic changes can be observed in the stimulation of a myecyte
1. Na enters the cell (action potential)
2. Inflow of Ca and outflow of K (platau)
3. Continuation of K outflow after Ca inflow stops (repolarization)
Causes of bradycardia
Sleep, common faint, increased age, beta-blockers, calcium channel blockers
Systemic pathophysiological changes associated with heart failure
Decreased output
Increased backup flow
Activation of SNS
RAAS activation
Release of antidiuretic hormone
Cytokine release
Release of cardiac specific enzymes (troponin, CK)
Cell death, fibrosis
Which factors induces the protein synthesis of contractile proteins associated with heart failure hypertrophy

And through which intracellular mediators do they act
Angiotensin II, TNF-a, norepinephrine

acts through c-fos, c-jun, c-myc
What is believed to be the mediator of pain in angina?
Adenosine
Blocking adenosine-receptors with aminophylline has shown to reduve pain
What are the three classical signs of pericardial tamponade (Becks triad)
Muffled heart sounds
Hypetension
Increased jugular venous pressure
Explain the timeline of changes in an ischemic heart cell from start of ischemia to death of cell
10 sec: cells are ischemic
60 sec: functional changes, normal morphology
20 min: borderline cell still alive and can become normal if bloodflow is restored
60 min: cell is definetly dead and necrosis cannot be reversed by restoration of blood flow
What intracellular changes occur in myecytes during ischemia
decreased ATP, decreased contractility, glycogenolysis, acidosis, extracellular hyperkalemia, lactic acidosis, edema, free radical formation
What is a stunned heart
Ischemic heart that is morphologically normal, but is functionally not able to contract