First aid Cardiology Flashcards
coronary blood flows peaks in
early diastole
coronary artery occlusion most common
LAD
most posterior part of the heart is:
Left atrium
enlargement:
compress the esophagus –dysphagia
compress the left recurrent laryngeal nerve, branch of the vagus and cause hoarseness
Fick principle cardiac output
CO= rate of O2 consumption/arteriol O2 content-venous oxygen content
MAP
MAP = CO x TPR MAP = 2/3 diastolic pressure + 1/3 the systolic pressure
SV
SV = EDV - ESV
During exercise
increased SV and HR to keep CO, but as SV plateaus later in exercise only HR increases to maintain CO
What can cause an increased pulse pressure?
hyperthyroidism aortic regurg arteriosclerosis obstructive sleep apnea (increased sympathetic tone) exercise
decrease in pulse pressure
aortic stenosis
cardiogenic shock
cardiac tamponade
advanced heart failure
myocardial oxygen demand
Increases: increased after load (arterial pressure) Increased contractility Increased HR Increased ventricular diameter (increased wall tension)
hydralazine
arterial vasodilator, decrease afterload
Viscosity
increase:
polycythemia, hyperproeteinemic states (MM) abd hereditary spherocytosis
decrease:
anemia
Resistance
R = delta P/ flow Q
= 8(viscosity)(length)/pi r^4
S3
in early diastole during rapid ventricle filling phase. Associated with increase filling pressures (mitral regurg, CHF) and more common in dilated ventricles, slosh slosh (but normal in children and pregnant females)
S4
atrial kick!
in late diastole . high atrial pressure, associated with ventricular hypertrophy. Left atrium must push against a stiff LV wall
a wave JVP
atrial contraction
C wave JVP
RV contraction (closed tricuspid valve bulges into RA)
x descent JVP
atrial relaxation and downward displacement of TV during ventricular contraction, absent in tricuspid regurgitation
v wave JVP
increase RA pressure due to filling against a closed tricuspid valve
y descent
blood flow from RA to RV
Normal splitting
S1, A2P2 inspiration leads to a drop in intrathoracic P, increases venous return, increased RV sv and RV ejection time, delayed closing of pulmonc valve
wide splitting
S1 A2 P2
seen in conditions that delay RV emptying (pulmonary stenosis, right bundle branch block).
Delay in RV emptying causes delayed pulmonic sound (regardless of breath). An exaggerated of normal splitting
fixed splitting
S1 A2 P2
ASD left to right shunt
increase RA and RV volumes, increase flow through pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed
paradoxical splitting
S1 P2 A2
Seen in conditions that delay LV emptying (aortic stenosis, LBBB)
normal in order of valve closure is reversed so that the P2 sound occurs before a delayed A2 sound. Therefore on inspiration, P2 closes later and moves closer to A2 thereby paradoxically ELIMINATING the split
ASD murmur
best heard in the pulmonic area
commonly presents as a pulmonary flow murmur (increased flow through the pulmonary valve) and a diastolic murmur (increased flow across the tricuspid)
NO murmur from blood flow ACROSS the actual ASD because there is no increased pressure gradient
the murmur will later progress to a louder diastolic murmur of pulmonary regurgitation from dilation of the pulmonary artery
hand grip (increases the systemic vascular resistance)
increase intensist:
-MR, AR, VSD
Decrease intensity:
AS, hypertrophic cardiomyopathy murmurs
MVP: increase in intensity, but a later onset of click/murmer
Valsalva (phase 2), standing (decrease venous return)
decrease intensity: most murmurs including AS Increase: hypertrophic cardiomyapthy murmur MVP: decrease intensity, have an earlier onset of click/murmer
rapid squatting (increased venous return increases preload ) after prolongued squatting increase after load
decrease intensity of:
hypertrophic cardiomyopathy murmer
increase intensity of:
AS
MVP: increase intensity and later onset click/murmer
systolic sounds
Aortic/pulmonic stenosis, mitral/tricuspid regurg, VSD
Diastolic heart sounds
aortic/pulmon regurg and mitral/tricuspid stenosis
Mitral regurg
holosystolic, high pitched blowing murmur
loudest at apex, radiates to axilla, enhanced by maneuvers that in TPR (squatting and hand grip)
MR is often due to ischemic heart disease, MVP or LV dilation
Tricuspid regurg
loudest at tricuspid area
holosystolic, high pitched blowing murmur
radiates to right sternal border
enhanced by maneurmers that increase RA return (inspiration)
TR commonly caused by RV dilation.
Rheumatic fever and infective endocardidtis can cause either MR or TR
Aortic stenosis
Crscendo-decrescendo systolic ejection murmur.
LV» aortic pressure during systole
loudest at heart base, radiates to carotids
pulses parvus et tardus - pulses are weak with a delayed peak.
can lead to syncope, angina and dyspnea on exertion
often due to age related calcific stenosis or bicuspid aortic valve
VSD
holosytolic, harsh sounding murmer, loudest in the tricuspid area, accentuated with hand grip maneurver due to afterload
mitral valve prolapse MVP
laste systolic crescendo murmer with midsystolic click (MC; due to sudden tensing of chordae tendineae
best heard over apex
loudest just before S2
usually benign
can predispose to infective endocarditis
can be caused by myxomatous degeneration, RF, or chordae rupture
occurs earlier with maneurvers that decrease venous return (valsalva or standing)
This is because those maneuvers which decrease the volume of the left ventricle (Valsalva, standing) will cause the prolapse to occur sooner and more severely, while those that increase venous return and diastolic filling (squatting) and thereby enhance the ventricular volume, help to maintain tension along the chordae and to keep the valve shut
AR
high pitched blowing early diastolic decresendo murmur.
wide pulse pressure when chronic
can present with bounding pupses and head bobbing
often due to aortic root dilatio, biscuspid aortic valve, endocarditis or RF. the murmer inscreases with hand trap, vasodilators decrease the intensist of the murmur
Mitral stenosis
follows opening snap (due to abrupt halt in leaflet motion in diastole after rapid oepning due to fusion at leaflet tips).
delayed rumbling late diastolic murmur
decrease interval between S2 and opening snap correlates with increased severity. LA»LV pressure
often occurs secondary to RF
Chronic MS can result in LA dilation.
enhanced by maneurvers that increase LA return (expiration)
respiration and Left heart
During inspiration, expansion of the lungs and pulmonary tissues causes pulmonary blood volume to increase, which transiently decreases the flow of blood from the lungs to the left atrium. Therefore, left ventricular filling actually decreases during inspiration. In contrast, during expiration, lung deflation causes flow to increase from the lungs to the left atrium, which increases left ventricular filling. The net effect of increased rate and depth of respiration, however, is an increase in left ventricular stroke volume and cardiac output.
PDA
Continuous machine like murmur across systole and diastole
loudest at S2
often due to congenital rubella or prematurity
best hear at the left infraclavicular area (pulmonic valve region)
1 big box
0.2 s or 200 ms
1 small box
40 ms
box heart rate
1 300 2 150 3 100 4 45 5 60 6 50 7 43 8 37 9 33 beats/min
1 full stip is 10 seconds
so counts the complexes and multiply by 6 to bet bpm
P wave
atrial depolarization, atrial repolarization is masked by the QRS
PR interval
-conduction delay through the AV node (normally less than 200 ms) (less than a big box)
QRS
ventricular depolarization (less that 120 ms)
T wave
ventricular depolarization
ST segment
isoelectric, ventricles depolarized
QT
mechanical contraction of the ventricles
u wave
caused by hypokalemia, bradycardia
speed of conduction -
purkinje> atria> ventricles> Av node PAVA
pacemakers
SA> AV> bundle of his> purkinje/ventricles
conduction pathway
SA, atria, AV done then to common bundle, then bundle branches then purkinje fibers and finally ventricles
Torsades de pointes
-polymorphic ventricular tach
-characterized by shifting sinusoidal waveforms on ECG
-can progress to V fibb
-Long QT interval predisposes to torsades de pointes
-caused by drugs that decrease K and Mg
Treat with MgSO4
Drugs that prolong QT
Some Risky Meds Can Prolong QT: Sotalol Risperidone Macrolides Chloroquine Protease inhibitors (-navir) Quinidine (Class 1a) Thiazides
Romano-ward syndrome
congenital long QT syndrome
inherited disorder of myocardial repolarization, typically due to ion channel defects, increases risk of suddencardiac death due to torsades de points
Autosomal DOMINANT
pure cadiac phenotypes
Jervell and Lange-Nielsen syndrome
congenital long QT syndrome
inherited disorder of myocardial repolarization, typically due to ion channel defects, increases risk of suddencardiac death due to torsades de points
Autosomal RECESSIVE
sensorineural deafness!
wolff-parkinson white syndrom
abnormal fast accessory conduction pathway from atria to ventricle via the bundle of kent, bypasses the rate slowing AV node
- as a result ventricles begin to partially depolarize earlier, giving rise to characteristic delta wave and shortened PR interval
- may result in supraventricular tach
afibb
irregular irregular
no discrete P
irregularily spaced QRS
atrial flutter
back to back atrial depolarization waves
sawtooth appearense
use 1a, 1C or III.
v fibb
a completely erratic rhythm with no identifiable waves. fatal arrhythmia without immediate CPR and defibrillation
AV block 1st degree
PR interval is prolonged > 200 ms
AV block 2nd degree mobitz type 1 (wenckebach)
progressive legnthing of PR interval until a beat is DROPPED, usually asymptomatic
AV block 2nd degree mobitz type II
dropped beats that are NOT processed by a change in length of PR.
often found in 2:1 block, where there are 2 or more P waves to 1 QRS response
often treated with pacemaker
AV 3rd degree block
atria and ventricles beat independantly of each other, both P waves and QRS complexes are present, although the P waves bear no relation to the QRS complexes. The atrial rate is faster than the ventricular rate.
Lyme disease can result in 3rd degree heart block
Lyme disease
3rd degree heart block
atrial naturetic peptide
- released from atrial mycoses with stretch
- vasodilation
- decreased Na reabsorption at renal CT
- contricts efferent, dilates afferent renal via cGMP –> diuresis contributing to the aldosterone escape
B-type (brain) natriuretic peptide
released from ventricular myocytes in response to increased tension
-longer half life, similiar to ANP
good test for HF, good NPV
-available in recombinant form Nesiritide for treatment of heart failure
Aortic arch receptors
transmit via vagus nerve to solitary nucleus of medulla
Carotid sinus (dilated region at carotid bifurcation)
transmits via glossopharyngeal nerve to solitary nucleus to medulla
Baroreceptors in hypotension
- decreased in Atrial P, decreased stretch, decreased afferent baroreceptor firing (vagus to solitary nucleus of medulla) , increased efferent firing sympathetic firing (post ganglionic, via spine etc) and decreased efferent parasymp stimulation (vagus).
leads to vasoconstriction, increased HR, increased contractility, increased BP
Carotid massage
increased P on carotid sinus, increases stretch, increased baroreceptor firing, increased AV node refractory period, decreased HR.
Carotid sinus massage: increase pressure on carotid artery –> increase stretch –> increase afferent CN IX firing –> signal thru nucleus tractus solitarus in medulla–> increase parasympathetic outflow to heart via CN X firing—> decrease heart
Cushing reaction
increased intracranial pressure constricts arterioles, this leads to cerebral ischemia and reflex increase in sympathetic tone in perufusion pressure HTN. Increase stretch and reflex baroreceptors induced bradycardia (parasympathetic vagus)
HTN, bradycardia and respiratory depression
note increase vagus –> acid, ulcers
Peripheral carotid and aortic bodies are stimulated
-decrease in PO2 ( hyperventilation
Central chemoreceptors are stimulated by
changes in pH and PCO2 of brain interstitial fluid
Edema
excess fluid outflow into interstitium commonly caused by:
- increased hydrostatic capilliary pressure (Pc in heart failure)
- decreased plasma proteins, decreased plasma onctoc (Pi c , nephrotic syndome, liver failure)
- increased permiability factor (K) caused by toxins, infections, burns
- Increased interstitial fluid colloid osmotic pressure (interstitial oncotic pressure, like a lymphatic blockage
R to L shunsts
early cyanosis, often diagnosed prenatally or become evident immediately after birth. usually require urgent surgical repair and or maintenance of PDA
Truncus arteriousus (1 vessel) Transposition (2 sitched vessels) Tricuspid atresia Tetrology of Fallot Total anomalous pulmonary venous return
Total anomalous pulmonary venous return
pulmonary veins drain right into right heart circulation (SVC, coronary sinus etc) associated with an ASD and sometimes PDA to allow R to Left shunt
tricuspid atresia
no tricuspid, requires both an ASD and VSD for viability
terology of fallot
caused by anterosuperior displacement of the infundibular septum. most common cause of early childhood cyanosis
- Pulmonary infundibular stenossis
- RVH - boot shaped heart
- Overring aorta
- VSD (right to left due to pulmonary stenosis)
Squatting increases SVR which would decrease the R to L shunt and improves cyanosis
ASD
distinct from PFO in that septa are missing tissue (septum secundum) rather than unfused
-loud S1 and fixed split S2 (more filling of RA and RV, delated closing of pulmonic valve).
Eisenmenger syndrome
uncorrected L to R shunt (VSD, ASD, PDA) eventually increased pulmonary blood flow and pathologica remodeling of vasculature leading to pulmonary arteriolar HTN. RVH to compensate the shunt becomes R to L this will cause late cyanosis, clubbing and polycythemia
Coarcatation of aorta:
infantile type
associated with bisupid aortic valve and other heart defects:
aortic narrowing is proximal to insertion of ductus arteriousus (pre ductal). Associated with Turner syndrome
can present with close ductus arterioles
Coarcatation of aorta:
associated with bisupid aortic valve and other heart defects:
aorta narrowing is distal to ligamentum arteriosusm (post ductal). assoc with notching of ribs due to collateral circulation, HTN in upper extremities and weak, delayed pulses in lower extremities
xanthoma
lipid laden histiocyte in the skin
corneal arcus
lipid in cornea , appears early in life with hypercholesterolemia. commonly in elderly
arteriolosclerosis
arterioles:
hyaline (thickening of small arteues in essential HTN or DM)
hyperplastic onion skinning as seen in severe HTN
aortic aneurism
localized pathologic dilation of the aorta, may cause pain, which is a sign of leaking, dissection, or imminent rupture
AAA
HTN male, >50 years, assoc. atherosclerosis
Thoracic AA
associated with cystic medial degenration due to HTN (older) or Marfan (younger)
assoc. 3 syphyilis (obliterative endarteritis of the vasa vasorum)
Aortic dissection
longitudinal intraluminal tear forming a false lumer. assoct with HTN, bicuspid aortic valve and inhere tied connective tissue disorders like Marfan
tearing chest pain, sudden onset, radiating to back
stable angina
secondary to atherosclerosis, resolves at rest
variant angina (pinzmetal)
occurs at rest! secondary to coroanry arter spasm, known triggers at tobacco, cocaine, triptans but trigger is often unknown
treat with calcium channel blockers, nitrates and smoking cessation
MI 4-12 hours
Gross changes: Dark discoloration
Microscopic Changes: early coagulative necrosis, release of necrotic cell contents into blood, edema, hemmorrhage and wavy fibers
Complications:
arrhythmia, HF, cardiogenic shock, death
MI 1-3 days
Gross changes: hyperemia, yellow pallor
Microscopic Changes: tissue surrounding infarct shows accute inflammation with neutrophils, extensive coagulative necrosis
Complications:
fibrinous pericarditis presents with chest pain and friction rub
MI 3-14 days
Gross changes: hyperemic border, central yellow brown softening-maximally yellow and soft for ten days
Microscopic Changes: macrophages then granulation tissue at margins
Complications:
free wall rupture: tamponade; papillary muscle rupture –> mitral regurg; intraventricular spetal rupture due to macrophages mediated structural degradation
LV pseudoaneurism (mural thrombus plugs hole in myocardium time bomb)
MI 1-3 weeks
Gross changes: red border emmerges as granulation tissue enters from edge of infarct
Microscopic Changes: granulation tissue with plum fibroblasts, collagen and blood vessel
Complications:
MI 2 weeks to months
Gross changes:white scar
Microscopic Changes: fibrosis and contracted scar complete
Complications:
aneurism, mural thrombosis and dressler syndrome (resulting in fibrinous pericarditis from autoimmune phenomena , several weeks post MI)
MI 12-24 hours
Gross changes:
Microscopic Changes: neutrophil migration starts
reperfusion injury may cause contraction bands due to free radical damage
Complications:arrhythmia, HF, cardiogenic shock, death
CK-MB
useful in diagnosing reinfarction following acute MI because levels return to normal in 48 hours
troponin 1
rises after 4 hours, remains elevated for 7-10 days
ST elevation
STEMI acute transmural infarction
ST depression
subendocardial infarct (subendo is especially vulnerable to ischemia)
MI Anterior wall (LAD)
V1-V4
MI Anteriospetal (LAD)
V1-V4
Anteriolateral (LAD or LCX)
V4-V6
Lateral Wall (LCX)
I avL
Inferior wall (RCA)
II, III, aVF
Dilated cardiomyopathy
systolic dysfuction ensures. Eccentric hypertrophy (sarcomeres added in series) Idiopathic or congenital -Wet beriberi Coxsackie B Chagas Cocaine use Doxorubicin hemochromatosis peripartum cardiomyopathy
HF, S3, dilated
Hypertrophic cardiomyopathy
60-70% familial, autosomal dominant
commonly the b-myosin heavy chain mutation
rarely assoc. Friedrich ataxia
cause of sudden death in young athlets
findings: S4, systolic murmer
diastolic dysfuction ensues
marked ventricular hypertrophy, often septal predominance
hypertropied septum to close to anterior mitral leaflet can cause an outflow obsturction leading to dyspnea and possible syncope
Restrictive/infiltraive cardiomyopathy
diastolic dysnfuction ensues
major causes:
sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastos (thick fibroelastic tissue in endocardium of young children, loffler syndrome, hemachromatosis
loffler syndrome
endomyocardial fibrosis with prominent eosinophillic infiltrate
systolic dysfunction
low EF, poor contractility, often secondary to ischemia heart disease or dilated cardiomyopathy
diastolic dysfunction
normal EF and contractility, impaired relaxation, decreased compliance
CHF reducing mortality
ACE inhibitors, B blockers (except in actue decompensated HF), ARB, spirinolactone.
hemosiderin-laden macrophages
heart failure cells in the lungs
Bacterial endocarditis Acute
s.aureus
Bacterial endocarditis Subacute
viridans step, smaller vegetations on congenitally abnormal or diseased valves
Bacterial endocarditis culture negative
coxiella bunetti, bartonella spp
Bacterial endocarditis prosthetic valves
s. epidermidis
Bacterial endocarditis nonbacterial secondary to:
malignancy (colon cancer s bovis), hypercoagulable state, lupus (mantic/thrombotic endocarditis)
Bacterial endocarditis, which valves?
Mitral valve!
Tricuspid valve in IV drug abuse (s. aureus, pseudomonas, candida)
Bacterial endocarditis clinical findings
- Fever
2 Roth spots (round white spots on retina surrounded by hemorrhage) - Osler nodes (tender raised lesions on fingers or toe pads)
- Janeway lesions (small painless eythematous lesions on palm or sole)
- Murmer
- Anemia
- splinter hemmorages on nail bed
RF which valves?
Mitral>aortic»tricuspid
early lesion is MR late is MS
RF histo and titers
ASO titers Aschoff bodies (granuloma with giant cells and anitschkow cells (enlarged macrophages with ovoid, wavy, rod-like nucleus.
Type II hypersensitivity: antibodies to M protein cross react with self antigens.
RF clinical
fever erythema marginatum valvular damage increased ESR red hot joints subcutanoues nodules St. Vitus dance syndenham chorea
Acute pericarditis
sharp pain, aggravated by inspiration, and relieved by sitting up and leaning foward. Presents with friction rub, ECG WIDESPREAD St-segmant elevation and/or PR depression
fibrinous pericarditis
Caused by: dressler syndrome (AI, 7 weeks ish post MI) uremia radiation loud friction rub!
serous pericarditis
viral pericarditis: resolve spont.
noninfectious inflammatory disease: RA, SLE
Suppurative/purulent pericarditis
pneumococcus, streptococcus
pulses paradoxus
decrease in systolic blood pressure by >/ 10 mmHg during inspiration cardiac tamponade asthma obstructive sleep apnea pericarditis croup
cardiac tamponade
compression of heart by fluid, leading to decreased CO
equilibration of diastolic pressures in all 4 chambers
findings:
Beck triad (hypotension, distended neck veins, distant heart sounds).
increased HR
pulsus peridoxus
kussmual sign
ECG shows low voltage QRS and eletrical alternates
Kussmaul sign
(paradoxical rise in jugular venous pressure (JVP) on inspiration) during cardiac tamponade
Cardiac most common tumor
metastasis (melanoma, lymphoma)
Myxoma
most common primary cardiac tumor in adults
90% in atria, LA
ball valve obstruction
rhadomyomas
most frequent primary in kids
assoc. tuberous sclerosis
